Overlap and Associations of Psychiatric and Sleep Disorders, Exams of Psychiatry

Download Overlap and Associations of Psychiatric and Sleep Disorders and more Exams Psychiatry in PDF only on Docsity! Binesca ATI my Hay BOARD REVIEW pyar em Ty MONTE eee ema eM mele] The best rapid, last-minute review New Rebecca Schmidt Psychiatry BOARD REVIEW Third Edition Rebecca A. Schmidt, MD President and Chief Executive Adult, Child, and Adolescent Psychiatric Associates of Omaha Assistant Clinical Professor Department of Psychiatry Creighton University School of Medicine Omaha, Nebraska CONTENTS Contributors...................................................................................................................... ix Introduction......................................................................................................................xi SECTION I. GENERAL INFORMATION 1. Classification of Mental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2. Psychiatric Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 3. Neuropsychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 4. Psychological Sciences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 5. Quantitative and Experimental Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 SECTION II. PSYCHOPATHOLOGY 6. Schizophrenia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 7. Other Psychotic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 8. Mood Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 9. Anxiety Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 10. Somatoform Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 11. Factitious and Dissociative Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .103 12. Sexuality Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .111 13. Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .121 14. Sleep Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131 15. Impulse Control Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 16. Personality Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 v vi Contents ... SECTION III. SPECIAL TOPICS 17. Psychiatric Issues Related to Acquired Immunodeficiency Syndrome (AIDS) . . . . . . . . . . . . .163 18. Consultation Liaison Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171 19. Mental Disorders Due to a General Medical Condition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183 20. Geriatric Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189 21. Substance Abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201 22. Suicide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .213 23. Forensic and Ethical Issues in Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217 24. Noncompliance with Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .223 25. Cultural Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .229 SECTION IV. SELECT TOPICS IN CHILD PSYCHIATRY 26.Normal Growth and Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .235 ❍ How does the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), compare to the International Classification of Diseases, 10th Revision (ICD-10)? The ICD-10, which is the official system used in Europe, and the DSM-IV were developed in a coordinated fashion. The terms in both classification systems and codes correlate and are fully compatible, although the wording may differ. All the DSM-IV categories are found in ICD-10, but not all ICD-10 categories are found in DSM-IV. ❍ What is the official nomenclature of American psychiatry? The DSM-IV, published in 1994, is the official nomenclature for psychiatry (as well as other mental health professions) in the United States. The DSM-IV is a result of a three-stage revision process, including reviews of scientific literature, data reanalyses, and field trials of diagnostic criteria. ❍ The original Diagnostic and Statistical Manual of Mental Disorders, published in 1952 by the American Psychiatric Association, was essentially developed as an adaptation of what publication? The Medical 203, a classification system established after World War II by the U.S. Army. Developed by William C. Menniger and others, the Medical 203 was heavily influenced by the theories of Adolph Meyer, who proposed that mental health disorders were a result of one’s “reactions” to their environment. ❍ How did the DSM-II differ from the DSM-I ? Use of the term “reaction” was discontinued, but use of the term “neurosis” was continued. CHAPTER1 Classification of Mental Disorders ❍ Define the difference between “psychosis” and “neurosis.” According to American Psychiatric Association terminology, the word “psychosis” indicates severe impairment in reality testing and includes delusions and hallucinations, without insight. The DSM-IV does not include use of the term “neurosis” in its official nomenclature, but the term is generally accepted to mean a disorder with prominent anxiety and no psychotic features. (The ICD-10 does include a category of “neurotic” disorders.) On a side note, suggested omission of neurosis from the DSM-III, almost caused the APA Board of Trustees to not approve the DSM- III for publication in the late 1970s. ❍ How did the DSM-III, published in 1980, differ from the DSM-I and DSM-II ? The DSM-III represented the first widespread use of diagnostic criteria (descriptors) to define mental health disorders in a manner that did not imply etiology. In addition, a multiaxial assessment system was introduced to help “plan treatment and predict outcome.” 3 ❍ ... CHAPTER1 Classification of Mental Disorders 5 How does a health care professional describe a mental disorder secondary to a medical condition, such as major depression secondary to hypothyroidism? Mental disorders, which are attributable to an underlying medical condition, are listed under Axis I (i.e., mood disorder due to hypothyroidism). The medical condition is also listed on Axis III. ❍ What does “not otherwise specified” (NOS) mean? In the DSM-IV, NOS is used if the patient’s symptoms do not meet criteria for a specific diagnosis—the symptoms are either below the threshold of the criteria or present in mixed or atypical manner. The term NOS is also used when the clinician is uncertain about the etiology of a patient’s symptoms (i.e., depression which is primary vs. depression which is secondary to cocaine use). ❍ What is meant by “diagnostic hierarchy”? DSM-IV uses a hierarchical scheme to approach diagnoses. This means that certain diagnoses preclude others, such as a substance-induced depression preempting a diagnosis of major depressive disorder. Other hierarchical considerations are when a more pervasive disorder (such as schizophrenia) preempts a less pervasive disorder. Exclusionary criteria are specifically listed as part of the DSM-IV criteria and are also reflected in the DSM-IV decision trees in the back of the manual. ❍ What is the time criterion for substance-induced disorders? For a disorder to be considered directly related to substance use, the DSM-IV indicates that the symptoms develop within a month of the substance use. There are times when the symptoms persist beyond 1 month. “Substances” can include medications. ❍ What are the key features of a defined “mental disorder”? To be defined as a disorder, the symptoms must be associated with distress and disability or with the risk of “suffering, death, pain, disability, or an important loss of freedom.” The symptoms must not be limited to a culturally accepted response to stressors (such as acute bereavement). ❍ ❍ Does the DSM-IV include any conditions that are not “psychiatric disorders” at this time? The DSM-IV includes a section on “Other Conditions That May Be a Focus of Clinical Attention.” This section includes new or controversial categories under study. Examples of diagnoses in this section include caffeine withdrawal, premenstrual dysphoric disorder, and mixed anxiety-depressive disorder. ❍ When should a health care professional use his or her clinical judgment in using the DSM-IV? Always! The DSM-IV is meant as a guide and not as a rigid document. The sequential changes in the DSM-IV, with resulting changes in criteria and even the addition or deletion of entire diagnoses, indicate the limitations of the categorical approach and the need for clinical judgment to always be part of a diagnosis. ❍ What is a “V code”? A “V code” is a code used to describe a clinical condition that may be important in the overall clinical presentation but not a disorder. Examples of V codes include partner or sibling relational problems, problems related to abuse or neglect, and phase of life problems or bereavement. “No disorder” on Axis I or Axis II is also listed as a V code (V71.09). ❍ 6 Psychiatry Board Review ... What is the use of rating scales in psychiatry? Rating scales allow the quantitative measure of a patient’s symptoms or functioning. Scales add data to the clinical database and are helpful in measuring treatment effects over time. Rating scales may be clinician rated or patient rated. ❍ What is the Brief Psychiatric Rating Scale (BPRS)? The BPRS is a rating scale that assigns number values to 18 different symptoms. The BPRS addresses more severe problems, such as psychosis, and is often used as an outcome measure in clinical trials of antipsychotic medications. ❍ What is the Hamilton Anxiety Scale (HAM-A)? The HAM-A is a rating scale that is clinician rated. It assesses a variety of somatic and psychological symptoms of anxiety. The Hamilton Depression Scale (HAM-D) is a clinician-rated depression scale that similarly assesses and assigns a numerical value to the degree of depression found in a patient. Both of these scales are frequently used in the clinical setting as well as in clinical trials of interventions for depression and anxiety. ❍ What is the Beck Depression Inventory (BDI)? The BDI is a rating scale that is patient rated. The questions on the BDI target cognitive symptoms