Psychiatry in Neurology


General Psychiatry

  • 1.

    When referring to brain dysfunction (neurologic and psychiatric disorders), why are the terms focal and functional preferred over organic and inorganic ?

    Using the terms organic and inorganic to refer to neurologic and psychiatric disorders, respectively, follows from the dualistic (Cartesian) model—an antiquated model that regards mind and brain as two distinct entities, which somehow are unified. A modern neuroscience-based view is that mind is a verb; mind is what the brain does via the integration of mainly frontal and limbic cortical–subcortical circuits and distributed networks working in parallel processing. Disruption of the function of these circuits and networks underlies mental disorders.

  • 2.

    What is the Diagnostic and Statistical Manual for Psychiatric Disorders (DSM)?

    In the United States, the DSM, now in its 5th edition (DSM-5), is the most widely used clinical diagnostic schemata for psychiatric disorders. While the earliest form of the DSM was intended solely as a research tool, it has since undergone revisions to improve the validity of its diagnostic constructs and, by incorporating developmental, medical, psychological, and psychosocial factors, expand in clinical utility and is used to inform treatment selection, patient education, and prognosis and to facilitate clinical communication.

  • 3.

    Does the DSM describe specific diseases?

    Diagnoses in the DSM are based on sign and symptom clusters (phenomenology) involving cognitive, emotional, and/or behavioral dysfunction and are more akin to syndromes than diseases; the clinical presentation and course, rather than a specific etiopathology, defines the diagnosis. As such, there is often overlap among diagnostic criteria, and many disorders are considered to exist on a spectrum (and/or dimensions) ranging from normal experience/response to persistent and pervasive pathology (i.e., personality disorders).

  • 4.

    At what point do symptoms (e.g., sad feelings) become a disorder (e.g., major depressive disorder) as defined in the DSM?

    Generally, to meet diagnostic criteria of a disorder the symptoms must result in distress and disruption of functional ability of the individual (e.g., interference with work). Allowances are made for culturally/religiously normative behaviors or sociopolitical deviance (DSM-5, p 20 ).

  • 5.

    Why are psychiatric diagnoses generally “diagnoses of exclusion”?

    A multitude of etiopathologic origins can underlie psychiatric phenomenology. While the etiopathology may be known in some cases, psychiatric disorders are often complex and idiopathic. Care should be taken to evaluate for and exclude known medical causes of the phenomenology before a psychiatric diagnosis is made.

  • 6.

    What are some interviewing techniques for eliciting sensitive information (e.g., sexual trauma history, suicidality, or current substance abuse)?

    • Start with open-ended questions and an empathic and nonjudgmental demeanor.

    • Consider follow-up with structured, systematic questions (employ structured interviews and/or screening tools as appropriate); straightforward questions are preferred.

    • Ease disclosure of sensitive information by use of normalization and symptom assumption (phrasing questions to imply a behavior is normal, understandable, or to be expected).

  • 7.

    How can you foster patient alliance in difficult situations, e.g., patients with somatic symptom disorders (SSDs)?

    • Listen first and empathically and nonjudgmentally reflect the patient’s understanding and concerns and validate the patient’s experience of symptoms.

    • Avoid use of unnecessary stigmatizing labels or colloquial jargon (e.g., “it’s all in your head”) and empathize with the real experience of symptoms (e.g., psychogenic nonepileptic seizures are still seizures, they’re just not caused by epilepsy).

      Post RM: Neural substrates of psychiatric syndromes. In Mesulam MM (ed): Principles of behavioral and cognitive neurology, 2nd ed. New York: Oxford University Press, 2010, pp 406-438.

      Georgiopoulos AM, Donovan AL: The DSM-5: a system for psychiatric diagnosis. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, pp 165-170.

    • Find common goals (your goal should be the patient’s improvement), and focus on these rather than convincing him or her of your diagnosis.

    • Anchor proposed interventions in known or presumed pathophysiologic mechanisms as appropriate (i.e., use psychoeducation).

    • Encourage use of a symptom diary, and focus on reduction rather than elimination of symptoms.

    • Encourage frequent follow-up with a single provider (you if appropriate).

    • Maintain vigilance for changing psychological, social, and biological factors (including routine health maintenance and screening for development of medical disorders).

  • 8.

    What is motivational interviewing?

    Motivational interviewing is a technique based on the Stages of Change Model developed initially to help patients with substance addiction address their ambivalence (mixed feelings) regarding their addiction and desire to quit. It has since been applied to a variety of situations in which fostering the intrinsic (within the patient) motivation to change is the goal (such as improving patient compliance with treatments).

  • 9.

