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KAPLAN & SADOCK’S POCKET HANDBOOK OF CLINICAL PSYCHIATRY

SEVENTH EDITION

Samoon Ahmad, M.D.

KAPLAN & SADOCK’S POCKET HANDBOOK

OF CLINICAL PSYCHIATRY

SEVENTH EDITION

KAPLAN & SADOCK’S POCKET HANDBOOK

OF CLINICAL PSYCHIATRY

SEVENTH EDITION

S amoon A hmad , MD Clinical Professor Department of Psychiatry NYU Grossman School of Medicine New York, New York

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Seventh Edition

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Dedicated to my wife Kim, son Daniel, and my parents, Naseem and Riffat

Preface

This is the second book in the Kaplan and Sadock series for which I have had the privilege of being the sole author. Previously, I had served as a coauthor of the sixth edition of this book with Benjamin J. Sadock, MD, and Virginia A. Sadock, MD. The book was originally the brainchild of Harold Kaplan and Ben Sadock, who recognized that a busy clinician (especially one in training), a medical stu dent, or a mental health professional looking for quick and easily accessible in formation could not delve into larger textbooks while in the clinic. What they needed was a quick reference for necessary guidance in everyday clinical issues. They produced the first edition of the pocket handbook to satisfy this need. This is a book that I still own to this day. As I sat down to write the preface for this book, I browsed through my coveted first edition of the Pocket Handbook of Clinical Psychiatry , which was published in 1990—a couple of years before I started my residency. However, it was my go-to reference book throughout those 4 years. As I skimmed through the preface of the first edition, I came across the fol lowing sentence that struck me: “The Pocket Handbook represents a distillation in that it provides brief summaries of psychiatric disorders, which include key as pects of their etiology, epidemiology, and treatment.” I realized that the authors’ description of the purpose of this book has consistently remained the same for the last 33 years, even after seven editions, and that its success is a testament to the readership who have enjoyed its up-to-date, succinct, and brief descriptions of all psychiatric disorders and treatments. It is extremely useful in clinical set tings, where time is of the essence in obtaining information. After my residency I was very fortunate to contribute to various textbooks of Kaplan and Sadock’s series and to eventually become not only close profes sional colleagues but also close friends with Ben and Virginia. As I take the helm as the author of the seventh edition of this book, I cannot imagine being in this role without the invaluable and unparalleled guidance from the two of them. Their mentorship, friendship, teachings, and advice have been a constant source of encouragement and I am grateful and indebted for their everlasting support. Goals of This Book Similar to the most recent edition of the Pocket Handbook of Psychiatric Drug Treatment , the goal of this book is to serve as an updated guide to working cli nicians who need a quick and trusted reference source. To achieve this goal, the book has been updated with the latest information on dozens of psychiatric disorders and incorporates the text revisions to the fifth edition of the Diagnos tic and Statistical Manual of Mental Disorders ( DSM-5-TR ), as these revisions were published in 2022. Moreover, the book has also been reorganized in a way

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that follows a set template so that information is easier to find than in previous editions. Organization of This Book Though updated, the format of the seventh edition is not radically different from previous editions, and chapters follow closely along with the organization of DSM-5-TR . Readers will find that the information presented in each chapter fol lows a similar template where each condition is given its own section and broken up into the following subsections: epidemiology; comorbidity; etiology; labora tory and psychological tests; pathophysiology; diagnosis, signs, and symptoms; specifications (when appropriate); differential diagnosis; course and prognosis; and treatment. While there are several chapters where adherence to the template was not feasible, most of the book is organized in this fashion. New Additions to This Book Some of the new chapters that have been added to the seventh edition break with this pattern because they do not describe conditions, but rather the science behind novel therapies that were traditionally considered outside the parameters of psy chiatry. These therapies include treatment with cannabis, ketamine, and psyche delics such as psilocybin and 3,4-methylenedioxymethamphetamine (MDMA). A new chapter has also been included that provides information about the SARS-CoV-2 virus, long COVID, and the psychosocial impact of the COVID-19 pandemic—with subsections describing the unique challenges for children, se niors, and patients with psychiatric issues. The chapter on COVID-19 also de scribes issues like clinician burnout and changes in medical pedagogy. The new edition also includes a section on emerging trends in psychiatry. No doubt, there has been a lot of interest in the potential of artificial intelligence and generative text, but advancements in scanning, brain mapping, and virtual reality also have enormous clinical implications. Similarly, the fields of immu nology, endocrinology, neurology, and psychiatry are all converging in the study of the gut microbiome and the gut-brain axis. The purpose of mentioning these emerging trends is not to provide the clinician with expertise but to whet their intellectual appetite and encourage personal research. Purpose of This Series As with previous editions of the Pocket Handbook of Clinical Psychiatry and the companion book, the Pocket Handbook of Psychiatric Drug Treatment , the purpose of this book is to be an easy-to-navigate source of information that phy sicians, nurses, and other individuals who work in the field of mental health can access while in the field. My hope is that improvements in organization and the addition of visual aids, such as color-coded thumb tabs, will ultimately make it easier to find and retrieve information, upholding the original intent of the series and better serving the clinician and the patient.