and, compared to the HAM-D, has much less emphasis on somatic symptoms. The BDI has wide use both in the clinical setting (where it is easily administered to patients) and in research of depression. ❍ What are some of the advantages to using the DSM-IV approach? With the DSM-IV, the reliability of diagnosis is improved (although never perfect). That is, two observers of the same patient would be likely to agree on the diagnosis. The use of the DSM-IV also facilitates history taking because then the clinician is aware of which specific symptoms to target in the interview. In addition, differential diagnosis is facilitated by the DSM-IV approach, since the criteria are explicit and overlaps are addressed in the “rule out” part of each diagnostic table. ❍ What are some of the disadvantages of the DSM-IV approach? The diagnoses, although field tested and based on research, are still relatively arbitrary. In the quest for certainty, clinicians may develop a false sense of security in ❍ different levels of adaptation. This scale is under study for possible inclusion into the axes. This page intentionally left blank ❍ What are the three types of clinical psychiatric evaluations according to the American Psychiatric Association (APA)? The general psychiatric evaluation, the emergency psychiatric evaluation, and the clinical psychiatric consultation. ❍ What are the goals of a general psychiatric evaluation according to the APA? To establish a diagnosis, generate a case formulation, develop a treatment plan, and ascertain if any symptoms (such as suicidal ideation) need emergency treatment. Development of an empathic rapport is also essential to initiating and maintaining treatment compliance. ❍ How do the goals of an emergency psychiatric evaluation differ from the goals of a general psychiatric evaluation? Not much, in reality. However, out of necessity, there is a greater emphasis on safety and willingness to participate in treatment during the emergency psychiatric evaluation. In the event that a person is unable to maintain his or her own safety (and/or others), and unwilling to participate in an appropriate level of care, involuntary commitment processes are indicated. ❍ What is the essential component of the clinical psychiatric consultation? The reason for the evaluation. If you do not answer the question the consulting physician, court, therapist, or caseworker is asking, you will not be consulted again. When the reason for the psychiatric consultation is vague, it is best to ascertain (from the person/institution requesting the evaluation) the exact reason for the evaluation (i.e., psych 2C = call 2U). CHAPTER2 Psychiatric Assessment 11 Psychiatry Board Review ... ❍ ❍ What information should be included in the history of present illness? The severity and duration of current symptoms, as well as identifiable stressors. Pertinent negatives as well as statements regarding dangerousness to self and others should also be included. ❍ True/False: A substance abuse history is not a component of the psychiatric evaluation. False. A substance abuse history is critical to every psychiatric evaluation, even if it is negative. The use of substances during any psychiatric illness does tend to expand the differential diagnosis and is a major risk factor in dangerousness to self or others. ❍ Past psychiatric history should include what information? The past psychiatric history should include information about any inpatient psychiatric hospitalizations, the reason for hospitalization, and diagnoses, if available. Information about index hospitalizations are often very helpful as to the severity of illness and diagnosis, especially if the patient is presenting for treatment in a stable condition. In addition, prior outpatient services by psychiatrists and other mental health providers should be included, as well as a history of previous medication trials and the response thereof. ❍ ... CHAPTER2 Psychiatric Assessment 11 Why is past medical history an essential component of the psychiatric evaluation? Past medical history is essential in ruling out medical causes of psychiatric symptoms, as well as assessing for medication interactions that may be present. In addition, a medical illness may be a major stressor, particularly when that illness is disabling or disfiguring. ❍ What information should be included in a developmental history? Information regarding birth history, developmental milestones, relationships, and level of functioning in those relationships are the items that are generally included in a developmental history. ❍ What clinical implications does a family history of psychiatric disorders? A positive psychiatric family history may help with establishing risk factors for particular diagnoses, predicting response to various medications, and in developing a greater understanding of the patient’s past and current family milieu. ❍ What is one of the best means for evaluating the distribution of mental illness in a family? A genogram. ❍ What does the occupational and social history tell the examiner about a patient’s level of functioning? An occupational and social history gathers information about a person’s ability to “work and love.” The ability to hold a job for a period of time demonstrates an ability to structure daily activities, meet expectations, relate adequately with peers and supervisors, and take on a certain minimum level of responsibility. The ability to have a long-term relationship indicates an ability to attend to someone else’s needs, control impulses, and make a commitment. ❍ List some questions pertaining to a patient’s religious background. Questions to ask about the role of religion in a person’s life could include some of the following: Were there conflicts between the patient’s and parent’s religious beliefs? How large a role does religion play in the patient’s life? How do the parent’s religious ❍ beliefs impact on the patient’s attitude toward emotions, conflict, and psychiatric treatment? ❍ An extensive legal history can lead one to consider which two diagnoses? Antisocial personality disorder, and alcohol and/or substance dependence. ❍ Is physical examination included in a psychiatric evaluation? Yes. Particularly because some physical findings may be directly related to the patient’s psychiatric condition or psychotropic medication side effects. ❍ What conditions can cause increased psychomotor activity? Anxiety, akathesia, hyperactivity associated with attention deficit hyperactivity disorder, elevated mood, agitation during psychotic episodes, confusional states due to delirium or dementia, and iatrogenic causes. ❍ ... CHAPTER2 Psychiatric Assessment 13 Name five risk factors for suicide. Previous attempts, seriousness of attempts, a history of alcohol or drug usage, lack of social support, and presence of an Axis I disorder. ❍ Does the risk of suicide increase with direct questioning about suicide? There is no evidence that it increases risk, and it is likely to increase communication and trust with the patient. ❍ While interviewing a potentially violent patient, what precautions should be taken? Do not interview the patient alone. Leave the door to the interview room open, and sit between the patient and the door to allow for unrestricted exit. ❍ What factors are involved in assessing acute dangerousness? History of violent behavior, current violent ideation, a realistic and premeditated plan, and intent. ❍ Name three kinds of normal perceptual disturbances? Illusions, hypnagogic hallucinations, and hypnopompic hallucinations. ❍ Should a patient’s delusions be directly confronted? No, the patient will generally become more defensive and even more fixed in their beliefs. ❍ What exactly is a delusion? A delusion is a false belief not based on reality. ❍ List five types of delusions? Paranoid, somatic, delusions of infidelity, delusions of poverty, and delusions of grandeur are five types of delusions. Other types of delusions include, but are not limited to those of control (thought withdrawal, thought broadcasting, thought insertion, thought control), erotomania, nihilistic delusions, and bizarre delusions. ❍ In general, delusions can form about anything or anyone, and may not fit into any particular type of delusion. ❍ How is concentration assessed on a mental status examination? By patient report, behavioral observation, serial 7’s (or 3’s if there are educational or developmental deficits noted), or by spelling the word “world” backward. ❍ In a patient who is disoriented, which sphere is the last to be affected; which is the first? Orientation to person; orientation to time. ❍ What is the best way to infer a patient’s level of intellectual functioning? By considering the patient’s vocabulary and ability to interpret proverbs. 18 Psychiatry Board Review ... ❍ What is considered to be a normal digit span? The majority of people are able to recall seven digits forward and five to seven digits backward. ❍ What are the essential differences between delirium and dementia? Delirium is characterized by an acute state of confusion, disorientation, and varying levels of consciousness, while dementia is a gradual or step-wise decline in intellectual functioning. ❍ What are the characteristic features and course of delirium? Delirium is characterized by an acute onset of impaired consciousness, with global impairment of cognitive functions. The course is usually brief and fluctuating, and rapid improvement occurs when the underlying etiology resolves. ❍ How can agitation be distinguished from anxiety in the geriatric population? Agitated individuals do not generally complain of a sense of impending doom or dread. ❍ In distinguishing between schizophrenia and bipolar disorder, what single finding on mental status examination would most likely lead to a diagnosis of schizophrenia? Flat affect. 