    What are the stages in the Stages of Change Model and are they clinically valid?

    The Stages of Change Model, while heuristically valuable, has not been found to validly reflect any actual sequentially discrete sequence of change. The stages in the model are as follows:

    • Precontemplation: characterized by denial and minimization

    • Contemplation: characterized by thinking about change

    • Preparation: characterized by making preparations to do something

    • Action: characterized by actually implementing concrete actions directed at the problem

    • Maintenance: characterized by implementing change-maintaining actions

  • 10.

    What is the difference between classical and operant conditioning?

    In classical conditioning, a conditioned stimulus (such as a bell ringing) is paired with a stimulus that is already hard-wired to evoke a response (such as food evoking salivation) until the conditioned stimulus evokes the same response. In operant conditioning, behavior is reinforced by reward and the best way to do this is with positive reinforcement given at an intermittent (variable) schedule (like how casinos reward gambling).

  • 11.

    What are the major types of psychotherapies and which types may be better for patients with cognitive limitations?

    Supportive therapy ( Table 29-1 ) aims to bolster existing adaptive (healthy) coping skills and is well suited for nearly all patients, even those with cognitive limitations. Psychoeducation—teaching patients about brain function and the relevant aspects of their psychiatric disorder and treatments—is also appropriate for nearly all patients and can be empowering and facilitate adaptive coping. Psychotherapies that require higher levels of cognitive input on the part of the patient (as well as extensive training on the part of the therapist) include psychoanalysis, psychodynamic psychotherapy, interpersonal psychotherapy, cognitive behavioral therapy (CBT), dialectical behavioral therapy (DBT), and group and couples therapy.

    Table 29-1
    Select Supportive Therapy Techniques
    Adapted from Abernethy R, Schlozman S. An overview of the psychotherapies. In Stern TA, Fava M, Wilens TE, Rosenbaum JF, editors. Massachusetts General Hospital Comprehensive Clinical Psychiatry. London, Elsevier, p. 104 ( Box 10-4 ), 2016.
    Aim to enhance the patient’s self-esteem; praise and encourage use of strengths.
    Keep the therapy focused in a constructive direction rather than encouraging the patient to say whatever comes to mind.
    Aim to allay any anxiety generated by the therapy itself.
    Respond to the patient’s questions with appropriate answers.
    Make suggestions and give advice.
    Use clarification and confrontation but generally avoid interpretation.

    Gerstenblith T, Kontos N: Somatic symptom disorders. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, pp 255-264.

    Miller WR, Rollnick S: Motivational interviewing: preparing people for change, 2nd ed. New York: Guilford Press, 2002.

    Flashman LA, McAllister TW: Environmental and behavioral interventions. In Arciniegas DB, Anderson CA, Filley CM (eds): Behavioral neurology & neuropsychiatry. New York: Cambridge University Press, 2013, p 612.

    Littell JH, Girvin H: Stages of change: a critique. Behav Modif 26:223-273, 2002.

  • 12.

    What basic workup is recommended for patients presenting with psychiatric signs and symptoms and what additional exams or tests may be considered?

    See Table 29-2 .

    Table 29-2
    Laboratory Tests and Other Studies Useful for Psychiatric Symptom Workup
    Data from American Psychiatric Association: Psychiatric evaluation of adults, 2nd ed. Am J Psychiatry 163(6 Suppl):3–36, 2006; Freudenreich O, Schulz S, Goff DC. Initial medical work-up of first-episode psychosis: a conceptual review. Early Interv Psychiatry 3(1):10–18, 2009.
    Test Purpose/Clinical Situation/When to Consider
    Physical exam: including complete neurologic exam, vital signs, height and weight (BMI), waist circumference All patients; observe for focal deficits; exclude medical problems; establish a baseline; monitoring
    Basic labs: CBC, BMP, calcium, phosphorus, LFTs, lipids, UA, pregnancy test, hemoglobin A1c, vitamin B12, folate, vitamin D, blood alcohol level, thiamine, urine toxicology screen Routine evaluation of most psychiatric complaints (evaluate for medical illness and substance use) and baseline and routine monitoring of pharmacologic treatments
    Prescription drug levels Sub- or supratherapeutic effects (e.g., toxicity)
    Medication levels Sub- or supratherapeutic effects (e.g., toxicity); especially for medications with narrow therapeutic windows such as lithium, valproate, clozapine, and tricyclic antidepressants
    Thyroid function tests (TFTs) Mood or anxiety symptoms, dementia, lithium monitoring
    Serology for HIV , syphilis (FTA-Abs), hepatitis C, and Lyme Routine screening; suspicion of infectious etiology
    ESR, antinuclear antibodies, consider other serum or CSF antibody studies (e.g., anti-NMDAR antibodies) Evaluate for inflammatory, autoimmune, and paraneoplastic disorders
    Ceruloplasmin Evaluate for Wilson’s disease
    Genetic analysis Rule out a genetic disorder (e.g., Huntington’s disease). Pharmacology selection (identification of cytochrome P450 or COMT hyper- or hypometabolizers)
    Electrocardiogram (ECG) For monitoring of QT interval effects of medications and arrhythmias contributing to panic symptoms
    Chest X-ray (CXR) Delirium and paraneoplastic workup
    Lumbar puncture (LP) CNS infections, autoimmune encephalopathy; consider in delirium and psychosis workup
    Neuroimaging (CT, MRI, PET, etc.) Evaluate for CNS pathology (e.g., stroke, tumor, demyelination, atrophy, proteinopathies, etc.)
    Electroencephalography (EEG) Confusion, history, or clinical suspicion for seizure, narcolepsy, or head injury
    Polysomnography (sleep study) Sleep apnea, restless legs syndrome, etc.
    Neuropsychologic testing Assess intelligence, memory, language, executive function, and better characterize psychiatric diagnosis
    Bolded items are recommended for general workup for most psychiatric symptoms, baseline, and treatment monitoring.