Of note this book was written entirely by a human with no assistance from generative AI tools.

Acknowledgments

My gratitude for the opportunity to reach all of you and the wider psychiatric and medical communities with this update is immeasurable. None of this would have been possible without my esteemed mentor and colleague Benjamin J. Sadock, MD, Menas S. Gregory professor of psychiatry, NYU Grossman School of Medicine. He is the veritable great whose eternal support and guidance remain the driving force behind my thinking and writing. As with the recently published eighth edition of the Pocket Handbook of Psychi atric Drug Treatment , Ben gave me the opportunity to step into his shoes as this edition’s author. I remain eternally indebted to Ben and his wife Virginia—also a prior coauthor. I am profoundly appreciative of their wise and kind counsel and the time we have spent together over the years. Maryanne Badaracco, MD, director and chief of psychiatry, Bellevue Hospital, has been deeply supportive of my pursuit of academic excellence during my 30-year career at Bellevue. I additionally extend my gratitude to Charles Marmar, MD, Lucius R. Littauer professor and chair of the Depart ment of Psychiatry, NYU Grossman School of Medicine, for his leadership and encouragement. Jay Fox, my research and editorial assistant, deserves my utmost respect and appreciation for his continued collaboration and commitment. I am extremely fortunate to be able to depend on you, Jay. Thanks to my publisher and team at Wolters Kluwer for their unwavering support. Our process remains seamless and timely, and for that I owe each and many of you thanks, especially Chris Teja, acquisitions editor. Last, thank-you to my family for your love and trust. I am so fortunate to have you by my side. Samoon Ahmad, MD Clinical Professor, Department of Psychiatry NYU Grossman School of Medicine New York, New York

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Contents

Preface vi Acknowledgments viii

Chapter 1: Classification in Psychiatry Chapter 2: Psychiatric History and Mental Status Examination Chapter 3: Medical Assessment and Laboratory Testing in Psychiatry Chapter 4: Medical Comorbidity and Management Chapter 6: Major Neurocognitive Disorders Chapter 7: Major or Minor Neurocognitive Disorder due to Another Medical Condition (Amnestic Disorder) Chapter 8: Mental Disorders due to Another Medical Condition Chapter 9: Substance-Related and Addictive Disorders Chapter 10: Schizophrenia Spectrum and Other Psychotic Disorders Chapter 11: Schizophreniform, Schizoaffective, Delusional, and Other Psychotic Disorders Chapter 5: Brain Imaging

38 58 79 85

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222 243 292

Chapter 12: Mood Disorders Chapter 13: Anxiety Disorders

Chapter 14: Obsessive-Compulsive and Related Disorders

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Chapter 16: Dissociative Disorders

351 367 385 416

Chapter 17: Somatic Symptom and Related Disorders

Chapter 18: Personality Disorders Chapter 19: Sexual Dysfunction

Contents

Chapter 20: Gender Dysphoria

441 448 464

Chapter 21: Feeding and Eating Disorders

Chapter 22: Normal Sleep and Sleep-Wake Disorders Chapter 23: Disruptive, Impulse-Control, and Conduct Disorders Chapter 24: Consultation-Liaison Psychiatry Chapter 25: Suicide, Violence, and Emergency Psychiatric Medicine

480 487

500 523 574 593 603 620 737 756 767 774 783 796 809 835

Chapter 26: Child Psychiatry Chapter 27: Geriatric Psychiatry Chapter 28: End-of-Life Care Issues

Chapter 29: Psychotherapies

Chapter 30: Psychopharmacologic Treatment and Nutritional Supplements

Chapter 31: Cannabis

Chapter 32: Psychedelics and Entactogens

Chapter 33: Ketamine

Chapter 34: Brain Stimulation Therapies Chapter 35: Forensic Psychiatry and Ethics in Psychiatry Chapter 37: The COVID-19 Pandemic Chapter 38: The Future of Psychiatry Glossary of Signs and Symptoms 847 Index 872 About the Author 912 Chapter 36: Medication-Induced Movement Disorders

