Psychology Responses homework help

Psychology Responses homework help

Response 1:

Resiliency

Respond to at least two colleagues in one or more of the following ways:

        

·      Add to your colleague’s suggestion for applying resiliency to Talia’s case by suggesting an adaptation of the strategy.

·      Critique your colleague’s suggested application of resiliency to social work practice, stating whether you might use the strategy in your own practice, and why

·      Be sure to support your responses with specific references to the resources. If you are using additional articles, be sure to provide full APA-formatted citations for your references.
 

Colleague 1: B

Nineteen year old Talia Johnson was the victim of a rape at a fraternity party (Plummer, Makris and Brocksen, 2014).  This week’s video depiction highlights Talia’s struggle with navigating her way back into the life she knew prior to the sexual assault (Laureate Education, 2013).  The social worker has a glimpse into her daily life, particularly as she struggles with her parent’s understandable discomfort with their daughter remaining on campus (Laureate Education, 2013).  Talia views her current situation as stagnant and not easily changeable.  During these situations, the professional charged with helping the client achieve the best positive outcomes when pairing their innate resiliency with a Strengths Based Perspective (Zastrow and Kirst- Ashman, 2016).  Zastrow and Kirst-Ashman recognize the importance of emphasizing one’s resiliency, particularly when faced with undeniable adversity (Zastrow and Kirst-Ashman, 2016).

 

While this may be proven as an effective approach, convincing a client who is experiencing consistent feelings of helplessness and hopelessness, is certainly not an easy feat.  Therefore, the focus of this approach should remain small, manageable tasks seen through to completion (Zastrow and Kirst-Ashman, 2016).  In Talia’s case, perhaps suggesting she schedules agreed upon times to speak with her mother would alleviate the stress she feels by receiving the numerous phone calls (Laureate Education, 2013).  The premise behind this suggestion is that when Talia starts seeing small daily success, she may start “buying in” to the fact that she, too, can come back from the trauma that has placed her where she is.  Thus, her acceptance of her own resiliency, while her innate strengths are continually highlighted by the social worker, will only add to her achievement of positive outcomes (Zastrow and Kirst – Ashman, 2016).

 

By applying this concept of resiliency to Talia’s case, it is clear how this would be an effective approach within my own future social work practice.  Every client with whom a social worker comes in contact, has some innate level of resiliency.  Finding the opportunities to point out resiliency, even in its simplest form, becomes the responsibility of the professional charged with guiding the client toward the desired outcomes.   For example, when a client drives a car for the first time after being involved in a car accident, this can be identified as  form of resiliency and the first step in achieving their goals.  The ultimate goal would be for the client to recognize this resiliency within himself, but until this time the social worker can serve as the client’s “strength identifier.”

 

Laureate Education (Producer). (2013). Johnson family: Episode 5 [Video file]. Retrieved from https://class.waldenu.edu

 

Plummer, S. -B., Makris, S., & Brocksen, S. M. (Eds.). (2014). Baltimore, MD: Laureate International Universities Publishing. [Vital Source e-reader

 

Zastrow, C. H., & Kirst-Ashman, K. K. (2016). Understanding human behavior and the social environment (10th ed.)Boston, MA:  Cengage Learning.

 

 

 

Colleague 2: J

Talia is a 19-year-old college student who was sexually assaulted at a frat party. After seeking help from campus resources and the services of a counselor, she has begun to experience high levels of anxiety and stress (Plummer, Makris, and Brocksen, 2014). While Talia has begun to resent her counselor for the coping mechanisms she has given Talia, Talia has nonetheless continued to do the things suggested for her, such as journaling, going to group meetings, and talking about her feelings (Laureate Education, 2013). As an observer, these behaviors exhibited by Talia all suggest that she is a resilient individual who refuses to let the things that have befallen her ruin her life permanently.

 

As a social worker, it can be a very difficult task to convince a client that they are resilient, especially when they feel like their life is falling apart. As mentioned by Zastrow and Kirst-Ashman (2016,) giving the individual small, manageable tasks to achieve can boost their confidence and encourage them to take on larger, more difficult tasks. The social worker in Talia’s case already has proof that she is resilient by Talia’s compliance and adherence to journaling and going to group meetings (Laureate Education, 2013).

 

In my own practice, using the concept of resiliency will only serve to increase my client’s self-esteem and self-worth. By giving clients small goals that they can achieve, I can build up their confidence and determination. I think it will also be important to still call clients resilient when they fail at a goal- by still coming to sessions and admitting failure, they are only improving themselves. This would also give them the chance to evaluate the goal or their performance and see what went wrong, what can be done to fix it, and when can it be tried again. Resiliency means to be able to keep going through adversity; it also means to be able to adapt and change with the situations at hand. By instilling this in clients, they can begin the healing process.

 

Laureate Education (Producer). (2013). Johnson family: Episode 5 [Video file]. Retrieved from https://class.waldenu.edu.

 

Plummer, S.-B., Makris, S., & Brocksen, S. M. (2013). The Johnson Family. In Sessions: Case Histories. Laureate Education, Inc.

Zastrow, C. H., & Kirst-Ashman, K. K. (2016). Understanding human behavior and the social environment (10th ed.)Boston, MA:  Cengage Learning.

 

 

 

 

 

Response 2:

 

Discussion: Micro vs. Macro Practice

 

·      Respond to at least two colleagues by identifying three reasons that macro practice should not be dominated by micro practice if social work policy is to effectively deal with the problems of oppressed and marginalized groups.

·      Support your response with specific references to the resources. Be sure to provide full APA citations for your references.
Colleague 1: D

Micro practice is to work with individuals.  Macro practice is to work at the organizational level.  Micro practice has come to dominate the social work profession because if we were to break down the macro and mezzo levels, we are left with individuals.  “Social workers have long recognized that micro and macro practice are complementary, but they have generally emphasized the micro, individual treatment aspect of the profession” (Popple & Leighninger, 2015, p. 7).  It has been discussed plenty that social workers find themselves working with individuals a majority of the time.  The root of the individual’s issues is based on things that are bigger than the individual (Popple & Leighninger, 2015, p. 7).

 

Popple, P. R., & Leighninger, L. (2015). The policy-based profession: An introduction to social welfare policy analysis for social workers. (6th ed.). Upper Saddle River, NJ: Pearson Education.

 

Colleague 2: R

The dichotomy between micro and macro social worker practice varies in the approaches used. Micro social worker practices are based on the ideas on how to better equip the individual to deal with societal needs and expectations. If there is an individual in need of services, the micro approach will link that individual to services to assist their individual underlying needs. The macro social worker approach attempts to have the community meet people at their levels of need. The idea behind the macro level approach to is discuss social worker and the needs of group of individual to larger organizations and agencies such as schools or child welfare agencies. In essence, and as mentioned in this week’s reading, the ideas of micro and macro practices are to compliment from one another. Understanding the needs of one might be just be the needs of the general population of that area, (Popple & Leighninger, 2015). Therefore becoming familiar and effective with using techniques on the micro level, might uncover solutions to bigger societal problems in communities.

 

 

Popple, P.R., & Leighninger, L. 2015. The police-based profession: Introduction to social welfare policy analysis for social workers. 6th ed. Upper Saddle River, NJ: Pearson Educations

 
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Nursing Paper Example on Agraphia: Understanding a Neurological Disorder

Nursing Paper Example on Agraphia: Understanding a Neurological Disorder

Agraphia, a neurological disorder characterized by impaired writing abilities, presents unique challenges to affected individuals. This condition, often arising from various underlying causes, significantly impacts communication and daily functioning. Understanding the etiology, signs, and symptoms of agraphia is crucial for accurate diagnosis and effective treatment. From strokes to traumatic brain injuries and neurodegenerative diseases, the causes of agraphia vary, highlighting the complexity of this condition. The pathophysiology involves disruptions in the brain’s language processing regions, leading to difficulties in forming letters, words, and coherent sentences. Diagnosing agraphia follows criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), ensuring standardized assessment and intervention approaches. Treatment regimens typically involve a multidisciplinary approach, focusing on improving writing skills and addressing underlying conditions. Patient education plays a vital role in empowering individuals to cope with challenges and maximize their quality of life despite the impact of agraphia. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Nursing Paper Example on Agraphia: Understanding a Neurological Disorder

Causes of Agraphia

Agraphia stems from various underlying causes, each contributing to the impairment of writing abilities. One common cause is stroke, where disruption of blood flow to the brain leads to damage in areas responsible for language processing and production. Specifically, damage to regions such as Broca’s area in the left hemisphere can result in agraphia. Traumatic brain injury is another significant cause, often affecting neural pathways involved in writing due to physical trauma or shearing forces. Neurodegenerative diseases, such as Alzheimer’s, gradually deteriorate cognitive functions, including writing skills, as the disease progresses.

In addition to these primary causes, other factors can contribute to the development of agraphia. Brain tumors may exert pressure on brain structures responsible for language processing, leading to impairments in writing abilities. Infections affecting the brain, such as encephalitis or meningitis, can also result in agraphia through inflammation and damage to neural tissue. Furthermore, psychiatric disorders like schizophrenia or bipolar disorder may manifest with symptoms of agraphia, highlighting the complex interplay between mental health and cognitive functions.

In some cases, the exact cause of agraphia remains unknown, posing challenges in diagnosis and treatment. These idiopathic cases underscore the need for comprehensive evaluation and ongoing research to elucidate underlying mechanisms.

Overall, the causes of agraphia encompass a wide range of neurological, neurodegenerative, traumatic, and sometimes idiopathic factors. Understanding the specific cause is crucial for tailoring treatment approaches and addressing underlying conditions to improve writing skills and overall functional abilities in individuals affected by agraphia. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Signs and Symptoms

Agraphia manifests through distinct signs and symptoms that affect an individual’s ability to write coherently. One prominent sign is impaired handwriting, characterized by illegible or disjointed writing that may be difficult to decipher. Individuals with agraphia often struggle to form letters and words correctly, resulting in irregular or distorted scripts.

Nursing Paper Example on Agraphia: Understanding a Neurological Disorder

Spelling difficulties are another common symptom of agraphia, wherein individuals may have trouble spelling words correctly or consistently. This difficulty extends beyond mere typographical errors and may involve fundamental challenges in recalling and representing letter sequences accurately.

In addition to handwriting and spelling impairments, individuals with agraphia may experience difficulty composing coherent sentences. This symptom manifests as disjointed or fragmented written expression, with sentences lacking proper syntax and organization. Consequently, written communication may be challenging to comprehend and may lack clarity and cohesion.

Moreover, agraphia can impact both written and oral language abilities, affecting overall communication skills. Individuals may struggle to express themselves effectively through writing or verbal communication, leading to frustration and communication breakdowns.

Furthermore, the severity of symptoms can vary widely among individuals with agraphia, ranging from mild to profound impairment. Some individuals may experience relatively mild difficulties with occasional spelling errors or handwriting inconsistencies, while others may struggle significantly with fundamental aspects of writing and language production.

Overall, recognizing these signs and symptoms is essential for timely diagnosis and intervention. Healthcare professionals rely on thorough assessments of writing skills, including handwriting samples and spelling tests, to evaluate the presence and severity of agraphia. By identifying and addressing these symptoms, individuals with agraphia can receive appropriate support and interventions to improve their writing abilities and enhance overall communication skills. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Etiology of Agraphia

The etiology of agraphia encompasses various underlying factors that contribute to the impairment of writing abilities. One primary cause is stroke, which occurs when disruption of blood flow to the brain leads to damage in regions crucial for language processing and production. Ischemic strokes, resulting from blockages in blood vessels supplying the brain, and hemorrhagic strokes, caused by bleeding into the brain tissue, can both precipitate agraphia.

Traumatic brain injury (TBI) represents another significant etiological factor, often resulting from physical trauma or shearing forces affecting the brain. TBI can disrupt neural pathways involved in writing, leading to agraphia. The severity and location of the injury influence the extent of impairment and recovery potential.

Neurodegenerative diseases, such as Alzheimer’s disease, progressively deteriorate cognitive functions, including writing skills, as the disease advances. These conditions involve the accumulation of abnormal proteins and neuronal loss, particularly in brain regions crucial for language processing.

Additionally, brain tumors can contribute to the development of agraphia by exerting pressure on or infiltrating brain structures responsible for language production. The location and size of the tumor determine the specific impairments observed.

Infections affecting the brain, such as encephalitis or meningitis, can lead to agraphia through inflammation and damage to neural tissue. Psychiatric disorders, including schizophrenia and bipolar disorder, may also manifest with symptoms of agraphia, highlighting the intricate interplay between mental health and cognitive functions.

In some cases, the etiology of agraphia remains idiopathic, with no identifiable cause despite thorough evaluation. These cases underscore the complexity of the disorder and the need for ongoing research to elucidate underlying mechanisms and inform treatment approaches. Understanding the specific etiological factors contributing to agraphia is crucial for tailoring interventions and addressing underlying conditions to improve writing skills and overall functional abilities in affected individuals. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Pathophysiology

The pathophysiology of agraphia involves disruptions in the brain’s intricate network of language-processing regions, leading to difficulties in writing and related language functions. Damage to specific brain areas crucial for language production and coordination, such as Broca’s area in the left hemisphere, plays a central role in the development of agraphia.

In cases of stroke-induced agraphia, ischemic or hemorrhagic events disrupt blood flow to the brain, resulting in localized damage to language centers. Ischemic strokes, caused by arterial blockages, deprive brain regions of oxygen and nutrients, leading to neuronal dysfunction and cell death. Hemorrhagic strokes, characterized by bleeding into brain tissue, exert pressure on surrounding structures, disrupting neural connectivity and function.

Traumatic brain injury (TBI) disrupts neural pathways involved in writing due to physical trauma or shearing forces affecting the brain. TBI can result in diffuse axonal injury, neuronal loss, and glial scarring, impairing communication between brain regions responsible for language processing and production.

Neurodegenerative diseases, such as Alzheimer’s, involve the progressive accumulation of abnormal proteins and neuronal loss, particularly in brain regions crucial for language processing. These pathological changes disrupt synaptic transmission and neural communication, impairing writing skills as the disease advances.

Furthermore, alterations in neurotransmitter systems, including acetylcholine and dopamine, may contribute to the pathophysiology of agraphia. Imbalances in these neurotransmitters disrupt neuronal signaling and synaptic plasticity, affecting cognitive functions such as language processing and writing abilities.

Overall, the pathophysiology of agraphia involves complex interactions between structural brain damage, neural connectivity disruptions, and neurotransmitter imbalances. Understanding these underlying mechanisms is crucial for developing targeted treatment approaches and addressing the specific needs of individuals with agraphia. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

DSM-5 Diagnosis

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), provides criteria for diagnosing agraphia as a neurocognitive disorder. To receive a diagnosis of agraphia, individuals must exhibit significant impairment in writing abilities that cannot be attributed to intellectual disabilities or other neurological conditions. The impairment must cause clinically significant distress or functional impairment in daily life activities.

According to DSM-5 criteria, the diagnosis of agraphia requires the presence of specific symptoms, including impaired handwriting, spelling difficulties, and difficulty composing coherent sentences. These symptoms must persist despite efforts to improve writing skills, such as remedial education or cognitive rehabilitation.

Additionally, the DSM-5 emphasizes the importance of ruling out other potential causes of writing impairments, such as intellectual disabilities, language disorders, or motor coordination deficits. A comprehensive evaluation, including standardized assessments of writing skills, neurological examinations, and medical history review, is essential to differentiate agraphia from other conditions.

Furthermore, the diagnosis of agraphia considers the severity and impact of symptoms on daily functioning. Clinicians assess the extent to which impaired writing abilities interfere with communication, academic or occupational performance, and social interactions.

Overall, the DSM-5 diagnosis of agraphia requires careful consideration of specific criteria and comprehensive evaluation to differentiate it from other neurocognitive disorders. By adhering to standardized diagnostic criteria, healthcare professionals can accurately identify agraphia and develop tailored treatment plans to address the unique needs of individuals affected by this condition. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Treatment Regimens and Patient Education

Treatment regimens for agraphia typically involve a multidisciplinary approach tailored to individual needs. Speech therapists play a crucial role in implementing structured writing exercises and strategies to improve handwriting, spelling, and sentence construction. These interventions may include practicing letter formation, word recognition, and sentence composition through repetitive exercises and task-specific training. Additionally, speech therapists employ techniques such as modeling, cueing, and feedback to facilitate learning and reinforce correct writing behaviors.

Nursing Paper Example on Agraphia: Understanding a Neurological Disorder

Occupational therapists may also be involved in the treatment of agraphia, focusing on fine motor skills and coordination to enhance writing proficiency. Occupational therapy interventions may include activities to improve grip strength, hand-eye coordination, and motor planning necessary for handwriting. Furthermore, adaptive equipment and assistive devices, such as specialized writing utensils or keyboard adaptations, may be recommended to accommodate individual needs and enhance writing performance.

Cognitive rehabilitation techniques, including memory training and attentional exercises, may complement speech and occupational therapy interventions to address underlying cognitive deficits contributing to agraphia. These interventions aim to improve cognitive functions such as attention, working memory, and executive functioning, which are essential for effective writing and language processing.

In addition to formal therapy sessions, individuals with agraphia benefit from practicing writing skills in daily life activities and real-world contexts. Encouraging individuals to engage in writing tasks relevant to their personal interests and daily routines promotes skill generalization and functional independence.

Patient education plays a vital role in empowering individuals with agraphia to understand their condition and actively participate in treatment. Educating individuals and their families about the nature of agraphia, its underlying causes, and available treatment options fosters understanding and collaboration in the rehabilitation process. Providing strategies and resources to support writing skills, such as visual aids, mnemonic devices, and assistive technologies, enables individuals to overcome challenges associated with agraphia and maximize their functional abilities.

Moreover, educating individuals about compensatory strategies, such as breaking down writing tasks into smaller components or using alternative communication methods, empowers them to navigate daily life with confidence and adapt to their unique needs. By equipping individuals with knowledge and resources, patient education facilitates active participation in treatment and enhances the overall quality of life for individuals with agraphia. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

Conclusion

Agraphia poses significant challenges to individuals affected by this neurological disorder, impacting their ability to write coherently and communicate effectively. Understanding the multifaceted etiology, signs, and symptoms of agraphia is essential for accurate diagnosis and tailored treatment interventions. The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) provides criteria for diagnosing agraphia, guiding healthcare professionals in evaluating and managing this condition effectively. Treatment regimens for agraphia involve a multidisciplinary approach, incorporating speech therapy, occupational therapy, and cognitive rehabilitation to address underlying impairments and improve writing skills. Additionally, patient education plays a crucial role in empowering individuals with agraphia to understand their condition, learn compensatory strategies, and actively participate in treatment. By combining clinical expertise with patient-centered care and support, healthcare professionals can help individuals with agraphia navigate challenges and maximize their quality of life despite the impact of this disorder. (Nursing Paper Example on Agraphia: Understanding a Neurological Disorder)

References

https://www.ncbi.nlm.nih.gov/books/NBK560722/

 
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Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder

Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder

Agnosia, a neurological condition shrouded in mystery, presents a perplexing phenomenon where individuals struggle to recognize and interpret sensory stimuli despite intact sensory organs. This enigmatic disorder challenges the conventional understanding of sensory perception, highlighting the intricacies of the human brain’s processing capabilities. While rare, Agnosia’s impact on affected individuals is profound, disrupting fundamental aspects of daily life such as recognizing familiar faces, objects, or sounds. Understanding the complexities of Agnosia is essential for healthcare professionals tasked with diagnosis and management, as well as for individuals and their caregivers navigating the challenges it presents. This paper endeavors to delve into the depths of Agnosia, exploring its causes, signs and symptoms, etiology, pathophysiology, DSM-5 diagnosis, treatment regimens, patient education, and offering insights into this intricate neurological condition. Through unraveling the mysteries of Agnosia, we aim to shed light on its complexities and pave the way for improved understanding and management strategies. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder

Causes of Agnosia

Agnosia arises from various neurological disruptions that interfere with the brain’s ability to process sensory information accurately. One primary cause is brain injury, often resulting from traumatic incidents such as car accidents, falls, or sports-related injuries. In these cases, the impact can lead to damage in specific brain regions responsible for sensory perception, triggering Agnosia.

Another contributing factor is cerebrovascular accidents, commonly known as strokes, which disrupt blood flow to the brain, leading to tissue damage. Depending on the affected area, strokes can impair sensory processing regions, causing Agnosia.

Furthermore, brain tumors can exert pressure on brain structures, causing compression or damage that disrupts sensory pathways, resulting in Agnosia. Neurodegenerative diseases such as Alzheimer’s disease, which progressively damages brain cells, can also contribute to Agnosia by affecting regions crucial for sensory processing.

Additionally, infectious diseases like encephalitis or meningitis can lead to inflammation of the brain, causing damage to sensory processing areas and subsequent Agnosia. Genetic factors may also play a role, as certain hereditary conditions predispose individuals to neurological abnormalities that can manifest as Agnosia.

Moreover, toxins or chemicals, whether ingested or environmental, can damage the brain and disrupt sensory processing, contributing to Agnosia. Drug abuse, particularly substances that affect neurotransmitter function, can also lead to neurological impairments and Agnosia.

Agnosia can stem from various causes, including brain injury, stroke, tumors, neurodegenerative diseases, infectious diseases, genetic factors, toxins, and drug abuse. Understanding these diverse etiological factors is crucial for diagnosing and managing Agnosia effectively, as each case may require specific approaches to treatment and intervention. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Signs and Symptoms

Agnosia presents a spectrum of signs and symptoms that vary depending on the type and severity of the condition. Visual Agnosia, for instance, may manifest as difficulty recognizing familiar objects, faces, or places despite intact vision. Individuals may struggle to identify common items such as keys, utensils, or household items, leading to challenges in daily activities.

Auditory Agnosia, on the other hand, affects the interpretation of sounds and speech. Affected individuals may have difficulty understanding spoken language, distinguishing between voices, or recognizing familiar tunes or melodies. This can lead to communication difficulties and social isolation.

Tactile Agnosia involves impaired recognition of textures, temperatures, or shapes through touch. Individuals may struggle to identify objects by touch alone, such as distinguishing between fabrics or perceiving the shape of items placed in their hands.

Furthermore, there are specific subtypes of Agnosia, such as Prosopagnosia, characterized by the inability to recognize faces, even those of close friends or family members. This can lead to social awkwardness and challenges in interpersonal relationships.

In some cases, individuals with Agnosia may exhibit anosognosia, a lack of awareness or recognition of their sensory deficits. They may deny or minimize their difficulties, leading to frustration and misunderstandings with others.

Overall, the signs and symptoms of Agnosia can significantly impact daily functioning, interpersonal relationships, and overall quality of life. Understanding these manifestations is crucial for accurate diagnosis and tailored interventions to help affected individuals cope with their sensory perception deficits effectively. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Etiology of Agnosia

The etiology of Agnosia is multifaceted, involving a complex interplay of neurological factors that disrupt sensory processing pathways in the brain. One primary contributor to Agnosia is brain injury, which can result from traumatic incidents such as falls, sports-related injuries, or motor vehicle accidents. These injuries can lead to structural damage or lesions in specific brain regions responsible for sensory perception, causing Agnosia.

Cerebrovascular accidents, commonly known as strokes, represent another significant etiological factor in Agnosia. Strokes disrupt blood flow to the brain, leading to tissue damage in critical sensory processing areas, thereby impairing sensory recognition and interpretation.

Moreover, brain tumors can exert pressure on brain structures, causing compression or damage that disrupts sensory pathways, leading to Agnosia. Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, or dementia, can also contribute to Agnosia by progressively damaging brain cells and affecting regions crucial for sensory processing.

Infectious diseases, including encephalitis or meningitis, can lead to inflammation of the brain, causing damage to sensory processing areas and subsequent Agnosia. Additionally, genetic factors may play a role in predisposing individuals to neurological abnormalities that manifest as Agnosia.

Furthermore, exposure to toxins or chemicals, whether ingested or environmental, can damage the brain and disrupt sensory processing, contributing to Agnosia. Drug abuse, particularly substances that affect neurotransmitter function, can also lead to neurological impairments and Agnosia.

Understanding the diverse etiological factors underlying Agnosia is crucial for accurate diagnosis and targeted interventions to address the underlying causes and mitigate its impact on affected individuals’ sensory perception and daily functioning. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Pathophysiology of Agnosia

Agnosia stems from disruptions in the neural pathways responsible for processing sensory information in the brain. These disruptions can arise from various etiological factors, including brain injury, stroke, tumors, neurodegenerative diseases, and genetic predispositions.

The pathophysiology of Agnosia involves abnormalities in specific brain regions involved in sensory perception, including the primary sensory cortices and associated higher-order processing areas. Structural damage or lesions in these regions impede the transmission and interpretation of sensory signals, leading to impaired recognition and interpretation of sensory stimuli.

In cases of visual Agnosia, for example, lesions in the occipital and temporal lobes, particularly the ventral visual pathway, disrupt the processing of visual information essential for object recognition. Similarly, lesions affecting the auditory cortex or associated pathways can result in auditory Agnosia, impairing the interpretation of sounds and speech.

Tactile Agnosia may arise from lesions in somatosensory processing areas, such as the parietal lobe, hindering the recognition of textures, shapes, or temperatures through touch. The pathophysiology of Agnosia varies depending on the type and location of brain damage, with specific regions implicated in each subtype.

Furthermore, neurodegenerative diseases like Alzheimer’s disease or Parkinson’s disease contribute to Agnosia through progressive damage to brain cells and disruption of neural pathways involved in sensory processing. Genetic factors may also influence the pathophysiology of Agnosia, predisposing individuals to structural or functional abnormalities in sensory processing regions.

Overall, the pathophysiology of Agnosia involves complex disruptions in neural pathways and brain regions responsible for sensory perception, highlighting the intricate nature of this neurological disorder and the diverse mechanisms underlying its manifestation. Understanding these pathophysiological mechanisms is essential for guiding diagnostic and therapeutic approaches to manage Agnosia effectively. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

DSM-5 Diagnosis

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), classifies Agnosia under the broader category of Neurocognitive Disorders. Diagnosis of Agnosia involves a comprehensive assessment to evaluate sensory perception deficits and their impact on daily functioning.

Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder

Clinical interviews play a crucial role in gathering information about the onset, duration, and progression of sensory recognition difficulties. Healthcare professionals also conduct neurological examinations to assess sensory modalities and identify any associated neurological deficits.

Neuropsychological testing is an essential component of the diagnostic process, involving specialized assessments to evaluate sensory recognition abilities across different modalities. These tests may include tasks to assess visual object recognition, auditory discrimination, tactile perception, and other sensory processing abilities.