    Recommended in the routine workup of first-break psychosis. BMI , Body mass index; CBC , complete blood count; BMP , basic metabolic panel (including electrolytes, glucose, blood urea nitrogen, creatinine); LFTs , liver function tests; UA , urinalysis; HIV , human immunodeficiency virus (e.g., immunoassay); CSF , cerebrospinal fluid; ESR , erythrocyte sedimentation rate; FTA-Abs , fluorescent treponemal antibody absorption (RPR is insufficient); NMDAR , N -methyl- d -aspartate receptor; COMT , Catechol-O-methyltransferase; CNS , central nervous system; CT , computed tomography; MRI , magnetic resonance imaging; PET , positron emission tomography.

  • 13.

    What is the biopsychosocial model?

    In the biopsychosocial model, one of several frameworks used for psychiatric case formulations, biological (e.g., genetic, medical, pharmacologic), psychological (e.g., abuse history, coping strengths or weaknesses, adaptive and maladaptive defenses), and social (e.g., relationship or work stressors and supports) factors, are considered as contributors to the clinical presentation and as potential avenues for intervention.

  • 14.

    What is the typical age of onset for major psychiatric disorders and how might this knowledge change management?

    Psychiatric disorders typically begin to manifest in adolescence to early adulthood, with roughly 75% of cases having a first onset before age 24 years. For example, the typical age of onset of schizophrenia is between 15 and 35 years of age, and onset after 45 years of age is rare. Increased diagnostic suspicion and keeping a lower threshold for further workup to rule out other (neurologic or medical) causes is necessary before diagnosing a psychiatric disorder in a patient presenting outside of the typical age range.

Mental Status Exam

  • 15.

    How is the mental status exam (MSE) performed and what are its main components?

    The MSE is continuously performed throughout the encounter via observation of the patient. You can always perform an MSE; it is not appropriate to document “unable to perform” a MSE as this means the patient was not observed. If the patient does not participate in the encounter (due to disordered consciousness, refusal, or other reason), then that is an important observation to note as part of the MSE ( Table 29-3 ).

    Table 29-3
    The Main Components of the Mental Status Exam (MSE)
    From American Psychiatric Association: Psychiatric evaluation of adults. 2nd ed. Am J Psychiatry 163: (6 Suppl):3–36, 2006.
    Appearance and Apparent age, body habitus, appropriateness of dress, grooming, hygiene, and distinguishing features
    Behavior Demeanor, posture/position, level of distress, degree of eye contact, attitude, psychomotor activity, gait, abnormal movements
    Speech and Coherence, rate, rhythm, volume, tone, and prosody
    Language Fluency, repetition, comprehension, naming
    Mood and affect Subjective and objective components of each, quality and range
    Thought process and Logicality, linearity, goal-directedness (inferred from speech)
    Thought content Suicidality, homicidality, delusions, obsessions, and usually also including perceptions: illusions and hallucinations)
    Sensorium and Level of consciousness and its stability
    Cognition Orientation, attention, concentration, intelligence, abstraction, executive function, construction (visuospatial)
    Memory and Registration and immediate, delayed, and autobiographical recall
    Fund of knowledge In relation to sociocultural and educational background
    Insight and Awareness of problems/behaviors including causes and ramifications; motivation to change
    Judgment Rationality of decisions made based on careful thought
    Note: A variety of component headings and subcomponents are used in clinical practice, and this list is a suggestion of components and is not intended to be exhaustive.