21 Psychiatry Board Review ... ❍ What are the most common psychiatric presentations of frontal lobe tumors? Irresponsibility, childishness, indifference toward others, disinhibition, facetiousness, inappropriate sexual behavior, and witzelsucht—a tendency to make light of everything, albeit with a sarcastic, angry edge to the humor. Previous cognitive skills are preserved and formal intelligence is unaffected, but “executive functioning” can be severely disrupted. Right frontal damage is associated with euphoria; left frontal damage with akinesia, abulia, and flattened affect. ❍ What percentage of frontal lobe tumors present with psychiatric symptoms? Ninety percent. ❍ What is the most common psychiatric presentation of temporal lobe tumors? Cancer in the temporal lobes often presents with a schizophrenia-like illness, but can also cause depressed mood, apathy, irritability, euphoria and hypomania (because of interference in the connections between the temporal and frontal lobes/limbic system), lability and intensification of premorbid personality traits, anxiety, and panic attacks. ❍ How can temporal lobe tumors be distinguished from schizophrenia? Temporal lobe tumors will often be associated with visual, olfactory, and tactile hallucinations as well as auditory hallucinations, while affect is typically spared. The psychosis will usually present as repeated “spells,” staring behavior or dreamlike episodes, and there can also be episodic mood swings. Tumors in the dominant lobe are associated with receptive aphasia or deficits in the ability to learn and remember verbal information; those in the nondominant lobe with disruption in the discrimination of nonspeech sounds. ❍ What is the psychiatric presentation of parietal lobe tumors? Symptoms of parietal lobe tumors are often more cognitive than behavioral. There is often a marked lack of awareness of deficits or even frank denial on the part of the patient (anosognosia or “neglect syndrome”), and the often-bizarre neurologic presentation can lead to incorrect diagnoses of conversion or somatization disorders. ❍ How about occipital tumors? Also fairly silent psychiatrically, fewer than 20% of occipital tumors have an initial behavioral presentation. The characteristic visual hallucinations tend to be simple and unformed, often little more than flashes of light, but can be associated with agitation, 22 Psychiatry Board Review ... ❍ irritability, fatigue, suspiciousness, and prosopagnosia (an inability to recognize familiar faces). Homonymous hemianopsia is common. ❍ What is the psychiatric presentation of diencephalic tumors? Tumors of the thalamus, hypothalamus and the area surrounding the third ventricle often interrupt the cortical–striatal–pallidal–thalamic–cortical loop, affecting many frontal functions and presenting as a frontal lobe syndrome. Hypothalamic tumors can cause hyperphagia, daytime somnolence, or anorexia nervosa. Diencephalic tumors often cause a subcortical dementia affecting memory and causing slowing of thought processes, apathy, abulia, depression, and inability to manipulate acquired knowledge. Interruption of CSF flow by tumor growth can cause hydrocephalus and consequent generalized cognitive dysfunction. ... CHAPTER3 Neuropsychiatry 23 ❍ What are the five signs that should lead one to suspect a brain tumor in a psychiatric patient? Seizures, especially if focal or new onset (this is the initial manifestation of 50% of brain tumors), headaches (especially if dull, new onset, poorly localized, nocturnal or positional, present on awakening, and worsening with time), nausea and vomiting, sensory changes (especially visual changes, vertigo, or unilateral hearing loss), and focal neurological signs (such as weakness, ataxia, or localized sensory loss). ❍ What procedures may aid the diagnosis of a brain tumor? CT scans are good for identifying small soft-tissue mass lesions and concomitant calcifications, obstructive hydrocephalus, and midline shift. They may not reveal very small tumors, however, and can miss isodense tumors and carcinomatosis (diffuse meningeal involvement). MRIs have better resolution and are thus better at revealing very small tumors; the drawbacks are cost, the inability to detect calcifications, and the restriction of subjects to those without metal in their heads. Cisternography, in which dye is injected into the ventricles, can aid in the differential diagnosis of intraventricular tumors and tumor-associated hydrocephalus. Skull x-rays can diagnose craniopharyngiomas, pituitary tumors, and “empty sella” syndrome, but bone scans are better at detecting bony metastases. Chest x-rays are useful for detecting primary neoplasms of the lung, the most frequent source of brain metastases. A lumbar puncture is useful only for diagnosing meningeal carcinomatosis or leukemia if other tests are unrevealing, and requires a preliminary CT scan or MRI if there is any suspicion of increased intracerebral pressure. EEGs are frequently normal, but sometimes there are diffuse or focal spikes or slow waves, either continuous or paroxysmal. Angiography is useful for establishing the vascular supply of a tumor prior to surgery. Neuropsychiatric testing, formerly used to localize the lesion before the advent of modern imaging, now is useful to establish the extent of the dysfunction, provide a baseline measurement of cognitive function, and help to optimize rehabilitation posttreatment. The advantages of SPECT, PET, BEAM, and MEG scans over the above diagnostic tests are as yet unclear. ❍ How should therapy be altered if a patient with preexisting psychiatric disease presents with a brain tumor? Clinicians should be especially aware of drug–drug interactions, drugs that cause delirium, and those that cause seizures, because patients with cranial neoplasms become more sensitive to all three. Drug dosages should be decreased (use 1–5 mg of haloperidol, for example, instead of 10–20 mg) and serum levels should be monitored. To decrease the risk of delirium, it is better to substitute haloperidol, carbamazepine, valproate, or benzodiazepines for lithium. Likewise, SSRIs, MAOIs, or secondary amines are better tolerated than TCAs, high-potency neuroleptics are safer than low- potency, and the antiparkinsonian agents amantadine or diphenhydramine much less likely to cause anticholinergic delirium than benztropine, trihexyphenidyl, or 26 Psychiatry Board Review ... ❍ ❍ What patterns of psychopathology are common in those with a seizure disorder? There are three patterns of psychopathology associated with seizure disorders, but they are poorly characterized and overlap. The first pattern is characterized by perceptual changes, alterations in consciousness, and poor memory of events. The second is more chronic, associated with paranoia, simple auditory hallucinations, and perceptual changes. The third is characterized by persistent depersonalization and/or visual distortions. ❍ How can a seizure be distinguished from a pseudoseizure? The distinction can sometimes be tricky, as patients often have both. ... CHAPTER3 Neuropsychiatry 27 Seizure Pseudoseizure Related to sleep deprivation No relation to sleep Marked by incontinence No incontinence Patient sustains injuries (tongue biting, head trauma, broken bones) Injuries unusual Abrupt onset and termination Gradual onset and termination Triggered by interpersonal stress No “epileptic personality” exists Positive findings on MMPI Elevated serum prolactin levels Prolactin levels normal at 15–30 min postseizure Bizarre, purposeful movements—pelvic thrusts side- to-side movements Reflexes impaired Intact reflexes Seizure exacerbated by restraint Loss of consciousness Consciousness preserved during seizure No autonomic instability No postictal changes (such as lethargy) No amnesia for seizure Extremity movements are out of phase ❍ What are some other terms for “pseudoseizure”? Conversion reaction, hysteroepilepsy, and nonepileptic seizure (the preferred term). ❍ How can a seizure disorder be distinguished from schizophrenia? Altered mentation from a seizure tends to be ego-dystonic, and the patient can talk about the symptoms in a detached manner. There is generally no evidence of interictal changes on the mental status examination, and the premorbid social histories are generally good. The seizure disorder is characterized with abrupt rather than gradual alterations in personality, mood, and ability to function that are unresponsive to psychiatric or psychological intervention. The patient generally does not quite meet DSM-IV criteria for schizophrenia. ❍ How can a seizure disorder be distinguished from a panic disorder? Often a difficult distinction, because both conditions have overlapping symptoms— depersonalization, fear, d´eja vu` and jamais vu, dizziness, illusions, paresthesias, ... CHAPTER3 Neuropsychiatry 28 chills, and flushes, which are in part mediated by a similar underlying limbic dysfunction (the temporal lobe modulates fear, for example) and amenable to similar pharmacologic intervention, i.e., benzodiazepines. However, in panic disorders, consciousness is preserved, an EEG will be normal, there are seldom olfactory hallucinations, family history is usually positive, there are no automatisms, and a positive response is found not to anticonvulsants but to antidepressants (which would typically worsen complex partial symptoms). In addition, panic attacks usually last longer than seizures, and agoraphobia is a prominent symptom in panic but not seizure. ... CHAPTER3 Neuropsychiatry 31 ❍ What tests can help diagnose Parkinson’s? PET scans show decreased uptake in the striatum, while CT scan and MRI show decreased volume in the substantia nigra of advanced cases. EEG shows nonspecific slowing. ❍ What percentage of patients with Parkinson’s disease manifest dementia? From 10% to 40%, the risk rising with age. Other risk factors for dementia in Parkinson’s disease are family history, depression, and motor disability. ❍ What are some treatments for