The DSM-5 criteria for Agnosia emphasize the presence of significant impairment in recognizing or identifying familiar objects, faces, sounds, or other sensory stimuli despite intact sensory organs. The deficits must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Additionally, the diagnosis of Agnosia requires ruling out other potential etiologies for sensory recognition difficulties, such as sensory deficits due to primary sensory organ dysfunction or cognitive impairments unrelated to sensory processing.

Overall, the DSM-5 diagnosis of Agnosia involves a comprehensive evaluation of sensory perception deficits and their impact on daily functioning, guided by specific criteria outlined in the diagnostic manual. Accurate diagnosis is essential for implementing targeted interventions and support strategies to help individuals with Agnosia cope with their sensory recognition difficulties effectively. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Treatment Regimens and Patient Education for Agnosia

Effective management of Agnosia involves a multidisciplinary approach encompassing various treatment regimens and patient education strategies to address the complex nature of sensory recognition deficits.

Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder

Treatment Regimens:

  1. Sensory Rehabilitation Techniques: Occupational therapists and rehabilitation specialists employ sensory retraining techniques to improve sensory perception and recognition abilities. These may include repetitive exposure to sensory stimuli, sensory discrimination exercises, and multisensory integration activities to enhance sensory processing skills.
  2. Assistive Devices: Utilizing assistive devices such as magnifiers, auditory aids, or tactile cueing devices can facilitate sensory recognition and compensate for deficits. These devices aim to enhance sensory input and improve functional independence in daily activities.
  3. Cognitive-Behavioral Therapies: Psychologists or cognitive therapists may employ cognitive-behavioral techniques to address emotional and psychological challenges associated with Agnosia. Therapy sessions focus on coping strategies, stress management, and cognitive restructuring to alleviate distress and enhance coping skills.
  4. Environmental Modifications: Modifying the environment to reduce sensory overload and enhance accessibility can improve functional abilities for individuals with Agnosia. This may involve simplifying surroundings, organizing objects, and providing clear cues to facilitate recognition and navigation.
  5. Medication: In some cases, medication may be prescribed to manage underlying conditions contributing to Agnosia, such as neurodegenerative diseases or neurological disorders. Pharmacological interventions aim to alleviate symptoms and slow disease progression, although their efficacy in treating Agnosia specifically may vary.

Patient Education:

  1. Understanding Agnosia: Providing comprehensive education about Agnosia helps individuals and their caregivers understand the nature of the condition, its causes, and implications. Education sessions include information about sensory recognition deficits, associated challenges, and available treatment options.
  2. Compensatory Strategies: Educating individuals about compensatory strategies and adaptive techniques to cope with sensory recognition difficulties is essential. This includes teaching techniques to enhance sensory perception, improve daily functioning, and maintain independence.
  3. Support Networks: Encouraging individuals to engage with support networks, such as support groups or online communities, can provide emotional support, practical advice, and share experiences with others facing similar challenges.
  4. Advocacy and Resources: Providing information about advocacy resources, disability services, and community support organizations helps individuals access necessary resources and navigate healthcare and social systems effectively.
  5. Regular Follow-Up: Emphasizing the importance of regular follow-up appointments with healthcare providers ensures ongoing monitoring of Agnosia symptoms, adjustment of treatment regimens as needed, and support for individuals and their caregivers throughout their journey with the condition.

By implementing comprehensive treatment regimens and patient education strategies, healthcare professionals can support individuals with Agnosia in managing their sensory recognition deficits, improving functional abilities, and enhancing overall quality of life. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

Conclusion

Agnosia presents a complex neurological challenge characterized by impaired sensory recognition despite intact sensory organs. Through exploring its causes, signs and symptoms, etiology, pathophysiology, DSM-5 diagnosis, treatment regimens, and patient education, we gain valuable insights into this enigmatic disorder. The causes of Agnosia encompass diverse neurological factors such as brain injury, stroke, tumors, and neurodegenerative diseases. Its signs and symptoms manifest across various sensory modalities, affecting daily functioning and interpersonal relationships. Understanding the etiology and pathophysiology of Agnosia guides accurate diagnosis and targeted interventions. The DSM-5 criteria assist in identifying sensory recognition deficits, while treatment regimens encompass sensory rehabilitation, assistive devices, cognitive-behavioral therapies, and environmental modifications. Patient education plays a pivotal role in empowering individuals and their caregivers to cope with Agnosia effectively, fostering adaptive strategies, accessing support networks, and advocating for resources. By addressing Agnosia comprehensively, healthcare professionals can improve outcomes and enhance the quality of life for individuals navigating this challenging neurological condition. (Nursing Paper Example on Understanding Agnosia: An Overview of a Neurological Disorder)

References

https://www.ncbi.nlm.nih.gov/books/NBK493156/

 
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Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care

Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care

Encephalitis, a neurological disorder characterized by inflammation of the brain, affects millions worldwide, making it a significant public health concern. This essay aims to provide a comprehensive overview of encephalitis, focusing on its causes, symptoms, etiology, pathophysiology, DSM-5 diagnosis, treatment regimens, and patient education. Understanding encephalitis is vital due to its diverse etiologies and complex clinical presentations, which necessitate prompt diagnosis and appropriate management. By exploring the intricacies of this disorder, we can enhance our knowledge of its underlying mechanisms and improve therapeutic approaches. With a deeper understanding of encephalitis, healthcare professionals can better support patients in navigating their diagnosis, treatment, and recovery journey. Thus, this essay serves as a valuable resource for healthcare providers and individuals seeking to comprehend and address the challenges posed by encephalitis. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care

Causes

Encephalitis has various causes, spanning infectious and non-infectious origins. Viral infections are predominant culprits, with herpes simplex virus (HSV) and varicella-zoster virus (VZV) being common offenders. These viruses can directly invade the brain, triggering an inflammatory response and leading to encephalitis. Additionally, other viral agents such as enteroviruses, arboviruses (e.g., West Nile virus), and influenza viruses can also induce encephalitis.

Bacterial infections like Lyme disease, caused by Borrelia burgdorferi, can result in neuroborreliosis, leading to encephalitis in some cases. Moreover, certain parasitic infections, such as toxoplasmosis and malaria, can cause encephalitis through indirect mechanisms.

Non-infectious triggers, including autoimmune reactions, can also contribute to encephalitis. Autoimmune encephalitis occurs when the body’s immune system mistakenly attacks healthy brain tissue, leading to inflammation and neurological dysfunction. Conditions like anti-NMDA receptor encephalitis and autoimmune limbic encephalitis exemplify this mechanism.

Environmental factors such as exposure to toxins or chemicals may also precipitate encephalitis. For instance, exposure to heavy metals like lead or mercury can trigger neuroinflammation, potentially leading to encephalitis.

Furthermore, immunocompromised individuals, such as those with HIV/AIDS or undergoing immunosuppressive therapy, are at higher risk of developing encephalitis due to their weakened immune defenses.

Understanding the diverse array of causes underlying encephalitis is crucial for accurate diagnosis and targeted treatment. Differentiating between infectious and non-infectious etiologies guides clinicians in selecting appropriate therapeutic interventions and optimizing patient outcomes. Thus, a comprehensive understanding of encephalitis causes is essential for effective management and improved prognosis.

Signs and Symptoms

Encephalitis manifests through a spectrum of signs and symptoms, often varying in severity and presentation. The hallmark features typically include fever, headache, and altered mental status, which may range from mild confusion to profound disorientation or coma. These cognitive changes often accompany behavioral alterations, including irritability, agitation, or personality changes.

Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care

Neurological manifestations of encephalitis can encompass a wide array of symptoms, such as seizures, focal neurological deficits, and impaired consciousness. Seizures may manifest as generalized convulsions or focal motor seizures, further complicating the clinical picture.

In some cases, patients may exhibit psychiatric symptoms, including psychosis, hallucinations, or delusions, reflecting the profound impact of encephalitis on brain function. Additionally, movement disorders such as tremors, ataxia, or dyskinesias may arise due to disruption of neural circuits within the basal ganglia or cerebellum.

Furthermore, encephalitis can lead to autonomic dysfunction, presenting as fluctuations in blood pressure, heart rate, or temperature regulation. These autonomic disturbances contribute to the overall clinical complexity of encephalitis and may pose challenges in management.

Children with encephalitis may exhibit distinct symptoms, including irritability, lethargy, poor feeding, or developmental regression. Early recognition of these pediatric-specific signs is critical for prompt diagnosis and intervention.

It is essential to recognize the broad spectrum of signs and symptoms associated with encephalitis, as timely identification facilitates early initiation of appropriate treatment and improves clinical outcomes. Vigilance for subtle neurological changes, particularly in high-risk populations, is paramount for early intervention and preventing potential complications. Thus, a comprehensive understanding of encephalitis symptoms is essential for timely diagnosis and effective management. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

Etiology

Encephalitis encompasses a diverse etiology, reflecting the multifaceted nature of this neurological disorder. Viral infections stand as predominant etiological factors, with herpes simplex virus (HSV) and varicella-zoster virus (VZV) accounting for a significant proportion of cases. These viruses gain access to the central nervous system (CNS) via neuronal pathways, causing direct neuronal injury and triggering an inflammatory response within the brain.

Other viral agents, including enteroviruses, arboviruses (e.g., West Nile virus), and influenza viruses, can also precipitate encephalitis through various mechanisms. These viruses may disseminate hematogenously or via peripheral nerves, leading to CNS invasion and subsequent neuroinflammation.

Bacterial infections represent another important etiological category, with pathogens such as Borrelia burgdorferi (causing Lyme disease) and Mycobacterium tuberculosis capable of inducing encephalitis. These bacteria may infiltrate the CNS through hematogenous spread or direct extension from adjacent structures, inciting an inflammatory cascade within the brain parenchyma.

Parasitic infections, though less common, can also contribute to encephalitis pathogenesis. Toxoplasma gondii and Plasmodium species (causing malaria) are notable examples, with encephalitis arising secondary to parasitic invasion of the CNS and subsequent inflammatory response.

Non-infectious etiologies, particularly autoimmune reactions, are increasingly recognized as significant contributors to encephalitis. Autoimmune encephalitis encompasses a spectrum of disorders characterized by immune-mediated attacks on neuronal antigens, leading to neuroinflammation and neurological dysfunction.

Furthermore, environmental factors such as exposure to toxins or chemicals may precipitate encephalitis by eliciting neuroinflammatory responses within the brain. Understanding the diverse etiological factors underlying encephalitis is crucial for accurate diagnosis and targeted therapeutic interventions, ultimately improving patient outcomes and guiding preventive strategies. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care

Pathophysiology

The pathophysiology of encephalitis involves a complex interplay of inflammatory cascades, immune responses, and neuronal dysfunction, culminating in neurological impairment. Viral encephalitis typically begins with viral invasion of the central nervous system (CNS), facilitated by hematogenous dissemination or neuronal spread from peripheral sites of infection. Upon entering the CNS, viruses target neurons, glial cells, and endothelial cells, initiating a robust immune response characterized by cytokine release and activation of resident immune cells.

This inflammatory milieu triggers endothelial cell activation and disruption of the blood-brain barrier (BBB), allowing infiltration of immune cells into the brain parenchyma. Activated microglia and infiltrating macrophages release pro-inflammatory mediators, exacerbating neuroinflammation and promoting neuronal injury.

In addition to direct viral-induced damage, immune-mediated mechanisms contribute to neuronal dysfunction in encephalitis. Autoimmune encephalitis, for instance, results from antibodies targeting neuronal antigens, leading to synaptic dysfunction, neuronal excitotoxicity, and impaired neurotransmission.

The ensuing neuronal injury and inflammation disrupt neural circuits and neurotransmitter pathways, manifesting clinically as altered mental status, seizures, and focal neurological deficits. Moreover, disruption of the BBB facilitates the entry of neurotoxic substances and exacerbates neuroinflammation, further exacerbating neuronal injury.

The pathophysiological processes underlying encephalitis are dynamic and multifactorial, involving a delicate balance between viral replication, immune responses, and neuronal damage. Understanding these mechanisms is crucial for developing targeted therapeutic strategies aimed at mitigating neuroinflammation, preserving neuronal function, and optimizing patient outcomes. Further research into the pathophysiology of encephalitis is warranted to unravel its complexities and identify novel therapeutic targets for intervention. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

DSM-5 Diagnosis

Diagnosing encephalitis entails a comprehensive evaluation based on clinical presentation, laboratory findings, and neuroimaging studies, as outlined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The DSM-5 provides criteria for diagnosing neurocognitive disorders, including those resulting from infectious or inflammatory etiologies such as encephalitis.

The DSM-5 criteria emphasize the presence of significant cognitive decline from a previous level of functioning, which may manifest as impaired memory, executive function, attention, or language skills. Additionally, individuals with encephalitis may exhibit disturbances in consciousness, orientation, perception, or behavior, reflecting the multifaceted nature of the disorder.

Laboratory investigations play a crucial role in confirming the diagnosis of encephalitis. Cerebrospinal fluid (CSF) analysis reveals lymphocytic pleocytosis, elevated protein levels, and sometimes the presence of specific pathogens or antibodies indicative of viral or autoimmune etiologies. Serological tests for viral antibodies and polymerase chain reaction (PCR) assays can identify viral pathogens circulating in the CNS.

Neuroimaging studies, particularly magnetic resonance imaging (MRI) of the brain, may demonstrate characteristic findings such as focal or diffuse signal abnormalities in the affected brain regions. These imaging findings complement clinical and laboratory assessments, aiding in confirming the diagnosis of encephalitis and guiding treatment decisions.

The DSM-5 diagnosis of encephalitis underscores the importance of a multidisciplinary approach involving neurologists, infectious disease specialists, and psychiatrists. By integrating clinical, laboratory, and imaging data, healthcare professionals can accurately diagnose encephalitis and initiate timely interventions to optimize patient outcomes. Moreover, adherence to DSM-5 criteria ensures consistency and precision in diagnosing encephalitis across diverse clinical settings, facilitating effective management and support for affected individuals. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

Treatment Regimens and Patient Education

Treatment of encephalitis necessitates a multifaceted approach aimed at addressing the underlying cause, managing symptoms, and preventing complications. Antiviral therapy is the mainstay of treatment for viral encephalitis, targeting specific viral pathogens such as herpes simplex virus (HSV) or varicella-zoster virus (VZV). Intravenous administration of antiviral medications like acyclovir or ganciclovir is initiated promptly upon suspicion of viral encephalitis to mitigate viral replication and reduce neuronal damage.

In cases of bacterial encephalitis, antibiotic therapy targeting the causative pathogen is imperative. Prompt initiation of antibiotics like ceftriaxone or penicillin G is crucial to combat bacterial invasion of the central nervous system (CNS) and prevent systemic complications.

In autoimmune encephalitis, immunomodulatory therapy aims to suppress the aberrant immune response directed against neuronal antigens. Treatment may involve corticosteroids, intravenous immunoglobulin (IVIG), or immunosuppressive agents like rituximab or cyclophosphamide to attenuate neuroinflammation and preserve neuronal function.

Supportive care plays a pivotal role in managing complications and promoting recovery in patients with encephalitis. This includes close monitoring of vital signs, maintenance of adequate hydration, seizure management, and addressing nutritional needs. In severe cases with neurological sequelae, rehabilitation therapy may be necessary to optimize functional outcomes and enhance quality of life.

Patient education is integral to the management of encephalitis, empowering individuals and their caregivers to navigate the challenges associated with the condition. Patients should be educated about the importance of adhering to prescribed medications, attending follow-up appointments, and recognizing warning signs of disease progression or relapse. Furthermore, patients and caregivers should receive guidance on strategies to optimize brain health, including adequate rest, nutrition, and cognitive stimulation.

Moreover, raising awareness about encephalitis within the community is crucial to promoting early recognition and timely intervention. Educational initiatives aimed at healthcare providers, schools, and the general public can facilitate prompt referral to specialized care centers and improve outcomes for individuals affected by encephalitis.

The treatment of encephalitis involves a comprehensive approach encompassing specific antiviral or antibiotic therapy, immunomodulatory interventions, and supportive care measures. Patient education is paramount in empowering individuals and caregivers to actively participate in disease management and promote optimal outcomes. By addressing both the medical and educational aspects of encephalitis, healthcare providers can enhance the quality of care and support for affected individuals and their families. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

Conclusion

Encephalitis is a complex neurological disorder with diverse causes, symptoms, and treatment regimens. This essay has provided a comprehensive overview, emphasizing the importance of understanding its multifaceted etiology, including viral, bacterial, autoimmune, and environmental factors. The discussion of signs and symptoms underscored the varied clinical presentations, highlighting the need for early recognition and intervention. Additionally, the exploration of pathophysiology elucidated the intricate interplay of inflammatory processes and neuronal dysfunction underlying encephalitis. The DSM-5 diagnosis section outlined the criteria for accurate identification, guiding clinicians in diagnostic evaluation and treatment planning. Furthermore, the treatment regimens and patient education section emphasized the multidisciplinary approach to management, incorporating antiviral, antibiotic, and immunomodulatory therapies alongside supportive care measures. By addressing both the medical and educational aspects, healthcare providers can optimize outcomes for individuals affected by encephalitis, underscoring the importance of timely intervention and comprehensive support. (Nursing Paper Example on Understanding Encephalitis: Causes, Symptoms, Treatment, and Patient Care)

References

https://www.ncbi.nlm.nih.gov/books/NBK470162/

 
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Psych 635 Shaping And Chaining, Reinforcement Schedules And One-Trial Learning Week 3

HEALTH AND SPORTS PSYCHOLOGY REVIEW

Running head: HEALTH AND SPORTS PSYCHOLOGY REVIEW

1

HEALTH AND SPORTS PSYCHOLOGY REVIEW

2

Health and Sports Psychology Review

Psych 635

February 9, 2015 Health and Sports Psychology Review

The foundation of sports psychology centers on helping players maximize their performance and strengthen motor learning skills, by learning techniques to overcome mental blocks. The first publication of sports psychology focused on how spectators influence athletes competing in competitive bicycling (Brown & Mahoney, 1984). Health and sports psychology focuses on the influences of athletics and the psychological and physiological impact it has on humans. A sports psychologist assists athletes through the application of shaping and chaining, reinforcement schedules, and one-trial learning techniques in teaching new technical skills.

Shaping and Chaining

As a sports psychologist, one must comprehend the concepts of shaping and chaining when teaching and implementing unfamiliar technical skills to athletes. Before a behavior arises, an athlete cannot associate his or her skills and performance to a behavior, therefore shaping is only useful when linking behaviors that can help athletes perform adequately and comprehensively. “The basic operant conditioning method of behavioral change is shaping, or differential reinforcement of successive approximations to the desired form or rate of behavior” (Schunk, 2012). The process of shaping identifies behaviors not yet present, and assists athletes retrieve a specific behavior, mindset, and skill expansion. The process of shaping in sports psychology consists of the identification of the current abilities of an athlete, identification of a behavior, identification of possible reinforcement within an athlete’s environment, dividing the goal into smaller goals, and ultimately, guide the athlete to his or her desired behavior through the use of reinforcements (Schunk, 2012). For instance, when an athlete complains of weak leg muscles, he or she can begin with leg muscle development that fosters strength, stamina, and confidence. Once an athlete works toward a desired behavior, he or she will need to continue to reinforce the behavior until the desired results are achieved. A good example of this is hurdles.

Hurdles is a type of sports activity that requires athletes to run and leap over a bar at pre-determined intervals thus building leg muscles, strength and increasing versatility. An athlete accomplishing a hurdles race builds confidence and physical strength. By receiving corrective feedback, an athlete can achieve his or her desired goal. A sports psychological can assist an athlete by monitoring speed, versatility, and strength and encouraging an athlete to do more, go faster, and untimely achieve their goal.

According to B.F. Skinner, “Chaining is the process of producing or altering some of the variables that serve as stimuli for future responses” (Schunk, 2012, p. 99). Chaining identifies when an athlete desired skill acquisition without reinforcement of successful elements of monitor behavior an athlete cannot improve or achieve higher performance (Greene, 2012). “The operant principle of chaining has been widely researched and implemented with motor skill acquisition and improvement, therefore, in order to ensure proper motor learning, reinforcement of specific behaviors must occur” (Greene, 2012, p.1). Every step offers a signal of action for the next step; a chain is a sequence of cues and behaviors, therefore when one’s behavior in a chain of reactive step generates another signal for the next course of action. Chaining is very useful for sports psychologists when assisting athletes enhance performance and achieve their goals. For example, when an athlete is struggling while training for an event, or merely has a desire to improve his or her performance, a sports psychologist can develop a plan for the athlete to follow on a daily, weekly, and monthly basis. When an athlete follows these guidelines, he or she is creating a chain. Many times athletes develop psychological hindrances that prevent them from performing at an optimal level, therefore a sport psychologist can analyze those factors and examine methods of motivation, enhancing, or eliminating self-esteem issues and offer encouragement throughout stages of progress. Shaping and chaining is a useful tool for sport psychologists in assisting athletes by focusing on the psychological and physiological factors athletes need to succeed.

Reinforcement Schedules

Primarily known for his theory of operant conditioning, B.F. Skinner believed behaviors were dependent on the after-effect of a response called operant behavior. In operant conditioning, scheduling reinforcements are crucial components of learning. There are two types of reinforcement schedules: continuous and partial reinforcement. The schedule of frequency for behavioral reinforcement has a significant impact on the intensity and timeline of the desired response. Continuous reinforcement is more effective during the initial stages of learning to develop a solid connection of the behavior and response. This occurs through the presentation of reinforcement every time an undesired or desired behavior appears. Partial reinforcement is the response of reinforcement only part of the time rather than continuously. Reinforcement schedules can help athletes learn new technical skills through reward or punishment. These schedules help ensure an athlete’s dedication and focus toward his or her goals. When an individual suffers from a psychological or physiological issue, positive reinforcement is pure joy such as an enjoyable evening with friends or a day without working out, therefore the experience is pleasurable and desirable. The negative reinforcement and punishment stage is when the joy is taken away or controlled (consequence). For example, an extra workout, or additional laps around the track or denial of participating in an upcoming event. Although it is important for sports psychologists to provide a positive and encouraging environment for their clients, it is also important to use negative reinforcement to motivate athletes to improve perform.

One-Trial Learning Techniques

The one-trial learning technique involves learning by a single paired response and stimulus, not repetitive responses. If a child places his or her hand on a hot stove and burns it, the child will most likely not do so again fearing the pain from the first experience. Sports psychologists can use one-trial learning techniques to teach athletes the type of mistakes not to make more than once, therefore avoiding time and health consuming hindrances. Many times injuries can happen to athletes causing financial, physiological, and psychological setbacks. When an athlete heals, he or she learns from that one-time error, to avoid such a task or move. Many times athletes over-exert themselves and the one-trial learning technique teaches them to realize and respect their limitations. For example, when long-distance runners decide to push themselves to beat their current time or a competitor’s, they may be doing more good than harm, therefore if they pull a ligament or become sore or unable to run on schedule, they will have learned from this learning technique.

Conclusion

According to Division 47 of the American Psychological Association (2013),

Sports psychology, includes a range of topics that include motivation to continue and achieve, psychological considerations in sport injury and rehabilitation, counseling techniques with athletes, assessing talent, exercise adherence and well-being, self-perceptions related to achieving, expertise in sport, youth sport and performance enhancement and self-regulation techniques (para.1).

Health and sports psychology focuses on an extensive spectrum of clinical, scientific, and adapted subject matter regarding exercise and sports. This field of science focuses on the psychological vision of applying motivation and performance improvement and the comprehension of improving mental and physical health. Among these applied techniques are shaping and chaining, reinforcement schedules, and one-trail learning techniques to assist athletes achieving optimal psychological and physiological health.

References

American Psychological Association. (2013). Purpose and goals. Retrieved from http://www.apa.org/divisions/div47/APA%20Div%2047%20(2)/about_purposeandgoals. html

Browne, M. A., & Mahoney, M. J. (1984). Sport psychology. Annual Review of Psychology,

35(1), 605.

Greene, L. M. (2012). Mastery chaining and modeling to improve dart throwing skill acquisition. (Order No. 3549416, Hofstra University). ProQuest Dissertations and Theses, 85. Retrieved from http://search.proquest.com/docview/1283383949?accountid=458. (1283383949).

Schunk, D. H. (2012). Learning theories: An educational perspective (6th ed.). Boston, MA: Pearson Education.

 
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Initial Assessment homework help

Initial Assessment homework help

Prior to beginning work on this discussion, please read Chapters 2, 6, and 7 in DSM-5 Made Easy: The Clinician’s Guide to Diagnosis.  Additionally, please watch the video Beer Is Cheaper than Therapy: Fort Hood’s PTSD Problem .  (https://fod.infobase.com/OnDemandEmbed.aspx?Token=49272&aid=18596&Plt=FOD&loid=0&w=640&h=480&ref)

For this discussion, the patient for whom you wrote your transcript in the Week One Initial Call discussion has come to your office for a 15-minute initial assessment. As part of the intake process, you have asked the patient to fill out a biographical form that contains the same information included in the case study. Based on this information, propose three questions you would ask the patient to determine a diagnosis and treatment plan.

Provide a transcript of this brief initial session including your three questions and the answers you would expect the prospective patient to give. Beneath the transcript, provide a rationale for each of the three questions you proposed. Include the case study title you chose for your Week One Initial Call discussion post.

Examine your colleague’s transcript, and write an evaluation of the prospective patient’s apparent symptoms and presenting problem(s) within the context of a theoretical orientation. Theoretical orientations are based on the personality theories you learned about in PSY615, and are referred to as “approaches” in Abnormal and Clinical Psychology: An Introductory Textbook.

Remember that symptoms may not be explicitly mentioned by the patient, but they may be inferred by the patient’s presenting problem(s). Summarize views of these symptoms from at least two historical perspectives. For instance, how have these symptoms have been conceptualized and understood, historically? Finally, suggest diagnostic manuals and handbooks besides the DSM-5 that might be used to assess this patient.