  • 16.

    What is the difference between mood and affect?

    The terms mood and affect are sometimes used to represent the patient’s subjective (reported emotional feelings) and objective (observed emotional expression), respectively. However, the DSM describes both mood and affect as emotional feelings with objective and subjective components and differentiates them temporally—whether the emotion is persistent (days to weeks) or temporary (seconds to hours), respectively. Thus, mood is the persistent “emotional climate,” and affect is the transient “emotional weather.” This use more appropriately describes the phenomenology of emotion and helps to distinguish mood disorders from affect disorders. For example, the colloquial “mood swings” occurring over seconds to hours are better described as affective lability.

    Yeung AS, Chang TE: Psychiatric epidemiology. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, p 663.

    Sadock BJ, Sadock VA, Belkin GS (eds): Kaplan & Sadock’s pocket handbook of clinical psychiatry, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2010, p 143.

  • 17.

    What are some psychiatric or neurologic conditions associated with disordered affect?

    Affective lability may be one feature of some mood disorders (e.g., bipolar disorders) and personality disorders (e.g., borderline personality disorder), but these disorders should not be diagnosed on the basis of this feature alone . Pathologic laughing and crying (also called pseudobulbar affect ) can result from disruption of afferents (especially brain stem [i.e., bulbar] serotonergic afferents) to paralimbic regions by various disorders including amyotrophic lateral sclerosis, multiple sclerosis, traumatic brain injury, Alzheimer’s disease, and others. Witzelsucht (pathologic punning) is associated with frontal lobe injury. Ictal laughing (gelastic epilepsy) or crying (dacrystic or quiritarian epilepsy) are associated with complex partial seizures.

  • 18.

    Name and describe some abnormal thought processes and the dysfunction or disorders associated with each.

    See Table 29-4 .

    Table 29-4
    Abnormal Thought Processes and Associated Disorders
    Thought process Description Associated Dysfunction
    Tangential Logical and linear but not goal directed Impaired attention and memory
    Circumferential or circumstantial Talking around a topic, overinclusive; gets to the point eventually Executive dysfunction
    Preservation Repetition of words or phrases; stuck on a theme or idea; difficulty shifting set Autism, catatonia, frontal lobe injury
    Flight of ideas Generally logical but nonlinear and not goal directed (like the seemingly erratic flight of a bird); often seen with uninterruptible, “pressured” speech Bipolar mania
    Loosening of associations Statements are not logically connected to each other; the listener has to “connect the dots” Psychotic disorders
    Derailment The logical link between trains of thought is suddenly and completely disconnected Psychotic disorders
    Thought blocking A sudden prolonged pause as though the thought was blocked perhaps by some other internal stimuli Psychotic disorders
    Clang associations Excessive alliteration or rhyming; words are linked by sounds rather than meaning Psychotic disorders, Tourette syndrome

  • 19.

    Why use screening tools, rating scales, and structured interviews?

    Screening tools, rating scales, and structured interviews can help guide the evaluation, ensure important screening questions are asked, and facilitate patient report that might not have spontaneously volunteered. Some are validated measures of symptom severity and help anchor the diagnosis and treatment response to quantifiable data (rather than just clinical impressions) and may be used for research purposes as well. Some (e.g., Patient Health Questionnaire-9 [PHQ-9], and the Neuropsychiatric Inventory-Q [NPI-Q]) are self-report measures and can be filled out by the patient prior to the visit. Some require a clinician to administer and may be brief and focused (e.g., Beck Depression Inventory) or long and thorough (e.g., the Structured Clinical Interview for DSM-5 Disorders [SCID-5]).

    Arciniegas DB: Emotion. In Arciniegas DB, Anderson CA, Filley CM (eds): Behavioral neurology & neuropsychiatry. New York: Cambridge University Press, 2013, pp 270-273.

  • 20.

    Name some examples of bedside screening tools and structured interviews.

    See Table 29-5 .