Dissociative Disorders

Introduction Dissociation is defined as an unconscious defense mechanism involving the seg regation of any group of mental or behavioral processes from the rest of the per son’s psychic activity. This mechanism is central to the pathology of dissociative disorders, which involve a disruption in one or more mental functions, such as memory, identity, perception, consciousness, or motor behavior. The disturbance may be sudden or gradual, transient, or chronic, and the signs and symptoms of the disorder are very often caused by psychological trauma. Unlike trauma- and stressor-related disorders (Chapter 15), traumatic experience is not part of the diagnostic criteria for any dissociative disorders. Within this chapter, there are three specific dissociative disorders: disso ciative amnesia, dissociative identity disorder (DID), and depersonalization/ derealization disorder, as well as a category for other specified or unspecified dissociative disorders. Dissociative fugue , which was included as a major diag nostic category in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) , became a specifier within dissociative amnesia in DSM-5 and DSM-5-TR . Trauma Exposure Unfortunately, exposure to traumatic events is relatively common. Within the United States, 40.8% to 82.7% of individuals are exposed to trauma over the course of their lifetimes though not all populations are affected evenly. Individ uals from resource-poor communities are more likely to experience stress and trauma than individuals who come from more affluent society. Additional factors that can increase one’s risk of exposure to traumatic events are gender, age, race, ethnicity, sexual orientation, marital status, and education level. Dissociative Amnesia Dissociative amnesia occurs when the patient is unable to recall an important memory which is usually traumatic or stressful but retains the capacity to learn new material. The process of dissociation is believed to be a psychological de fense mechanism governed by the limbic system and associated with instances where one “freezes” during a stress response rather than responding with aggres sion (fight), flight, or an attempt to win over a belligerent actor (fawn). There is no medical explanation for the occurrence, nor is the condition caused by a drug. The different types of dissociative amnesia are listed in Table 16-1 .

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Epidemiology Of all the dissociative disorders, dissociative amnesia is the most common, with a 12-month prevalence of approximately 2%. It is far more common in women than men, occurs more often in adolescents and young adults than in older adults, and increases in incidence in the wake of natural disasters and wars. Comorbidity Common comorbidities of dissociative amnesia include posttraumatic stress dis order (PTSD), somatic symptom disorder, conversion disorder, and dependent or avoidant personality disorders. Etiology Dissociative amnesia typically occurs following extreme emotional trauma, par ticularly in the wake of physical or sexual abuse. Dissociative amnesia can also occur following traumatic brain injury (TBI) in the absence of emotional trauma. Laboratory and psychological tests There are no laboratory tests for dissociative amnesia, though blood and urine tests can be useful to rule out the use of substances that may have caused the am nesia. Patient responses during a clinical evaluation will oftentimes be sufficient for a diagnosis (see Table 16-2 ). Pathophysiology Tonic immobility, a rigid state of paralysis that is often associated with the opos sum (ie, “playing possum”), is a response to stress that appears to be closely associated with dissociative amnesia. When the body is in this unresponsive state, it may result in reduced neural network activity, including connectivity between the hippocampus and neocortical areas, thereby resulting in memory fragmentation. Tests involving functional magnetic resonance imaging (fMRI) in patients with dissociative amnesia have shown reduced hippocampal activity and increased activity in the prefrontal cortex while testing for recall. Diagnosis, signs, and symptoms Patients who suffer from dissociative amnesia have an inability to recall vital autobiographical details of an event. The DSM-5-TR diagnostic criteria for dis sociative amnesia note that the forgotten information is usually of a traumatic or stressful nature but does not require it (see Table 16-3 ). Dissociative amnesia TABLE 16-1. Types of Dissociative Amnesia Localized amnesia: Inability to recall events related to a circumscribed period of time Selective amnesia: Ability to remember some, but not all, of the events occurring during a circum scribed period of time Generalized amnesia: Failure to recall one’s entire life Continuous amnesia: Failure to recall successive events as they occur Systematized amnesia: Failure to remember a category of information, such as all memories relating to one’s family or to a particular person