Morrison, J. (2014). DSM-5 made easy: The clinician’s guide to diagnosis. New York, NY: The Guilford Press.Retrieved from https://redshelf.com

 

“CHAPTER 6 Trauma- and Stressor-Related Disorders

 

“Trauma- and Stressor-Related Disorders Quick Guide to Trauma- and Stressor-Related Disorders Various types of stress and trauma are responsible for the disorders we’ll consider in this chapter. By now, you know the drill: The link indicates where a more detailed discussion begins. Primary Trauma- and Stressor-Related Disorders Reactive attachment disorder. There is evidence of pathogenic care in a child who habitually doesn’t seek comfort from parents or surrogates. Disinhibited social engagement disorder. There is evidence of pathogenic care in a child who fails to show normal reticence in the company of strangers. Posttraumatic stress disorder. These adolescents or adults repeatedly relive a severely traumatic event, such as combat or a natural disaster. Posttraumatic stress disorder in preschool children. Children repeatedly relive a severely traumatic event, such as car accidents, natural disasters, or war. Acute stress disorder. This condition is much like posttraumatic stress disorder, except that it begins during or immediately after the stressful event and lasts a month or less. Adjustment disorder. Following a stressor, an individual develops symptoms that disappear once the cause of stress has subsided. Other specified, or unspecified, trauma- and stressor-related disorder. Patients whose stress or trauma appears related to other presentations may be classified in one of these categories. Other Problems Related to Trauma or Stress Problems related to abuse or neglect. An astonishing number of Z-codes (V-codes in ICD-9) cover the categories of difficulties that arise from neglect or from physical or sexual abuse of children or adults. Separation anxiety disorder. The patient becomes anxious when separated from parent, other attachment figure, or home. INTRODUCTION Another new chapter for the DSMs incorporates certain diagnoses formerly listed as anxiety, developmental, or adjustment disorders. The unifying factor here is that something traumatic or stressful in the patient’s history appears to be at least partly responsible for the symptoms that develop. It is part of a trend toward grouping together patients of any age who have the right mix of symptoms, rather than separating patients by developmental stage. Many diagnoses include statements about what is not causative, but here is the only full DSM-5 section that presumes any etiology at all, let alone one rooted in the psychology of a pathological developmental process. In the instances of reactive attachment and disinhibited social engagement disorders, there must be evidence of pathogenic care; for posttraumatic stress disorder (PTSD) and its cousins, a horrific event; for adjustment disorder a stressful—well, stressor. The respective criteria sets permit us to check off the fulfilled criteria and go on our way, perhaps thinking that we’ve solved the puzzle. While we rejoice that we’ve successfully determined a cause–effect relationship, nagging at the back of our minds must be a sense that there is more to the story. Otherwise, why do some people become symptomatic while others, exposed to the (as nearly as we can tell) exact same stimulus, go untrammeled on their way? Furthermore, studies have demonstrated that, sooner or later, significant stressors will visit the majority of us. Shouldn’t we conclude that the stimulus in question is necessary, but not sufficient, for the outcome observed? At least this DSM-5 chapter has herded most of these etiology-specific diagnoses into one corral, where we can keep a watchful eye on them. F43.10 [309.81] Posttraumatic Stress Disorder Many people who survive severely traumatic events will develop PTSD. Survivors of combat are the most frequent victims, but it is also encountered in those who have experienced other disasters, both natural and contrived. These include rape, floods, abductions, and airplane crashes, as well as the threats that may be posed by a kidnapping or hostage situation. Children can have PTSD as a result of inappropriate sexual experience, whether or not actual injury has occurred. PTSD can be diagnosed even in those who have only learned about severe trauma (or its threat) suffered by someone to whom they are close—children, spouses, other close relatives. One or two in every 1,000 patients who have undergone general anesthesia have afterwards reported awareness of pain, anxiety, helplessness, and the fear of impending death during the procedure; up to half of them may subsequently develop PTSD symptoms. Implicitly excluded from the definition are stressful experiences of ordinary life, such as bereavement, divorce, and serious illness. Awakening from anesthesia while your surgery is still in progress, however, would qualify as a traumatic event, as would learning about a spouse’s sudden, accidental death or a child’s life-threatening illness. Watching TV images of a calamity would not be a sufficient stressor (except if the viewing was related to the person’s job). After some delay (symptoms usually don’t develop immediately after the trauma), the person in some way relives the traumatic event and tries to avoid thinking about it. There are also symptoms of physiological hyperarousal, such as an exaggerated startle response. Patients with PTSD also express negative feelings such as guilt or personal responsibility (“I should have prevented it”). Aside from the traumatic event itself, other factors may play a role in the development of PTSD. Individual factors include the person’s innate character structure and genetic inheritance. Relatively low intelligence and low educational attainment are positively associated with PTSD. Environmental influences include relatively low socioeconomic status and membership in a minority racial or ethnic group. In general, the more horrific or more enduring the trauma, the greater will be the likelihood of developing PTSD. The risk runs to one-quarter of the survivors of heavy combat and two-thirds of former prisoners of war. Those who have experienced natural disasters such as fires or floods are generally less likely to develop symptoms. (Overall lifetime prevalence of PTSD is estimated at about 9%, though European researchers usually report lower overall rates.) Older adults are less likely to develop symptoms than are younger ones, and women tend to have somewhat higher rates than do men. About half the patients recover within a few months; others can experience years of incapacity. In children, the general outline is pretty much the same as the five general points given in the list of typical symptoms, though the emphasis on symptom numbers differs, as discussed below. Mood, anxiety, and substance use disorders are frequently comorbid. A new specifier reflects findings that in perhaps 12–14% of patients, dissociation is important in the development and maintenance of PTSD symptoms. Essential Features of Posttraumatic Stress Disorder Something truly awful has happened. One patient has been gravely injured or perhaps sexually abused; another has been closely involved in the death or injury of someone else; a third has only learned that someone close experienced an accident or other violence, whereas emergency workers (police, firefighters) may be traumatized through repeated exposure. As a result, for many weeks or months these patients: • Repeatedly relive their event, perhaps in nightmares or upsetting dreams, perhaps in intrusive mental images or dissociative flashbacks. Some people respond to reminders of the event with physiological sensations (racing heart, shortness of breath) or emotional distress. • Take steps to avoid the horror: refusing to watch films or television or to read accounts of the event, or pushing thoughts or memories out of consciousness. • Turn downbeat in their thinking: with persistently negative moods, they express gloomy thoughts (“I’m useless,” “The world’s a mess,” “I can’t believe anyone.”) They lose interest in important activities and feel detached from other people. Some experience amnesia for aspects of the trauma; others become numb, feeling unable to love or experience joy. • Experience symptoms of hyperarousal: irritability, excessive vigilance, trouble concentrating, insomnia, or an intensified startle response. The Fine Print The D’s: • Duration (1+ months) • Distress or disability (work/educational, social, or personal impairment) • Differential diagnosis (substance use and physical disorders [especially traumatic brain injury], mood and anxiety disorders, normal reactions to stressful events) Coding Notes Specify if: With delayed expression. Symptoms sufficient for diagnosis didn’t accumulate until at least six months after the event. With dissociative symptoms: Depersonalization. This indicates feelings of detachment, as though dreaming, from the patient’s own mind or body. Derealization. To the patient, the surroundings seem distant, distorted, dreamlike, or unreal. Barney Gorse “They’re gooks! The place is staffed with gooks!” Someone sitting behind Barney Gorse had dropped a book onto the tile floor, and that had set him off. Now he had backed into a corner in the waiting room of the mental health clinic. His pupils were widely dilated, and perspiration stood out on his forehead. He was panting heavily. He pointed a shaky finger at the Asian student who stood petrified on the other side of the room. “Get this goddamn gook out of here!” He made a fist and lumbered off in the direction of the student. “Hang on, Barney. It’s OK.” Barney’s new therapist took him firmly by the elbow and led him to a private office. They sat there in silence for a few minutes, while Barney’s breathing gradually returned to normal and the clinician reviewed his chart. Barney Gorse was 39 now, but he had been barely 20 when his draft number came up and he joined the Ninth Infantry Division in Vietnam. At that time President Nixon was “winding down the war,” which made it seem all the more painful when Barney’s squad was hit by mortar fire from North Vietnamese regulars. He had never talked about it, even during “anger displacement” group therapy with other veterans. Whenever he was asked to tell his story, he would fly into a rage. But something truly devastating must have happened to Barney that day. The reports mentioned a wound in the upper thigh; he had been the only member of his squad to survive the attack. He had been awarded a Purple Heart and a full pension. Barney hadn’t been able to remember several hours of the attack at all. And he had always been careful to avoid films and television programs about war. He said he’d had enough of it to last everybody’s lifetime; in fact, he had gone to some lengths to avoid thinking about it. He celebrated his discharge from the Army by getting drunk, which was how he remained for 6 years. When he finally sobered up, he turned to drugs. Even they hadn’t been enough to obliterate the nightmares that still haunted him; he awakened screaming several times a week. Sudden noises would startle him into a panic attack. Now, thanks to disulfiram and a chaplain in the county jail where he had been held as a persistent public nuisance, Barney had been clean and sober for 6 months. On the condition that he would seek treatment for his substance use, he had been released. The specialists in substance misuse treatment had quickly recognized that he had other problems, and that had led him here. Last week when they met, the therapist had reminded him again that he needed to dig into his feelings about the past. Barney had responded that he didn’t have any feelings; they’d dried up on him. For that matter, the future didn’t look so good, either: “Got no job, no wife, no kids. I just wasn’t meant to have a life.” He got up and put his hand on the doorknob to leave. “It’s no use. I just can’t talk about it.” Evaluation of Barney Gorse Let’s summarize and restate the criteria that must be fulfilled to diagnose PTSD. 1. There must be severe trauma (criterion A). Barney’s occurred in the context of combat, but a variety of civilian stressors can also culminate in death, serious injury, or sexual abuse. Two features must be present for the stressor to be considered sufficiently traumatic: (a) It must involve the fact or threat of death, severe wounds or injuries, or sexual violation; and (b) it must be personally experienced by the patient in some way—through direct observation (not viewed on TV), through personal involvement, or through information obtained after the fact that it involved a relative or close friend. A first responder (police officer, ambulance attendant) could also qualify through repeated exposure to consequences of the horrific event (think workers at Ground Zero shortly after 9/11). Divorce and death of a spouse from cancer, though undeniably stressful, are relatively commonplace and expected; they don’t qualify. 2. Through some intrusive mechanism, the patient relives the stress. Barney had flashbacks (B3), during which he imagined himself actually back in Vietnam. He also experienced rather intense responses to an external cue (seeing a staff member who, to him, resembled a Viet Cong soldier). Less dramatic forms of recollection include recurrent ordinary memories, dreams, and any other reminder of the event that results in distress or physiological symptoms. 3. The patient attempts (wittingly or not) to achieve emotional distance from the stressful event by avoiding reminders of the trauma. The reminders can be either internal (feelings, thoughts) or external (people, places, activities). Barney refused to watch movies and TV programs or to talk about Vietnam (C). 4. The patient experiences expressions (two or more) of negative mood and thoughts related to the trauma. Barney’s included amnesia for much of his time in combat (D1), a persistently negative frame of mind (“I wasn’t meant to have a life”—D4), and the lack of positive mood states (his feelings had “dried up” on him, D7). 5. Finally, for PTSD, patients must have at least two symptoms of heightened arousal and reactivity associated with the traumatic event. Barney suffered from insomnia (E6) and a severe startle response (E4); others may experience general irritability, poor concentration, or excessive vigilance. As with all symptoms, the clinician would have to determine that these symptoms of arousal had not been apparent before Barney’s Vietnam trauma. Barney’s symptoms had persisted far longer than the required minimum of 1 month (F); were obviously stressful and impaired his functioning in a number of areas (G); and could not be attributed to the direct effects of substance use—now that he’d been clean and sober for half a year (H). The experience of severe trauma in combat and the typical symptoms would render any other explanation for Barney’s symptoms unlikely. A patient with intermittent explosive disorder might become aggressive and lose control, but wouldn’t have the history of trauma. Still, clinicians must always be alert to the possibility of another medical condition (H) that might produce anxiety symptoms and could be diagnosed instead of or in addition to PTSD. For example, head injuries would be relatively common among veterans of combat or other violent trauma; we’d have to mention and code any accompanying brain injury. Situational adjustment disorder shouldn’t be confused with PTSD: The severity of the trauma would be far less, and the effects would be transient and less dramatic. In PTSD, comorbidity is the rule rather than the exception. Barney had used drugs and alcohol; his clinician would have gathered additional information about use of other substances and mentioned them in his diagnostic summary. Of combat veterans who have PTSD, half or more also have a problem with a substance use disorder, and use of multiple substances is common. Anxiety disorders (phobic disorders, generalized anxiety disorder) and mood disorders (major depressive disorder and dysthymia) are likewise common in this population. Dissociative amnesia may also occur. Any coexisting personality disorder would be explored, but it is hard to make a definitive diagnosis when a patient is acutely ill from PTSD. Malingering is also a diagnosis to consider whenever there appears to be a possibility of material gain (insurance, disability, legal problems) resulting from an accident or physical attack. Although the vignette is imprecise on this point, Barney’s symptoms probably began by the time he was discharged from the military, so he would not rate the specifier with delayed onset. The vignette doesn’t provide encouragement to add with prominent dissociation. I’d give him a GAF score of 35. Pending further information on substance use, Barney’s diagnosis would read as follows: F43.10 [309.81] Posttraumatic stress disorder F10.20 [303.90] Alcohol use disorder, moderate, in early remission Z60.2 [V60.3] Lives alone Z56.9 [V62.29] Unemployed There is still considerable controversy over the specifier with delayed expression. Many experts deny that symptoms of PTSD can begin many months or years after the trauma. Nonetheless, it is there to use, should you ever find it appropriate. Posttraumatic Stress Disorder in Preschool Children There can be no doubt that preschool children are sometimes exposed to traumatic events. Mostly, these are car accidents, natural disasters, and war—in short, all the benefits contemporary life has to offer. The question is, do very young children respond with typical PTSD symptoms? The best evidence would seem to indicate that they do, but with a likelihood much lower (0–12%) than for older children. Table 6.1 compares the DSM-5 criteria for PTSD in young children, PTSD in adults, and acute stress disorder (to be discussed next). The revamped criteria for PTSD in young children are, as we would hope, more sensitive to symptoms in this age group. Based on interviews with parents, they yield rates in children who have survived severe burns of 25% and 10% at 1 month and 6 months, respectively. TABLE 6.1. Comparison of PTSD in Preschool Children, PTSD in Adults, and Acute Stress Disorder Child PTSD Adult PTSD Acute Stress Disorder Trauma Direct experience Direct experience Direct experience Witness (not just TV) Witness Witness Learn of Learn of Repeat exposure (not just TV) Learn of Repeat exposure (not just TV) Intrusion symptoms (1/5)a Intrusion symptoms (1/5) All symptoms (9/14) • Memories • Memories • Memories • Dreams • Dreams • Dreams • Dissociative reactions • Dissociative reactions • Dissociative reactions • Psychological distress• Physiological reactions • Psychological distress• Physiological reactions • Psychological distress or physiological reactions Avoid/Neg. emotions (1/6) Avoidance (1/2) • Avoids memories • Avoids memories • Avoids memories • Avoids external reminders • Avoids external reminders • Avoids external reminders Negative emotions (2/7) • Altered sense of reality of self or surroundings • Amnesia • Amnesia • Negative beliefs • Distortion → self-blame • Negative emotional state • Negative emotional state • Decreased interest • Decreased interest • Social withdrawal • Detached from others • Decreased positive emotions • No positive emotions • No positive emotions Physiological (2/5) Physiological (2/6) • Irritable, angry • Irritable, angry • Irritable, angry • Reckless, self-destructive • Hypervigilance • Hypervigilance • Hypervigilance • Startle • Startle • Startle • Poor concentration • Poor concentration • Poor concentration • Sleep disturbance • Sleep disturbance • Sleep disturbance Duration >1 month >1 month 3 days–1 month Purchasers of this ebook can download a copy of this table from www.guilford.com/morrison2-forms. aFractions indicate the number of symptoms required of the number possible in the following list. F43 [308.3] Acute Stress Disorder Based on the observation that some people develop symptoms immediately after a traumatic stress, acute stress disorder (ASD) was devised several decades ago. Even then, this wasn’t exactly new information; something similar was noted as far back as 1865, just after the U.S. Civil War. For many years it was termed “shell shock.” Like PTSD, ASD can also be found among civilians. Overall rates of ASD, depending on the nature of the trauma and personal characteristics of the individual, center on 20%. Though the number and distribution of symptoms is different, the criteria embody the same elements required for PTSD: • Exposure to an event that threatens body integrity • Reexperiencing the event • Avoidance of stimuli associated with the event • Negative changes in mood and thought • Increased arousal and reactivity • Distress or impairment The symptoms usually begin as soon as the patient is exposed to the event (or learns about it), but they must be experienced farther out than 3 days after the stressful event to fulfill the criterion for duration. This gets us to a period of time beyond the stressful event itself and its immediate aftermath. Should symptoms last longer than 1 month, they are no longer acute and no longer constitute ASD. Then many patients will be rolled over into a diagnosis of PTSD. This is the fate of as many as 80% of patients with ASD. However, patients with PTSD don’t usually enter through the ASD doorway; most are identified farther along the road than one month. Essential Features of Acute Stress Disorder Something truly awful has happened—grave injury or sexual abuse, or perhaps the traumatic death or injury of someone else. (It could have come about through learning another has experienced violence or injury, or through repeated exposure for an emergency worker.) As a result, for up to a month the patient experiences many symptoms such as intrusive memories or bad dreams; dissociative experiences such as flashbacks or feeling unreal; the inability to experience joy or other love; amnesia for parts of the event; attempts to avoid reminders of the event (refusing to watch films or television or to read accounts of the event); pushing thoughts or memories out of consciousness. The patient may also experience symptoms of hyperarousal: irritability, hypervigilance, trouble concentrating, insomnia, or an intense startle response. The Fine Print The D’s: • Duration (3 days to 1 month) • Distress or disability (work/educational, social, or personal impairment) • Differential diagnosis (substance use and physical disorders (especially traumatic brain injury), panic disorder, mood disorders, dissociative disorders, PTSD) Marie Trudeau Marie Trudeau and her husband, André, sat in the intake interviewer’s office. Marie was the patient, but she spent most of the time rubbing the knuckles of one hand and gazing vacantly into the room. André did most of the talking. “I just can’t believe the change in her,” he said. “A week ago, she was completely normal. Never had anything like this in her life. Heck, she’s never had anything wrong with her. Then, all of a sudden, boom! She’s a mess.” At André’s exclamation, Marie jerked around to face him and rose half out of her chair. For a few seconds she stood there, frozen except for her gaze, which darted from one side of the room to the other. “Aw, geez, I’m sorry, honey. I forgot.” He put his arm around her. Grasping her shoulders firmly but gently, he eased her back into the chair. He held her there until she began to relax her grip on his arm. A week earlier, Marie had just finished her gardening and was sitting in the back yard with a lemonade, reading a book. When she heard airplane engines, she looked up and saw two small planes flying high overhead, directly above her. “My God,” she thought, “they’re going to collide!” As she watched in horror, they did collide. She could see perfectly. The sun was low, highlighting the two planes brilliantly against the deep blue of the late afternoon sky. Something seemed to have been torn off one of them—the news media later reported that the right wing of one plane had ripped right through the cockpit of the other. Thinking to call 911, Marie picked up her portable phone, but she didn’t dial. She could only watch as two tiny objects suddenly appeared beside the stricken airplanes and tumbled toward her in a leisurely arc. “They weren’t objects, they were people.” It was the first time she had spoken during the interview. Marie’s chin trembled, and a lock of hair fell across her eye. She didn’t try to brush it back. As she continued to watch, one of the bodies hurtled into her yard 15 feet from where she was sitting. It buried itself 6 inches deep in the soft earth behind her rose bushes. What happened next, Marie seemed to have blanked out completely. The other body landed in the street a block away. Half an hour later, when the police knocked on her door, they found her in the kitchen peeling carrots for supper and crying into the sink. When André arrived home an hour after that, she seemed dazed. All she would say was “I’m not here.” In the 6 days since, Marie hadn’t improved much. Although she might start a conversation, something would appear to distract her, and she would usually trail off in midsentence. She couldn’t focus much better on her work at home. Amy, their 9-year-old daughter, seemed to be taking care of her. Sleep had slipped to a restless struggle, and three nights running Marie had awakened from a dream, trying to cry out but managing only a terrified squeak. She kept the blinds in the kitchen closed, so she wouldn’t even have to look into the back yard. “It’s like someone I saw in a World War II movie,” André concluded. “You’d think she’d been shell-shocked.” Evaluation of Marie Trudeau Anxiety and depressive symptoms are nearly universal following a severe stress. Usually these are relatively short-lived, however, and do not include the full spectrum of symptoms required for ASD. This diagnosis should only be considered when major symptoms last 3 days or more after personal exposure to a horrific event. Such an event was the plane crash Marie witnessed (criterion A2). She was dazed (B6) and emotionally unresponsive (B5), and could not recall what had happened during part of the accident (B7). When she could sleep at all (B10), she had nightmares (B2); she also avoided looking into the back yard (B9), startled easily (B14), and even in the interviewer’s office appeared hypervigilant (B12). From her inability to finish conversations, we infer poor concentration (B13), as she was distracted by intrusive recollections of the event (B1). As far as we are aware, she had had none of these symptoms (DSM-5 requires 9 of the 14 symptoms listed in criterion B) prior to witnessing the accident. Since then, just a week earlier (C), she had been unable to carry on with her work at home (D). Would any other diagnosis be possible? According to André, Marie’s previous health had been good, reducing the likelihood of another medical condition (E). We aren’t told whether she used alcohol or drugs, though the fact that she was drinking lemonade at the time of the crash could suggest that she did not. (OK, I’m definitely out on a limb here; her clinician needs to rule out a substance use disorder.) Brief psychotic disorder would be ruled out by the lack of delusions, hallucinations, or disorganized behavior or speech. Patients with ASD are likely to have severe depressive symptoms (“survivor’s guilt”), to the point that a concomitant diagnosis of major depressive disorder may sometimes be justified; Marie deserves further investigation along those lines. Until then, with a GAF score of 61, her diagnosis would be straightforward: F43.0 [308.3] Acute stress disorder Adjustment Disorder Patients with adjustment disorder (AD) may be responding to one stress or to many; the stressor may happen once or repeatedly. If the stressor goes on and on, it can even become chronic, as when a child lives with parents who fight continually. In clinical situations, the stressor has usually affected only one person, but it can affect many (think flood, fire, and famine). However, almost any relatively commonplace event could be a stressor for someone. Those most often cited for adults are getting married or divorced, moving, and financial problems; for adolescents, they are problems at school. Whatever the nature of the stressor, patients feels overwhelmed by the demands of something in the environment. As a result, they develop emotional symptoms such as low mood, crying spells, complaints of feeling nervous or panicky, and other depressive or anxiety symptoms—which must not, however, meet criteria for any defined mood or anxiety disorder. Some patients have mainly behavioral symptoms—especially ones we might think of as conduct symptoms, such as driving dangerously, fighting, or defaulting on responsibilities. The course is usually relatively brief; DSM-5 criteria specify that the symptoms must not persist longer than 6 months after the end of the stressor or its consequences. (Some studies report that a large minority of patients continue to have symptoms longer than the 6-month limit.) Of course, if the stressor is one that will be ongoing, such as a chronic illness, it may take a very long time for the patient to adjust. Although AD has been reported in 10% or more of adult primary care patients, and in huge percentages of mental health patients, one recent study found a prevalence of only 3%; many of these patients were being inappropriately treated with psychotropic medications, and in only two cases had the AD diagnosis been made. The discrepancies probably rest on the rather poorly developed criteria and on the (mistaken) view of AD as a residual diagnosis. AD is found in all cultures and age groups, including children. It may be more firmly anchored in adults than in adolescents, whose early symptoms often evolve into other, more definitive mental disorders. The reliability and validity of AD tend to be quite low. In a recent study, in under two-thirds of patients receiving the clinical diagnosis of AD could it be subsequently confirmed with ICD-10 criteria. Personality disorders or cognitive disorders may make a person more vulnerable to stress, and hence to AD. Patients in whom AD is diagnosed often misuse substances as well. Essential Features of Adjustment Disorder A stressor causes someone to develop depression, anxiety, or behavioral symptoms—but the response exceeds what you’d expect for most people in similar circumstances. After the stressor has ended, the symptoms might drag on, but not longer than 6 more months. The Fine Print The D’s: • Duration (starts within 3 months of stressor’s onset, stops within 6 months of stressor’s end) • Distress or disability (work/educational, social, or personal impairment) • Differential diagnosis (just about everything you can name: substance use and physical disorders, mood and anxiety disorders, trauma-related disorders, somatic symptom disorder, psychotic disorders, conduct and other behavior disorders, milder reactions to life’s stresses, normal bereavement) Coding Notes Specify: F43.21 [309.0] With depressed mood. The patient is mainly tearful, sad. F43.22 [309.24] With anxiety. The patient is mainly nervous, tense, or fearful of separation. F43.23 [309.28] With mixed anxiety and depressed mood. Symptoms combine the preceding. F43.24 [309.3] With disturbance of conduct. The patient behaves inappropriately or unadvisedly, perhaps violating societal rules, norms, or the rights of others. F43.25 [309.4] With mixed disturbance of emotions and conduct. The clinical picture combines emotional and conduct symptoms. F43.20 [309.9] Unspecified. Use for other maladaptive stress-related reactions, such as physical complaints, social withdrawal, work or academic inhibition. Specify if: Acute. The condition has lasted less than 6 months. Persistent (or chronic). 6+ months duration of symptoms, though still not lasting more than 6 months after the stressor has ended. Clarissa Wetherby “I know it’s temporary, and I know I’m overreacting. I sure don’t want to, but I just feel upset!” Clarissa Wetherby was speaking of her husband’s new work schedule. Arthur Wetherby was foreman on a road-paving crew whose current job was to widen and resurface a portion of the interstate highway just a few miles from the couple’s house. Because the section the crew was working on involved an interchange with another major highway, the work had to be done at night. For the past 2 months, Arthur had slept days and gone to work at 8:00 P.M. Clarissa worked the day shift as cashier in a restaurant. Except on weekends, when he tried to revert to a normal sleep schedule so he could be with her, they hardly ever saw one another. “I feel like I’ve been abandoned,” she said. The Wetherbys had been married only 3 years, and they had no children. Each partner had been married once before; each was 35. Neither drank or used drugs. Clarissa’s only previous encounter with the mental health system had occurred 7 years earlier, when her first husband had left her for another man. “I respected his right not to continue living a lie,” she said, “but I felt terribly alone and humiliated.” Clarissa’s symptoms now were much as they had been then. Most of the time when she was at work, she felt “about normal” and maintained good interest in what she was doing. But when alone at home in the evenings, she would be overwhelmed by waves of sadness. These left her virtually immobilized, unable even to turn on the television for company. She often cried to herself and felt guilty for giving in to her emotions. “It’s not as if someone had died, after all.” Although she had some difficulty getting to sleep at night, she slept soundly in the morning. Her weight was constant, her appetite was good, and she had no suicidal ideas or death wishes. She did not report any problems with her concentration. She denied ever having mania symptoms. The previous time she’d sought help, she had remained depressed and upset until a few weeks after the divorce was final. Then she seemed suddenly able to put it behind her and begin dating once again. “I know I’ll feel better, once Arthur gets off that schedule,” she said. “I guess it just makes me feel worthless, playing second fiddle to an overpass.” Evaluation of Clarissa Wetherby As she herself recognized, Clarissa’s reaction to the stress of her husband’s work schedule might be considered extreme by some observers. That is one of the important points of this diagnosis: The patient’s misery seems disproportionate to the apparent degree of the stress that has caused it (criterion B1). Her history provides a clue as to the source of her reaction: She was reminded of that awful time when her previous husband abandoned her—for good, and under circumstances that she considered humiliating. It is important, however, always to consider carefully whether a patient’s reaction occurs as a nonpathological response to a genuine danger, which was not the case with Clarissa. The time course of Clarissa’s symptoms was right for AD: They developed shortly after she learned about Arthur’s new work schedule (A). Although we have no way of knowing how long this episode might last, her previous episode ended after a few months, when the aftermath of her divorce had subsided (E). Of course, bereavement didn’t enter into her differential diagnosis (D). Note that AD is not intended as a residual diagnosis, though it is often used that way. Nonetheless, it does come at the end of a long differential diagnosis that comprises every other condition listed in DSM-5 (C). For Clarissa, the symptoms of mood disorder were the most prominent. She had never been manic, so could not qualify for a bipolar disorder. She had low mood, but only when alone in the evenings (not most of the day). She maintained interest in her work (rather than experiencing loss of interest in nearly all activities). Without at least one of these symptoms, there could not be a diagnosis of major depressive disorder, regardless of her guilt feelings, low energy, and trouble getting to sleep at night. Of course, her symptoms had lasted far less than 2 years, ruling out dysthymia. Although she remained fully functional at work, she was seriously distressed, fulfilling the severity requirement. The question of PTSD (and acute stress disorder) often arises in the differential diagnosis of AD. Each of those diagnoses requires that the stressor threaten serious harm and that the patient react with a variety of responses; Clarissa did not fulfill these conditions. She similarly did not have symptoms that would suggest generalized anxiety disorder, another diagnosis prominent in the differential for AD. A personality disorder may worsen (and hence become more apparent) with stress, but there is no hint that Clarissa had any lifelong character pathology. I’d assign her a GAF score of 61. F43.21 [309.0] Adjustment disorder, with depressed mood, acute Although some data support the utility of AD, which has been used clinically for decades, I recommend reserving it as a diagnosis of “almost last resort.” There are several reasons for this warning. For one thing, we probably too often use it when we simply have no better idea of what is going on. For another, the DSM-5 criteria do not tell us how we are to differentiate ordinary events from those that are stressful enough to cause depression, anxiety, or aberrant behavior. I suspect that an event is singled out solely on the basis that it causes and emotional or behavioral problem, and that seems to me a tad circular. F94.1 [313.89] Reactive Attachment Disorder F94.2 [313.89] Disinhibited Social Engagement Disorder In two apparently rare but extremely serious disorders, children who have been mistreated (by accident or design) respond by becoming either extremely withdrawn or pathologically outgoing. For neither disorder do we have a lot of information, placing these two among the least well understood of mental disorders that affect children (or adults, for that matter). Each disorder is conceived as a reaction to an environment in which the child experiences caregiving that is inconstant (frequent change of parent or surrogate) or pathological (abuse, neglect). One of two patterns then develops. In reactive attachment disorder (RAD), even young infants withdraw from social contacts, appearing shy or distant. Inhibited children will resist separation by tantrums or desperate clinging. In severe cases, infants may exhibit failure-to-thrive syndrome, with head circumference, length, and weight hovering around the 3rd percentile on standard growth charts. By contrast, a child’s response in disinhibited social engagement disorder (DSED) borders on the promiscuous. Small children eschew normal wariness and boldly approach strangers; instead of clinging, they may instead appear indifferent to the departure of a parent. In both subtypes, the abnormal responses are more obvious when the main caregiver is absent. Factors that indicate increased risk for either RAD or DSED include being reared in an orphanage or other institution; protracted hospitalizations; multiple and frequent changes in caregivers; severe poverty; abuse (the gamut of physical, emotional, and sexual); and a family riven by death, divorce, or discord. Complications associated with these disorders include stunted physical growth, low self-esteem, delinquency, anger management issues, eating disorders, malnutrition, depression or anxiety, and later substance misuse. In either disorder, a constant, nourishing relationship with a sensitive caregiver is required to reestablish adequate physical and emotional growth. Without such a remedy, the conditions tend to persist into adolescence. There has been almost no follow-up into adult life; despite a dearth of reliable information, you will (of course) find websites. DSM-IV listed these two conditions as subcategories of one disorder. Because of differences in symptoms, course, treatment response, and other correlates, DSM-5 now treats them as separate diagnoses—despite their supposed common etiology. However, some children will appear withdrawn when very young, then become disinhibited later, whereas others have symptoms of both conditions simultaneously. The upshot is that some observers find the dichotomy a bit forced. Essential Features of Reactive Attachment Disorder Adverse child care (abuse, neglect, caregiving insufficient or changed too frequently) has apparently caused a child to withdraw emotionally; the child neither seeks nor responds to soothing from an adult. Such children will habitually show little emotional or social response; far from having positive affect, they may experience periods of unprovoked irritability or sadness. The Fine Print The presumption of causality stems from the temporal relationship of the traumatic child care to the disturbed behavior. The D’s: • Demographics (begins before age 5; child has developmental age of at least 9 months) • Differential diagnosis (autism spectrum disorder, intellectual disability, depressive disorders) Coding Notes Specify if: Persistent. Symptoms are present longer than 1 year. Severe. All symptoms are present at a high level of intensity. Essential Features of Disinhibited Social Engagement Disorder Adverse child care (abuse, neglect, caregiving insufficient or changed too frequently) has apparently caused a child to become unreserved in interactions with strange adults. Such children, rather than showing typical first-acquaintance shyness, will little hesitate to leave with a strange adult; they don’t “check in” with familiar caregivers, and readily become excessively familiar. In so doing, they may cross normal cultural and social boundaries. The Fine Print The presumption of causality stems from the temporal relationship of the traumatic child care to the disturbed behavior. The D’s: • Demographics (child has developmental age of at least 9 months) • Differential diagnosis (autism spectrum disorder, intellectual disability, ADHD) Coding Notes Specify if: Persistent. Symptoms are present longer than 1 year. Severe. All symptoms are present at a high level of intensity. F43.8 [309.89] Other Specified Trauma- or Stressor-Related Disorder This diagnosis will serve to categorize those patients for whom there is an evident stressor or trauma, but who for a specific, stated reason don’t fulfill criteria for any of the standard diagnoses already mentioned above. DSM-5 gives several examples, including two forms of adjustment-like disorders (one form with delayed onset and another with prolonged duration relative to adjustment disorder). Others are as follows: Persistent complex bereavement disorder. For at least a year, a patient experiences intense grief for someone close who has died. There may be yearning and preoccupation of thoughts for the person, or continuing ruminations over the circumstance of death. A number of other symptoms express the patient’s loss of identity and reactive distress. Proposed criteria and discussion are given in Section III of DSM-5 on page 789. Various cultural syndromes. You’ll find a number of these in an appendix in DSM-5, page 833. F43.9 [309.9] Unspecified Trauma- or Stressor-Related Disorder This diagnosis will serve to categorize those patients for whom there is an evident stressor or trauma, but who don’t fulfill criteria for any of the standard diagnoses already mentioned above, and for whom you do not care to specify the reasons why the criteria are not fulfilled.”