    Table 29-5
    Select Screens, Rating Scales, and Structured Interviews
    Adapted from Roffman JL, Mischoulon D, Fava M. Diagnostic rating scales. In Stern TA, Fava M, Wilens TE, Rosenbaum JF, editors. Massachusetts General Hospital Comprehensive Clinical Psychiatry. London, Elsevier, p. 64 ( Table 6-1 ), 2016.
    General diagnostic instruments SCID-5 Structured Clinical Interview for DSM-5 Disorders
    MINI Mini-International Neuropsychiatric Interview
    SCAN Schedules for Clinical Assessment in Neuropsychiatry
    NPI-Q Neuropsychiatric Inventory (brief self-assessment version)
    Mood disorders HAM-D Hamilton Depression Rating Scale
    MADRS Montgomery–Asberg Depression Rating Scale
    BDI Beck Depression Inventory
    Y-MRS Young Mania Rating Scale
    Anxiety disorders HAM-A Hamilton Anxiety Rating Scale
    BAI Beck Anxiety Inventory
    Y-BOCS Yale–Brown Obsessive Compulsive Scale
    BSPS Brief Social Phobia Scale
    CAPS Clinician Administered PTSD Scale
    Psychotic disorders PANSS Positive and Negative Syndrome Scale
    BPRS Brief Psychiatric Rating Scale
    AIMS Abnormal Involuntary Movement Scale
    BARS Barnes Akathisia Rating Scale
    Substance use disorders CAGE CAGE questionnaire
    DAST Drug Abuse Screening Test
    Cognitive and executive function screens MMSE Mini-Mental State Examination
    CDT Clock-Drawing Test
    DRS Dementia Rating Scale
    FAB Frontal Assessment Battery

  • 21.

    What combination of assessments is recommended for cognitive disorder screening?

    The Mini Mental State Exam (MMSE) with age- and education-normative corrections and supplemented with measures of spatial function (e.g., Clock-Drawing Test) and executive function (e.g., Frontal Assessment Battery [FAB]) form a reasonable cognitive screening battery recommended by the American Neuropsychiatric Association.

Capacity

  • 22.

    What is capacity, who evaluates for capacity, when is it evaluated, and how is it different from competency?

    Capacity—the patient’s ability to make a medical decision—is evaluated by the physician who is rendering the intervention and its evaluation should be part of every informed consent process (i.e., every medical decision) to varying degrees, based on the complexity and potential consequences of the decision. The patient may have capacity for some simple decisions (e.g., starting an antidepressant) but lack capacity for more complicated decisions (e.g., surgical interventions). In contrast, competency is a legal term for the ability to participate in legal proceedings (e.g., stand trial) and is determined by a judge, sometimes based on evaluations by physicians.

    Malloy PF, Cummings JL, Coffey CE, et al.: Cognitive screening instruments in neuropsychiatry: a report of the Committee on Research of the American Neuropsychiatric Association. J Neuropsychiatry Clin Neurosci 9:189-197, 1997.

  • 23.

    What are the essential components of capacity?

    The essential components of capacity (all of which are required) and special situations are recalled by the mnemonic CURVES : the patient must be able to C ommunicate a C hoice and express an adequate U nderstanding of the risks, benefits, alternatives, and consequences, and the choice must logically follow (i.e., be R easonable) from this understanding and the patient’s expressed V alue system. In E mergency situations when no S urrogate decision maker is available, life- or limb-saving interventions may be performed for a patient who lacks capacity.

  • 24.

    If the patient is found to lack decision-making capacity, who makes the decision(s)?

    If an advanced directive document (e.g., living will, health care power of attorney, physician orders for life-sustaining treatment, legal guardian, etc.) outlining the patient’s wishes for care and/or selection of surrogate decision maker is not available, then the duty of surrogate decision maker generally defaults to the next of kin in a hierarchy that varies somewhat by state but typically has the patient’s spouse at the top followed by adult children, then parents, then siblings and other family members.

  • 25.

    Is being psychotic grounds enough for involuntary hospitalization? What are the general civil involuntary commitment criteria?

    Having a mental illness alone is not grounds for involuntary hospitalization. In the United States, each state government defines the criteria for involuntary hospitalization in its mental health code, and these usually follow the American Psychiatric Association’s Model that requires six criteria to be met: (1) the patient has a mental illness that (2) is treatable by hospitalization, (3) poses a danger to others or self (including severe decompensation), (4) does not voluntarily consent, (5) lacks capacity, and (6) hospitalization is the least restrictive treatment. Involuntary (court-mandated) outpatient treatment is also possible.

Suicide

  • 26.

    What are the major risk factors for suicide?

    Some major risk factors for suicide are presented in Table 29-6 . The strongest risk factor for suicide is the presence of a psychiatric disorder, especially a mood disorder (∼50% of all suicides). Other risk factors include access to firearms (∼50% of suicides are by use of firearms), age in a bimodal fashion (15 to 24 years and 65+), and Caucasian and Native American race. Men are more likely to complete suicide though women make more attempts. Roughly one-quarter of suicide completions are in the context of alcohol intoxication. The presence of severe anxiety, panic attacks, insomnia, and major psychosocial loss increase the risk for imminent suicide. Prior suicide attempt is the best predictor of future suicide attempts.