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may take one of several forms: localized amnesia (loss of memory for the events over a short time); generalized amnesia (loss of memory for a whole lifetime of experiences); and selective or systematized amnesia (inability to recall some but not all events over a short time). Patients are capable of learning and remem bering new information, and their general cognitive functioning and language capacity are usually intact. The amnesia is not the result of a general medical condition or the ingestion of a substance. Onset of dissociative amnesia is often abrupt, and history usually shows pre cipitating trauma charged with painful emotions and psychological conflict. Pa tients are aware that they have lost their memory, and while some may be upset at the loss, others appear to be unconcerned or indifferent. Patients are usually alert before and after amnesia; however, some report a slight clouding of conscious ness during the period immediately surrounding the onset of amnesia. Depression and anxiety are common predisposing factors. Of note, amnesia may provide a primary or a secondary gain (ie, a woman who is amnestic about a stillbirth). TABLE 16-3. Diagnostic Criteria of Dissociative Amnesia • Failure to remember personal information (often pertaining to stressful experiences) that is more extreme than forgetting • The disturbance results in distress or impairment that is clinically significant. • The disturbance is not due to the physiologic effects of a substance or medical condition (eg, traumatic brain injury, epilepsy, Wernicke-Korsakoff syndrome). • The disturbance is not better explained by dissociative identity disorder or a trauma- and stressor related disorder. Note: Can be with or without dissociative fugue. TABLE 16-2. Mental Status Examination Questions for Dissociative Amnesia If answers are positive, ask the patient to describe the event. Make sure to specify that the symptom does not occur during an episode of intoxication. 1. Do you ever have blackouts? Blank spells? Memory lapses? 2. Do you lose time? Have gaps in your experience of time? 3. Have you ever traveled a considerable distance without recollection of how you did this or where you went exactly? 4. Do people tell you of things you have said and done that you do not recall? 5. Do you find objects in your possession (such as clothes, personal items, groceries in your grocery cart, books, tools, equipment, jewelry, vehicles, weapons, etc) that you do not remember acquir ing? Out-of-character items? Items that a child might have? Toys? Stuffed animals? 6. Have you ever been told or found evidence that you have talents and abilities that you did not know that you had? For example, musical, artistic, mechanical, literary, athletic, or other talents? Do your tastes seem to fluctuate a lot? For example, food preference, personal habits, taste in music or clothes, and so forth. 7. Do you have gaps in your memory of your life? Are you missing parts of your memory for your life history? Are you missing memories of some important events in your life? For example, weddings, birthdays, graduations, pregnancies, birth of children, and so on. 8. Do you lose track of or tune out conversations or therapy sessions as they are occurring? Do you find that, while you are listening to someone talk, you did not hear all or part of what was just said? What is the longest period of time that you have lost? Minutes? Hours? Days? Weeks? Months? Years? Describe. Adapted from Loewenstein RJ. An office mental status examination for complex chronic dissociative symptoms and multiple personality disorder. Psychiatr Clin North Am . 1991;14(3):567-604. Copyright © 1991 Elsevier. With permission.

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Dissociative fugue Dissociative fugue is now diagnosed as a subtype (specifier) of dissociative am nesia. It is characterized by sudden, unexpected travel away from home, with the inability to recall some or all of one’s past. This is accompanied by confusion about identity and, often, the assumption of an entirely new identity. With disso ciative fugue, memory loss is sudden and is associated with purposeful, uncon fused travel, often for extended periods of time (days to months or even years). Patients lose part or complete memory of their past life and are often unaware of the memory loss. They assume an apparently normal, nonbizarre new identity. However, perplexity and disorientation may occur. Once they suddenly return to their former selves, they recall the time antedating the fugue, but they are amnes tic for the period of the fugue itself. Though technically rare, with a prevalence rate of 0.2% in the general pop ulation, it happens far more frequently than clinical experience would suggest, and occurs most often during times of war, following natural disasters, and as a result of personal crises with intense internal conflict. As is the case with dissociative amnesia, psychiatric interview, drug-assisted in terview, and hypnosis help reveal to the clinician and the patient the psychological stressors that triggered the fugue episode. Psychotherapy helps patients incorporate the precipitating stressors into their psyches in a healthy and integrated manner. Differential diagnosis Loss of memory may result from numerous other medical conditions, as noted in Table 16-4 . What distinguishes dissociative amnesia from many other causes of memory loss is that it is not due to a neurologic or other medical condition. TABLE 16-4. Differential Diagnostic Considerations in Dissociative Amnesia Dementia Delirium Ordinary forgetfulness and nonpathologic amnesia Amnestic disorder due to a medical condition Anoxic amnesia Cerebral infections (eg, herpes simplex affecting temporal lobes) Cerebral neoplasms (especially limbic and frontal) Epilepsy Metabolic disorders (eg, uremia, hypoglycemia, hypertensive encephalopathy, porphyria) Postconcussion (posttraumatic) amnesia Postoperative amnesia Electroconvulsive therapy (or other strong electric shock) Substance-related amnesia (eg, ethanol, sedative-hypnotics, anticholinergics, steroids, lithium, β -adrenergic receptor antagonists, pentazocine, phencyclidine, hypoglycemic agents, cannabis, hallucinogens, methyldopa) Transient global amnesia Wernicke-Korsakoff syndrome Sleep-related amnesia (eg, sleepwalking disorder)

Dissociative identity disorders Other dissociative disorders Posttraumatic amnesia Posttraumatic stress disorder Acute stress disorder Somatoform disorders (somatization disorder, conversion disorder) Malingering and factitious amnesia (especially when associated with criminal activity)