 
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Psychology Chapter 1 Practice Problems homework help

Psychology Chapter 1 Practice Problems homework help

Name:

Chapter 1 Instructions

Practice Problem 12, 15, 19, 20, 21, & 22

Due Week 2 Day 6 (Sunday)

Follow the instructions below to submit your answers for Chapter 1 Practice Problem 12, 15, 19, 20, 21, & 22.

1. Save Chapter 1 Instructions to your computer.

2. Type your answers into the shaded boxes below. The boxes will expand as you type your answers.

3. Resave this form to your computer with your answers filled-in.

4. Attach the saved form to your reply when you turn-in your work in the Assignments section of the Classroom tab. Note: Each question in the assignments section will be listed separately; however, you only need to submit this form one time to turn-in your answers.

Read each question in your text book and then type your answers for Chapter 1 Practice Problem 12, 15, 19, 20, 21, & 22 in the corresponding spaces below.

12a. equal-interval –

12b. rank-order –

12c. nominal –

12d. ratio scale –

12e. continuous –

15. Type your answers to Practice Problem 15a in the shaded boxes below. The “X” represents the speed; “f” represents the frequency; and “%” represents the relative percentage for each score. Round to the nearest whole percentage. For example, if your remainder is .5 or greater, round up (i.e. 2.5 = 3). Note: Fill-in each box. Please do not delete any scores.

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19. Give an example, in words, of something having the distribution shapes listed below.

19a. bimodal –

19b. approximately rectangular –

19c. positively skewed –

20. Describe an example of a misleading graph: Note: Either copy and paste a graph in the first shaded box below, or fully describe the graph if it will not paste. You may also cut and paste a misleading graph onto a Word document and send as an attachment. Please do not include a link to a graph in lieu of pasting a graph onto a Word document. I will not navigate to a link to view your chosen graph.

In the second shaded box, discuss specific characteristics that make the graph misleading.

 

 

21a. Explain the idea of frequency table 1-10 below:

 

21b. Explain the meaning of the pattern of results below:

 

22a. Explain the idea of frequency table 1-11 below:

 

22b. Explain the meaning of the pattern of results below:

 
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Psychology Response homework help

Psychology Response homework help

1. Responded to message below. Should be at least 250 words. Responses should be informative and contribute to advancing knowledge of the topic. Include at least 2 APA-cited references.

Frank, Greitzer & Holimer (2011) makes powerful augments about the difficulties surrounding the trail before the fact. I agree with them. It really is difficult to determine if threats are bogus and if they should be taken seriously. However, once a threat is made it must be taken seriously and that it is highly possible for the individual to carry out their plan. It is also difficult to know the individual’s state of mind or if the individual has psychological issues. Frank, Greitzer & Holimer (2011) states, “there are several factors that should taken into consideration regarding picking up the trail before the fact, (a) the lack of sufficient real-world data that has “ground truth” adequate scientific verification and validate of proposed solutions; (b) the difficulty in distinguishing between malicious insider behavior and what can be described as normal or legitimate behavior (c) the potential quantity of data, and the resultant number of “associations” or relationships that may emerge produce enormous scalability challenges; and (d) despite ample evidence suggesting that in a preponderance of cases, the perpetrator exhibited observable ‘concerning behaviors’. All threats should be taken into account and noted as warning signals and reported to the proper authorities.

Sometimes the most damage is done by individuals who had a personal insight into the company or one who became disgruntled. They know the outs an ins of the organization and how to cause the most damage. I also agree that the methods and skills of the perpetrators have changed in recent years. With all of the new technology, the generations have become wiser and smarter. Therefore, all threats should be observed.

2. Responded to message below. Should be at least 250 words. Responses should be informative and contribute to advancing knowledge of the topic. Include at least 2 APA-cited references.

What Frank, Greitzer & Hohimer (2011) argue about difficulties of picking up the trail before the fact, in order to provide time to intervene and prevent an insider cyber attack?
I agree with Greitzer and Hohimer that insider threat is a serious concern for cyber security that has to be addressed successfully. Unfortunately this is much easier said than done. The nature of insider threat makes it very difficult to detect and as Grietzer and Hohimer (2011) point out, there is a lack of real world data, it is difficult to differentiate between normal and abnormal behavior, there would be scalability challenges in data collected and no one has really decided to tackle this issue with technology yet (p.27). This means that devising a way to identify an insider threat prior to that insider launching an attack is a task that will not be easy to complete. That doesn’t mean that this is not a goal that we should be working towards, quite the opposite actually. This is something that should be given attention and professionals should be working on methods that can help catch insider threats before the damage is done.
Do you agree with them? Why? Why not?
I do agree with Greitzer and Hohimer that insider threat is a big problem. I also agree that there is a lack of data that can be used to help identify patterns and help develop methods and technology that can catch insider threat early. I have to admit that much of what they discussed in the article was a bit over my head. I don’t fully understand how the technology they discussed would work and I also can’t say that I believe that a technological solution would the perfect solution for this issue. Humans can be very unpredictable. This means that any technology developed to be an early identifier of insider threat will not work every time. I do think that more often than not there will be indicators prior to an insider attack occurring but there is always that chance that someone just snaps. With that being said I do think that there should still be research and work done to mitigate the risk of insider attacks.

Quantification: 2 Pages

Assignment: Chapter 2 & Chapter 3

Question1:

(Problem 1): If a program has 471 bytes and will be loaded into page frames of 100 bytes each, and the instruction to be used is at byte 132, answer the following questions:

 

a. How many pages are needed to store the entire job?

b. Compute the page number and the exact displacement for each of the byte addresses where the data is stored. (note: page numbering starts at zero).

 

a) 471/100 + 1=5

b) To store page number: 3 bits

To store offset:7 bits

 

(Problem-2): Given that main memory is composed of only three page frames for public use and that a seven-page program (with Pages a, b, c, d, e, f, g) that requests pages in the following order:

a, c, a, b, a, d, a, c, b, d, e, f

(a). Using the FIFO page removal algorithm, indicate the movement of the pages into and out of the available page frames (called a page trace analysis). Indicate each page fault with an asterisk (*). Then compute the failure and success ratios.

(b). Increase the size of memory so it contains four page frames for public use. Using the same page requests as above and FIFO, do another page trace analysis and compute the failure and success ratios.

Given that main memory is composed of three page frames for public use and that a seven-page program (with pages a, b, c, d, e, f, g) requests pages in the following order: a, b, a, c, d, a, e, f, g, c, b, g

 

a.

page request a b a c d a e f g c b g
                         
page fault *  *    * * * * * * * *  
                         
page 1 a a a a d d d f f f b b
                         
page 2   b b b b a a a g g g g
                         
page 3       c c c e e e c c c
Total faults: 10   Failure: 10/12     83.33e %

Total faultless: 2 Success: 2/12 16.66e%

 

b

page request a b a c d a e f g c b g
                         
page fault *  *    *  *   * * * * *  
                         
page 1 a a a a a a e e e e b b
                         
page 2   b b b b b b f f f f f
                         
page 3       c c c c c g g g g
                         
page 4         d d d d d c c c
Total faults: 9   Failure: 9/12     75 %

Total faultless: 3 Success: 3/12 25%

 

 

 

 

 

 

 

 

Question2:

(Problem 1): Given the following information:

a. Use the best-fit algorithm to indicate which memory blocks are allocated to each of the three arriving jobs.

b. Use the first-fit algorithm to indicate which memory blocks are allocated to each of the three arriving jobs.

 

a) For the best fit algorithm, allocates the smallest free partition which meets the requirement without wasting much memory. So Job A needs 57k so it can fit in any block of the four. but it takes Block 3 so that much memory is not wasted.

Job B needs 920k it cannot fit in both Block 2 and block 1, but it has to use two blocks to fit. Even so much memory is wasted so it fits in Block 2 and takes remaining from other block.

Job C also fits in block 3

Job D can fit in Block 1 and 2 but it fits in block 1 as block 2 is used.

b) For the first fit algorithm, means pick the first block that meets the requirement.

For Job A, it takes first block 1

Job B it takes block 2 but does not fit so it has to wait for Job A

Job C it takes block 3 as per the requirement.

Job D it takes Block 4 but does not fit so it has to wait for other blocks as Job A or Job C to finish which has free space and then fits.

 

 

 

(Problem-2): Next-fit is an allocation algorithm that starts by using the first-fit algorithm but keeps track of the partition that was last allocated. Instead of restarting the search with Block 1, it starts searching from the most recently allocated block when a new job arrives. Using the following information:

 

 

Indicate which memory blocks are allocated to each of the three arriving jobs, and explain in your own words what advantages the next-fit algorithm could offer.

 

 

For Job A it takes for the block 1 and uses it 100k in it and then takes for block 2 for remaining to fit in it. The unused memory in block 2 would be 410k.

For job B it takes for the block 2 and use 50k so remains 360k

For job C it takes block 2 and uses 275k and the remaining memory of the block 2 is 85k

For job D, it takes block 2 which has 85k and uses it and then moves to block 3 uses it and for remaining 95k it moves to block 4 and uses 95k thus leaving 500k remaining unused in block 4.

The advantage of next fit is such that, when a new job is called it searches from the remaining block of memory so that much space is saved rather than wasting some amount of space in each block. Thus speed also is improved in next fit since if memory is released that is earlier in the heap for an application, it will check for that block first and fits there.

 
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Biological Psychology Worksheet

Biological Psychology Worksheet

Biological Psychology Worksheet

PSYCH/575 Version 3

1

University of Phoenix Material

Biological Psychology Worksheet

Answer the following questions with 50-to 100-word responses. Prepare to discuss your answers.

1. What are the core assumptions of the biopsychological approach?

Biopsychological approach is also known as physiological psychology, which focuses on the relationship between behaviors, biological makeup, and experiences (Carlson, 2010). Studies of the functions of the nervous system include examples of brain damage, by damaging or disconnecting conscious brain functions from the speech mechanisms in the left hemisphere (Carlson, 2010). The phenomenon of blindsight is partial damage to the visual system on one side of the brain (Carlson, 2010). The phenomenon of unilateral involves consciousness operations of the verbal mechanisms of the left hemisphere (Carlson, 2010). The understanding of the language functions of the brain will lead to an understanding of how the brain may be conscious of its own existence (Carlson, 2010).

2. What historical disciplines converge to create biological psychology?

Physiological psychologists use both reduction and generalization to explain behavior (Carlson, 2010). Generalization refers to the classification of phenomena according to their essential features so that general laws can be formulated (Carlson, 2010). Reduction refers to the description of phenomena in terms of more basic physical processes (Carlson, 2010). Generalizations use the traditional methods of psychology whereas reduction explains behaviors in terms of physiological events within the body primarily within the nervous system (Carlson, 2010). Physiological psychology builds upon the tradition of both experimental psychology and experimental physiology (Carlson, 2010).

3. What are some of the earliest examples of a biological approach to studying behavior?

The most popular example is the evolution of the Darwin’s theory, which is based upon the concepts of natural selection (Carlson, 2010). The theory suggests that it is important to have an understanding of the performing functions of organs, body parts, and behavior (Carlson, 2010). Changes in genetics may cause the production of different proteins, which alters physical characteristics (Carlson, 2010). After the changes confer with a selective advantage, the new genes will be transmitted to other members of the species (Carlson, 2010). Behaviors may also evolve, through the selective advantage of alterations in the structure of the nervous system (Carlson, 2010). Examples of homo neanderthalis evolving into homo sapiens is the perfect study.

4. What are some examples of modern careers that have resulted from studying biological psychology? Include an overview of the careers.

A career in physiological psychology must be obtained with a graduate degree and serve years as junior scientist. Physiological psychology includes the study of neuroscience (Carlson, 2010). A career as a Neuroscientists concerns there study with all aspects of the nervous system: its anatomy, chemistry, physiology, development, and functioning (Carlson, 2010). The research of neuroscientists ranges from the study of molecular genetics to the study of social behavior (Carlson, 2010). Most professional physiological psychologists are employed by colleges and universities, where they are engaged in teaching and research (Carlson, 2010).

5. How is biological psychology viewed by other professionals in psychology today?

The field provides a unique forum for the collaboration and interaction of professionals unparalleled in other areas of scientific and clinical study (Rosenzweig, Breedlove & et al, 2001). Biological psychology contributes to the advancement of empirical and theoretical perspectives (Rosenzweig, Breedlove & et al, 2001). The diverse professionals include representation of investigators trained in the areas of anatomy, anthropology, behavioral medicine, biochemistry, clinical neuropsychology, endocrinology, genetics, molecular biology, paleontology, psychiatry, and psychophysiology (Rosenzweig, Breedlove & et al, 2001). Working together, the professionals study the structural and functional aspects of behavior across species, explore the developmental processes of biology and behavior across the life span, and utilize findings to formulate practical applications that promote human health while respecting each other views and opinions (Rosenzweig, Breedlove & et al, 2001).

Reference:

Carlson, N. R. (2010). Physiology of behavior. (10th ed.). Boston, MA: Allyn & Bacon.

Rosenzweig, M.R., Breedlove, S.M. & Leiman, A.L. (2001). Biological Psychology: An Introduction to Behavioral, Cognitive, and Clinical Neuroscience. (3rd ed.). Sunderland, MA.

 
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Dissociative Disorders And Trauma Assignment help

Dissociative Disorders And Trauma Assignment help

8 somatic symptom and dissociative disorders

image1

learning objectives 8

·  8.1 What are somatic symptom disorders?

·  8.2 What is illness anxiety disorder?

·  8.3 What is conversion disorder (functional neurological symptom disorder)?

·  8.4 What is the difference between a factitious disorder and malingering?

·  8.5 What are the primary features of dissociative disorders?

·  8.6 What is depersonalization/derealization disorder?

·  8.7 What is dissociative amnesia?

·  8.8 What is dissociative identity disorder?

Have you ever had the experience, particularly during a time of serious stress, when you felt like you were walking around in a daze or like you just weren’t all there? Or have you known people who constantly complained about being sure they had a serious illness even though medical tests failed to show anything wrong? Both of these are examples of mild dissociative and somatic symptoms experienced at least occasionally by many people. However, when these symptoms become frequent and severe and lead to significant distress or impairment, a somatic symptom or dissociative disorder may be diagnosed. Somatic symptom disorders (formerly known as  somatoform disorders ) and dissociative disorders appear to involve more complex and puzzling patterns of symptoms than those we have so far encountered. As a result, they confront the field of psychopathology with some of its most fascinating and difficult challenges. Unfortunately, however, we do not know much about them—in part because many of them are quite rare and difficult to study.

As we have seen ( Chapter 6 ), both somatic symptom and dissociative disorders were once included with the various anxiety disorders (and neurotic depression) under the general rubric neuroses, where anxiety was thought to be the underlying cause of all neuroses whether or not the anxiety was experienced overtly. But in 1980, when DSM-III abandoned attempts to link disorders together on the basis of hypothesized underlying causes (as with neurosis) and instead focused on grouping disorders together on the basis of overt symptomatology, the anxiety, mood, somatic symptom, and dissociative disorders each became separate categories.

Somatic Symptom and Related Disorders

The somatic symptom disorders lie at the interface between abnormal psychology and medicine. They are a group of conditions that involve physical symptoms combined with abnormal thoughts, feelings, and behaviors in response to those symptoms (APA,  2013 ).  Soma  means “body,” and somatic symptom disorders involve patterns in which individuals complain of bodily symptoms that suggest the presence of medical problems but where there is no obvious medical explanation that can satisfactorily explain the symptoms such as paralysis or pain. Despite a wide range of clinical manifestations, in each case the person is preoccupied with some aspect of her or his health to the extent that she or he shows significant impairments in functioning.

In DSM-IV a great deal of emphasis was placed on the idea that the symptoms were medically unexplained. In other words, although the patient’s complaints suggested the presence of a medical condition no physical pathology could be found to account for them (Allen & Woolfolk,  2012 ; Witthöft & Hiller,  2010 ). In DSM-5 this idea is less prominent, because it is recognized that medicine is fallible and that a medical explanation for symptoms cannot always be provided. Nonetheless, medically unexplained symptoms are still a key part of some disorders (such as conversion disorder) that we will describe later.

Equally key to these disorders is the fact that the affected patients have no control over their symptoms. They are also not intentionally faking symptoms or attempting to deceive others. For the most part, they genuinely believe something is terribly wrong with them. Not surprisingly, these patients are frequent visitors to their primary-care physicians.

Sometimes, of course, people do deliberately and consciously feign disability or illness. Also placed in the somatic symptoms and related disorders category in DSM-5 is factitious disorder. In  factitious disorder  the person intentionally produces psychological or physical symptoms (or both). Although this may strike you as strange, the person’s goal is to obtain and maintain the benefits that playing the “sick role” (even to the extent of undergoing repeated hospitalizations) may provide, including the attention and concern of family and medical personnel. However, there are no tangible external rewards. In this way factitious disorder differs from malingering. In  malingering  the person is intentionally producing or grossly exaggerating physical symptoms and is motivated by external incentives such as avoiding work or military service or evading criminal prosecution (APA,  2013 ; Maldonado & Spiegel,  2001 ).

In our discussion, we will focus on four disorders in the somatic symptom and related disorders category. These are (1) somatic symptom disorder; (2) illness anxiety disorder; (3) conversion disorder; and (4) factitious disorder.

Somatic Symptom Disorders

This new diagnosis includes several disorders that were previously considered to be separate diagnoses in DSM-IV. The old disorders of (1) hypochondriasis, (2) somatization disorder, and (3) pain disorder have all now disappeared from DSM-5. Most of the people who would in the past have been diagnosed with any one of these disorders will now be diagnosed with a somatic symptom disorder. In each case, individuals must be experiencing chronic somatic symptoms that are distressing to them and they must also be experiencing dysfunctional thoughts, feelings, and/or behaviors. In the past, the diagnosis required evidence that the symptoms were medically unexplained. However, as we noted earlier, this is no longer required for the diagnosis (in part because it is very difficult to prove something is medically unexplainable). Instead the focus in DSM-5 is on there being at least one of the following three features: (1) disproportionate and persistent thoughts about the seriousness of one’s symptoms; (2) persistently high level of anxiety about health or symptoms; and/or (3) excessive time and energy devoted to these symptoms or health concerns (Allen & Woolfolk, 2013). Symptoms have to have persisted for at least six months.

Patients with somatic symptom disorder are usually seen in medical clinics. They are more likely to be female, nonwhite, and less educated than are people with symptoms that have an obvious medical basis. Patients with somatic symptom disorder frequently engage in illness behavior that is dysfunctional, such as seeking additional medical procedures or diagnostic tests when the physician fails to find anything physically wrong with them. Whereas most of us are relieved when tests do not reveal any problems, people with somatic symptom disorder are likely to think something was missed and therefore seek help from another physician, leading to needlessly high medical bills due to unnecessary tests, hospitalizations, and even surgeries. High levels of functional impairment are common, as is comorbid psychopathology—especially depression and anxiety.

Research suggests that people with somatic symptom disorders tend to have a cognitive style that leads them to be hyper-sensitive to their bodily sensations. They also experience these sensations as intense, disturbing, and highly aversive. Another characteristic of such patients is that they tend to think catastrophically about their symptoms, often overestimating the medical severity of their condition.

In the following sections, we will be discussing hypochondriasis, pain disorder, and somatization disorder. It’s important to note that in DSM-5, these disorders were technically dropped and are now part of the somatic symptom disorders. However, the history of and the research on these disorders is still important to understand.

Hypochondriasis

DSM-5 criteria for: Somatic Symptom Disorder

·  A. One or more somatic symptoms that are distressing or result in significant disruption of daily life.

·  B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following:

·  1. Disproportionate and persistent thoughts about the seriousness of one’s symptoms.