Parkinson’s and its associated neuropsychiatric symptoms? l-Dopa is a dopamine agonist that can help compensate for the bradykinesia and rigidity, as do anticholinergics, but there is no treatment for the postural instability except for physical and occupational therapy. Antidepressants work normally on Parkinson’s patients, but this population is very sensitive to the anticholinergic, sedating, and orthostatic effects of these drugs. ECT is effective for both the affective and motor symptoms. If antipsychotics must be used, atypicals with minimal extrapyramidal side effects will have the least effect on motor symptoms. Quetiapine and clozapine have been shown to be the most effective in controlling psychotic symptoms in Parkinson’s-related psychosis, while aripiprazole is minimally effective and can exacerbate motor function. Risperdal is generally poorly tolerated in these patients and should be avoided. Whenever the use of atypicals is indicated in patients with Parkinson’s disease, monitoring for neuroleptic malignant syndrome–like symptoms is essential, and can be very difficult to distinguish from baseline symptoms. Again, the use of typical neuroleptics such as haloperidol is generally contraindicated, although may be necessary when agitation becomes a safety issue. ❍ What symptoms can occur as a side effect of treating a patient with Parkinson’s disease? Anticholinergic drugs, while being the most effective in suppressing the parkinsonian tremor, are also the most prone to induce psychosis. Delusions are usually dose related, frequently persecutory, and preceded by vivid dreams or visual hallucinations. Risk factors for delusions are age and concurrent dementia. Thirty percent of treated Parkinson’s patients will hallucinate fully formed animal or human figures, typically at night and with the hallucinations associated with sleep disturbance. These differ from typical anticholinergic hallucinations in that they are less threatening, more fully formed, not combined with tactile or auditory stimuli, and not associated with delirium. Delirium occurs in 5% to 25% of patients as a medication side effect, with bromocriptine and pergolide particularly implicated. l-Dopa can cause anxiety. ... CHAPTER3 Neuropsychiatry 32 ❍ ❍ What is delirium? Delirium is a pattern of diffuse, reversible cognitive deficits with acute onset, and a waxing and waning course. The deficits can include delusions (20%–70%), perceptual disturbances, mood alterations, language (50%–90%) and thought disorders (95%), sleep/wake disturbance (50%–95%), hallucinations (30%), and psychomotor alterations. Disorientation is common, to time (80%), place (70%), and person (20%). Twenty percent of hospital patients will become delirious, and if elderly, the 1-year mortality will be 40%. Some clinicians distinguish between acute confusional state, a disorder of attention associated with frontostriatal dysfunction, and acute agitated delirium, a disorder of emotion associated with middle temporal gyrus dysfunction, but many patients present with a mixed picture. 33 Psychiatry Board Review ... ❍ What is the etiology of delirium? The anticholinergic hypothesis of delirium holds that it is a result of decreased levels of acetylcholine. Medications or medical conditions causing decreased oxidative metabolism of glucose in the brain decrease the levels of acetyl CoA and thus acetylcholine, causing mental status changes. However, cholinergic medications can cause delirium also. Both decreased glucose and hypoxia can increase dopamine activity, while GABA levels are decreased in delirium tremens. Other neurotransmitters have also been implicated. Delirium is a final common pathway that can result from intoxication, withdrawal, metabolic dysfunction, infection, concussion or cerebral contusion, epilepsy (ictal, postictal, or interictal), neoplasm, cerebral vascular disease, hematologic processes, hypersensitivity reactions, or exposure to excessive radiation or electricity. Small thalamic lesions can also cause delirium. Delirium is sometimes divided into hyperactive or hypoactive delirium on the basis of psychomotor symptoms, but the difference is not standardized and the two cannot be distinguished on the basis of cognitive impairment or EEG findings, although hyperactive delirium is associated with a somewhat better prognosis. ❍ What are the risk factors for delirium? Risk factors for delirium include polypharmacy, multiple medical problems, alcohol and sedative/hypnotic dependence, severe burns, status postsurgery (particularly hip replacement and cardiotomy), HIV/AIDS, hypoxemia, organ insufficiency, preexisting brain disease, and increased age. ❍ What are risk factors for delirium in the elderly? In addition to the ones already listed, additional risk factors for delirium in the elderly include dementia, low albumin levels, few social interactions, age above 80 years, infection (especially UTI), visual impairment, fractures, fever/hypothermia, and thiamine deficiency. ❍ What laboratory tests can help diagnose delirium? An EEG will show slowing for both hypo- and hyperactive delirium, but this can precede or lag behind clinical changes. Alpha activity is decreased, and delta and theta activity is increased, with slowing of both peak and mean activity. TBI delirium and hepatic encephalopathy shows decreased blood flow globally on SPECT, particularly to the frontal lobes. Delirium tremens, in contrast, shows low-voltage fast activity on EEG, and is associated with increased cerebral blood flow. Evoked potentials will be abnormal in delirium. ❍ How is delirium best treated? ... CHAPTER3 Neuropsychiatry 36 ❍ ❍ What neuropsychiatric symptoms occur in Alzheimer’s? Personality alterations include passivity and disengagement, loss of enthusiasm and energy, and decreased affection. Patients become emotionally coarse, labile, insensitive, excitable, and unreasonable, and often self-centered, resistive, and disinhibited. Delusions occur in 30% to 50%, usually in the middle of the illness, typically with themes of theft, infidelity of spouse, or abandonment. “Phantom boarder” and the Capgras syndrome are common. Patients with delusions do not necessarily have more severe illness, but they do tend to be more behaviorally disturbed and difficult to manage, and manifest a more rapid intellectual decline. Hallucinations are not common, found in only 10% of Alzheimer’s sufferers, and mostly visual, consisting of people from the past, intruders, animals, objects, or scenes. Hallucinations are more likely to be secondary to concurrent delirium, or alternately, Lewy body dementia. Auditory hallucinations are usually persecutory and occur in the context of delusions. Mood changes are common, with tearfulness, feelings of worthlessness and thoughts of being a burden characteristic. Suicide is nevertheless rare. Elation occurs in one in five, angry outbursts in half. Forty percent manifest anxiety, usually in the form of excessive anticipatory concern surrounding upcoming events. Psychomotor symptoms include wandering and pacing (in the middle and late stages of the disease), assaultiveness (one in five), and most commonly, apathy, agitation, and anxiety. There are also frequent interruptions in sleep, decreased interest in food with anosmia, and decreased sexual activity. 37 Psychiatry Board Review ... ❍ What laboratory tests can help diagnose Alzheimer’s? Laboratory studies are useful in excluding other causes of dementia. Serum tests in patients with Alzheimer’s disease should be normal. CT scan and MRI show striking cortical atrophy, particularly in the medial temporal lobes. EEG may show theta and delta wave slowing, with maximal abnormality in the parietal lobes. PET scans show early abnormalities, in particular hypometabolism in the parietal lobes, later extending to the frontal lobes, with subcortical structures spared. SPECT scans are similar. Although measurement of more specific markers associated with Alzheimer’s is being developed, multiple studies have shown that a clinical diagnosis of dementia may be more sensitive and specific than these tests. ❍ What is the etiology of Alzheimer’s disease? Genetic contributions to Alzheimer’s disease include mutations on chromosomes 14 and 21, the latter of which contains the gene for the β-amyloid precursor protein. Alleles for the apo-E4 protein (chromosome 19) facilitate deposition of amyloid, leading to amyloid plaques, neurofibrillary tangles, and neuronal death through a mechanism that is not entirely clear. The presence of Alzheimer’s-like dementia symptoms in many individuals with Down’s syndrome over the age of 40 years supports the role of β-amyloid precursor protein in disease development, as these individuals have an extra 21st chromosome. Findings of increased aluminum in the senile plaques and neurofibrillary tangles have raised questions about the role of the metal in the etiology of the disease, but it does not appear related to dietary intake. Head injuries predispose patients to the later development of Alzheimer’s, and there are probably other, as yet unidentified, environmental factors. The indifference manifested by those with the disease is likely secondary to the temporal and parietal lobe damage, which also accounts for disorientation and lack of visuospatial skills; frontal lobe damage causes the disinhibition and lability. Delusions may be the result of temporoparietal alterations combined with an acetylcholine deficit. ❍ What is the treatment for Alzheimer’s disease? There is no cure, but several acetylcholinesterase inhibitors (e.g., donepezil, galantamine, and rivastigmine) may allay some symptoms of Alzheimer’s, but not delay progression. The NMDA receptor antagonist, memantine, is also available and can be used in lieu of or in combination with the existing acetylcholinesterase inhibitors. Again, the improvement seen with these medications is symptomatic only and the progression of the disease does not seem to be altered. It has been estimated that a treatment that could delay onset of Alzheimer’s disease by 5 years would halve the nursing home population in the United States. ❍ What are the symptoms of Pick’s disease? 