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Dissociative identity disorder Patients with DID also report lapses in memory, but will likely report additional dissociative symptoms and multiple episodes of memory lapses. Patients will likely also report a history of finding unexpected possessions and random fluctu

ations in abilities or skills. Posttraumatic stress disorder

Patients with PTSD are unable to consistently recall all or some details of the traumatic event, whereas patients with dissociative amnesia will not remember extended periods of time before and/or after the event. Of note, comorbidity of PTSD and dissociative amnesia is relatively common. Neurocognitive disorders Memory loss due to neurocognitive disorders (eg, seizure disorders, Alzheimer disease, and transient ischemic attack) is typically tied to additional deficits in cognition and disturbances in affect, attention, or behavior. Substance-related disorders Individuals with a long history of substance use disorder, especially alcohol, may experience blackouts during periods of extreme intoxication. If a longitudinal history reveals a pattern of memory deficits while the individual is intoxicated, it is likely that memory lapses are substance related. Substance-related disorders in the context of sexual assault Victims of sexual assault may also experience blackouts while voluntarily in toxicated or involuntarily intoxicated due to “date rape” drugs like γ -hydroxy butyrate (GHB). Should a sexual assault happen while the victim is intoxicated, it can be impossible to discern if the memory deficit is due to intoxication or Amnesia may follow a TBI. Unlike dissociative amnesia, memory deficits fol lowing TBI are usually accompanied by additional symptoms like disorientation and confusion. Neuroimaging abnormalities are also associated with TBI but not dissociative amnesia. Factitious disorder and malingering Some individuals may feign amnesia, especially if they stand to gain or to avoid legal or financial difficulties. If determined enough, some individuals may be able to maintain the deception indefinitely. Course and prognosis The symptoms of dissociative amnesia terminate abruptly. Recovery is complete with few recurrences. The condition may last a long time in some patients, es pecially in cases involving secondary gain. Disruptions in memory should be restored as soon as possible, or the repressed memory may form a nucleus in the unconscious mind where future amnestic episodes may develop. Recovery generally is spontaneous but is accelerated with treatment. dissociative amnesia as a result of trauma. Sequela related to traumatic brain injury

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Treatment Psychotherapy

Psychotherapy helps patients to incorporate the memories into their conscious state. Hypnosis is used primarily as a means to relax the patient sufficiently to recall forgotten information. Pharmacotherapy Drug-assisted interviews with short-acting benzodiazepines may be used to help patients recover their forgotten memories. Barbiturates like amobarbital (sodium amytal) and pentobarbital also known as truth serum have also been employed to interview patients though information extracted under their influence has never been accepted in court. One reason is that people may be more suggestible under their influence. In addition, some case studies suggest ketamine may be helpful. Dissociative Identity Disorder This condition, formerly known as multiple personality disorder, is usually the result of a traumatic event, most often physical or sexual abuse especially in childhood. This disorder involves the manifestation of two or more distinct per sonalities (often referred to as “alters”), which, when present, will dominate the person’s behaviors and attitudes as if no other personality existed. Symptoms may be covert and rarely resemble the dramatic transformations common in The 12-month prevalence of DID is believed to be between 1% and 2% but oc curs in 5% of patients with psychiatric disorder at nearly equal rates for men and women. Onset is most common in late adolescence and young adulthood, although symptoms may be present for 5 to 10 years before diagnosis. DID is more common in first-degree biologic relatives with the disorder. Comorbidity As DID tends to follow a traumatic experience, patients may also develop PTSD or another trauma- and stressor-related disorder. DID is also highly comorbid with depressive disorders, obsessive-compulsive disorder, substance-related disorders, conversion disorder, somatic symptom disorder, eating disorder, and sleep disorders. Comorbid personality disorders, particularly avoidant or border line personality disorders, are fairly common. Alterations in identity may affect the presentation of symptoms associated with comorbid disorders. Etiology DID is associated with severe sexual and psychological abuse in childhood and a lack of support from attachment figures or significant others. Severe psycho logical and physical abuse leads to a profound need to distance the self from horror and pain. Each personality expresses some necessary emotion or state (eg, rage, sexuality, flamboyance, competence) that the original personality dares not express. During abuse, the child attempts to protect themselves from trauma by dissociating from the terrifying acts, becoming, in essence, another person or fiction and film. Epidemiology

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persons who are not experiencing abuse and who could not be subjected to abuse. The dissociated selves become a long-term, ingrained method of self-protection from perceived emotional threats.