·  2. Persistently high level of anxiety about health or symptoms.

·  3. Excessive time and energy devoted to these symptoms or health concerns.

·  C. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Approximately 75 percent of people previously diagnosed with hypochondriasis will be diagnosed with somatic symptom disorder in DSM-5 (APA,  2013 ). In  hypochondriasis  the person is preoccupied either with fears of contracting a serious disease or with the idea that of having that disease even though they do not. These very distressing preoccupations are thought to all be based on a misinterpretation of one or more bodily signs or symptoms (e.g., being convinced that a slight cough is a sign of lung cancer). Of course the decision that a complaint is hypochondriacal and is based on a misinterpretation of bodily signs or symptoms can only be made after a thorough medical evaluation has failed to find a medical condition that could account for the signs or symptoms. Another typical feature of hypochondriasis is that the person cannot be reassured by the results of a medical evaluation. In other words, the fear or idea of having a disease persists despite lack of medical evidence. Indeed, these individuals are sometimes disappointed when no physical problem is found. The condition has to persist for at least 6 months for the diagnosis to be made so as to not diagnose relatively transient health concerns.

Not surprisingly, people with hypochondriasis usually first see a medical doctor for their physical complaints. Because they are never reassured for long and are inclined to suspect that their doctor has missed something, they sometimes shop for additional doctors, hoping one might discover what their problem really is. Because they repeatedly seek medical advice (e.g., Bleichhardt & Hiller,  2006 ; Fink et al.,  2004 ), it is hardly surprising that their annual medical costs are much higher than average (e.g., Fink et al.,  2010 ; Hiller et al.,  2004 ). People with hypochondriasis are generally resistant to the idea that their problem is a psychological one that might be best treated by a psychologist or psychiatrist.

Prior to DSM-5, hypochondriasis was one of the two most commonly seen somatic symptom disorders with a prevalence in general medical practices of 2 to 7 percent (APA,  2000 ). Hypochondriasis occurs about equally often in men and women and can start at almost any age, although early adulthood is the most common age of onset. Hypochondriasis is regarded as a persistent disorder if left untreated, although its severity can fluctuate over time. Individuals with hypochondriasis often also suffer from mood disorders, panic disorder, or other types of somatic symptom disorders (Creed & Barsky,  2004 ). This is one reason why hypochondriasis is now not differentiated from other somatic symptom disorders in DSM-5.

MAJOR CHARACTERISTICS

Individuals with hypochondriasis tend to be highly preoccupied with bodily functions (e.g., heart beats or bowel movements), or with minor physical abnormalities (e.g., a small sore or an occasional cough), or with vague and ambiguous physical sensations (such as a “tired heart” or “aching veins”). They attribute these symptoms to a particular disease and often have intrusive thoughts about it. The diagnoses they make for themselves include cancer, exotic infections, AIDS, and numerous other diseases.  image2 Watchthe Video Henry: Hypochondriasis on MyPsychLab

Although people with hypochondriasis are usually in good physical condition, they are sincere in their conviction that the symptoms they detect represent real illness. In other words, they are not malingering—consciously faking symptoms to achieve a specific goals such as winning a personal injury lawsuit. Not surprisingly, given their tendency to doubt the soundness of their doctors’ conclusions (i.e., that they have no medical problem) and recommendations, the relationships they have with their doctors are often marked by conflict and hostility.

The following case captures the typical clinical picture in hypochondriasis. It also demonstrates that a high level of medical sophistication does not necessarily protect someone from developing this or a related disorder.

An “Abdominal Mass” This 38-year-old physician/radiologist initiated his first psychiatric consultation after his 9-year-old son accidentally discovered his father palpating (examining by touch) his own abdomen and said, “What do you think it is this time, Dad?” The radiologist describes the incident and his accompanying anger and shame with tears in his eyes. He also describes his recent return from a 10-day stay at a famous out-of-state medical diagnostic center to which he had been referred by an exasperated gastroenterologist colleague who had reportedly “reached the end of the line” with his radiologist patient. The extensive physical and laboratory examinations performed at the center had revealed no significant physical disease, a conclusion the patient reports with resentment and disappointment rather than relief.

The patient’s history reveals a long-standing pattern of overconcern about personal health matters, beginning at age 13 and exacerbated by his medical school experience. Until fairly recently, however, he had maintained reasonable control over these concerns, in part because he was embarrassed to reveal them to other physicians. He is conscientious and successful in his profession and active in community life. His wife, like his son, has become increasingly impatient with his morbid preoccupation about life-threatening but undetectable diseases.

In describing his current symptoms, the patient refers to his becoming increasingly aware, over the past several months, of various sounds and sensations emanating from his abdomen and of his sometimes being able to feel a “firm mass” in its left lower quadrant. His tentative diagnosis is carcinoma (cancer) of the colon. He tests his stool for blood weekly and palpates his abdomen for 15 to 20 minutes every 2 to 3 days. He has performed several X-ray studies of himself in secrecy after hours at his office.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 88–90). Washington, DC: (Copyright © 2002). American Psychiatric Association.

CAUSAL FACTORS

Our knowledge of causal factors involved in somatic symptom disorders, including hypochondriasis, is quite minimal. This is especially true when compared to knowledge about the mood and anxiety disorders discussed in the preceding chapters. Currently, cognitive-behavioral views of hypochondriasis are perhaps most widely accepted. These have as a central tenet that it is a disorder of cognition and perception. Misinterpretations of bodily sensations are currently a defining feature of the syndrome, but in the cognitive-behavioral view these misinterpretations also play a causal role. It is believed that an individual’s past experiences with illnesses (in both him- or herself and others, and as observed in the mass media) lead to the development of a set of dysfunctional assumptions about symptoms and diseases that may predispose a person to developing hypochondriasis (Marcus et al.,  2007 ; Salkovskis & Warwick,  2001 ). These dysfunctional assumptions might include notions such as, “Bodily changes are usually a sign of serious disease, because every symptom has to have an identifiable physical cause” or “If you don’t go to the doctor as soon as you notice anything unusual, then it will be too late” (Salkovskis & Bass,  1997 , p. 318; see also Marcus et al.,  2007 ).

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Dissociative Disorders And Trauma Assignment help

Individuals with hypochondriasis are preoccupied with unrealistic fears of disease. They are convinced that they have symptoms of physical illness, but their complaints typically do not conform to any coherent symptom pattern, and they usually have trouble giving a precise description of their symptoms.

Because of these dysfunctional assumptions, individuals with hypochondriasis seem to focus excessive attention on symptoms, with experimental studies showing that these individuals do in fact have an attentional bias for illness-related information (Owens et al.,  2004 ; see also Jasper & Witthöft,  2011 ). Although their physical sensations probably do not differ from those in normal controls (Marcus et al.,  2007 ), they perceive their symptoms as more dangerous than they really are and judge a particular disease to be more likely or dangerous than it really is. Once they have misinterpreted a symptom, they tend to look for confirming evidence and to discount evidence that they are in good health; in fact, they seem to believe that being healthy means being completely symptom-free (Rief et al.,  1998a ). They also perceive their probability of being able to cope with the illness as extremely low (Salkovskis & Bass,  1997 ) and see themselves as weak and unable to tolerate physical effort or exercise (Rief et al.,  1998a ). All this tends to create a vicious cycle in which their anxiety about illness and symptoms results in physiological symptoms of anxiety, which then provide further fuel for their convictions that they are ill.

If we also consider the secondary reinforcements that individuals with hypochondriasis obtain by virtue of their disorder, we can better understand how such patterns of thought and behavior are maintained in spite of the misery these individuals often experience. Most of us learn as children that when we are sick special comforts and attention are provided and, furthermore, that we may be excused from a number of responsibilities. Barsky and colleagues ( 1994 ) found that their patients with hypochondriasis reported much childhood sickness and missing of school. People with hypochondriasis also tend to have an excessive amount of illness in their families while growing up, which may lead to strong memories of being sick or in pain (Pauli & Alpers,  2002 ), and perhaps also of having observed some of the secondary benefits that sick people sometimes reap (Cote et al.,  1996 ; Kellner,  1985 ).

Interestingly, one study retested patients with hypochondriasis 4 to 5 years later and found that those who had remitted at follow-up had acquired significantly more (real) major medical problems than their nonremitting counterparts (Barsky et al.,  1998 ). In other words, it appears that hypochondriacal tendencies were reduced by the occurrence of serious medical conditions. The authors suggested that having a serious medical illness “served to legitimize the patients’ complaints, sanction their assumption of the sick role, and lessen the skepticism with which they had previously been regarded …. As one noted, ‘Now that I know Dr. X is paying attention to me, I can believe him if he says nothing serious is wrong’” ( p. 744 ).

TREATMENT OF HYPOCHONDRIASIS

More than a dozen studies on cognitive-behavioral treatment of hypochondriasis have found that it can be a very effective treatment for hypochondriasis (e.g., Barsky & Ahern,  2004 ; Tyrer,  2011 ; see also Hedman et al.,  2011 , for an example of Internet-based Cognitive Behavioral Therapy). The cognitive components of this treatment approach focus on assessing the patient’s beliefs about illness and modifying misinterpretations of bodily sensations. The behavioral techniques include having patients induce innocuous symptoms by intentionally focusing on parts of their body so that they can learn that selective perception of bodily sensations plays a major role in their symptoms. Sometimes they are also directed to engage in response prevention by not checking their bodies as they usually do and by stopping their constant seeking of reassurance. The treatment is relatively brief (6 to 16 sessions) and can be delivered in a group format. In these studies such treatment produced large changes in hypochondriacal symptoms and beliefs as well as in levels of anxiety and depression.

Somatization Disorder

The DSM-IV diagnosis of somatization disorder is another disorder that has now been subsumed into the broader category of somatic symptom disorder in DSM-5 Somatization disorder  is characterized by many different physical complaints. To qualify for the diagnosis, these had to begin before age 30, last for several years, and not be adequately explained by independent findings of physical illness or injury. They also had to have led to medical treatment or to significant life impairment. Not surprisingly, somatization disorder has long been seen most often among patients in primary medical care settings (Guerje et al.,  1997 ; Iezzi et al.,  2001 ). Indeed, patients with this variant of somatic symptom disorder are enormously costly to health care systems because they often have multiple unnecessary hospitalizations and surgeries (Barsky et al.,  2005 ; Hiller et al.,  2003 ).

The DSM-IV-TR (APA,  2000 ) criteria required that patients report a large number of symptoms across a wide range of domains (e.g., 4 pain symptoms, two gastrointestinal symptoms, one sexual symptom and one neurological-type symptom). Thus, to qualify for a diagnosis of somatization disorder, a patient had to have experienced at least 8 out of 33 specified symptoms (Rief & Barsky,  2005 ). Over time, the rather arbitrary nature of this became increasing apparent and the formal diagnostic criteria began to be modified by many researchers and clinicians (e.g., Rief & Broadbent,  2007 ). Following suit, in DSM-5 the long and complicated symptom count is no longer required and somatization disorder is now considered to be just another variant of somatic symptom disorder.

Another advantage of the recent change in DSM-5 is that it is no longer necessary for us to be concerned about whether somatization disorder and hypochondriasis are really two different and distinct disorders. There are indeed significant similarities between the two conditions. They also sometimes co-occur (Mai,  2004 ). Some years ago leading researchers in this area expressed concerns about whether somatization disorder and hypochondriasis could really be regarded as separate disorders (e.g., Creed & Barsky,  2004 ). Combining them both into a common category in DSM-5 and considering them to be variants of somatic symptom disorder is probably a wise move.

The main features of somatization disorder are illustrated in the following case summary, which also involves a secondary diagnosis of depression.

Not-Yet-Discovered Illness This 38-year-old married woman, the mother of five children, reports to a mental health clinic with the chief complaint of depression, meeting diagnostic criteria for major depressive disorder …. Her marriage has been a chronically unhappy one; her husband is described as an alcoholic with an unstable work history, and there have been frequent arguments revolving around finances, her sexual indifference, and her complaints of pain during intercourse.

The history reveals that the patient … describes herself as nervous since childhood and as having been continuously sickly beginning in her youth. She experiences chest pain and reportedly has been told by doctors that she has a “nervous heart.” She sees physicians frequently for abdominal pain, having been diagnosed on one occasion as having a “spastic colon.” In addition to M.D. physicians, she has consulted chiropractors and osteopaths for backaches, pains in her extremities, and a feeling of anesthesia in her fingertips. She was recently admitted to a hospital following complaints of abdominal and chest pain and of vomiting, during which admission she received a hysterectomy. Following the surgery she has been troubled by spells of anxiety, fainting, vomiting, food intolerance, and weakness and fatigue. Physical examinations reveal completely negative findings.

DEMOGRAPHICS, COMORBIDITY, AND COURSE OF ILLNESS

Somatization disorder usually begins in adolescence and is believed by many to be about three to ten times more common among women than among men. It also tends to occur more among less educated individuals and in lower socioeconomic classes. The lifetime prevalence has been estimated to be between 0.2 and 2.0 percent in women and less than 0.2 percent in men (APA,  2000 ). Somatization disorder very commonly co-occurred with several other disorders including major depression, panic disorder, phobic disorders, and generalized anxiety disorder. It has generally been considered to be a relatively chronic condition with a poor prognosis, although sometimes the disorder remits spontaneously (e.g., Creed & Barsky,  2004 ).

CAUSAL FACTORS IN SOMATIZATION DISORDER

Despite its prevalence in medical settings, researchers are still not certain about the developmental course and specific etiology of somatization disorder. There is evidence that somatization disorder runs in families and that there is a familial linkage between antisocial personality disorder in men (see  Chapter 10 ) and somatization disorder in women. That is, one possibility is that some common, underlying predisposition, probably at least partly genetically based, leads to antisocial behavior in men and to somatization disorder in women (Cale & Lilienfeld,  2002b ; Guze et al.,  1986 ; Lilienfeld,  1992 ). Moreover, somatic symptoms and antisocial symptoms in women tend to co-occur (Cale & Lilienfeld,  2002b ). However, we do not yet have a clear understanding of this relationship. One possibility is that the two disorders are linked through a common trait of impulsivity.

It has also become clear that people with somatization disorder selectively attend to, and show perceptual amplification of, bodily sensations. They also tend to see bodily sensations as somatic symptoms (Martin et al.,  2007 ). Like patients with hypochondriasis, they tend to catastrophize about minor bodily complaints (taking them as signs of serious physical illness) and to think of themselves as physically weak and unable to tolerate stress or physical activity (Martin et al.,  2007 ; Rief et al., 1998).

TREATMENT OF SOMATIZATION DISORDER

Somatization disorder was long considered to be extremely difficult to treat, and general practitioners experienced a great deal of uncertainty and frustration in working with these patients. However, in the past 15 years some treatment research has begun to suggest that a certain type of medical management along with cognitive-behavioral treatments may be quite helpful and that general practitioners can be educated in how to better manage and treat somatization patients and be less frustrated by them (Rosendal et al.,  2005 ; see also Edwards & Edwards,  2010 ). One moderately effective treatment involves identifying one physician who will integrate the patient’s care by seeing the patient at regular visits (thereby trying to anticipate the appearance of new problems) and by providing physical exams focused on new complaints (thereby accepting her or his symptoms as valid). At the same time, however, the physician avoids unnecessary diagnostic testing and makes minimal use of medications or other therapies (Looper & Kirmayer,  2002 ; Mai,  2004 ). Several studies have found that these patients show substantial decreases in health care expenditures over subsequent months and sometimes an improvement in physical functioning (although not necessarily in psychological distress; e.g., Rost et al.,  1994 ). This type of medical management can be even more effective when combined with cognitive-behavioral therapy that focuses on promoting appropriate behavior, such as better coping and personal adjustment, and discouraging inappropriate behavior such as illness behavior and preoccupation with physical symptoms (e.g., Bleichhardt et al.,  2004 ; Mai,  2004 ).

Pain Disorder

The third DSM-IV diagnosis subsumed into the new category of somatic symptom disorder is pain disorder.  Pain disorder  is characterized by persistent and severe pain in one or more areas of the body that is not intentionally produced or feigned. Although a medical condition may contribute to the pain, psychological factors are judged to play an important role. Indeed psychological factors play a role in all forms of pain. The pain disorder may be acute (duration of less than 6 months) or chronic (duration of over 6 months). When working with patients with pain disorder it is very important to remember that the pain that is experienced is very real and can hurt as much as pain that comes from other sources. It is also important to note that pain is always, in part, a subjective experience that is private and cannot be objectively identified by others.

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When one physician integrates a patient’s care, the physical functioning of patients with somatization disorder may improve. Why should this be?

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The experience of pain is always subjective and private, making pain impossible to assess with pinpoint accuracy. Pain does not always exist in perfect correlation with observable tissue damage or irritation. Psychological factors influence all forms of pain.

The prevalence of pain disorder in the general population is unknown. It is definitely quite common among patients at pain clinics. It is diagnosed more frequently in women than in men and is very frequently comorbid with anxiety or mood disorders, which may occur first or may arise later as a consequence of the pain disorder. People with pain disorder are often unable to work (they sometimes go on disability) or to perform some other usual daily activities. Their resulting inactivity (including an avoidance of physical activity) and social isolation may lead to depression and to a loss of physical strength and endurance. This fatigue and loss of strength can then exacerbate the pain in a kind of vicious cycle (Bouman et al.,  1999 ; Flor et al.,  1990 ). In addition, the behavioral component of pain is quite malleable in the sense that it can increase when it is reinforced by attention, sympathy, or avoidance of unwanted activities (Bouman et al.,  1999 ). Finally, there is suggestive evidence that people who have a tendency to catastrophize about the meaning and effects of pain may be the ones most likely to progress to a state of chronic pain (Seminowicz & Davis,  2006 ).

TREATMENT OF PAIN DISORDER

Perhaps because it is a less complex and multifaceted disorder than somatization disorder, pain disorder is usually easier to treat. Indeed, cognitive-behavioral techniques have been widely used in the treatment of both physical and more psychological pain syndromes. Treatment programs generally include relaxation training, support and validation that the pain is real, scheduling of daily activities, cognitive restructuring, and reinforcement of “no-pain” behaviors (Simon,  2002 ). Patients receiving such treatments tend to show substantial reductions in disability and distress, although changes in the intensity of their pain tend to be smaller in magnitude. In addition, antidepressant medications (especially the tricyclic antidepressants) and certain SSRIs have been shown to reduce pain intensity in a manner independent of the effects the medications may have on mood (Aragona et al.,  2005 ; Simon,  2002 ).

ILLNESS ANXIETY DISORDER

Illness anxiety disorder is new to DSM-5. In this newly identified disorder, people have high anxiety about having or developing a serious illness. This anxiety is distressing and/or disruptive but there are very few (mild) somatic symptoms. (see the DSM-5 criteria box below).

It is estimated that around 25 percent of people who would have been diagnosed with hypochondriasis in DSM-IV will be diagnosed with illness anxiety disorder in DSM-5 (APA,  2013 ).

Conversion Disorder (Functional Neurological Symptom Disorder)

DSM-5 criteria for: Illness Anxiety Disorder

·  A. Preoccupation with having or acquiring a serious illness.

·  B. Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.

·  C. There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.

·  D. The individual performs excessive health-related behaviors (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).

·  E. Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of time.

·  F. The illness-related preoccupation is not better explained by another mental disorder, such as somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmorphic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Conversion disorder  is one of the most intriguing and baffling patterns in psychopathology, and we still have much to learn about it. It involves a pattern in which symptoms or deficits affecting the senses or motor behavior strongly suggest that the patient has a medical or neurological condition. However, upon a thorough medical examination, it becomes apparent that the pattern of symptoms or deficits cannot be fully explained by any known medical condition. A few typical examples include partial paralysis, blindness, deafness, and pseudoseizures. The person is not intentionally producing or faking the symptoms, Rather, psychological factors are often judged to play an important role because symptoms usually either start or are exacerbated by preceding emotional or interpersonal conflicts or stressors.

Early observations dating back to Freud suggested that most people with conversion disorder showed very little of the anxiety and fear that would be expected in a person with a paralyzed arm or loss of sight. This seeming lack of concern (known as la belle indifférence—French for “the beautiful indifference”) in the way the patient describes what is wrong was thought for a long time to be an important diagnostic criterion for conversion disorder. However, more careful research later showed that la belle indifférenceactually occurs in only about 20 percent of patients with conversion disorder, so it was dropped as a criterion from recent editions of the DSM (Stone et al.,  2006 , 2011).

The term conversion disorder is relatively recent. Historically this disorder was one of several disorders that were grouped together under the term  hysteria .

Freud used the term conversion hysteria for these disorders (which were fairly common in his practice) because he believed that the symptoms were an expression of repressed sexual energy—that is, the unconscious conflict that a person felt about his or her repressed sexual desires. However, in Freud’s view, the repressed anxiety threatens to become conscious, so it is unconsciously converted into a bodily disturbance, thereby allowing the person to avoid having to deal with the conflict. For example, a person’s guilty feelings about the desire to masturbate might be solved by developing a paralyzed hand. This is not done consciously, of course, and the person is not aware of the origin or meaning of the physical symptom. Freud also thought that the reduction in anxiety and intrapsychic conflict was the “primary gain” that maintained the condition, but he noted that patients often had many sources of “secondary gain” as well, such as receiving sympathy and attention from loved ones. Authors of DSM-5 had many suggestions for changing the name of this disorder (e.g., to psychogenic, functional, and dissociative). In the end, a conservative approach was taken and the term conversion disorder was retained, although this is now followed in parentheses by “Functional neurological symptom disorder” (Stone et al., 2011).

PRECIPITATING CIRCUMSTANCES, ESCAPE, AND SECONDARY GAINS

Freud’s theory that conversion symptoms are caused by the conversion of sexual conflicts or other psychological problems into physical symptoms is no longer accepted outside psychodynamic circles. However, many of Freud’s astute clinical observations about primary and secondary gain are still incorporated into contemporary views of conversion disorder. Although the condition is still called a conversion disorder, the physical symptoms are usually seen as serving the rather obvious function of providing a plausible bodily “excuse” enabling an individual to escape or avoid an intolerably stressful situation without having to take responsibility for doing so. Typically, it is thought that the person first experiences a traumatic event that motivates the desire to escape the unpleasant situation, but literal escape may not be feasible or socially acceptable. Moreover, although becoming sick or disabled is more socially acceptable, this is true only if the person’s motivation to do so is unconscious.

Thus, in contemporary terms, the  primary gain  for conversion symptoms is continued escape or avoidance of a stressful situation. Because this is all unconscious (i.e., the person sees no relation between the symptoms and the stressful situation), the symptoms go away only if the stressful situation has been removed or resolved. Relatedly, the term  secondary gain , which originally referred to advantages that the symptom(s) bestow beyond the “primary gain” of neutralizing intrapsychic conflict, has also been retained. Generally, it is used to refer to any “external” circumstance, such as attention from loved ones or financial compensation, that would tend to reinforce the maintenance of disability.

DSM-5 criteria for: Conversion Disorder

·  A. One or more symptoms of altered voluntary motor or sensory function.

·  B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions.

·  C. The symptom or deficit is not better explained by another medical or mental disorder.

·  D. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Given the important role often attributed to stressful life events in precipitating the onset of conversion disorder, it is unfortunate that little is actually known about the exact nature and timing of these psychological stress factors (Roelofs et al.,  2005 ). However, one study compared the frequency of stressful life events in the recent past in patients with conversion disorder and depressed controls and did not find a difference in frequency between them. Moreover, the greater the negative impact of the preceding life events, the greater the severity of the conversion disorder symptoms (Roelofs et al.,  2005 ). Another study compared levels of a neurobiological marker of stress (lower levels of brain-derived neurotropic factor) in individuals with conversion disorder versus major depression versus no disorder. Both those with depression and those with conversion disorder showed reduced levels of this marker relative to the nondisordered controls (Deveci et al.,  2007 ). This also provides support for the link between stress and the onset of conversion disorder.

DECREASING PREVALENCE AND DEMOGRAPHIC CHARACTERISTICS

Conversion disorders were once relatively common in civilian and (especially) military life. In World War I, conversion disorder was the most frequently diagnosed psychiatric syndrome among soldiers; it was also relatively common during World War II. Conversion disorder typically occurred under highly stressful combat conditions and involved men who would ordinarily be considered stable. Here, conversion symptoms—such as paralysis of the legs—enabled a soldier to avoid an anxiety-arousing combat situation without being labeled a coward or being subject to court-martial.

Conversion disorders are found in approximately 50 percent of people referred for treatment at neurology clinics. The prevalence in the general population is unknown, but even the highest estimates have been around only 0.005 percent (APA,  2013 ). Interestingly, this decreased prevalence seems to be closely related to our growing sophistication about medical and psychological disorders: A conversion disorder apparently loses its defensive function if it can be readily shown to lack a medical basis. When it does occur today, it is most likely to occur in rural people from lower socioeconomic circles who are medically unsophisticated. For example, a highly unusual “outbreak” of cases of severe conversion disorder involving serious motor weakness and wasting symptoms was reported in five 9- to 13-year-old girls living in a small, poor, rural Amish community. Each of these girls had experienced substantial psychosocial stressors including behavioral problems, dys-functional family dynamics, and significant community stress from a serious local church crisis (see Cassady et al.,  2005 ). Fortunately, after the caregivers of these girls were educated regarding the psychological nature of the symptoms and given advice to stick with one doctor, minimize stress, and avoid reinforcement of the “sick role,” four of the five girls showed significant improvement over the next 3 months. In the fifth case, the family refused to acknowledge the psychological component of the illness, holding to the belief that the symptoms were caused by parasites.

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Conversion disorders were fairly common during World War I and World War II. The disorder typically occurred in otherwise “normal” men during stressful combat conditions. The symptoms of conversion disorder (e.g., paralysis of the legs) enabled a soldier to avoid high-anxiety combat situations without being labeled a coward or being court-martialed.

Conversion disorder occurs two to three times more often in women than in men (APA  2013 ). It can develop at any age but most commonly occurs between early adolescence and early adulthood (Maldonado & Spiegel,  2001 ). It generally has a rapid onset after a significant stressor and often resolves within 2 weeks if the stressor is removed, although it commonly recurs. In many other cases, however, it has a more chronic course. Like most other somatic symptom disorders, conversion disorder frequently occurs along with other disorders, especially major depression, anxiety disorders, and other forms of somatic symptom or dissociative conditions.

RANGE OF CONVERSION DISORDER SYMPTOMS

The range of symptoms for conversion disorder is practically as diverse as it is for physically based ailments. In describing the clinical picture in conversion disorder, it is useful to think in terms of four categories of symptoms: (1) sensory, (2) motor, (3) seizures, and (4) a mixed presentation of the first three categories (APA,  2013 ).