    Table 29-6
    Risk Factors for Suicide
    Adapted from Weintraub BR, Brezing C, Lagomasino I, et al. The suicidal patient. In Stern TA, Fava M, Wilens TE, Rosenbaum JF, editors. Massachusetts General Hospital Comprehensive Clinical Psychiatry. London, Elsevier, p. 590 (Box 53-1), 2016.
    Psychiatric illness (major depression [comorbid anxiety raises risk], bipolar disorder, drug dependence, alcoholism, schizophrenia, personality disorders, panic disorder)
    Neurologic disorders (Huntington’s disease, epilepsy, multiple sclerosis, stroke, TBI)
    Race (Caucasian and Native American)
    Marital status (widowed, divorced, or separated; especially divorced men)
    Living alone
    Recent personal loss
    Unemployment
    Financial/legal difficulties
    Comorbid medical illness (having chronic illness, pain, or terminal illness)
    History of suicide attempts or threats
    Male gender
    Advancing age
    Family history of suicide
    Recent hospital discharge
    Firearms in the household
    Hopelessness
    TBI , Traumatic brain injury.

    Chow GV, Czarny MJ, Hughes MT, Carrese JA: CURVES: a mnemonic for determining medical decision-making capacity and providing emergency treatment in the acute setting. Chest 137(2):421-427, 2010.

    Cai X, Robinson J, Muehlschlegel S, et al.: Patient preferences and surrogate decision making in neuroscience intensive care units. Neurocrit Care 23(1):131-141, 2015.

    Appelbaum PS: Special section on APA’s model commitment law: an introduction and key provision of APA’s model law. Hosp Community Psychiatry 36(9):966-968, 1985.

  • 27.

    What psychiatric diagnoses carry the highest risk for suicide completion? What about suicide attempts and suicidal gestures? What about neurologic disorders?

    The suicide completion rates are highest for depression (∼15%) and schizophrenia (∼10%). The presence of anxiety, mixed-manic state, or eating disorder (especially anorexia nervosa) elevates the risk. Persons with borderline personality disorder frequently engage in “parasuicidal gestures” and are also at high risk for suicide completion (4 to 10%). Suicide is common in Huntington’s disease (8% to 20%) and may be predicted in at-risk individuals with soft neurologic signs. Suicide risk is also increased for neurocognitive disorders (delirium and dementia), stroke, traumatic brain injury, multiple sclerosis (up to 7×), and epilepsy (∼5×)—especially temporal lobe epilepsy and complex partial seizures (up to 25×).

  • 28.

    How do you screen for suicide and safety?

    Direct, straightforward, and empathic questioning regarding suicidal and homicidal ideation and intent and other safety issues is recommended. Several reliable and valid structured instruments are available to facilitate the suicide risk assessment. These include the Beck Scale for Suicidal Ideation (BSS), Beck Hopelessness Scale (BHS), Reasons for Living Inventory (RFL), and the Columbia-Suicide Severity Rating Scale (C-SSRS).

  • 29.

    How do you manage suicide risk?

    Table 29-7 presents some essential components of suicide risk management.

    Table 29-7
    Management of Suicide Risk
    Adapted from Brendel RW, Brezing C, Lagomasino I, et al. The suicidal patient. In Stern TA, Fava M, Wilens TE, Rosenbaum JF, editors. Massachusetts General Hospital Comprehensive Clinical Psychiatry. London, Elsevier, p. 590 (Box 53-1), 2016.
    • Stabilize the medical situation

    • Create a safe environment

      • Remove potential means for self-harm

      • Provide frequent supervision (hospitalize involuntarily if necessary)

    • Identify and treat underlying mental illness

    • Identify and modify other contributing factors

  • 30.

    What two psychotropic medications have the best evidence to support their role in reducing suicide risk?

    Lithium (in patients with bipolar disorder) and clozapine (in patients with schizophrenia or schizoaffective disorder) have been shown to significantly reduce the risk of suicide and, despite their reputations for adverse effects, actually result in prolonged survival. Clozapine even has a Food and Drug Administration (FDA) indication for reducing suicide risk in patients with schizophrenia or schizoaffective disorder.

  • 31.

    Why did the FDA issue a black box warning for an increased risk of suicidality for antiepileptic drugs (AEDs)? Do AEDs increase the risk for depression and suicide in epilepsy?

