Introduction Medical Psychiatry: Cognitive Disorders and ƒ Delirium: A syndrome, not a disease ƒ Many underlying causes Somatoform Disorders ƒ Reversible global impairment of cognitive processes ƒ Impairment of: consciousness, Cynthia L. Gauss, MD cognitive function, awareness VCU School of Medicine Inova Campus

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Disturbed Functioning Time Course

ƒ Cognitive: perceiving, thinking, ƒ Rapid onset – hours to days remembering ƒ Brief fluctuating course ƒ Arousal and attention: involves ƒ Rapid resolution, once underlying reticular activating system causes identified and treated ƒ Psychiatric symptoms: mood, perception, and behavior ƒ Patients with delirium: longer ƒ Neurologic symptoms: asterixus, hospital stays, more likely to die nystagmus

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Many Different Names Epidemiology ƒ Delirium is a common disorder ƒ Acute brain syndrome ƒ General population: 0.4% age 18 and ƒ Acute confusional state older, 1.1% age 55 and older ƒ Metabolic encephalopathy ƒ 10-30% hospitalized medically ill ƒ Toxic psychosis ƒ 30% surgical and cardiac ICU pts. ƒ Toxic encephalopathy ƒ 40-50% patients s/p hip surgery ƒ Sundowning ƒ 90% postcardiotomy patients ƒ ICU psychosis ƒ 30-40% hospitalized patients with AIDS 5 6

1 Risk Factors Other Risk Factors

ƒ Age: 30-40% hospitalized elderly ƒ ƒ Pre-existing brain damage Pain ƒ ƒ History of delirium Malnutrition ƒ ƒ Alcohol, drug dependence Dehydration ƒ Poor mobility ƒ Diabetes ƒ ƒ Cancer Sleep deprivation ƒ ƒ Sensory impairment Male gender ƒ Young children

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Etiology CNS Causes

ƒ Central nervous system illness ƒ Epilepsy ƒ Systemic disease, metabolic ƒ Brain trauma disturbance ƒ Meningitis ƒ Intoxication or withdrawal from ƒ Tumor substances or medications ƒ Vascular disease

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Systemic Illness Drugs, Poisons ƒ Anticholinergic ƒ Endocrine ƒ Vitamin ƒ Phencyclidine dysfunction deficiencies ƒ Anticonvulsants ƒ Phenytoin ƒ Antihypertensive ƒ Liver (hepatic ƒ Infection ƒ Ranitidine encephalopathy) (fever,sepsis) ƒ Antiparkinsonian ƒ Salicylates ƒ Antipsychotics ƒ Kidney (uremic ƒ Electrolyte ƒ Opiates ƒ Cardiac glycosides encephalopathy) imbalance ƒ Sedatives ƒ Cimetidine ƒ Lung disease ƒ Trauma (head, ƒ Steroids ƒ Clonidine ƒ Cardiovascular body) ƒ Disulfiram ƒ Heavy metals disease ƒ Postoperative ƒ Carbon monoxide states ƒ Insulin

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2 DSM-IV-TR Criteria Of Pathophysiology Delirium

ƒ Cholinergic dysfunction: possible ƒ Disturbance of consciousness (i.e., common denominator reduced clarity of awareness of the ƒ Excess dopamine: believed to lead to environment with reduced ability to agitation, psychosis focus, sustain or shift attention) ƒ Involvement of reticular activating formation leads to problems with attention

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DSM-IV-TR Criteria Of 5 Types Delirium ƒ Delirium due to a general medical ƒ A change in cognition (such as memory condition deficit, disorientation, language ƒ Substance intoxication delirium disturbance or the development of a perceptual disturbance that is not better ƒ Substance withdrawal delirium accounted for by a preexisting established ƒ Delirium due to multiple etiologies or evolving dementia. ƒ The disturbance develops over a short ƒ Delirium not otherwise specified period of time (usually hours to days) and (unknown cause or due to causes tends to fluctuate during the course of the not listed, such as sensory day. deprivation)