Sensory Symptoms or Deficits Conversion disorder can involve almost any sensory modality, and it can often be diagnosed as a conversion disorder because symptoms in the affected area are inconsistent with how known anatomical sensory pathways operate. Today the sensory symptoms or deficits are most often in the visual system (especially blindness and tunnel vision), in the auditory system (especially deafness), or in the sensitivity to feeling (especially the anesthesias). In the anesthesias, the person loses her or his sense of feeling in a part of the body. One of the most common is glove anesthesia, in which the person cannot feel anything on the hand in the area where gloves are worn, although the loss of sensation usually makes no anatomical sense.

With conversion blindness, the person reports that he or she cannot see and yet can often navigate about a room without bumping into furniture or other objects. With conversion deafness, the person reports not being able to hear and yet orients appropriately upon “hearing” his or her own name. Such observations lead to obvious questions: In conversion blindness (and deafness), can affected people actually not see (or hear), or is the sensory information received but screened from consciousness? In general, the evidence supports the idea that the sensory input is registered but is somehow screened from explicit conscious recognition (explicit perception).

Motor Symptoms or Deficits Motor conversion reactions also cover a wide range of symptoms (e.g., Maldonado & Spiegel,  2001 ; see also Stone et al., 2010). For example, conversion paralysis is usually confined to a single limb such as an arm or a leg, and the loss of function is usually selective for certain functions. For example, a person may not be able to write but may be able to use the same muscles for scratching, or a person may not be able to walk most of the time but may be able to walk in an emergency such as a fire where escape is important. The most common speech-related conversion disturbance is aphonia, in which a person is able to talk only in a whisper although he or she can usually cough in a normal manner. (In true, organic laryngeal paralysis, both the cough and the voice are affected.) Another common motor symptom, called globus hystericus, is difficulty swallowing or the sensation of a lump in the throat (Finkenbine & Miele,  2004 ).

Seizures Conversion seizures, another relatively common form of conversion symptom, involve pseudoseizures, which resemble epileptic seizures in some ways but can usually be fairly well differentiated via modern medical technology (Bowman & Markand,  2005 ; Stonnington et al.,  2006 ). For example, patients with pseudoseizures do not show any EEG abnormalities and do not show confusion and loss of memory afterward, as patients with true epileptic seizures do. Moreover, patients with conversion seizures often show excessive thrashing about and writhing not seen with true seizures, and they rarely injure themselves in falls or lose control over their bowels or bladder, as patients with true seizures frequently do.

The following case of conversion disorder clearly shows how “functional” a conversion disorder may be in the overall life circumstances of a patient despite its exacting a certain cost in illness or disability.

A Wife with “Fits” Mrs. Chatterjee, a 26-year-old patient, attends a clinic in New Delhi, India, with complaints of “fits” for the last 4 years. The “fits” are always sudden in onset and usually last 30 to 60 minutes. A few minutes before a fit begins, she knows that it is imminent, and she usually goes to bed. During the fits she becomes unresponsive and rigid throughout her body, with bizarre and thrashing movements of the extremities. Her eyes close and her jaw is clenched, and she froths at the mouth. She frequently cries and sometimes shouts abuses. She is never incontinent of urine or feces, nor does she bite her tongue. After a “fit” she claims to have no memory of it. These episodes recur about once or twice a month. She functions well between the episodes.

Both the patient and her family believe that her “fits” are evidence of a physical illness and are not under her control. However, they recognize that the fits often occur following some stressor such as arguments with family members or friends …. She is described by her family as being somewhat immature but “quite social” and good company. She is self-centered, she craves attention from others, and she often reacts with irritability and anger if her wishes are not immediately fulfilled. On physical examination, Mrs. Chatterjee was found to have mild anemia but was otherwise healthy. A mental status examination did not reveal any abnormality … and her memory was normal. An electroencephalogram showed no seizure activity.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 469–70). Washington, DC. (Copyright © 2002). American Psychiatric Association.

IMPORTANT ISSUES IN DIAGNOSING CONVERSION DISORDER

Because the symptoms in conversion disorder can simulate a variety of medical conditions, accurate diagnosis can be extremely difficult. It is crucial that a person with suspected conversion symptoms receive a thorough medical and neurological examination. Unfortunately, however, misdiag-noses can still occur. Nevertheless, as medical tests (especially brain imaging) have become increasingly sophisticated, the rate of misdiagnoses has declined substantially from in the past, with estimates of misdiagnoses in the 1990s at only 4 percent down from nearly 30 percent in the 1950s (e.g., Stone et al.,  2005 ).

Several other criteria are also commonly used for distinguishing between conversion disorders and true neurological disturbances:

·  • The frequent failure of the dysfunction to conform clearly to the symptoms of the particular disease or disorder simulated. For example, little or no wasting away or atrophy of a “paralyzed” limb occurs in conversion paralyses, except in rare and long-standing cases. image7

Virtually all the symptoms of conversion disorder can be temporarily reduced or reproduced by hypnotic suggestion.

·  • The selective nature of the dysfunction. As already noted, in conversion blindness the affected individual does not usually bump into people or objects, and “paralyzed” muscles can be used for some activities but not others.

·  • Under hypnosis or narcosis (a sleeplike state induced by drugs), the symptoms can usually be removed, shifted, or re-induced at the suggestion of the therapist. Similarly, a person abruptly awakened from a sound sleep may suddenly be able to use a “paralyzed” limb.

TREATMENT OF CONVERSION DISORDER

Our knowledge of how best to treat conversion disorder is very limited because few well-controlled studies have yet been conducted (e.g., Bowman & Markand,  2005 ; Looper & Kirmayer,  2002 ). However, it is known that some hospitalized patients with motor conversion symptoms have been successfully treated with a behavioral approach in which specific exercises are prescribed in order to increase movement or walking, and then reinforcements (e.g., praise and gaining privileges) are provided when patients show improvements. Any reinforcements of abnormal motor behaviors are removed in order to eliminate any sources of secondary gain. In one small study using this kind of treatment for 10 patients, all had regained their ability to move or walk in an average of 12 days, and for seven of the nine patients available at approximately 2-year follow-up, the improvements had been maintained (Speed,  1996 ). At least one study has also used cognitive-behavior therapy to successfully treat psychogenic seizures (LaFrance et al.,  2009 ). Some studies have used hypnosis combined with other problem-solving therapies, and there are some suggestions that hypnosis, or adding hypnosis to other therapeutic techniques, can be useful (Looper & Kirmayer,  2002 ; Moene et al.,  2003 ).

Distinguishing Somatization, Pain, and Conversion Disorders from Malingering and Factitious Disorder

DSM-5 criteria for: Factitious Disorder

Factitious Disorder Imposed on Self

·  A. Falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception.

·  B. The individual presents himself or herself to others as ill, impaired, or injured.

·  C. The deceptive behavior is evident even in the absence of obvious external rewards.

·  D. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Earlier we mentioned that the DSM distinguishes between malingering and factitious disorder on the basis of the feigning person’s apparent goals. Malingering is diagnosed if the person is intentionally producing or grossly exaggerating physical symptoms and is motivated by external incentives such as avoiding work or obtaining financial compensation. Factitious disorder is diagnosed if the person intentionally produces psychological or physical symptoms, the person’s goal being simply to obtain and maintain the personal benefits that playing the “sick role” (even undergoing repeated hospitalizations) may provide, including the attention and concern of family and medical personnel. In factitious disorder, frequently these patients surreptitiously alter their own physiology—for example, by taking drugs—in order to simulate various real illnesses. Indeed, they may be at risk for serious injury or death and may even need to be committed to an institution for their own protection. The World Around Us box above describes a particularly pathological variation on this theme. In the past, severe and chronic forms of factitious disorder with physical symptoms were called “Munchausen’s syndrome,” where the general idea was that the person had some kind of “hospital addiction” or a “professional patient” syndrome.

the WORLD around us: Factitious Disorder Imposed on Another (Munchausen’s Syndrome by Proxy)

In a somewhat bizarre variant of factitious disorder called factitious disorder imposed on another (or Munchausen’s syndrome by proxy), the person seeking medical help or consulting a mental health professional has intentionally produced a medical or psychiatric illness (or appearance of an illness) in another person who is under his or her care (usually a child; e.g., Pankratz,  2006 ). In a typical instance, a mother presents her own child for treatment of a medical condition she has deliberately caused, disclaiming any knowledge of its origin. Of course, the health of such victims is often seriously endangered by this repeated abuse, and the intervention of social service agencies or law enforcement is sometimes necessary. In as many as 10 percent of cases, this atypical form of child abuse may lead to a child’s death (Hall et al.,  2000 ).

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Over a period of 20 months, Jennifer, 8, shown here with her mother, Kathy Bush, was taken to the hospital more than 130 times, underwent 40 surgeries, and amassed over $3 million in medical expenses. Doctors and nurses testified that Jennifer’s condition always worsened after her mother visited her daughter at the hospital behind closed doors. In addition, Jennifer’s health had significantly improved since being removed from her mother’s care. The jury was convinced that Kathy Bush was responsible for causing Jennifer’s illnesses. Bush was arrested and diagnosed with Munchausen’s syndrome by proxy.

This disorder may be indicated when the victim’s clinical presentation is atypical, when lab results are inconsistent with each other or with recognized diseases, or when there are unduly frequent returns or increasingly urgent visits to the same hospital or clinic. The perpetrators (who often have extensive medical knowledge) tend to be highly resistant to admitting the truth (McCann,  1999 ), and it has been estimated that the average length of time to confirm the diagnosis is 14 months (Rogers,  2004 ). If the perpetrator senses that the medical staff is suspicious, he or she may abruptly terminate contact with that facility, only to show up at another one to begin the entire process anew. Compounding the problem of detection is the fact that health care professionals who realize they have been duped may be reluctant to acknowledge their fallibility for fear of legal action. Misdiagnosing the disorder when the parent is in fact innocent can also lead to legal difficulties for the health care professionals (McNicholas et al.,  2000 ; Pankratz,  2006 ). One technique that has been used with considerable success is covert video surveillance of the mother and child during hospitalizations. In one study, 23 of 41 suspected cases were finally determined to have factitious disorder by proxy, and in 56 percent of those cases video surveillance was essential to the diagnosis (Hall et al.,  2000 ).

It is sometimes possible to distinguish between a conversion (or other somatic symptom) disorder and malingering, or factitiously “sick-role-playing,” with a fair degree of confidence, but in other cases it is more difficult to make the correct diagnosis. Persons engaged in malingering (for which there are no formal diagnostic criteria) and those who have factitious disorder are consciously perpetrating frauds by faking the symptoms of diseases or disabilities, and this fact is often reflected in their demeanor. In contrast, individuals with conversion disorders (as well as with other somatic symptom disorders) are not consciously producing their symptoms, feel themselves to be the “victims of their symptoms,” and are very willing to discuss them, often in excruciating detail (Maldonado & Spiegel,  2001 , p. 109). When inconsistencies in their behaviors are pointed out, they are usually unperturbed. Any secondary gains they experience are byproducts of the conversion symptoms themselves and are not involved in motivating the symptoms. On the other hand, persons who are feigning symptoms are inclined to be defensive, evasive, and suspicious when asked about them; they are usually reluctant to be examined and slow to talk about their symptoms lest the pretense be discovered. Should inconsistencies in their behaviors be pointed out, deliberate deceivers as a rule immediately become more defensive. Thus conversion disorder and deliberate faking of illness are considered distinct patterns.

in review

·  ● What are the primary characteristics of hypochondriasis, and how does the cognitive-behavioral viewpoint explain their occurrence?

·  ● What are the symptoms of somatization disorder and of pain disorder?

·  ● What are sources of primary and secondary gains involved in conversion disorders, and how is conversion disorder distinguished from malingering and from factitious disorder?

Dissociative Disorders

Dissociative disorders  are a group of conditions involving disruptions in a person’s normally integrated functions of consciousness, memory, identity, or perception (APA,  2013 ; Spiegel et al.,  2013 ). Included here are some of the more dramatic phenomena in the entire domain of psychopathology: people who cannot recall who they are or where they may have come from, and people who have two or more distinct identities or personality states that alternately take control of the individual’s behavior.

The term  dissociation  refers to the human mind’s capacity to engage in complex mental activity in channels split off from, or independent of, conscious awareness (Kihlstrom,  1994  2001  2005 ). The concept of dissociation was first promoted over a century ago by the French neurologist Pierre Janet (1859–1947). We all dissociate to a degree some of the time. Mild dissociative symptoms occur when we daydream or lose track of what is going on around us, when we drive miles beyond our destination without realizing how we got there, or when we miss part of a conversation we are engaged in. As these everyday examples suggest, there is nothing inherently pathological about dissociation itself. Dissociation only becomes pathological when the dissociative symptoms are “perceived as disruptive, invoking a loss of needed information, as producing discontinuity of experience” or as “recurrent, jarring involuntary intrusions into executive functioning and sense of self” (Spiegel et al., 2011, p. E19).

Much of the mental life of all human beings involves automatic nonconscious processes that are to a large extent autonomous with respect to deliberate, self-aware direction and monitoring. Such unaware processing extends to the areas of implicit memory and implicit perception, where it can be demonstrated that all persons routinely show indirect evidence of remembering things they cannot consciously recall ( implicit memory ) and respond to sights or sounds as if they had perceived them (as in conversion blindness or deafness) even though they cannot report that they have seen or heard them ( implicit perception ; Kihlstrom,  2001  2005 ; Kihlstrom et al.,  1993 ). As we learned in  Chapter 3 , the general idea of unconscious mental processes has been embraced by psychodynamically oriented clinicians for many years. But only in the past 30 years has it also become a major research area in the field of cognitive psychology (though without any of the psychodynamic implications for why so much of our mental activity is unconscious).

In people with dissociative disorders, however, this normally integrated and well-coordinated multichannel quality of human cognition becomes much less coordinated and integrated. When this happens, the affected person may be unable to access information that is normally in the forefront of consciousness, such as his or her own personal identity or details of an important period of time in the recent past. That is, the normally useful capacity of maintaining ongoing mental activity outside of awareness appears to be subverted, sometimes for the purpose of managing severe psychological threat. When that happens, we observe the pathological dissociative symptoms that are the cardinal characteristic of dissociative disorders. Like somatic symptom disorders, dissociative disorders appear mainly to be ways of avoiding anxiety and stress and of managing life problems that threaten to overwhelm the person’s usual coping resources. Both types of disorders also enable the individual to deny personal responsibility for his or her “unacceptable” wishes or behavior. In the case of DSM-defined dissociative disorders, the person avoids the stress by pathologically dissociating—in essence, by escaping from his or her own autobiographical memory or personal identity. The DSM-5 recognizes several types of pathological dissociation. These include depersonalization/derealization disorder, dissociative amnesia, dissociative fugue (a subtype of dissociative amnesia) and dissociative identity disorder.

Depersonalization/Derealization Disorder

Two of the more common kinds of dissociative symptoms are derealization and depersonalization. We mentioned these in  Chapter 6  because they sometimes occur during panic attacks. In  derealization  one’s sense of the reality of the outside world is temporarily lost, and in  depersonalization  one’s sense of one’s own self and one’s own reality is temporarily lost. As many as 50-74 percent of us have such experiences in mild form at least once in our lives, usually during or after periods of severe stress, sleep deprivation, or sensory deprivation (e.g., Khazaal et al.,  2005 ; Reutens et al.,  2010 ). But when episodes of depersonalization or derealization become persistent and recurrent and interfere with normal functioning,  depersonalization /  derealization disorder  may be diagnosed.

In this disorder, people have persistent or recurrent experiences of feeling detached from (and like an outside observer of) their own bodies and mental processes. They may even feel they are, for a time, floating above their physical bodies, which may suddenly feel very different—as if drastically changed or unreal. During periods of depersonalization, unlike during psychotic states, reality testing remains intact. The related experience of derealization, in which the external world is perceived as strange and new in various ways, may also occur. As one leader in the field described it, in both states “the feeling puzzles the experiencers: the changed condition is perceived as unreal, and as discontinuous with his or her previous ego-states. The object of the experience, self (in depersonalization) or world (in derealization), is commonly described as isolated, lifeless, strange, and unfamiliar; oneself and others are perceived as ‘automatons,’ behaving mechanically, without initiative or self-control” (Kihlstrom,  2001 , p. 267). Often people also report feeling as though they are living in a dream or movie (Maldonado et al.,  2002 ). In keeping with such reports, research has shown that emotional experiences are attenuated or reduced during depersonalization—both at the subjective level and at the level of neural and autonomic activity that normally accompanies emotional responses to threatening or unpleasant emotional stimuli (Lemche et al.,  2007 ; Phillips & Sierra,  2003 ; Stein & Simeon,  2009 ). After viewing an emotional video clip, participants with depersonalization disorder showed higher levels of subjective and objective memory fragmentation than controls (Giesbrecht et al.,  2010 ). Memory fragmentation is marked by difficulties forming an accurate or coherent narrative sequence of events, which is consistent with earlier research suggesting that time distortion is a key element of the experience of depersonalization (Simeon et al.,  2008 ).

DSM-5 criteria for: Depersonalization/Derealization Disorder

·  A. The presence of persistent or recurrent experiences of depersonalization, derealization, or both:

·  1. Depersonalization: Experiences of unreality, detachment, or being an outside observer with respect to one’s thoughts, feelings, sensations, body, or actions (e.g., perceptual alterations, distorted sense of time, unreal or absent self, emotional and/or physical numbing).

·  2. Derealization: Experiences of unreality or detachment with respect to surroundings (e.g., individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, or visually distorted).

·  B. During the depersonalization or derealization experiences, reality testing remains intact.

·  C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  D. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, medication) or another medical condition (e.g., seizures).

·  E. The disturbance is not better explained by another mental disorder, such as schizophrenia, panic disorder, major depressive disorder, acute stress disorder, posttraumatic stress disorder, or another dissociative disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

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Dissociative Disorders And Trauma Assignment help

People with derealization symptoms experience the world as hazy and indistinct.

A number of researchers have noted elevated rates of comorbid anxiety and mood disorders as well as avoidant, borderline, and obsessive-compulsive personality disorders (e.g., Hunter et al.,  2003 ; Mula et al.,  2007 ; Reutens et al.,  2010 ). Another study of over 200 cases found that the disorder had an average age of onset of 23. Moreover, in nearly 80 percent of cases, the disorder has a fairly chronic course (with little or no fluctuation in intensity; Baker, Hunter, et al.,  2003 ).

The case of the foggy student below is fairly typical.

A Foggy Student A 20-year-old male college student sought psychiatric consultation because he was worried that he might be going insane. For the past 2 years he had experienced increasingly frequent episodes of feeling “outside” himself. These episodes were accompanied by a sense of deadness in his body. In addition, during these periods he was uncertain of his balance and frequently stumbled into furniture; this was more apt to occur in public, especially if he was somewhat anxious. During these episodes he felt a lack of easy, natural control of his body, and his thoughts seemed “foggy” as well ….

The patient’s subjective sense of lack of control was especially troublesome, and he would fight it by shaking his head and saying “stop” to himself. This would momentarily clear his mind and restore his sense of autonomy, but only temporarily, as the feelings of deadness and of being outside himself would return. Gradually, over a period of several hours, the unpleasant experiences would fade …. At the time the patient came for treatment, he was experiencing these symptoms about twice a week, and each incident lasted from 3 to 4 hours. On several occasions the episodes had occurred while he was driving his car and was alone; worried that he might have an accident, he had stopped driving unless someone accompanied him.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 270–71). Washington, DC. (Copyright © 2002). American Psychiatric Association.

The lifetime prevalence of depersonalization/derealization disorder is unknown but has been estimated at 1 to 2 percent of the population (Reutens et al.,  2010 ). Moreover, occasional depersonalization/derealization symptoms are not uncommon in a variety of other disorders such as schizophrenia, borderline personality disorder, panic disorder, acute stress disorder, and posttraumatic stress disorder (PTSD) (Hunter et al.,  2003 ). Although severe depersonalization/derealization symptoms can be quite frightening and may make the victim fear imminent mental collapse, such fears are usually unfounded. Sometimes, however, feelings of depersonalization are clearly early manifestations of impending decompensation and the development of psychotic states ( Chapter 13 ). In either case, professional assistance in dealing with the precipitating stressors and in reducing anxiety may be helpful. Unfortunately, however, as of yet there are no clearly effective treatments—either through medication or psychotherapy.

Dissociative Amnesia and Dissociative Fugue

Retrograde amnesia is the partial or total inability to recall or identify previously acquired information or past experiences; by contrast, anterograde amnesia is the partial or total inability to retain new information (Gilboa et al.,  2006 ; Kapur,  1999 ). Persistent amnesia may occur in several disorders, such as dissociative amnesia and dissociative fugue. It may also result from traumatic brain injury or diseases of the central nervous system. If the amnesia is caused by brain pathology, it most often involves failure to retain new information and experiences (anterograde amnesia). That is, the information contained in experience is not registered and does not enter memory storage (Kapur,  1999 ).

On the other hand,  dissociative amnesia  is usually limited to a failure to recall previously stored personal information (retrograde amnesia) when that failure cannot be accounted for by ordinary forgetting. The gaps in memory most often occur following intolerably stressful circumstances—wartime combat conditions, for example, or catastrophic events such as serious car accidents, suicide attempts, or violent outbursts (Maldonado & Spiegel,  2007 ; Spiegel et al., 2011). In this disorder, apparently forgotten personal information is still there beneath the level of consciousness, as sometimes becomes apparent in interviews conducted under hypnosis or narcosis (induced by sodium amytal, or so-called truth serum) and in cases where the amnesia spontaneously clears up.  image10 Watch the Video Sharon: Dissociative Amnesia on MyPsychLab

Amnesic episodes usually last between a few days and a few years. Although many people experience only one such episode, some people have multiple episodes in their lifetimes (Maldonado & Spiegel,  2007 ; Staniloiu & Markowitsch,  2010 ). In typical dissociative amnesic reactions, individuals cannot remember certain aspects of their personal life history or important facts about their identity. Yet their basic habit patterns—such as their abilities to read, talk, perform skilled work, and so on—remain intact, and they seem normal aside from the memory deficit (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Thus the only type of memory that is affected is episodic (pertaining to events experienced) or autobiographical memory (pertaining to personal events experienced). The other recognized forms of memory—semantic (pertaining to language and concepts), procedural (how to do things), and short-term storage—seem usually to remain intact, although there is very little research on this topic (Kihlstrom,  2005 ; Kihl-strom & Schacter,  2000 ). Usually there is no difficulty encoding new information (Maldonado & Spiegel,  2007 ).

DSM-5 criteria for: Dissociative Amnesia

·  A. An inability to recall important autobiographical information, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting.

Note: Dissociative amnesia most often consists of localized or selective amnesia for a specific event or events; or generalized amnesia for identity and life history.

·  B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  C. The disturbance is not attributable to the physiological effects of a substance (e.g., alcohol or other drug of abuse, a medication) or a neurological or other medical condition (e.g., partial complex seizures, transient global amnesia, sequelae of a closed head injury/traumatic brain injury, other neurological condition).

·  D. The disturbance is not better explained by dissociative identity disorder, posttraumatic stress disorder, acute stress disorder, somatic symptom disorder, or major or mild neurocognitive disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

In rare cases a person may retreat still further from real-life problems by going into an amnesic state called a  dissociative fugue , which, as the term implies (the French word fugue means “flight”), is a defense by actual flight—a person is not only amnesic for some or all aspects of his or her past but also departs from home surroundings. This is accompanied by confusion about personal identity or even the assumption of a new identity (although the identities do not alternate as they do in dissociative identity disorder). During the fugue, such individuals are unaware of memory loss for prior stages of their life, but their memory for what happens during the fugue state itself is intact (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Their behavior during the fugue state is usually quite normal and unlikely to arouse suspicion that something is wrong. However, behavior during the fugue state often reflects a rather different lifestyle from the previous one (the rejection of which is sometimes fairly obvious). Days, weeks, or sometimes even years later, such people may suddenly emerge from the fugue state and find themselves in a strange place, working in a new occupation, with no idea how they got there. In other cases, recovery from the fugue state occurs only after repeated questioning and reminders of who they are. In either case, as the fugue state remits, their initial amnesia remits—but a new, apparently complete amnesia for their fugue period occurs. In DSM-5 dissociative fugue is considered to be a subtype of dissociative amnesia rather than a separate disorder as it was in DSM-IV.

The pattern in dissociative amnesia and dissociative fugue is essentially similar to that in conversion symptoms, except that instead of avoiding some unpleasant situation by becoming physically dysfunctional, a person unconsciously avoids thoughts about the situation or, in the extreme, leaves the scene (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Thus people experiencing dissociative amnesia and fugue are typically faced with extremely unpleasant situations from which they see no acceptable way to escape. Eventually the stress becomes so intolerable that large segments of their personalities and all memory of the stressful situations are suppressed.

Several of these aspects of dissociative fugue are illustrated in the following case.

A Middle Manager Transformed into a Short-Order Cook Burt Tate, a 42-year-old short-order cook in a small-town diner, was brought to the attention of local police following a heated altercation with another man at the diner. He gave his name as Burt Tate and indicated that he had arrived in town several weeks earlier. However, he could produce no official identification and could not tell the officers where he had previously lived and worked. Burt was asked to accompany the officers to the emergency room of a local hospital so that he might be examined ….

Burt’s physical examination was negative for evidence of recent head trauma or any other medical abnormality …. He was oriented as to current time and place, but manifested no recall of his personal history prior to his arrival in town. He did not seem especially concerned about his total lack of a remembered past ….

Meanwhile, the police … discovered that Burt matched the description of one Gene Saunders, a resident of a city some 200 miles away who had disappeared a month earlier. The wife of Mr. Saunders … confirmed the real identity of Burt, who … stated that he did not recognize Mrs. Saunders.

Prior to his disappearance, Gene Saunders, a middle-level manager in a large manufacturing firm, had been experiencing considerable difficulties at work and at home. A number of stressful work problems, including failure to get an expected promotion, the loss of some of his key staff, failure of his section to meet production goals, and increased criticism from his superior—all occurring within a brief time frame—had upset his normal equanimity. He had become morose and withdrawn at home and had been critical of his wife and children. Two days before he had left, he had had a violent argument with his 18-year-old son, who had declared his father a failure and had stormed out of the house to go live with friends.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 254–55). Washington, DC. (Copyright © 2002). American Psychiatric Association.