    The FDA’s black box warning is based on a 2008 meta-analysis finding of a nearly twofold increase in suicidal ideation or behavior associated with AED use. This issue has remained controversial due to the study’s limitations and the fact that epilepsy itself increases the risk for depression and suicide. A more recent systematic review and large population-based study found that AED use may actually decrease the risk of suicide for people with epilepsy. However, AED use was associated with increased risk of suicide-related behavior for people with depression or other disorders (but not bipolar disorder). Several AEDs (e.g., barbiturates, felbamate, levetiracetam, tiagabine, topiramate, vigabatrin, zonisamide) may be particularly prone to inducing depression. The best predictor of suicide in epilepsy is comorbid depression, and this necessitates routine screening and treatment for patients with depression.

Sadock BJ, Sadock VA, Belkin GS (eds): Kaplan & Sadock’s pocket handbook of clinical psychiatry, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2010, pp 332-335.

Gehl C, Paulsen JS: Behavior and personality disturbances. In Daroff RB, Bradley WG (eds): Bradley’s neurology in clinical practice. Philadelphia: Elsevier, 2012, pp 83-86.

Homaifar B, Matarazzo B, Wortzel HS: Therapeutic risk management of the suicidal patient: augmenting clinical suicide risk assessment with structured instruments. J Psychiatr Pract 19(5):406-409, 2013.

Griffiths JJ, Zarate CA Jr., Rasimas JJ: Existing and novel biological therapeutics in suicide prevention. Am J Prev Med 47(3 Suppl 2):S195-S203, 2014.

Ferrer P, Ballarín E, Sabaté M, et al.: Antiepileptic drugs and suicide: a systematic review of adverse effects. Neuroepidemiology 42(2):107-120, 2014.

Arana A, Wentworth CE, Ayuso-Mateos JL, Arellano FM: Suicide-related events in patients treated with antiepileptic drugs. N Engl J Med 363:542-551, 2010.

Other Psychiatric Emergencies

  • 32.

    What are the potentially life-threatening causes of delirium and how can they be recalled?

    The potentially life-threatening causes of delirium are outlined in Table 29-8 and can be recalled by the mnemonic WHHHHIIMPS.

    Table 29-8
    Potentially Life-Threatening Causes of Delirium
    Adapted from Prager LM, Ivkovic A. Emergency psychiatry. In Stern TA, Fava M, Wilens TE, Rosenbaum JF, editors. Massachusetts General Hospital Comprehensive Clinical Psychiatry. London, Elsevier, p. 943 (Table 88-1), 2016.
    Condition Diagnostics Treatment
    W ernicke’s encephalopathy Clinical triad: change in mental status, gait instability, ophthalmoplegia Thiamine 500 mg IM (may see improvement over the course of hours)
    H ypoxia Oxygen saturation/ABGs Treat etiology
    H ypoglycemia Blood glucose PO/IV administration of glucose, dextrose, sucrose, or fructose
    H ypertensive encephalopathy Blood pressure Antihypertensive medication
    H yperthermia/hypothermia Temperature Cooling or warming interventions
    I ntracerebral hemorrhage MRI/CT Per hemorrhage type/location
    I nfectious process (e.g., sepsis, bacteremia, subacute bacterial endocarditis) Infectious workup Treat infectious agent/site
    M eningitis/encephalitis LP, MRI Antibiotic medication
    M etabolic (e.g., chemical derangements, renal failure, hepatic failure, thyroid dysfunction) Laboratory investigations Per derangement
    P oisoning/toxic reaction (e.g., environmental exposures, medications, alcohol, illicit substances) Toxicology panel Per toxin
    S tatus epilepticus EEG IV benzodiazepines and/or anticonvulsants
    ABGs , Arterial blood gases; CT , computed tomography; EEG , electroencephalogram; IM , intramuscular; IV , intravenous; LP , lumbar puncture; MRI , magnetic resonance imaging; PO , oral (per os).

  • 33.

    What are some of the core features of catatonia and malignant catatonia?

    Catatonia is a peculiar syndrome of seemingly opposite features such as severe psychomotor retardation (stupor) or agitation; excessive and strange activity such as grimacing, odd mannerisms; repetitive, nongoal-directed stereotypies; maintenance of postures spontaneously (posturing), or with passive induction (catalepsy) that may be altered even with resistance from the examiner (waxy flexibility), or resisted with equal and opposite force (gegenhalten); or withdrawal from interaction (negativism) or communication (mutism), or the mimicking of movements or speech (echopraxia and echolalia). Catatonia is denoted as malignant when autonomic lability (fever, widely variable heart rate or blood pressure) is present.

  • 34.

    How is neuroleptic malignant syndrome (NMS) related to catatonia and how are these conditions treated?