Laboratory and psychological tests There are no laboratory tests for DID. Pathophysiology The pathophysiology of DID is poorly understood. Diagnosis, signs, and symptoms

Diagnosis requires the presence of two distinct personality states (alters). Origi nal personality is generally amnestic for and unaware of alters. The median num ber of alters ranges from 5 to 10, although data suggest an average of 8 alters for men and 15 for women. Usually, two or three alters are evident at diagnosis and others are recognized during the course of treatment (see Table 16-5 ). TABLE 16-5. Mental Status Examination Questions for Dissociative Identity Disorder Symptoms If answers are positive, ask the patient to describe the event. Make sure to specify that the symptom does not occur during an episode of intoxication. 1. Do you act so differently in one situation compared to another situation that you feel almost like you were two different people? 2. Do you feel that there is more than one of you? More than one part of you? Side of you? Do they seem to be in conflict or in a struggle? 3. Does that part (those parts) of you have its (their) own independent way(s) of thinking, perceiving, and relating to the world and the self? Have its (their) own memories, thoughts, and feelings? 4. Does more than one of these entities take control of your behavior? 5. Do you ever have thoughts or feelings, or both, that come from inside you (outside you) that you cannot explain? That do not feel like thoughts or feelings that you would have? That seem like thoughts or feelings that are not under your control (passive influence)? 6. Have you ever felt that your body was engaged in behavior that did not seem to be under your control? For example, saying things, going places, buying things, writing things, drawing or creating things, hurting yourself or others, and so forth? That your body does not seem to belong to you? 7. Do you ever feel that you have to struggle against another part of you that seems to want to do or to say something that you do not wish to do or to say? 8. Do you ever feel that there is a force (pressure, part) inside you that tries to stop you from doing or saying something? 9. Do you ever hear voices, sounds, or conversations in your mind? That seem to be discussing you? Commenting on what you do? Telling you to do or not do certain things? To hurt yourself or others? That seem to be warning you or trying to protect you? That try to comfort, support, or soothe you? That provide important information about things to you? That argue or say things that have nothing to do with you? That have names? Men? Women? Children? 10. I would like to talk with that part (side, aspect, facet) of you (of the mind) that is called the “angry one” (the Little Girl, Janie, who went to Atlantic City last weekend and spend lots of money, etc). Can that part come forward now, please? 11. Do you frequently have the experience of feeling like you are outside yourself? Inside yourself? Beside yourself, watching yourself as if you were another person? 12. Do you ever feel disconnected from yourself or your body as if you (your body) were not real? 13. Do you frequently experience the world around you as unreal? As if you are in a fog or daze? As if it were painted? Two-dimensional? 14. Do you ever while looking in the mirror not recognize who you see? See someone else there? Adapted from Loewenstein RJ. An office mental status examination for complex chronic dissociative symptoms and multiple personality disorder. Psychiatr Clin North Am . 1991;14(3):567-604. Copyright © 1991 Elsevier. With permission.

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Transition from one original personality to the alter or from one alter to an other tends to be abrupt. During a specific personality state/alter, patients are amnestic about other states and events that took place when another personality was dominant. Some personalities may be aware of aspects of other personali ties; each personality may have its own set of memories and associations, and each generally has its own name or description. Different personalities may have different physiologic characteristics (eg, different eyeglass prescriptions) and different responses to psychometric testing (eg, different IQ scores). Alters may be of different sexes, ages, or races than the original personality. One or more of the alters may exhibit signs of a coexisting psychiatric disorder (eg, mood disor der, personality disorder). Signs of DID are listed in Table 16-6 . The diagnostic criteria for DID require a discontinuity in agency and sense of self, as well as alters’ ability to assume control over patients’ executive function ing. Criterion A also notes that each alter possesses unique characteristics with respect to things like memory, behavior, and perception. Criterion B requires the existence of multiple episodes of amnesia, while Criterion C requires these disruptions lead to distress or impairment. Disturbances should not be part of a normal cultural or religious tradition (Criterion D) or better explained by another condition or due to the use of a substance (Criterion E). Differential diagnosis For a list of differential diagnosis, see Table 16-7 . Psychotic disorders DID may be mistaken for hallucinations associated with psychotic disorders like schizophrenia, particularly if the patient is capable of communicating with an alternate personality, in which case the clinician may assume the alter is merely a voice the patient hears instead of a separate identity. A key distinction between psychotic hallucinations and dissociative experiences is that the former do not TABLE 16-6. Signs and Symptoms of Dissociative Identity Disorder 1. Reports of time distortions, lapses, and discontinuities 2. At least two distinct personality states (can be described/experienced as “being possessed by” another) 3. Discontinuous identity (eg, dichotomies in memory, behavior, or consciousness) 4. Persistent gaps in memory and personal information 5. Fantasy play in children is excluded. 6. Being recognized by others or called by another name by people whom the patient does not recognize 7. Notable changes in the patient’s behavior reported by a reliable observer: The patient may call themselves by a different name or refer to themselves in the third person. 8. Other personalities are elicited under hypnosis or during amobarbital sodium interviews. 9. Use of the word “we” in the course of an interview 10. Discovery of writings, drawings, or other productions or objects (eg, identification cards, clothing) among the patient’s personal belongings that are not recognized or cannot be accounted for 11. Headaches 12. Hearing voices originating from within and not identified as separate 13. History of severe emotional or physical trauma as a child (usually before the age of 5 y) Used with permission of Elsevier Science &Technology Journals from Cummings JL. Dissociative states, depersonalization, multiple personality, episodic memory lapses. In: Cummings JL, ed. Clinical Neuropsychiatry . Grune & Stratton; 1985:122; permission conveyed through Copyright Clearance Center, Inc.