MEMORY AND INTELLECTUAL DEFICITS IN DISSOCIATIVE AMNESIA AND FUGUE

Unfortunately, very little systematic research has been conducted on individuals with dissociative amnesia and fugue. What is known comes largely from intensive studies of the memory and intellectual functioning of isolated cases with these disorders, so any conclusions should be considered tentative pending further study of larger samples with appropriate control groups. What can be gathered from a handful of such case studies is that these individuals’ semantic knowledge (assessed via the vocabulary subtest of an IQ test) seems to be generally intact. The primary deficit these individuals exhibit is their compromised episodic or autobiographical memory (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Indeed, several studies using brain-imaging techniques have confirmed that when people with dissociative amnesia are presented with autobiographical memory tasks, they show reduced activation in their right frontal and temporal brain areas relative to normal controls doing the same kinds of tasks (Kihlstrom,  2005 ; Markowitsch,  1999 ). In a recent review of nine cases of dissociative amnesia for which brain imaging data were available, the authors concluded there was evidence of significant changes in the brains of these patients, mostly centered on subtle loss of function in the right anterior hemisphere—changes similar to those seen in the brains of patients with organic memory loss (Staniloiu & Markowitsch,  2010 ).

However, several cases (some nearly a century old) have suggested that implicit memory is generally intact. For example, Jones (1909, as cited in Kihlstrom & Schacter,  2000 ) studied a patient with dense amnesia and found that although he could not remember his wife’s or daughter’s names, when asked to guess what names might fit them, he produced their names correctly. In a more contemporary case (Lyon, 1985, as cited in Kihlstrom & Schacter,  2000 ), a patient who could not retrieve any autobiographical information was asked to dial numbers on a phone randomly. Without realizing what he was doing, he dialed his mother’s phone number, which then led to her identifying him. In one particularly fascinating contemporary case of dissociative fugue, Glisky and colleagues ( 2004 ) describe a German man who had come to work in the United States several months before he had experienced a traumatic incident in which he had been robbed and shot. After the trauma, he wandered along unfamiliar streets for an unknown period of time. Finally, he stopped at a motel and asked if the police could be called because he did not know who he was (and had no ID because he’d been robbed) and could not recall any personal details of his life. He spoke English (with a German accent) but could not speak German and did not respond to instructions in German (which he denied that he spoke). In spite of his extensive loss of autobiographical memory (and the German language), when given a variety of memory tasks, he showed intact implicit memory. Especially striking was his ability to learn German–English word pairs, which he learned much faster than did normal controls, suggesting implicit knowledge of German even though he had no conscious knowledge of it.

Some of these memory deficits in dissociative amnesia and fugue have been compared to related deficits in explicit perception that occur in conversion disorders. This has convinced many people that conversion disorder should be classified with dissociative disorders rather than with somatic symptom disorders. This issue is discussed in more detail in the Thinking Critically About DSM-5 box below.

Dissociative Identity Disorder (Did)

DSM-5 THINKING CRITICALLY about DSM-5: Where Does Conversion Disorder Belong?

Starting with Freud and Janet, and for a large portion of the twentieth century prior to the publication of DSM-III in 1980, conversion disorders were classified together with dissociative disorders as subtypes of hysteria. When it was determined that DSM-III would rely heavily on overt behavioral symptoms rather than on presumed underlying etiology (namely, repressed anxiety) for classifying disorders, the decision was made to include conversion disorder with the other somatic symptom disorders. This was because its symptoms were physical ones with no demonstrable medical basis. However, as Kihlstrom ( 1994  2001  2005 ) and others have pointed out, this ignores some very important differences between conversion disorders and other somatic symptom disorders. The most important overall difference is that conversion symptoms (but not those of the other somatoform disorders) are nearly always pseudoneurological in nature (blindness, paralysis, anesthesias, deafness, seizures, etc.), mimicking some true neurological syndromes, just as most of the dissociative disorders do.

The disorders we currently classify as dissociative disorders (such as dissociative amnesia and DID) involve disruptions in explicit memory for events that have occurred, or who or what one’s identity is, or both. However, it is clear that events occurring during a period of amnesia or in the presence of one identity are indeed registered in the nervous system because they influence behavior indirectly even when the person cannot consciously recollect them (i.e., implicit memory remains at least partially intact in dissociative disorders). Similarly, Kihlstrom and others have argued that the conversion disorders involve disruptions in explicit perception and action. That is, people with conversion disorders have no conscious recognition that they can see or hear or feel, or no conscious knowledge that they can walk or talk or feel. However, patients with conversion disorder can see, hear, feel, or move when tricked into doing so or when indirect physiological or behavioral measures are used (see Janet,  1901  1907 ; Kihlstrom,  1994  2001  2005 ). Thus Kihlstrom ( 1994  2001  2005 ) and others made a compelling argument that in future editions, the term conversion disorder should be dropped and the sensory and motor types of the syndrome should be reclassified as forms of dissociative disorders. This way, the central feature of all dissociative disorders would be a disruption of the normally integrated functions of consciousness (memory, perception, and action). Such a proposal is also consistent with observations that dissociative symptoms and disorders are quite common in patients with conversion disorder (e.g., Sar et al.,  2004 ). This proposal was seriously considered and heavily debated by the DSM-5 task force. In the end, the proponents for moving conversion disorder into the dissociative disorders category did not succeed and in DSM-5 conversion disorder (at least for now) is still listed as a somatic symptom disorder.

Dissociative identity disorder (DID) , formerly known as multiple personality disorder is a dramatic dissociative disorder in which a patient manifests two or more distinct identities that alternate in some way in taking control of behavior. There is also an inability to recall important personal information that cannot be explained by ordinary forgetting. Each identity may appear to have a different personal history, self-image, and name, although there are some identities that are only partially distinct and independent from other identities. In most cases the one identity that is most frequently encountered and carries the person’s real name is the  host identity . Also in most cases, the host is not the original identity, and it may or may not be the best-adjusted identity. The  alter identities  may differ in striking ways involving gender, age, handedness, handwriting, sexual orientation, prescription for eyeglasses, predominant affect, foreign languages spoken, and general knowledge. For example, one alter may be carefree, fun-loving, and sexually provocative, and another alter quiet, studious, serious, and prudish. Needs and behaviors inhibited in the primary or host identity are usually liberally displayed by one or more alter identities. Certain roles such as a child and someone of the opposite sex are extremely common.

Much of the reason for abandoning the older diagnostic term multiple personality disorder in favor of DID was the growing recognition that it had misleading connotations, suggesting multiple occupancy of space, time, and people’s bodies by differing, but fully organized and coherent, “personalities.” In fact, alters are not in any meaningful sense personalities but rather reflect a failure to integrate various aspects of a person’s identity, consciousness, and memory (Spiegel, 2006). The term DID better captures this. Indeed Spiegel (one prominent theorist in this area) has argued that “the problem is not having more than one personality, it is having less than one” (Spiegel, 2006, p. 567).

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Chris Sizemore was the inspiration for the book and movie Three Faces of Eve, which explore her multiple personality disorder (now known as DID). After her recovery, Sizemore worked as an advocate for the mentally ill.

DSM-5 criteria for: Dissociative Identity Disorder

·  A. Disruption of identity characterized by two or more distinct personality states, which may be described in some cultures as an experience of possession. The disruption in identity involves marked discontinuity in sense of self and sense of agency, accompanied by related alterations in affect, behavior, consciousness, memory, perception, cognition, and/or sensory-motor functioning. These signs and symptoms may be observed by others or reported by the individual.

·  B. Recurrent gaps in the recall of everyday events, important personal information, and/or traumatic events that are inconsistent with ordinary forgetting.

·  C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.

Note: In children, the symptoms are not better explained by imaginary playmates or other fantasy play.

·  E. The symptoms are not attributable to the physiological effects of a substance (e.g., blackouts or chaotic behavior during alcohol intoxication) or another medical condition (e.g., complex partial seizures).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Alter identities take control at different points in time, and the switches typically occur very quickly (in a matter of seconds), although more gradual switches can also occur. When switches occur in people with DID, it is often easy to observe the gaps in memories for things that have happened—often for things that have happened to other identities. But this amnesia is not always symmetrical; that is, some identities may know more about certain alters than do other identities. Sometimes one submerged identity gains control by producing hallucinations (such as a voice inside the head giving instructions). In sum, DID is a condition in which normally integrated aspects of memory, identity, and consciousness are no longer integrated. Additional symptoms of DID include depression, self-mutilation, frequent suicidal ideation and attempts, erratic behavior, headaches, hallucinations, posttraumatic symptoms, and other amnesic and fugue symptoms (APA,  2013 ; Maldonado et al.,  2002 ). Depressive disorders, PTSD, substance-use disorders, and borderline personality disorder are the most common comorbid diagnoses (Maldonado & Spiegel,  2007 ). One recent study found that among patients with diagnoses of DID, the average number of comorbid diagnoses (based on structured diagnostic interviews) was five, with PTSD being the most common (Rodewald et al.,  2011 ).

DID usually starts in childhood, although most patients are in their teens, 20s, or 30s at the time of diagnosis (Maldonado & Spiegel,  2007 ). Approximately three to nine times more females than males are diagnosed as having the disorder, and females tend to have a larger number of alters than do males (Maldonado & Spiegel,  2007 ). Some believe that this pronounced gender discrepancy is due to the much greater proportion of childhood sexual abuse among females than among males (see  Chapter 12 ), but this is a highly controversial point.

Many of these features are illustrated in the case of Mary Kendall below.

the WORLD around us: DID, Schizophrenia, and Split Personality: Clearing Up the Confusion

The general public has long been confused by the distinction between DID and schizophrenia. It is not uncommon for people diagnosed with schizophrenia to be referred to as having a “split personality.” We have even heard people say such things as, “I’m a bit schizophrenic on this issue” to mean that they have more than one opinion about it!

Although this misuse of the term split personality actually began among psychiatric professionals, today it reflects the public’s general misunderstanding of schizophrenia, which does not involve a “split” or “Jekyll and Hyde” personality at all. The original confusion may have stemmed from the term schizophrenia, which was first coined by a Swiss psychiatrist named Bleuler. Schizien is German for “split,” and phren is the Greek root for “mind.” The notion that schizophrenia is characterized by a split mind or personality may have arisen this way (see McNally,  2007 , for a historical review of how this confusion arose).

However, this is not at all what Bleuler intended the word schizophrenia to mean. Rather, Bleuler was referring to the splitting of the normally integrated associative threads of the mind—links between words, thoughts, emotions, and behavior. Splits of this kind result in thinking that is not goal-directed or efficient, which in turn leads to the host of other difficulties known to be associated with schizophrenia.

It is very important to remember that people diagnosed with schizophrenia do not have multiple distinct identities that alternately take control over their mind and behavior. They may have a delusion and believe they are someone else, but they do not show the changes in identity accompanied by changes in tone of voice, vocabulary, and physical appearance that are often seen when identities “switch” in DID. Furthermore, people with DID (who are probably closer to the general public’s notion of “split personality”) do not exhibit such characteristics of schizophrenia as disorganized behavior, hallucinations coming from outside the head, and delusions, or incoherent and loose associations (e.g., Kluft,  2005 ).

Mary and Marian Mary, a 35-year-old divorced social worker, had … in her right forearm and hand … chronic pain. Medical management of this pain had proved problematic, and it was decided to teach her self-hypnosis as a means whereby she might control it. She proved an excellent hypnotic subject and quickly learned effective pain control techniques.

Her hypnotist/trainer, a psychiatrist, describes Mary’s life in rather unappealing terms. She is said to be competent professionally but has an “arid” personal and social life …. She spends most of her free time doing volunteer work in a hospice ….

In the course of the hypnotic training, Mary’s psychiatrist discovered that she seemed to have substantial gaps in her memory. One phenomenon in particular was very puzzling: She reported that she could not account for what seemed an extraordinary depletion of the gasoline in her car’s tank. She would arrive home from work with a nearly full tank, and by the following morning as she began her trip to work would notice that the tank was now only half-full. When it was advised that she keep track of her odometer readings, she discovered that on many nights on which she insisted she’d remained at home the odometer showed significant accumulations of up to 100 miles. The psychiatrist, by now strongly suspecting that Mary had a dissociative disorder, also established that there were large gaps in her memories of childhood. He shifted his focus to exploring the apparently widespread dissociative difficulties.

In the course of one of the continuing hypnotic sessions, the psychiatrist again asked about “lost time,” and was greeted with a response in a wholly different voice tone that said, “It’s about time you knew about me.” Marian, an apparently well-established alter identity, went on to describe the trips she was fond of taking at night … Marian was an extraordinarily abrupt and hostile “person,” the epitome in these respects of everything the compliant and self-sacrificing Mary was not. Marian regarded Mary with unmitigated contempt, and asserted that “worrying about anyone but yourself is a waste of time.”

In due course some six other alter identities emerged …. There was notable competition among the alters for time spent “out,” and Marian was often so provocative as to frighten some of the more timid others, which included a 6-year-old child ….

Mary’s history, as gradually pieced together, included memories of physical and sexual abuse by her father as well as others during her childhood …. Her mother was described … as having abdicated to a large extent the maternal role, forcing Mary from a young age to assume these duties in the family.

Four years of subsequent psychotherapy resulted in only modest success in achieving a true “integration” of these diverse trends in Mary Kendall’s selfhood.

Source: Adapted with permission from DSM-IV-TR Casebook (pp. 56–57). Washington, DC. (Copyright © 2002). American Psychiatric Association.

The number of alter identities in DID varies tremendously and has increased over time (Maldonado & Spiegel,  2007 ). One early review of 76 classic cases reported that two-thirds of these cases had only two personalities and most of the rest had three (Taylor & Martin,  1944 ). More recent estimates are that about 50 percent now show over 10 identities with some respondents claiming as many as a hundred. This historical trend of increasing multiplicity suggests the operation of social factors, perhaps through the encouragement of therapists, as we discuss below (e.g., Kihlstrom,  2005 ; Lilienfeld et al.,  1999 ; Piper & Merskey,  2004a  2004b ). Another recent trend is that many of the reported cases of DID now include more unusual and even bizarre identities than in the past (such as being an animal) and more highly implausible backgrounds (e.g., ritualized satanic abuse in childhood).

PREVALENCE—WHY HAS DID BEEN INCREASING?

Owing to their dramatic nature, cases of DID receive a great deal of attention and publicity in fiction, television, and motion pictures. But in fact, until relatively recently, DID was extremely rare—or at least rarely diagnosed—in clinical practice. Prior to 1979, only about 200 cases could be found in the entire psychological and psychiatric literature worldwide. By 1999, however, over 30,000 cases had been reported in North America alone (Ross,  1999 ), although as we will discuss later, many researchers believe that this is a gross overestimate (e.g., Piper & Merskey,  2004b ). Because their diagnosed occurrence in both clinical settings and in the general population increased enormously in recent years, prevalence estimates in the general population vary. One study of 658 people in upstate New York estimated a 1.5 percent prevalence (Johnson et al.,  2006 ), but it is possible that no such estimates are valid, given how hard it is to make this diagnosis reliably. (For example, recall that Mary’s DID was uncovered only in the course of hypnotic sessions for pain management.)

Many factors probably have contributed to the drastic increase in the reported prevalence of DID (although in an absolute sense it is still very rare, and most practicing psychotherapists never see a person with DID in their entire careers). For example, the number of cases began to rise in the 1970s after the publication of Flora Rhea Schreiber’s Sybil ( 1973 ) This increased public awareness of the condition. (Ironically, however, the case has now been thoroughly discredited (see Borch-Jacobsen,  1997 ; Paris,  2012 ; Rieber,  1999 ). At about the same time, the diagnostic criteria for DID (then called multiple personality disorder) were clearly specified for the first time with the publication of DSM-III in 1980. This seems to have led to increased acceptance of the diagnosis by clinicians, which may have encouraged reporting of it in the literature. Clinicians were traditionally (and often still are today) somewhat skeptical of the astonishing behavior these patients often display.

Another reason why the diagnosis was made more frequently after 1980 is that the diagnostic criteria for schizophrenia were tightened in DSM-III. People who had perhaps been inappropriately diagnosed with schizophrenia could now receive the more appropriate diagnosis of multiple personality disorder. In addition, beginning in about 1980, prior scattered reports of instances of childhood abuse in the histories of adult patients began building into what would become a crescendo. As we will see later, many controversies arose regarding how to interpret such findings, but it is definitely true that these reports of abuse in patients with DID drew a great deal of attention to this disorder, which in turn may have increased the rate at which it was being diagnosed.

Finally, it is almost certain that some of the increase in the prevalence of DID is artifactual and has occurred because some therapists looking for evidence of DID in certain patients may suggest the existence of alter identities (especially when the person is under hypnosis and very suggestible; e.g., Kihlstrom,  2005 ; Piper & Merskey,  2004b ). The therapist may also subtly reinforce the emergence of new identities by showing great interest in these new identities. Nevertheless, such factors cannot account for all cases of diagnosed DID, which has been observed in most parts of the world, even where there is virtually no personal or professional knowledge of DID, including rural Turkey (Akyuz et al.,  1999 ; see also Maldonado & Spiegel,  2007 ) and Shanghai, China (Xiao et al.,  2006 ).

EXPERIMENTAL STUDIES OF DID

Much of what is known about DID comes from patients’ self-reports and from therapists’ or researchers’ clinical observations. Indeed, only a small number of experimental studies of people with DID have been conducted to corroborate clinical observations. Moreover, most of these studies have been conducted on only one or a few cases, although very recently a few larger studies have been done that include appropriate control groups (e.g., Dorahy et al.,  2005 ; Huntjens et al.,  2003  2007 ). In spite of such shortcomings, most of the findings from these studies are generally consistent with one another and reveal some very interesting features of DID.

The primary focus of these studies has been to determine the nature of the amnesia that exists between different identities. As we have already noted, most people with DID have at least some identities that seem completely unaware of the existence and experiences of certain alter identities, although other identities may be only partially amnesic of some alters (e.g., Elzinga et al.,  2003 ; Huntjens et al.,  2003 ). This feature of DID has been corroborated by studies showing that when one identity (Identity 1) is asked to learn a list of word pairs, and an alter identity (Identity 2) is later asked to recall the second word in each pair using the first word as a cue, there seems to be no transfer to Identity 2 of what was learned by Identity 1. This interpersonality amnesia with regard to conscious recall of the activities and experiences of at least some other identities has generally been considered a fundamental characteristic of DID (Kihlstrom,  2001  2005 ; Kihlstrom & Schacter,  2000 ). Nevertheless, several interesting recent studies, each with about 20 DID patients, have challenged any idea that this interpersonality amnesia is complete, instead sometimes finding partial transfer of explicit memory across identities in certain tasks (Huntjens et al.,  2003  2007 , 2012; see also Dorahy & Huntjens,  2007 , for a review).

As noted earlier, there are kinds of memory other than simply what can be brought to awareness (explicit memory). As with dissociative amnesia and fugue, there is evidence that Identity 2 has some implicit memory of things that Identity 1 learned. That is, although Identity 2 may not be able to recall consciously the things learned by Identity 1, these apparently forgotten events may influence Identity 2’s experiences, thoughts, and behaviors unconsciously (Kihlstrom,  2001  2005 ). This might be reflected in a test asking Identity 2 to learn the list of words previously learned by Identity 1. Even though Identity 2 could not consciously recall the list of words, Identity 2 would learn that list more rapidly than a brand-new list of words, an outcome that suggests the operation of implicit memory (e.g., Eich et al.,  1997 ; Elzinga et al.,  2003 ; see Kihlstrom,  2001  2005 , for reviews).

Related studies on implicit transfer of memories have shown that emotional reactions learned by one identity often transfer across identities, too. Thus, even though Identity 2 may not be able to recall an emotional event that happened to Identity 1, a visual or auditory reminder of the event (a conditioned stimulus) administered to Identity 2 may elicit an emotional reaction even though Identity 2 has no knowledge of why it did so (e.g., Ludwig et al.,  1972 ; Prince,  1910 ). Moreover, one study by Huntjens and colleagues ( 2005 ) had 22 DID patients in Identity 1 learn to reevaluate a neutral word in a positive or negative manner through a simple evaluative conditioning procedure in which neutral words are simply paired with positive or negative words; the neutral words then come to take on positive or negative connotations. When Identity 2 was later asked to emerge, he or she also categorized the formerly neutral word in the same positive or negative manner as learned by Identity 1, showing implicit memory for the reevaluation of the word learned by Identity 1 (although complete subjective amnesia was reported by Identity 2). Nevertheless, other sophisticated studies have made it clear that implicit memory transfer across personalities does not always occur, particularly with certain kinds of implicit memory tasks where memory performance may be strongly influenced by the identity currently being tested (e.g., Dorahy,  2001 ; Eich et al.,  1997 ; Nissen et al.,  1988 ). However, the results that do show implicit memory transfer are very important because they demonstrate that explicit amnesia across identities cannot occur simply because one identity is trying actively to suppress any evidence of memory transfer. If this were possible, there would be no leakage of implicit memories across identities (Dorahy,  2001 ; Eich et al.,  1997 ).

An even smaller number of experimental studies have examined differences in brain activity when individuals with DID are tested with different identities at the forefront of consciousness. For example, in an early classic study, Putnam ( 1984 ) investigated EEG activity in 11 DID patients during different identities, and in 10 control subjects who were simulating different personality states, in order to determine whether there were different patterns of brain wave activity during different identities (real or simulated), as would be found if separate individuals were assessed. The study found that there were indeed differences in brain wave activity when the patients with DID were in different personality states and that these differences were greater than those found in the simulating subjects (see Kihlstrom et al.,  1993 ; Putnam,  1997 ).

One particularly interesting study by Reinders and colleagues ( 2006 ) examined subjective and cardiovascular activation patterns to both neutral and traumatic memories in 11 people diagnosed with DID. Each patient had one alter with a neutral identity such as the one active when they were functioning in everyday life, and each had another alter with a traumatic identity who had access to traumatic memories. As expected, when exposed to a script of neutral personal memories neither identity displayed much subjective or cardiovascular reactivity. However, when exposed to a script of personal memories of traumatizing events, responding differed in the two identity states. Specifically, the traumatic identity state (but not the neutral identity state) showed subjective and cardiovascular reactivity reflecting emotional distress to the personal traumatic memory. Such results could be seen as providing support for the idea that one function of certain alters is to protect the person from traumatic memories that a traumatic identity state has access to.

CAUSAL FACTORS AND CONTROVERSIES ABOUT DID

There are at least four serious, interrelated controversies surrounding DID and how it develops. First, some have been concerned with whether DID is a real disorder or is faked, and whether, even if it is real, it can be faked. The second major controversy is about how DID develops. Specifically, is DID caused by early childhood trauma, or does the development of DID involve some kind of social enactment of multiple different roles that have been inadvertently encouraged by careless clinicians? Third, those who maintain that DID is caused by childhood trauma cite mounting evidence that the vast majority of individuals diagnosed with DID report memories of an early history of abuse. But are these memories of early abuse real or false? Finally, if abuse has occurred in most individuals with DID, did the abuse play a causal role, or was something else correlated with the abuse actually the cause?

DID: Real or Faked? The issue of possible factitious or malingering origins of DID has dogged the diagnosis of DID for at least a century. One obvious situation in which this issue becomes critical is when it has been used by defendants and their attorneys to try to escape punishment for crimes (“My other personality did it”). For example, this defense was used, ultimately unsuccessfully, in the famous case of the Hillside Strangler, Kenneth Bianchi (Orne et al.,  1984 ), but it has probably been used successfully in other cases that we are unaware of (unaware because the person is not sent to prison but rather to a mental hospital in most cases). Bianchi was accused of brutally raping and murdering 10 young women in the Los Angeles area. Although there was a great deal of evidence that he had committed these crimes, he steadfastly denied it, and some lawyers thought perhaps he had DID. He was subsequently interviewed by a clinical psychologist, and under hypnosis a second personality, “Steve,” emerged. Steve confessed to the crimes, thereby creating the basis for a plea of “not guilty by reason of insanity” (see  Chapter 17 ). However, Bianchi was later examined even more closely by a renowned psychologist and psychiatrist specializing in this area, the late Martin Orne. Upon closer examination, Orne determined that Bianchi was faking the condition. Orne drew this conclusion in part because when he suggested to Bianchi that most people with DID have more than two identities, Bianchi suddenly produced a third (Orne et al.,  1984 ). Moreover, there was no evidence of multiple identities existing prior to the trial. When Bianchi’s faking the disorder was discovered, he was convicted of the murders. In other words, some cases of DID may involve complete fabrication orchestrated by criminal or other unscrupulous persons seeking unfair advantages, and not all prosecutors have as clever and knowledgeable an expert witness as Martin Orne to help detect this. Nevertheless, most researchers think that factitious and malingering cases of DID (such as the Bianchi case or cases in which the person has a need to be a patient) are relatively rare.

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FIGURE 8.1 Reported childhood abuse in five separate studies of DID patients (Total n = 843).

If DID Is Not Faked, How Does It Develop: Posttraumatic Theory or Sociocognitive Theory? Many professionals acknowledge that, in most cases, DID is a real syndrome (not consciously faked), but there is marked disagreement about how it develops and how it is maintained. In the contemporary literature, the original major theory of how DID develops is  posttraumatic theory  (Gleaves,  1996 ; Maldonado & Spiegel,  2007 ; Ross,  1997  1999 ). The vast majority of patients with DID (over 95 percent by some estimates) report memories of severe and horrific abuse as children (see  Figure 8.1  below). According to this view, DID starts from the child’s attempt to cope with an overwhelming sense of hopelessness and powerlessness in the face of repeated traumatic abuse. Lacking other resources or routes of escape, the child may dissociate and escape into a fantasy, becoming someone else. This escape may occur through a process like self-hypnosis (Butler et al.,  1996 ), and if it helps to alleviate some of the pain caused by the abuse it will be reinforced and occur again in the future. This notion is consistent with recent evidence that inducing a dissociative state in research participants can lead to decreased pain sensitivity (Ludascher et al.,  2009 ). Sometimes the child simply imagines the abuse is happening to someone else. If the child is fantasy prone, and continues to stay fantasy prone over time, the child may unknowingly create different selves at different points in time, possibly laying the foundation for multiple dissociated identities.

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Kenneth Bianchi, known as the “Hillside Strangler,” brutally raped and murdered 10 women in the Los Angeles area. Hoping to create a plea of “not guilty by reason of insanity,” Bianchi fabricated a second personality—“Steve”—who “emerged” while Kenneth was under hypnosis. A psychologist and psychiatrist specializing in DID determined he was faking the diagnosis, and Bianchi was subsequently convicted of the murders.

But only a subset of children who undergo traumatic experiences are prone to fantasy or self-hypnosis, which leads to the idea that a diathesis-stress model may be appropriate here. That is, children who are prone to fantasy and those who are easily hypnotizable may have a diathesis for developing DID (or other dissociative disorders) when severe abuse occurs (e.g., Butler et al.,  1996 ; Kihlstrom et al.,  1993 ). However, it should also be emphasized that there is nothing inherently pathological about being prone to fantasy or readily hypnotizable (Kihlstrom et al.,  1994 ).