38 Psychiatry Board Review ... ❍ Personality changes include apathy or disinhibition—patients become boisterous, irritable or overly familiar, show social and occupational withdrawal, and show decreased motivation and engagement. There can be some early, transient depression. One-third of patients will manifest elation, one-quarter will have delusions, and some may even show symptoms of the Kluver-Bucy syndrome with its consequent weight gain. Patients may be restless and¨ roam incessantly, and engage in complex repetitive acts and compulsive rituals. Memory, visuospatial, and mathematical skills are relatively spared, consistent with the pattern of cortical atrophy. The biggest deficits are in executive functioning (set shifting tasks, word-list generation, and response initiation) and language function. Pick’s patients usually have naming deficits, echolalia, impaired auditory comprehension, and poverty of speech, sometimes to the point of mutism. 41 Psychiatry Board Review ... ❍ What is Lewy body dementia? Also known as Lewy body disease, Lewy body variant of Alzheimer’s disease, diffuse Lewy body disease, diffuse cortical Lewy body disease, senile dementia of the Lewy body type (SDLBT), Lewy body dementia presents with parkinsonism, progressive dementia, mental status fluctuations, and paranoid ideation. It is notable for a delirium-like presentation with periods of mental coherence, making diagnosis difficult, and also visual hallucinations that are much more prevalent than in Alzheimer’s disease, typically of brightly colored animals or people, vivid and often frightening. The classic triad of Lewy body dementia is visual hallucinations, fluctuation of consciousness, and spontaneous parkinsonism. Patients with Lewy body dementia are unusually sensitive to neuroleptics, and therefore, must be started at very low doses. ❍ What characteristics distinguish vascular dementia from other dementias? Vascular dementias, which make up almost a third of all dementias depending on the population, present with focal neurological signs, stepwise deterioration, patchy intellectual deficits, abrupt onset and a history of cardiovascular disease, hypertension, or transient ischemic attacks. Common onset of over the age of 50 years, with males affected more than females, and death usually occurs in 6 to 8 years from cardiovascular disease or stroke. ❍ How can one diagnose vascular dementia? A definite diagnosis requires pathology, but a probable diagnosis can be made by noting the correlation between the dementia and corresponding cerebrovascular disease already diagnosed through imaging studies or the presence of focal neurological signs or stroke. The onset of the dementia should be within 3 months of the stroke. The profile of deficits varies depending on the location of the infarcts, slowness of cognition and impaired executive function are typical, as are decreased cognitive, memory, and visuospatial abilities. Language function is usually preserved. Laboratory tests are normal, but if the patient is young or lacks risk factors for stroke, an ANA, antiphospholipid antibody and lupus anticoagulant should be checked to rule out a treatable inflammatory vasculitis. CT scan can show cortical infarctions or evidence of periventricular ischemic changes, and an MRI, the technique of choice, will reveal small subcortical infarcts and white-matter changes. SPECT and PET scans should show multiple small areas of hypometabolism. History and physical is key, i.e., stepwise decline, abrupt onset, and focal signs. ❍ What causes vascular dementia? There are a number of different etiologies. Multi-infarct dementia, a term often used to refer to vascular dementia, is a result of many small-vessel infarcts affecting different areas of the brain. A strategic single infarct affecting the left angular gyrus 42 Psychiatry Board Review ... ❍ or medial thalamic nuclei will cause dementia, as will hypoperfusion from a hemorrhage or cardiac arrest, which causes border-zone ischemia. Binswanger’s disease is caused by white-matter changes, usually secondary to fibrinoid necrosis of the small vessels from hypertension. Hemorrhages, such as chronic subdurals, a ruptured cerebral aneurysm or subarachnoid hemorrhage, can also cause dementia. ❍ How does one treat vascular dementia? Control hypertension (or any other causes) and give aspirin, ticlopidine, or clopidogrel to decrease platelet aggregation. Baclofen is effective for poststroke spasticity, and nortriptyline for pseudobulbar affect. Mood disorders and psychosis can be treated in the usual manner. Patients also benefit from gait retraining and speech therapy if warranted. ... CHAPTER3 Neuropsychiatry 43 ❍ What is the relationship between stroke and depression? Thirty to fifty percent of stroke sufferers will become depressed, with 20% meeting criteria for major depression. The average duration of the depression is 1 year. There is an inverse relationship between the severity of the depression and the distance of the anterior border of a left-hemisphere lesion from the left frontal pole. Risk factors include preexisting subcortical atrophy, a family history of depression, lack of a meaningful life, and overprotection by a caregiver. Lesions of the left dorsolateral frontal cortex, left basal ganglia, or cerebellum/brainstem produce a transient depression rarely lasting more than 6 months. The test of growth hormone response to desipramine is 100% sensitive and 75% specific for poststroke depression, although this has yet to be recognized as a valid marker. ❍ What is the relationship between stroke and mania? Mania can occur with right basitemporal lesions, presumably reflecting the region’s close connection with the limbic system. Risk factors are subcortical atrophy and family history of bipolar disorder. ❍ What are the symptoms of progressive supranuclear palsy? There are several, both motor and cognitive. Patients will show profound bradykinesia, axial rigidity (neck and trunk more than limbs), and a pseudobulbar palsy (dysphagia, sialorrhea, and dysarthria). There are restrictions in gaze, vertical gaze more than horizontal (often leading to falls). Cognitive difficulties include deficits in verbal memory, calculating ability, and synthesis of complex information, with slowed central processing. There should be no agnosia, apraxia, or aphasia. Personality changes are consistent with impaired frontal function—apathy, emotional indifference, depression, irritability, forced inappropriate laughing or crying, outbursts of rage (often responsive to trazodone), or OCD-like symptoms. ❍ What laboratory tests can help in the diagnosis of progressive supranuclear palsy? Serum test results are normal. An EEG will be normal or show nonspecific findings, i.e., generalized background slowing or diffuse theta activity. CT scan and MRI will show diminished midbrain size with frontotemporal atrophy later on in the disease, PET scan reveals frontal hypometabolism, and SPECT shows a bilateral frontal hypoperfusion. ❍ What is the etiology of progressive supranuclear palsy? The exact etiology is unknown. There is decreased striatal dopamine formation and storage, and in the cortex, numbers of nicotinic acetylcholine receptors are 46 Psychiatry Board Review ... ❍ with the areas of the brain affected. One notable psychiatric symptom is the “alien hand” syndrome, in which the hand of the patient, while retaining full sensation, takes on a mind of it’s own. ❍ How does hydrocephalus present? There are two types: noncommunicating hydrocephalus, caused by an acute obstruction to CSF flow, which presents with the usual symptoms of increased intracranial pressure, headache, confusion, and ophthalmoplegia; and communicating hydrocephalus or normal-pressure hydrocephalus, caused by a deficiency in the resorption of CSF and responsible for 2% to 5% of all dementias. Normal-pressure hydrocephalus causes a characteristic triad of dementia, gait disturbance, and (later) incontinence. The dementia is frontal–subcortical in nature, characterized by deficits in attention, visuospatial skills, abstraction, judgment, and new learning. The gait slows, strides become shorter, and step height decreases, producing a characteristic “magnetic gait.” Incontinence is more likely to be urinary than fecal. ... CHAPTER3 Neuropsychiatry 47 ❍ What causes hydrocephalus? Subarachnoid hemorrhage, head trauma, encephalitis, meningitis, carcinomatous disease, and partial aqueductal obstruction, among others. ❍ How can normal-pressure hydrocephalus be diagnosed? A CT scan will show increased ventricular size, particularly anteriorly, with periventricular lucencies. A lumbar puncture will show no elevation of pressure and will be otherwise normal. Cisternography will show reflux into the ventricles, and no flow into the superior sagittal sinus where CSF is normally resorbed. ❍ What is the treatment for normal-pressure hydrocephalus? Shunting, either ventricle to peritoneum or lumbar subarachnoid to peritoneum. Not all patients improve, unfortunately. Good prognostic signs include a short duration of symptoms, a known etiology, gait disturbance presenting before dementia, visible periventricular changes on imaging, and a temporary improvement following the removal of 50 mL of CSF on lumbar puncture. ❍ What percentage of patients with Huntington’s disease present first with psychiatric symptoms and what are those symptoms? Fifty percent of Huntington’s patients will present first with emotional or cognitive symptoms such as depression, irritability, apathy, or hallucinations. ❍ What is the epidemiology of Huntington’s disease? It is an autosomal dominant trait with complete