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Dissociative Disorders

TABLE 16-7. Differential Diagnosis of Dissociative Identity Disorder Affective disorders Psychotic disorders Anxiety disorders Posttraumatic stress disorder Personality disorders Neurocognitive disorders Seizure disorders Somatic symptom disorders Factitious disorders Malingering Other dissociative disorders Deep-trance phenomena

involve a disruption of identity, whereas the latter do. Additionally, patients with DID will attribute dissociative experiences to alters rather than relying on delu sional explanations. Other specific dissociative disorder The existence of alters, disruptions in single identity narrative, and recurrent am nesia are core features of DID. Patients with other specific dissociative disorders may have similar symptoms, but their condition may not meet full criteria for DID. Posttraumatic stress disorder Patients can be diagnosed with both DID and PTSD. The dual diagnosis is rel atively common, as both conditions can oftentimes be traced back to trauma. A key distinction between the two is that dissociative symptoms may be present in PTSD (ie, dissociative flashbacks or dissociative amnesia based around the traumatic event), but patients with DID experience not only disruptions but also changes in identity states. Amnesias and intrusions are recurrent and not con nected to the traumatic events. Bipolar disorders Patients with DID may often be diagnosed with bipolar disorder, particularly bipolar II disorder, which involves cycling between hypomanic and depressive moods. The changes in personality can be mistaken for mood cycling. If patient displays changes in mood in conjunction with overt changes in identity, diagno sis of DID may be warranted. Major depressive disorder Patients with DID may experience comorbid depressive disorders in some per sonality states, but not all, thereby creating a complicated diagnostic situation. In this scenario, other specified depressive disorder with DID can be used to recognize the fluctuations in mood. Substance-/medication-induced disorders Patients with severe substance use disorders may seem to exhibit changes in person ality when under the influence of substances or experience blackouts, while patients with DID will experience dissociative experiences without the use of substances.

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Seizure disorders Several symptoms associated with DID may be observed in patients with sei zure disorders (eg, depersonalization/derealization, out-of-body experiences, disruptions in consciousness, amnesia), but patients with seizure disorders tend to achieve very low on dissociation scores while patients with DID score very high. Personality disorders Patients with DID may present identities with severe personality disorders, espe cially borderline personality disorder. Conversely, patients with borderline per sonality disorder may exhibit erratic mood and behaviors, as well as an inability to form stable interpersonal relationships. The key distinction is that patients with borderline personality disorder do not experience disruptions in conscious ness, memory, or identity narrative. Conversion disorder Although dissociative amnesia may occur with conversion disorder (also known as functional neurologic symptom disorder), the amnesia is limited in scope (eg, amnesia during a nonepileptic seizure). Additionally, patients with DID have dis ruptions in consciousness, memory, and identity narrative, whereas patients with conversion disorder will not. Facetious disorder and malingering Individuals who feign DID often stand to gain or to avoid legal or financial difficulties. Additionally, they oftentimes have no history of trauma, seem to almost enjoy “having” the disorder, and create superficial personalities that may be entirely innocent or entirely sadistic. Conversely, patients with DID typically are ashamed of the condition, have no ulterior motive, and report a history of trauma. CLINICAL HINT Do not confuse imaginary companions which begin in childhood and may persist through adulthood with an alter. The companion is recognized as a separate being that may or may not communicate with the patient; the companion is always known and never takes over the patient’s personality. Course and prognosis The earlier the onset of DID, the worse is the prognosis. It is chronic and the most severe of the dissociative disorders. Levels of impairment range from mod erate to severe, depending on the number, type, and chronicity of the various alters. Individual personalities may have their own separate mood disorders and personality disorders, with other dissociative disorders being the most common. Recovery is generally incomplete and unfortunately as many as two-thirds of patients with DID attempt suicide.