    NMS is considered to be a drug-induced form of malignant catatonia. These are medical emergencies with high fatality rates if not treated quickly. Electroconvulsive therapy (ECT) is the treatment of choice of these conditions. While arranging for ECT, discontinue use of any dopamine blocking agents (neuroleptics), initiate treatment with benzodiazepines, provide supportive treatment (e.g., hydration, antipyretics, and antihypertensives), and monitor vitals and creatine kinase levels.

    Fricchione GL, Beach SR, Huffman JC, et al.: Life-threatening conditions in psychiatry: catatonia, neuroleptic malignant syndrome, and serotonin syndrome. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, pp 608-617.

  • 35.

    How does serotonin syndrome (SS) develop? What features differentiate SS from catatonia?

    SS symptoms can emerge in the setting of serotonergic medication overdose, use of two or more serotonergic agents (e.g., selective serotonin reuptake inhibitors [SSRIs] with monoamine reuptake inhibitors, tramadol, or other agents that alter serotonin synthesis, release, catabolism, or reuptake), or when tumors (e.g., carcinoid, small-cell carcinoma) secrete serotonin-like substances. SS shares some features with catatonia but gastrointestinal (GI) symptoms (diarrhea), tremor, myoclonus, ocular clonus, and hyperreflexia set it apart.

Personality Disorders

  • 36.

    What are defense mechanisms?

    All people employ defense mechanisms to cope with internal and external conflicts and stressors. Some of these mechanisms are adaptive (promote functioning and strengthen relationships) while others are maladaptive. The clinician should remember that people (the clinician included) are generally trying to do the best they can with the ego resources and skills that they have.

  • 37.

    Briefly describe some common defense mechanisms. Which defense mechanism may interfere with delivery of care (i.e., which are maladaptive)?

    Generally maladaptive (immature and neurotic) defense mechanisms:

    • Reaction formation—substitution of diametrically opposite thoughts, feelings, behaviors

    • Projection—attribution to others (may be to a delusional extreme)

    • Projective identification—feelings are misattributed as justifiable and attributed also to others often to the point of and inducing projected feeling in others

    • Splitting—“black and white thinking”; compartmentalizing positive and negative attributes rather than integrating them into a cohesive whole

    • Idealization—regarding others as perfect or better than they really are

    • Acting out—unconscious expression in action of a wish or impulse

    • Dissociation—transient loss of or alteration of identity

    • Denial—rejection of reality

    • Displacement—redirection of impulses to a safer target

    Generally adaptive (mature) defense mechanisms:

    • Altruism—vicarious gratification through service to others

    • Anticipation—feeling in advance and considering consequences and alternative solutions

    • Humor—finding the humor in a stressful situation

    • Identification—modeling aspects of oneself after another’s example

    • Sublimation—feelings are converted or channeled into more socially acceptable forms

    • Suppression—difficult feelings are intentionally avoided to cope with the present reality

    • Others—mindfulness, acceptance, respect, tolerance

  • 38.

    What constitutes a personality disorder as defined in the DSM-5?

    “A personality disorder is an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment” (DSM-5, p 645).

    The diagnosis of personality disorders should be avoided while the patient is in a crisis; avoid throwing around pejorative labels for difficult patients.

  • 39.

    What are the major types, shared characteristics, and clusters of personality disorders?

    Paranoid, schizoid, and schizotypal personality disorders share odd or eccentric characteristics and are grouped together in cluster A. Borderline, histrionic, narcissistic, and antisocial personality disorders share dramatic, emotional, or erratic features and make up cluster B. Dependent, avoidant, and obsessive–compulsive personality disorders share anxious or fearful features and are grouped together in cluster C (DSM-5, p 646).

  • 40.

    How are personality disorders treated?

    Psychotherapies, including DBT (mainly used for borderline personality disorder), CBT, and psychodynamic therapy, as well as group therapy are the mainstay of treatment of personality disorders. Pharmacotherapy, if used, is typically symptom focused.

    Fricchione GL, Beach SR, Huffman JC, et al.: Life-threatening conditions in psychiatry: catatonia, neuroleptic malignant syndrome, and serotonin syndrome. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, pp 608-617.

    Blais MA, Smallwood P, Groves JE, et al.: Personality and personality disorders. In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds): Massachusetts General Hospital comprehensive clinical psychiatry. London: Elsevier, 2016, p 441.

  • 41.

    What personality characteristics may be associated with temporal lobe epilepsy?

    Classically, the temporal lobe epilepsy personality was described as humorless, hyposexual, overly concerned with religious questions, “sticky” in interpersonal relationships, and hypergraphic. This classic description has not reliably held up and is only occasionally found in patients with temporal lobe epilepsy.

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