penetrance, caused by an expanded and unstable CAG trinucleotide repeat in chromosome 4, which affects 5–7 out of 100,000 people, depending on the population studied. The principal causes of death, which typically occurs around 14 years after diagnosis, are pneumonia, trauma, and suicide. Family members of Huntington’s patients show increased psychopathology, but this is uncorrelated with the length of the trinucleotide repeat in asymptomatic carriers. ❍ What is the etiology of Huntington’s disease? Degeneration begins in the medial caudate nucleus (the degree of degeneration correlating with the degree of cognitive dysfunction) and proceeds laterally to the putamen and occasionally to the pallidum. Somatostatin levels are increased, and GABA and acetylcholine levels in the striatum are decreased. There are also smaller decreases in dopamine and neurokinin. Because the major sources of input to the ... CHAPTER3 Neuropsychiatry 48 ❍ caudate are the limbic system and motor cortex, emotional and motor symptoms tend to be intertwined. ❍ What are the signs and symptoms of Huntington’s disease? Initial motor symptoms are mild rigidity, restlessness, and tic-like jerks, exacerbated by emotional stress, mental concentration, and sleep deprivation, combined with slower writhing movements such as flexion and extension of the fingers (“piano playing”). There is an ulnar deviation of the hands on walking. Later symptoms include grimacing, nodding, head bobbing and rolling, a “dancing” gait; later still, akinesia, and dystonia. Abnormalities of articulation, coordination of limb movements and saccadic motions of the eyes are strongly correlated with intellectual and functional impairment. Cognitive deficiencies occur in visuospatial skills and memory, and skill acquisition is also impaired. Language skills are preserved except for fluency and prosody, with resulting impairment in interpersonal communication—patients will answer in single words or in short, infrequent phrases lacking emotional valence. ... CHAPTER3 Neuropsychiatry 51 ❍ What are the three basic patterns of traumatic brain injury? Contusions, diffuse axonal injury, and subdural hematomas are the three basic patterns of TBIs. Contusions, which usually affect the basal and polar areas of the temporal lobes, are typically the result of low-velocity injuries, such as falls. Contrecoup injuries result from abrupt pressure changes on the opposite side of the brain from the injury. Diffuse axonal injury is usually caused by acceleration or deceleration, and results in stretched axons and disrupted axonal transport, that causes axonal swelling and detachment and wallerian degeneration of the distal stump of the axon. The most vulnerable regions of the brain susceptible to axonal injury include the reticular formation, the superior cerebellar peduncles, the basal ganglia, hypothalamus, limbic fornices, and corpus callosum. Subdural hematomas, which have effects specific to location as well as more generalized effects on affect, arousal, and cognition, occur when an injury precipitates intracranial venous bleeding between the dura and the underlying cortex. ❍ What are the effects of TBI on brain chemistry? Initially, norepinephrine levels are elevated, with the degree of elevation correlating both with worse injuries and poorer outcome. The effect of TBI on other neurotransmitters is uncertain. Following the initial injury is secondary neurotoxicity from calcium influx, exotoxin release, phospholipase activation, and lipid peroxidation that further damages axons and neuronal systems. Free radicals and the neurotransmitter glutamate have both been implicated in causing further neuronal damages, and levels of both remain elevated for days postinjury. ❍ What laboratory tests can help in the diagnosis of TBI? CT scans may not show visible lesions until months after the injury. MRI is sensitive for frontal and temporal lesions that are often not visualized on CT scan, and can show diffuse axonal injury that do not show on CT scan. SPECT will show abnormalities that correlate with the degree of trauma. EEG can show abnormal foci or areas of seizure activity, particularly if measured under conditions of sleep deprivation, photic stimulation, or hyperventilation, or with anterotemporal or nasopharyngeal leads. ❍ What are the sequelae of traumatic brain injury? Sequelae of TBIs include slowed cognitive processing, deficits in attention and arousal, concentration, executive function, memory, personality changes (typically childishness, emotional lability, restlessness, decreased social contact, poverty of interests, and loss of spontaneity), anxiety, psychosis, and epilepsy. ... CHAPTER3 Neuropsychiatry 52 ❍ ❍ What are the prognostic indicators for recovery from TBI? Good prognostic indicators are high premorbid intelligence and preserved olfaction. Poor prognostic indicators are long posttraumatic amnesia, intoxication, chronic substance abuse, increased age, psychiatric history, learning disability, and a history of preexisting behavioral problems. ❍ What is the definition of a mild traumatic brain injury? Mild traumatic brain injury occurs when trauma to the head is characterized by a loss of consciousness less than 30 minutes, antero- or retrograde amnesia that lasts less than 24 hours, an altered mental status (dazedness, disorientation, or confusion) with a Glasgow Coma Score above 13, or focal neurological deficits. 53 Psychiatry Board Review ... ❍ Describe three “frontal lobe syndromes.” The orbitofrontal syndrome is characterized by impulsivity, disinhibition, hyperactivity, distractibility, and lability, while the dorsolateral syndrome is characterized by slowness, apathy, perseveration (negative symptoms), and is also known as akinetic mutism. The inferior orbital/anterior temporal syndrome is characterized by sudden outbursts of rage, withdrawal, fearfulness, and loss of inhibitions. ❍ What are the long-term neuropsychiatric sequelae of TBI? TBI causes increased deposition of β-amyloid protein, raising the risk of Alzheimer’s disease 10-fold in those who already have one copy of the apo-E gene. The incidence of postinjury depression is difficult to assess methodologically because of confounding with posttraumatic apathy and unknown premorbid states, but it seems to be from 10% to 40%. In the first year after injury, 10% will have suicidal ideation and 2% will attempt suicide (15% in the 5 years postinjury). More common is a sadness, described as “mourning” for the lost self. The risk of depression is related to a premorbid psychiatric history and the degree of neuropsychiatric impairment, but not to loss of consciousness, amnesia, or presence of skull fractures. Poor premorbid social adjustment predicts poor recovery of ADLs and social function postinjury. Left frontodorsolateral and left basal ganglia lesions are associated with a transient depression. Mania, by contrast, is correlated with lesions at the base of the right temporal lobe or in the right orbitofrontal cortex, has an incidence of 3% in the 10 years postinjury, and is associated with a positive family history of bipolar disorder. Up to 15% of TBI sufferers will develop symptoms indistinguishable from schizophrenia, especially those with left temporal lesions. One study of a 100 homeless schizophrenics found that 55 of them had a history of TBI. The risk of epilepsy is 1% with mild, 2% with moderate, and 12% with severe TBI. Factors that increase this risk include skull fractures, penetrating wounds (50% risk of epilepsy), chronic alcoholism, intracranial hemorrhage, and increased severity of injury. Often this epilepsy does not develop until many years later (as with Phineas Gage). Ten to thirty percent develop an anxiety disorder, but PTSD is rare thanks to posttraumatic amnesia. ❍ What is postconcussion syndrome? Even mild injury or brief loss of consciousness can lead to attentional and information- processing impairment. Somatic symptoms include headache (50%), dizziness, insomnia, and fatigue (25%). Cognitive symptoms include memory impairment and decreased concentration. Perceptual symptoms include tinnitus and sensitivity to sound and light. Emotional symptoms include anxiety, depression, and irritability. ❍ How does one treat postconcussion syndrome? ... CHAPTER3 Neuropsychiatry 56 ❍ associated with hemineglect, is characterized by the lack of interest in family and friends, minimization of physical disabilities, and enjoyment of foolish jokes. Finally, pseudobulbar affect is characterized by pathological laughing or crying unrelated to one’s inner emotional state (also known as pathological emotionalism or emotional lability). ❍ What is the epidemiology of HIV dementia? HIV dementia, also known as AIDS dementia complex, AIDS encephalopathy, subacute encephalitis, HIV encephalopathy, and HIV-1-associated minor cognitive/motor disorder (HAMCMD), will affect 30% persons infected by HIV. The median survival time postdiagnosis is 6 months. ❍ What is the etiology of AIDS dementia? It is caused by direct infection of the brain by HIV, which targets temporolimbic structures, the thalamus, and the basal ganglia, causing extensive atrophy (manifested through increased ventricular size rather than widened sulci). Neurons are not direct targets, but they are susceptible to associated neurotoxicity. The gp120 protein in the viral capsid binds irreversibly to calcium channels, increasing intracellular free calcium and increasing neurotoxin production. In addition, macrophages, once they have incorporated the viral genome into their own, are induced in the presence of cytokines and infectious byproducts to produce high levels of free radicals, quinolinic acid, TNF-α, IL-1β, interferon-γ , and arachidonic acid, which in turn increase intracellular calcium and nitric oxide. Neuronal apoptosis is also triggered by TNF-α and the viral tat protein. 