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Treatment Psychotherapy

Insight-oriented psychotherapy, often with hypnotherapy or drug-assisted inter viewing, is the most efficacious approach. Hypnotherapy is useful in obtaining additional history, identifying previously unrecognized alters, and fostering ab reaction. Psychotherapeutic treatment begins by confirming the diagnosis and by identifying and characterizing the various personalities. Goals of therapy include reconciliation of disparate, split-off affects by helping the patient understand that the original reasons for the dissociation (overwhelming rage, fear, and confusion secondary to abuse) no longer exist and that the affects can be expressed by one whole personality without the self being destroyed. However, despite these treat ment modalities, hospitalization may be necessary in some cases. Pharmacotherapy Drug-assisted interviewing is helpful in obtaining additional history and identi fying unrecognized identities. Antidepressant and antianxiety medications can be useful as adjuvants to psychotherapy. In select groups of patients, anticonvulsant medications, such as carbamazepine (Tegretol), have been helpful (see Table 16-8 ). Depersonalization/Derealization Disorder Depersonalization is defined as the persistent or recurrent feeling of detachment or estrangement from one’s self. The individual may report feeling like an au tomaton or watching themselves in a movie. Derealization is somewhat related and refers to feelings of unreality or of being detached from one’s environment. TABLE 16-8. Medications for Associated Symptoms in Dissociative Identity Disorder Medications and somatic treatments for posttraumatic stress disorder (PTSD), affective disorders, anxiety disorders, and obsessive compulsive disorder (OCD) Selective serotonin reuptake inhibitors (no preferred agent, except for OCD symptoms) Fluvoxamine (Luvox) (for OCD presentations) Clomipramine (Anafranil) (for OCD presentations) Tricyclic antidepressants Monoamine oxidase inhibitors (if patient can reliably maintain diet safely) Electroconvulsive therapy (for refractory depression with persistent melancholic features across all dissociative identity disorder alters) Mood stabilizers (more useful for PTSD and anxiety than mood swings)

Dissociative Disorders

Divalproex (Depakote) Lamotrigine (Lamictal) Oral or intramuscular benzodiazepines

Medications for sleep problems

Low-dose trazodone (Desyrel) Low-dose mirtazapine (Remeron) Low-dose tricyclic antidepressants Low-dose neuroleptics Benzodiazepines (often less helpful for sleep problems in this population) Zolpidem (Ambien) Anticholinergic agents (diphenhydramine [Benadryl], hydroxyzine [Vistaril])

Naltrexone (ReVia)

Medications for self-injury, addictions

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The patient may claim that the outside world lacks lucidity and emotional color ing and that they feel they are dreaming or dead. Epidemiology Though pathologic depersonalization/derealization is rare (lifetime prevalence is estimated to be between 0.8% and 2%), occasional isolated depersonaliza tion episodes are common and occur in 70% of a given population, with women more likely to experience episodes than men. The mean age of occurrence for the disorder is 16 years and rarely occurs in persons over the age of 40 years. The gender ratio of pathologic depersonalization/derealization is 1:1. Comorbidity Common comorbidities include unipolar depressive disorder and anxiety disorders. Etiology Predisposing factors include anxiety, depression, and severe stress. Depersonal ization/derealization disorder is frequently associated with anxiety disorders, de pressive disorders, and schizophrenia. It may also be caused by a psychological, neurologic, or systemic disease. Stress or trauma may precipitate depersonalization/derealization disorder. Additionally, episodes or extended periods of depersonalization/derealization are associated with an array of substances including alcohol, barbiturates, ben zodiazepines, scopolamine, β -adrenergic antagonists, marijuana, and virtually any phencyclidine (PCP)-like or hallucinogenic substance. Laboratory and psychological tests There are no laboratory tests for depersonalization/derealization disorder. Pathophysiology The pathophysiology of the disorder is not well understood. Diagnosis, signs, and symptoms A number of distinct components comprise the experience of depersonalization, including a sense of (1) bodily changes, (2) duality of self as observer and actor, (3) being cut off from others, and (4) being cut off from one’s own emotions. Pa tients experiencing depersonalization often have great difficulty expressing what they are feeling. Patients who are depersonalized may not adequately convey to the examiner the distress they experience and may try to express their subjective suffering with banal phrases such as “I feel dead,” “Nothing seems real,” or “I’m standing outside of myself.” While complaining bitterly about how this is ruining their life, they may nonetheless appear remarkably undistressed (see Table 16-9 ). TABLE 16-9. Signs and Symptoms of Depersonalization/Derealization Disorder • Persistent feelings of depersonalization or derealization without loss of reality testing • Depersonalization: feeling as though living outside one’s body, disconnected from sensations, emotions, and actions • Derealization: feeling detached from reality, as if in a dream

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