Increasingly, those who view childhood abuse as playing a critical role in the development of DID are beginning to see DID as perhaps a complex and chronic variant of posttraumatic stress disorder, which by definition is caused by exposure to some kind of highly traumatic event(s), including abuse (e.g., Brown,  1994 ; Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Anxiety symptoms are more prominent in PTSD than in DID, and dissociative symptoms are more prominent in DID than in PTSD. Nevertheless, both kinds of symptoms are present in both disorders (Putnam,  1997 ). Moreover, some (but not all) investigators have estimated that a very high percentage of individuals diagnosed with DID have a comorbid diagnosis of PTSD, suggesting the likelihood of some important common causal factors (Vermetten et al., 2006; see also Rodewald et al.,  2011 ).

At the other extreme from posttraumatic theory is  sociocognitive theory , which claims that DID develops when a highly suggestible person learns to adopt and enact the roles of multiple identities, mostly because clinicians have inadvertently suggested, legitimized, and reinforced them and because these different identities are geared to the individual’s own personal goals (Lilienfeld & Lynn,  2003 ; Lilienfeld et al.,  1999 ; Spanos,  1994  1996 ). It is important to realize that at the present time, the sociocognitive perspective maintains that this is not done intentionally or consciously by the afflicted individual but, rather, occurs spontaneously with little or no awareness (Lilienfeld et al.,  1999 ). The suspicion is that overzealous clinicians, through fascination with the clinical phenomenon of DID and unwise use of such techniques as hypnosis, are themselves largely responsible for eliciting this disorder in highly suggestible, fantasy-prone patients (e.g., Giesbrecht et al.,  2008 ; Piper, Merskey,  2004a  2004b ; Spanos,  1996 ).

Consistent with the sociocognitive hypothesis, Spanos et al. ( 1985 ) demonstrated that normal college students can be induced by suggestion under hypnosis to exhibit some of the phenomena seen in DID, including the adoption of a second identity with a different name that shows a different profile on a personality inventory. Thus people can enact a second identity when situational forces encourage it. Related situational forces that may affect the individual outside the therapist’s office include memories of one’s past behavior (e.g., as a child), observations of other people’s behavior (e.g., others being assertive and independent, or sexy and flirtatious), and media portrayals of DID (Lilienfeld et al.,  1999 ; Piper & Merskey,  2004b ; Spanos,  1994 ).

Sociocognitive theory is also consistent with evidence that most DID patients do not show unambiguous signs of the disorder before they enter therapy and with evidence that the number of alter identities often increases (sometimes dramatically) with time spent in therapy (Piper & Merskey,  2004b ). It is also consistent with the increased prevalence of DID since the 1970s, when the first popular accounts of DID reached the general public, and since 1980, when therapist awareness of the condition increased as well (Lilienfeld et al.,  1999 ; Piper & Merskey,  2004a ).

However, there are also many criticisms of sociocognitive theory. For example, Spanos and colleagues’ demonstration of role-playing in hypnotized college students is interesting, but it does not show that this is the way DID is actually caused in real life. For example, someone might be able to give a convincing portrayal of a person with a broken leg, but this would not establish how legs are usually broken. Moreover, the hypnotized participants in this and other experiments showed only a few of the most obvious symptoms of DID (such as more than one identity) and showed them only under short-lived, contrived laboratory conditions. No studies have shown that other symptoms such as depersonalization, memory lapses for prolonged periods, or auditory hallucinations can occur under similar laboratory conditions. Thus, although some of the symptoms of DID could be created by social enactment, there is no evidence that the disorder can be created this way (e.g., Gleaves,  1996 ).

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Former Georgia football star Herschel Walker has written a book, Breaking Free: My Life with Dissociative Identity Disorder (2008), in which he tells about his struggle with this disorder.

Are Recovered Memories of Abuse in DID Real or False? Case reports of the cruelty and torture that some DID patients suffered as children are gut-wrenching to read or hear. However, the accuracy and trustworthiness of these reports of widespread sexual and other forms of childhood abuse in DID have become a matter of major controversy. Critics (who are often proponents of sociocognitive theory) argue that many of these reports of DID patients, which generally come up in the course of therapy, may be the result of false memories, which are in turn a product of highly leading questions and suggestive techniques applied by well-meaning but inadequately skilled and careless psychotherapists (Lilienfeld et al.,  1999 ; Loftus & Davis,  2006 ; Yapko,  1994 ). It seems quite clear to many investigators that this sort of thing has happened, often with tragic consequences. Innocent family members have been falsely accused by DID patients and have sometimes been convicted and imprisoned. But it is also true that brutal abuse of children occurs far too often and that it can have very adverse effects on development, perhaps encouraging pathological dissociation (e.g., Maldonado & Spiegel,  2007 ; Nash et al.,  1993 ). In such cases, prosecution of the perpetrators of the abuse is indeed appropriate. Of course, the real difficulty here is in determining when the recovered memories of abuse are real and when they are false (or some combination of the two). This bitter controversy about the issue of false memory is more extensively considered in the Unresolved Issues section at the end of this chapter.

One way to document that particular recovered memories are real might be if some reliable physiological test could be developed to distinguish between them. Thus, some researchers are currently trying to determine whether there are different neural correlates of real and false memories that could be used to make this determination reliably. Another somewhat easier way to document whether a particular recovered memory is real would be to have independent verification that the abuse had actually occurred, such as through physician, hospital, and police records. A number of studies have indeed reported that they have confirmed the reported cases of abuse, but critics have shown that the criteria used for corroborating evidence are almost invariably very loose and suspect as to their validity. For example, Chu and colleagues ( 1999 ) simply asked their subjects, “Have you had anyone confirm these events?” (p. 751) but did not specify what constituted confirmation and had no way of determining if subjects were exaggerating or distorting the information they provided as confirming evidence (Loftus & Davis,  2006 ; Piper & Merskey,  2004a ). In another example of a flawed study, Lewis and colleagues ( 1997 ) studied 12 convicted murderers and then confirmed through medical, social service, and prison records that all 12 had been severely abused as children. Unfortunately, this study did not include a control group of otherwise comparable murderers who did not exhibit DID symptoms. Hence we cannot be certain that the childhood abuse of these subjects is not as much (or more) associated with violence or conviction for murder as with the development of DID specifically. Moreover, Lewis and colleagues should have carefully assessed for the possibility that some of the murderers might have been malingering (i.e., faking DID; Lilienfeld et al.,  1999 ). Thus, although this study may have been one of the most impressive attempts yet to document abuse independently in people with DID, it was significantly flawed and therefore highly inconclusive.

If Abuse Has Occurred, Does It Play a Causal Role in DID? Let us put the previous controversy about the reality of recovered memories of abuse aside for a moment and assume that severe abuse has occurred in the early childhood backgrounds of many people with DID. How can we determine whether this abuse has played a critical causal role in the development of DID (e.g., Piper & Merskey,  2004a )? Unfortunately, many difficulties arise in answering this question. For example, child abuse usually happens in family environments plagued by many other sources of adversity and trauma (e.g., various forms of psychopathology and extreme neglect and poverty). One or more of these other, correlated sources of adversity could actually be playing the causal role (e.g., Lilienfeld et al.,  1999 ; Nash et al.,  1993 ). Another difficulty of determining the role of abuse is that people who have experienced child abuse as well as symptoms of DID may be more likely to seek treatment than people with symptoms of DID who did not experience abuse. Thus the individuals in most studies on the prevalence of child abuse in DID may not be representative of the population of all people who suffer from DID. Finally, childhood abuse has been claimed by some to lead to many different forms of psychopathology including depression, PTSD, eating disorders, somatic symptom disorders, and borderline personality disorder, to name just a few. Perhaps the most we will ever be able to say is that childhood abuse may play a nonspecific role for many disorders, with other, more specific factors determining which disorder develops (see  Chapters 10  and  12 ).

Comments on a Few of These Controversies About DID As we have seen, numerous studies indicate that the separate identities harbored by DID patients are somewhat physiologically and cognitively distinct. For example, EEG activity of various alters may be quite different. Because such differences cannot in any obvious way be simulated (e.g., Eich et al.,  1997 ), it seems that DID must, in at least some cases, involve more than simply the social enactment of roles. Moreover, this should not be too surprising, given the widespread evidence of separate (dissociated) memory subsystems and nonconscious active mental processing, which indicates that much highly organized mental activity is normally carried on in all of us in the background, outside of awareness (e.g., Kihlstrom,  2005 ). Moreover, some people seem to be especially prone to pathological variants of these dissociative processes (Waller et al.,  1996 ; Waller & Ross,  1997 ).

We should also note that each of these controversies has usually been stated in a dichotomous way: Is DID real or faked? What causes DID—spontaneous social enactment of roles or repeated childhood trauma? Are recovered memories of abuse real or false? If abuse occurs, does it play a primary causal role? Unfortunately, however, such dichotomously stated questions encourage oversimplified answers. The human mind does not seem to operate in these dichotomous ways, and we need to address the complex and multifaceted nature of the dissociated mental processes that these often miserable and severely stressed patients are experiencing. Fortunately, theorists on both sides have begun to soften their positions a little, acknowledging that multiple different causal pathways are likely to be involved. For example, Ross ( 1997  1999 ), a long-time advocate for a strong version of posttraumatic theory, later acknowledged that some cases are faked and that some may be inadvertently caused by unskilled therapists in the course of treatment. In addition, other advocates of posttraumatic theory have recently acknowledged that both real and false memories do occur in these patients, noting that it is critical that a method for determining which is which be developed (e.g., Gleaves & Williams,  2005 ; Gleaves et al.,  2004 ). From the other side, Lilienfeld et al.,  1999 , who have been vocal advocates for Spanos’ sociocognitive theory since his death in  1994 , have acknowledged that some people with DID may have undergone real abuse, although they believe it occurs far less often, and is less likely to play a real causal role, than the trauma theorists maintain (see also Kihlstrom,  2005 ).

Sociocultural Factors in Dissociative Disorders

There seems little doubt that the prevalence of dissociative disorders, especially their more dramatic forms such as DID, is influenced by the degree to which such phenomena are accepted or tolerated either as normal or as legitimate mental disorders by the surrounding cultural context. Indeed, in our own society, the acceptance and tolerance of DID as a legitimate disorder have varied tremendously over time. Compared to relatively high reported rates of DID in Western cultures, a recent study of 893 patients diagnosed with some type of dissociative disorder over 10 years at a psychiatric hospital in India found no cases of DID (Chaturvedi et al.,  2010 ). Nevertheless, although its prevalence varies, DID has now been identified in all racial groups, socioeconomic classes, and cultures where it has been studied. For example, outside North America it has been found in countries ranging from Nigeria and Ethiopia to Turkey, India, China, Australia, and the Caribbean, to name a few (Maldonado et al.,  2002 ; Xiao et al.,  2006 ).

Many seemingly related phenomena, such as spirit possession and dissociative trances, occur very frequently in many different parts of the world where the local culture sanctions them (Krippner,  1994 ; Spiegel et al., 2011). When entered into voluntarily, trance and possession states are not considered pathological and should not be construed as mental disorders. But some people who enter into these states voluntarily because of cultural norms develop distress and impairment. In DSM-5, the diagnostic criteria for DID have been modified to that they now include certain phenomena associated with possession. A trance is said to occur when someone experiences a temporary marked alteration in state of consciousness or identity (but with no replacement by an alternative identity). It is usually associated with either a narrowing of awareness of the immediate surroundings, or stereotyped behaviors or movements that are experienced as beyond one’s control. A possession trance is similar except that the alteration of consciousness or identity is replaced by a new identity that is attributed to the influence of a spirit, deity, or other power. In both cases there is typically amnesia for the trance state. One study of 58 individuals from Singapore with this diagnosis, as well as 58 individuals with a diagnosis of major depression, found that conflicts over religious or cultural issues, prior exposure to trance states, and being a spiritual healer or healer’s helper were most predictive of who had dissociative trance disorder relative to major depression (Ng & Chan,  2004 ). A recent review of 402 cases of dissociative trance and possession disorders indicates that migration and struggles with acculturation are associated with these disorders (During et al.,  2011 ).

There are also cross-cultural variants on dissociative disorders, such as Amok, which is often thought of as a rage disorder. Amok occurs when a dissociative episode leads to violent, aggressive, or homicidal behavior directed at other people and objects. It occurs mostly in men and is often precipitated by a perceived slight or insult. The person often has ideas of persecution, anger, and amnesia, often followed by a period of exhaustion and depression. Amok is found in places such as Malaysia, Laos, the Philippines, Papua New Guinea, and Puerto Rico and among Navajo Indians.

Treatment and Outcomes in Dissociative Disorders

Unfortunately, virtually no systematic, controlled research has been conducted on treatment of depersonalization disorder, dissociative amnesia, and dissociative fugue, and so very little is known about how to treat them successfully. Numerous case histories, sometimes presented in small sets of cases, are available, but without control groups who are assessed at the same time or who receive nonspecific treatments it is impossible to know the effectiveness of the varied treatments that have been attempted (Kihlstrom,  2005 ).

As noted earlier depersonalization/derealization disorder is generally thought to be resistant to treatment (e.g., Simeon et al.,  1997 ), although treatment may be useful for associated psycho-pathology such as anxiety and depressive disorders. Some think that hypnosis, including training in self-hypnosis techniques, may be useful because patients with depersonalization disorder can learn to dissociate and then “reassociate,” thereby gaining some sense of control over their depersonalization and derealization experiences (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Many types of antidepressant, antianxiety, and antipsychotic drugs have also been tried and sometimes have modest effects. However, one randomized controlled study showed no difference between treatment with Prozac versus with placebo (Simeon et al.,  2004 ). One recent treatment showing some promise for the treatment of dissociative disorders involves administering rTMS (repetitive transcranial magnetic stimulation) to the temporo-parietal junction, an area of the brain highly involved in the experience of a unified self and body (Mantovani et al.,  2011 ). After three weeks of treatment, half of the subjects showed significant reductions in depersonalization, with nonresponders showing symptom reduction after an additional three weeks of treatment. In dissociative amnesia and fugue, it is important for the person to be in a safe environment, and simply removing her or him from what he or she perceives as a threatening situation sometimes allows for spontaneous recovery of memory. Hypnosis, as well as drugs such as benzodiazepines, barbiturates, sodium pentobarbital, and sodium amobarbital, is often used to facilitate recall of repressed and dissociated memories (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). After memories are recalled, it is important for the patient to work through the memories with the therapist so that the experiences can be reframed in new ways. However, unless the memories can be independently corroborated, they should not be taken at their face value (Kihlstrom,  2005 ).

For DID patients, most current therapeutic approaches are based on the assumption of posttraumatic theory that the disorder was caused by abuse (Kihlstrom,  2005 ). Most therapists set integration of the previously separate alters, together with their collective merging into the host personality, as the ultimate goal of treatment (e.g., Maldonado & Spiegel,  2007 ). There is often considerable resistance to this process by the DID patients, who often consider dissociation as a protective device (e.g., “I knew my father could get some of me, but he couldn’t get all of me”; Maldonado & Spiegel,  2007 , p. 781). If successful integration occurs, the patient eventually develops a unified personality, although it is not uncommon for only partial integration to be achieved. But it is also very important to assess whether improvement in other symptoms of DID and associated disorders has occurred. Indeed, it seems that treatment is more likely to produce symptom improvement, as well as associated improvements in functioning, than to achieve full and stable integration of the different alter identities (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ).

Typically the treatment for DID is psychodynamic and insight-oriented, focused on uncovering and working through the trauma and other conflicts that are thought to have led to the disorder (Kihlstrom,  2005 ). One of the primary techniques used in most treatments of DID is hypnosis (e.g., Kluft,  1993 ; Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Most DID patients are hypnotizable and when hypnotized are often able to recover past unconscious and frequently traumatic memories, often from childhood. Then these memories can be processed, and the patient can become aware that the dangers once present are no longer there. (One problem here is that such patients are suggestible under hypnosis, so much of what is recalled may not be accurate; see Kihlstrom,  2005 ; Loftus & Davis,  2006 ). Through the use of hypnosis, therapists are often able to make contact with different identities and reestablish connections between distinct, seemingly separate identity states. An important goal is to integrate the personalities into one identity that is better able to cope with current stressors. Clearly, successful negotiation of this critical phase of treatment requires therapeutic skills of the highest order; that is, the therapist must be strongly committed as well as professionally competent. Regrettably, not all therapists are.

Most reports in the literature are treatment summaries of single cases, and reports of successful cases should always be considered with caution, especially given the large bias in favor of publishing positive rather than negative results. Treatment outcome data for large groups of DID patients have been reported in only four studies we are aware of, and none of these included a control group, although it is clear that DID does not spontaneously remit simply with the passage of time, nor if a therapist chooses to ignore DID-related issues (Kluft,  1999 ; Maldonado et al.,  2002 ). For example, Ellason and Ross ( 1997 ) reported on a 2-year postdischarge follow-up of DID patients originally treated in a specialized inpatient unit. Of the original 135 such patients, 54 were located and systematically assessed. All these patients, and especially those who had achieved full integration, generally showed marked improvements in various aspects of their lives. However, only 12 of the 54 had achieved full integration of their identities. Such results are promising, but we must wonder about the clinical status of the 81 “lost” patients who may likely have done less well. Another 10-year follow-up study reported similar results in a smaller sample of 25 treated DID patients. Only 12 were located 10 years later; of these, six had achieved full integration, but two of those had partially relapsed (Coons & Bowman,  2001 ). In general it has been found that (1) for treatment to be successful, it must be prolonged, often lasting many years, and (2) the more severe the case, the longer that treatment is needed (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ).

in review

·  ● Describe the symptoms known as depersonalization and derealization, and indicate which disorder is primarily characterized by their appearance.

·  ● Describe dissociative amnesia and dissociative fugue, and indicate what aspects of memory are affected.

·  ● What are the primary symptoms of dissociative identity disorder (DID), and why is its prevalence thought to have increased?

·  ● Review the four major controversies surrounding DID that were discussed in this chapter.

UNRESOLVED issues: DID and the Reality of “Recovered Memories”

As we have seen in this chapter, many controversies surround the nature and origins of DID. None have been more bitter than those related to the truth value of “recovered” memories of childhood abuse, particularly sexual abuse, which posttraumatic theorists assert is the major causal factor in the development of DID. Indeed, a virtual chasm has developed between the “believers” (mostly but not exclusively private practitioners who treat people with DID) and the “dis-believers” (mostly but not exclusively the more academic and science-oriented mental health professionals). The disbelievers are very sympathetic to people suffering DID symptoms, but they have tended to doubt that the disorder is usually caused by childhood abuse and have challenged the validity or accuracy of recovered memories of abuse (see Loftus & Davis,  2006 , for a review of the recovered memory debate).

For 20 years, these controversies have moved beyond professional debate and have become major public issues, leading to countless legal proceedings. DID patients who recover memories of abuse (often in therapy) have often sued their parents for having inflicted abuse. But ironically, therapists and institutions have also been sued for implanting memories of abuse that they later came to believe had not actually occurred. Some parents, asserting they had been falsely accused, formed an international support organization—the False Memory Syndrome Foundation—and have sometimes sued therapists for damages, alleging that the therapists induced false memories of parental abuse in their child. Many families have been torn apart in the fallout from this remarkable climate of suspicion, accusation, litigation, and unrelenting hostility.

Whether DID originates in childhood abuse and whether recovered memories of abuse are accurate are basically separate issues, but they have tended to become fused in the course of the debate. Hence those who doubt the validity of memories of abuse are also likely to regard the phenomenon of DID as stemming from the social enactment of roles encouraged or induced—like the memories of abuse themselves—by misguided therapy (e.g., see Bjorklund,  2000 ; Lilienfeld et al.,  1999 ; Lynn et al.,  2004 ; Piper & Merskey,  2004a  2004b ). Believers, on the other hand, have usually taken both DID and the idea that abuse is its cause to be established beyond doubt (e.g., see Gleaves,  1996 ; Gleaves et al.,  2001 ; Ross,  1997  1999 ).

Much of the controversy about the validity of recovered memories is rooted in disagreements about the nature, reliability, and malleability of human autobiographical memory. With some exceptions, evidence for childhood abuse as a cause of DID is restricted to the “recovered memories” (memories not originally accessible) of adults being treated for dissociative experiences. Believers argue that before treatment such memories had been “repressed” because of their traumatic nature or had been available only to certain alter identities that the host identity was generally not aware of. Treatment, according to this view of believers, dismantles the repressive defense and thus makes available to awareness an essentially accurate memory recording of the past abuse.

Disbelievers counter with several scientifically well-supported arguments. For example, scientific evidence in support of the repression concept is quite weak (e.g., Kihlstrom,  2005 ; Loftus & Davis,  2006 ; Piper,  1998 ). In many alleged cases of repression, the event may have been lost to memory in the course of ordinary forgetting rather than repression, or it may have occurred in the first 3 to 4 years of life, before memories can be recorded for retrieval in adulthood. In many other cases, evidence for repression has been claimed in studies where people may simply have failed to report a previously remembered event, often because they were never asked or were reluctant to disclose such very personal information (Kihlstrom,  2005 ; Loftus & Davis,  2006 ; Pope et al.,  1998 ).

Even if memories can be repressed, there are very serious questions about the accuracy of recovered memories. Human memory of past events does not operate in a computer-like manner, retrieving with perfect accuracy an unadulterated record of information previously stored and then repressed. Rather, human memory is malleable, constructive, and very much subject to modification on the basis of events happening after any original memory trace is established (Loftus & Bernstein,  2005 ; Loftus & Davis,  2006 ; Schacter et al.,  2000 ).

Indeed, there is now good evidence that in certain circumstances, people are sometimes very prone to the development of false memories (see Wade et al.,  2007 , for a review). For example, a number of studies have now shown that when normal adult subjects are asked to imagine repeatedly events that they are quite sure had not happened to them before age 10, they later increase their estimate of the likelihood that these events actually had happened to them (Tsai et al.,  2000 ). Moreover, even in a relatively short time frame, adult subjects sometimes come to believe they have performed somewhat bizarre acts (e.g., kissing a magnifying glass), as well as common acts (e.g., flipping a coin), after simply having imagined they had engaged in these acts several times 2 weeks earlier (Thomas & Loftus,  2002 ). These and other studies clearly show that repeated imagining of certain events (even somewhat bizarre events) can lead people to have false memories of events that never happened (Loftus & Bernstein,  2005 ; Loftus & Davis,  2006 ). In addition, an experimental study by McNally and colleagues ( 2005 ) looked at individuals who reported either repressed or recovered memories of childhood sexual abuse and found some evidence that they had greater difficulty on at least some measures than normal controls in distinguishing between words that they had seen versus words that they had only imagined. This suggests that people with repressed or recovered memories of abuse may have greater difficulty distinguishing between what has actually happened to them and what they have imagined happened to them. However, a different study found that those who report recovered memories of childhood sexual abuse did not show increased difficulty retrieving non-abuse-related autobiographic memories compared to those who reported continuous memories of childhood sexual abuse or a control group reporting no childhood sexual abuse (Raymaekers et al.,  2010 ).

One fascinating study compared a group of people who had continuous memories of childhood abuse with two groups who had recovered memories of abuse. In one of the latter groups the memories had been recovered during therapy and in the other the memories had been recovered out of therapy. The researchers then attempted to corroborate these recovered memories, and found corroborative evidence for over half of those who had recovered memories outside of therapy and for none in the group who recovered their memories during therapy (Geraerts et al.,  2007 ).

Recently, McNally and Geraerts ( 2009 ) offered a different perspective on recovered memories, one that attempts to bridge the gap between the conviction that repression underlies recovered memories and the alternate conviction that all recovered memories are false. Their third perspective suggests that some recovered memories are genuine but were never actually repressed. Instead, some abuse victims may simply not have thought about their abuse for a long period of time, have been deliberately attempting to forget the abuse (suppression rather than repression), or may have forgotten prior instances when they did recall the abuse, resulting in the false impression that a recently surfaced memory had been repressed for years.

8 summary

·  8.1 What are somatic symptom disorders?

·  • Somatic symptom disorders lie at the interface of abnormal psychology and medicine. These are disorders in which psychological problems are manifested in physical symptoms. In response to the symptoms the person also experiences abnormal thoughts, feelings, and behaviors.

·  • Somatic symptom disorder occurs in individuals who have had multiple somatic complaints lasting at least 6 months. Even if the symptoms do not seem to have a medical explanation, the person’s suffering is regarded as authentic.

·  8.2 What is illness anxiety disorder?

·  • Illness anxiety occurs in individuals who are very anxious about having an illness even though there are no apparent symptoms.

·  8.3 What is conversion disorder (functional neurological symptom disorder)?

·  • Conversion disorder involves patterns of symptoms or deficits affecting sensory or voluntary motor functions leading one to think there is a medical or neurological condition, even though medical examination reveals no physical basis for the symptoms.

·  8.4 What is the difference between a factitious disorder and malingering?

·  • Individuals with factitious disorder intentionally produce medical or psychological symptoms (or both). They do this in the absence of external rewards in order to take on an illness role.

·  • Malingering involves the intentional production of symptoms or the exaggeration of symptoms. This is motivated by external factors such as a wish to claim insurance money, avoid work or military service, or to get leniency in a criminal prosecution.

·  8.5 What are the primary features of dissociative disorders?

·  • Dissociative disorders occur when the processes that normally regulate awareness and the multichannel capacities of the mind apparently become disorganized, leading to various anomalies of consciousness and personal identity.

·  8.6 What is depersonalization/derealization disorder?

·  • Depersonalization/derealization disorder occurs in people who experience persistent and recurrent episodes of derealization (losing one’s sense of reality of the outside world) and/or depersonalization (losing one’s sense of oneself and one’s own reality).

·  8.7 What is dissociative amnesia?

·  • Dissociative amnesia involves an inability to recall previously stored information that cannot be accounted for by ordinary forgetting and seems to be a common initial reaction to highly stressful circumstances. The memory loss is primarily for episodic or autobiographical memory.

·  8.8 What is dissociative identity disorder?

·  • In dissociative identity disorder, the person manifests at least two or more distinct identities that alternate in some way in taking control of behavior. Alter identities may differ in many ways from the host identity.

key terms

·  alter identities  281

·  conversion disorder  270

·  depersonalization  276

·  depersonalization/derealization disorder  276

·  derealization  276

·  dissociation  276

·  dissociative amnesia  278

·  dissociative disorders  276

·  dissociative fugue  278

·  dissociative identity disorder (DiD)  280

·  factitious disorder  264

·  factitious disorder imposed on another  275

·  host identity  281

·  hypochondriasis  265

·  hysteria  271

·  implicit memory  276

·  implicit perception  276

·  malingering  264

·  pain disorder  269

·  posttraumatic theory (of DID)  285

·  primary gain  271

·  secondary gain  271

·  sociocognitive theory (of DID)  286

·  soma  264

·  somatic symptom disorders  264

·  somatization disorder  268

·  somatoform disorders  264

 
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