57 Psychiatry Board Review ... ❍ What is the differential diagnosis for mental status changes in AIDS patients? The differential diagnosis for mental status changes in AIDS patients is extensive. Toxoplasmosis, the most prevalent AIDS-related CNS infection, presents as focal or diffuse cognitive or affective disturbance, with ring-enhancing lesions on imaging. It is diagnosed by biopsy. Cryptococcus neoformans, presents as meningitis with headache, altered mental status, nuchal rigidity, nausea, and vomiting. An LP and CSF analysis is diagnostic. Cytomegalovirus can cause encephalitis, retinitis, peripheral neuropathy, and demyelination, and is treated with intravenous foscarnet or ganciclovir. Herpes simplex causes temporal lobe encephalitis or encephalomyelitis; severity is correlated with the severity of immune dysfunction, and it is treated with intravenous acyclovir. Varicella zoster causes peripheral and cranial nerve inflammation, encephalitis, and vascular inflammation, also treated with intravenous acyclovir. Non-Hodgkin’s lymphoma, the primary CNS tumor in AIDS patients, causes altered mental status, hemiparesis, aphasia, seizures, and focal signs. Other CNS pathogens include syphilis, TB, adenovirus type II, papovavirus, MAC, metastatic Kaposi’s sarcoma, Candida, Aspergillus, Coccidioides, Rhizopus, Acremonium, Listeria, Nocardia, vasculitis, thrombotic emboli, and vasculotoxicity from AIDS medications. ❍ What diagnostic tests can aid in determining the etiology of mental status changes in AIDS patients? CT scan and MRI are both good for showing ring-enhancing lesions, with MRI particularly suited as it shows high-signal intensities in subcortical white and gray matter. PET imaging will show increased glucose metabolism in basal ganglia and thalamus early in the disease, with hypometabolism late, and can be used to assess response to treatment. SPECT has an uncertain role. A lumbar puncture and CSF analysis can show toxoplasmosis, cryptococcus, HSV, VZV, CMV, and HIV, the signs of which include virions, increased IgG, HIV-specific antibody, neopterin, increased numbers of mononuclear cells, β2-microglobulin (which is correlated with the severity of the dementia), and oligoclonal bands. EEG will show abnormal frontotemporal theta slowing in 25% of otherwise asymptomatic HIV-positive patients, and is thus very sensitive for early signs of the disease. Of those with AIDS, 65% will show intermittent or continuous theta or delta slowing. Evoked potentials are also abnormal even in the asymptomatic, and manifest delayed latency in the brainstem auditory and somatosensory evoked potentials. Polysomnography shows gross disturbances in sleep architecture. ❍ What are the symptoms of AIDS dementia? Impaired attention and concentration, mental slowing, impaired memory, slowed movements, incoordination, personality changes (irritability and lability) and, as the disease worsens, severe cognitive deficits, psychomotor slowing, seizures, muteness, 58 Psychiatry Board Review ... ❍ catatonia, psychosis, mania, ataxia, spasticity, hyperreflexia, and bladder and bowel incontinence occur. ❍ What psychiatric conditions are associated with AIDS dementia? The incidence of depression is uncertain given the confounding substance abuse histories of many AIDS sufferers, but appears to be about 30%, with a risk factor being a past history of depression. Suicidal ideation has been measured at 55% in the HIV-positive population. Mania, when it appears, can be from a right frontal tumor or infection, or as a side effect of zidovudine. Anxiety can be triggered by knowledge of the diagnosis, PCP prophylaxis, CNS infections, or pulmonary insufficiency, and can often result from the zidovudine or steroids used in treatment. Delirium is also common and difficult to reverse. 36 Psychiatry Board Review ... ❍ How is lupus best treated? The treatment of lupus includes the use of high dose steroids, which ironically worsen psychiatric symptoms, anticoagulation for symptoms related to antiphospholipid antibodies, and IV pulse cyclophosphamide for severe cases. Psychiatric disease can be treated symptomatically in the usual fashion. Note: This chapter is intended as an adjunct to preparation for the neurology section of ABPN boards. Multiple references are available for study, including the Neurology: Pearls of Wisdom review book. ❍ Name three kinds of learning (conditioning). Classical, operant, and observational (or modeling). ❍ According to classical conditioning, in order to achieve a conditioned response, what must be paired with the neutral object? An unconditioned stimulus. ❍ Classical conditioning is generally thought to be most relevant to which form(s) of psychopathology? Anxiety disorders (or specific forms such as panic, phobia, and obsessive–compulsive disorder). ❍ Which psychiatric disorder might be thought of as an example of “one trial learning”? Posttraumatic stress disorder (or acute stress disorder). ❍ What do we call that which we place after a behavior that increases the likelihood that a behavior will occur again or more frequently? A reinforcer (or reward). Negative or positive ❍ If you reward (or reinforce) someone for successive approximations toward some goal, what is this called? Shaping. CHAPTER4 Psychological Sciences ❍ Punishment stops behaviors from occurring, but it has undesirable consequences. Name three. 1. Emotional reactivity (sometimes including aggression) that may interfere with learning. 2. Avoidance of the punishment in ways that are unanticipated and negative. 3. It does not teach alternative desired behaviors, it only stops what is not desired. ❍ If you wish for a behavior to be maintained, even after reinforcements (or rewards) no longer follow the behavior, the behavior will be more likely to last longer under which initial reinforcement schedule: continuous or partial? Partial. 37 ... CHAPTER4 Psychological Sciences 66 ❍ What is the name given to treatment for social deficiencies in people with schizophrenia that is most heavily based on observational learning? Social skills training. ❍ Which experimental design was popularized by the behaviorists, and which can be readily employed in the clinical setting? Single subject design or multiple baseline single subject design, commonly known as N = 1 designs. ❍ Which behavioral approach has the best likelihood of success for treating obsessive–compulsive disorder—systematic desensitization, in vivo exposure, or reverse conditioning? In vivo exposure. ❍ If a parent intentionally ignores a child’s misbehavior, this is an example of which operant conditioning principle? Extinction. ❍ Define negative reinforcement. Negative reinforcement, by definition, is the application of an event that increases the probability of a target behavior occurring in the future. For example, when a fire truck comes by with the loud siren, one puts their fingers in their ears to eliminate the loud noise. Placing one’s fingers in the ears is negatively reinforced by the reduction of a painful noise. A teacher expelling a youth from a classroom when the child says a curse word is negatively reinforced by the elimination of the noxious stimulus (youth). It is also positively reinforced in the youth if he or she wants to escape the classroom. ❍ How many “bits” of information can be stored in immediate memory for the average human? Seven. This phenomenon is actually called the “seven plus or minus two phenomena.” That is why phone numbers and zip codes are about five to nine characters. ❍ To enhance the amount of retention, several pieces of information can be associated together to form a single “bit” in immediate memory. What is this process called? ... CHAPTER4 Psychological Sciences 67 ❍ Chunking. ❍ To enhance memory, various investigators have demonstrated that pieces of information can be associated together with one another according to various mental pictorial schemes or other cognitive techniques. What are such techniques called? Mnemonic devices. ❍ Jean Piaget developed four stages of cognitive development. What are these stages? (1) Sensorimotor, (2) preoperational, (3) concrete operations, and (4) formal operations. ❍ What did Piaget call the process in which an experience is integrated into existing cognitive structures? Assimilation. 68 Psychiatry Board Review ... ❍ What did Piaget call the process whereby cognitive structures change, based on new information that cannot be assimilated into existing structures (scheme)? Accommodation. ❍ According to Piaget, before the individual progresses to the preoperational stage, what must be achieved, and at about what age does this happen? Object permanence, which occurs between 18 and 24 months of age. ❍ Name the six stages of moral development, as formulated by Lawrence Kohlberg. (1) External reward and punishment stage, (2) bargaining or marketplace stage, (3) conformist stage, (4) law and order stage, (5) social contract stage, and (6) universal ethical principles stage. ❍ What are the most common individually administered intelligence tests? The Wechsler scales (specifically, the Wechsler Adult Intelligence Scale III, the Wechsler Intelligence Scale for Children, and the Wechsler Preschool and Primary Intelligence Scale-Revised). ❍ What are the means and standard deviations of all of the Wechsler scales? The means are 100 and the standard deviations are 15. ❍ What are the levels of mental retardation, based on IQ scores? Mild: 50/55 to 70 Moderate: 35/40 to 50/55 Severe: 20/25 to 35/40 Profound: less than 20/25 Note: because of the standard error of measurement, a given IQ test score should not be taken as absolute, and allowance is made in diagnosis for the test score to vary approximately five points in either direction. That is, a person may have an IQ of 65 on a given test, but be judged appropriately by a clinician to NOT be mentally retarded. ❍ Why did Alfred Binet originally develop an IQ test? To have an objective means of assessing mental retardation. ❍ What are the two most commonly used projective personality tests for adults? ... CHAPTER4 Psychological Sciences 71 ❍ ❍ What are the factors of the five-factor theory of personality, and why is this theory considered important? Neuroticism, extraversion, openness to experience, conscientiousness, and agreeableness. This theory is considered important because these factors have arisen consistently in many factor-analytic studies of personality traits, because the factors have been replicated across many cultures, and because the factors emerge even if the people rating others have almost no contact with the people they are rating, i.e., the factors seem to be intrinsic to all humans, forming an “implicit personality theory.” ❍ What is the most important factor in determining behavior, the situation or one’s personality traits? While on the average, situations exert more influence on behavior than personality traits, the combination of the personality traits and the situation under consideration is the most predictive model, based on empirical investigation. ❍ What are the three qualities of the psychotherapist considered by Carl Rogers to be the most important for the outcome of the psychotherapy? Empathy, warmth, and genuineness. 72 Psychiatry Board Review ... ❍ For which of the following disorders would psychotherapy alone most likely be an inappropriate treatment: major depression, posttraumatic stress disorder, or panic disorder? Major depression. ❍ What factor is in general most influential in the development of friendship relationships? Proximity. ❍ What is the next most influential factor in the development of friendship relationships with others? Personal similarity. ❍ Leon Festinger demonstrated that people tend to be consistent in the way they conduct themselves. When people’s inconsistencies are pointed out, it produces distress. In general, people will try to reduce perceived inconsistency in some way. What is the name of the theory associated with these findings? The theory of cognitive dissonance. ❍ Stanley Milgram conducted a now famous set of experiments in which he demonstrated that people under certain circumstances were willing to deliver (what they believed to be) painful electrical shocks to others. What phenomenon was Milgram studying in this set of experiments? Obedience to authority. Note: these studies caused such a stir with the APA that IRBs were created. Milgram was interested in general compliance related to Nazi Germany. ❍ What activity did Muzafer Sherif demonstrate to be most effective in reducing destructive intergroup rivalry or competition? Focusing attention on to a common enemy, which resulted in the groups joining together in cooperation. ❍ Philip Zimbardo tried to conduct studies of the behavior of prisoners and guards by having ordinary people role play prisoners or guards interacting with one another. Why did he have to halt his now famous Prison–Guard experiment? 73 Psychiatry Board Review ... ❍ The guards started abusing the prisoners. Note: important related to Labeling Theory. ❍ Name two intrinsic psychological motivational systems. Appetitive (or approach) and aversive (or avoidance). ❍ Paul Ekman demonstrated that several emotional expressions seem to be biologically based or at least intrinsic to all humans, i.e., they are universally understood by humans studied across many cultures. Name six such emotional expressions. Anger, fear, sadness, joy, disgust, and surprise. ❍ What are the two factors in Stanley Schacter’s two-factor theory of emotion? (1) Arousal or activation and (2) cognitive interpretation or attribution. Quantitative and CHAPTER5 Experimental Methods ❍ What is a direct interview? An important source of information about a subject is the direct interview, which is a person-to-person interaction. ❍ What are indirect surveys? Indirect surveys are structured self-report forms that may be used for gathering research data. However, they lack the clinical judgment of an experienced practitioner that is necessary in some instances. ❍ What is reliability? Reliability refers to whether or not the findings of the assessment instrument or diagnostic procedure are reproducible (i.e., whether or not the quality of the data is trustworthy or dependable). In psychometrics, reliability is a measure of the internal consistency and stability with which a measuring instrument performs its function. Generally, reliability roughly corresponds to the everyday concept of accuracy. ❍ What is interrater reliability? Interrater reliability means the results of the survey can be replicated when the instrument is used by different examiners. A measure of the consistency of rating, interrater reliability is equal to the correlation between the ratings given by different raters of the same people or stimulus. ❍ What is test-retest reliability? Test-retest reliability means the results of the survey can be replicated when the instrument is used on different occasions. A measure of a test’s reliability, or more specifically its stability, test-retest reliability is based on the correlation between scores of a group of respondents on two separate occasions. ❍ What is validity? Validity refers to whether the test measures what it is supposed to measure, or in other words, the soundness or adequacy of something or the extent to which it satisfies certain standards or conditions. In psychometrics, validity is the extent to which a test measures what it purports to measure, or the extent to which specified inference from the test’s sores are justified or meaningful. 45 46 Psychiatry Board Review ... ❍ What are the subcategories of validity? There are many. They include criterion validity, face validity (a priori validity), content validity, concurrent validity, internal validity, external validity, ecological validity, congruent validity, consensual validity, construct validity, content validity, convergent validity, incremental validity, intrinsic validity, predictive validity, and trait validity. ❍ What is bias? There are different types of biases. The first is construct bias, which occurs when what the construct measures is not identical across groups. Method bias refers to all sources of assessment problems emanating from an instrument or its administration, such as the influence of the person or the tester on the best outcome. Finally, item bias (or differential item functioning) refers to anomalies at the item level, such as a poor translation of words. ❍ What does the double-blind design method help with? The double-blind design is helpful in controlling experimenter effects and the influence of demand characteristics. Neither the experimenter nor the research participants or subjects know, until after the data have been collected, what participants received during the experiment. The double-blind method is often used with a placebo to avoid contamination of the results from biases and preconceptions on the part of the experimenter. ❍ What is randomization? Randomization of a sample is a method in which each member of the total group studied has an equal chance of being selected. It also helps eliminate bias. ❍ What is sensitivity? Sensitivity is the ability of an assessment instrument to detect the item/quality being measured. ❍ What is specificity? Specificity refers to the ability of an assessment instrument to assess only the variable chosen for study. ❍ What is predictive value? ❍ What is a t test? A statistical procedure designed to compare two sets of observations is the t test. ❍ What is a type I error? The false claim of a true difference because the observed difference is due entirely to chance is a type I error. In statistics, a type I error occurs by rejecting the null hypothesis when the null is true. The significance level determined from a statistical test is the probability of a type I error. ❍ What is a type II error? The false acceptance of the null hypothesis when, in fact, there is a true difference but the difference is so small that it falls within the acceptance region of the null hypothesis is a type II error. In statistics, a type II error occurs by failing to reject the null hypothesis when it is false. Note: type III error is a term used to refer to an error arising from a misinterpretation of the nature of the scores being compared in a significance test. 48 Psychiatry Board Review ... ❍ What are independent variables? Independent variables are those qualities that the experimenter systematically varies (e.g., time, age, sex, type of drug). ❍ What are dependent variables? Dependent variables are those qualities that measure the influence of the independent variable or the outcome of the experiment (e.g., the measurement of a person’s specific physiological reactions to a drug). ❍ What is the sensitivity of a test? Sensitivity is the proportion of patients with the condition in question that the test is able to detect. ❍ What is the specificity of a test? Specificity is the proportion of patients who do not have the condition that the test calls negative. ❍ What is the sensitivity in the following test? Disease No Disease Test + 90 20 Test − 10 80 Total 100 100 True Positive Sensitivity = True Positive + False Negative In the table shown in the question, it is clear that 90 people who were tested have the disease, which means they are true positive. Twenty people tested positive but have no disease so they are false positive. Eighty people tested negative and have no disease so they are true negative. Ten people have the disease but tested negative (hence, they are false negative). Know the formulas and fill in the numbers to get correct answers in % values. ❍ What is the specificity in the above test? True Nagative Sensitivity = True Negative + False Positive ❍ What is the positive predictive value in the above test? True Positive Positive predictive value = True Positive + False Positive