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Diagnosis Other Diagnostic Features

ƒ Most significant features: ƒ Disturbed psychomotor behavior – Decreased and fluctuating levels of ƒ Disturbance of sleep/wake cycles consciousness ƒ Mood alterations – Disturbance of attention ƒ Perceptual disturbance – Disorientation – Memory disturbance ƒ Disturbed thought processes ƒ Neurological abnormalities

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3 Diagnostic Procedures Diagnosis

ƒ Mental status exam, including mini- ƒ The main goal is to determine and mental status exam treat the underlying medical cause of the delirium. ƒ Longitudinal, systematic clinical assessments ƒ Physical exam ƒ Laboratory data

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Laboratory Data Differential Diagnosis ƒ Blood chemistries: ƒ Chest X-ray electrolytes, renal ƒ Drug screen ƒ Dementia and liver fx, ƒ EEG: slow waves glucose ƒ Brief psychotic disorder ƒ Blood, urine and ƒ Schizophreniform disorder ƒ CBC with diff CSF cultures ƒ Thyroid function ƒ B12 and folate ƒ Mood disorders ƒ RPR ƒ CAT scan of brain ƒ Anxiety disorders ƒ Urinalysis ƒ Lumbar puncture ƒ Malingering ƒ HIV ƒ EKG 21 22

Course And Prognosis Treatment ƒ Sudden onset ƒ Resolves over hours to weeks ƒ After treating underlying causes, ƒ The primary aim of treatment: treat usually resolves in 3-7 days the underlying medical cause of the delirium ƒ Most recover ƒ Treat the symptoms of delirium ƒ Others progress to stupor, coma or seizures ƒ Provide a safe and supportive environment ƒ 20-75% die during hospitalization ƒ 25% die within 6 months

ƒ 35% die within a year 23 24

4 Pharmacologic Treatment Behavioral Management ƒ Ensure safety: fall prevention, ƒ Minimize polypharmacy in general remove dangerous items, 1 to 1 ƒ Check medication levels sitter, avoid restraints ƒ Treat psychosis with Haldol (po and ƒ Consistent staff, family, friends IM) or atypical antipsychotics: ƒ Calm environment: avoid sensory Risperdol (po,IM,m-tabs) Zyprexa deprivation and over-stimulation (po, zydis, IM), Geodon (po, IM) or ƒ Regular orientation, explanations, Seroquel reassurances ƒ Avoid benzodiazepines alone, except ƒ Provide calendars, familiar objects, for alcohol, sedative withdrawal 25 nightlight, glasses, hearing aid 26

Dementia Epidemiology ƒ Global decrease of cognition in ƒ 8 to 10% over 65 develop dementia multiple domains ƒ 40% over age 80 develop dementia ƒ Stable level of consciousness ƒ Dementia of Alzheimer’s type ƒ Due to abnormalities in brain structure increases in prevalence with age ƒ Risk increases with age ƒ Annual cost: 80 to 100 billion $/year ƒ Leads to institutionalization ƒ 50% of nursing home patients have ƒ Often permanent Alzheimer’s ƒ 15% of dementias are reversible if ƒ 2 million people in nursing homes treated with dementia 27 28

Epidemiology Etiology

ƒ Dementia most commonly occurs ƒ Alzheimer’s dz ƒ Nutritional (B12, after age 60 ƒ Vascular dementia folate, thiamine ƒ Rare cases occurs in 40s or 50s ƒ Drugs, toxins deficiency, pellagra) (early-onset dementia) (including alcohol) ƒ Anoxia ƒ Alzheimer’s is leading cause ƒ Tumors ƒ Normal-pressure hydrocephalus ƒ Vascular dementia 2nd leading cause ƒ Infections (Creutzfeld-Jacob, ƒ Head trauma ƒ The two together make up 75% AIDS, neurosyphilis, ƒ Inflammatory dz meningitis) (Lupus, MS)

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5 Etiology Diagnosis: DSM-IV-TR

ƒ Neurodegenerative ƒ Metabolic ƒ Dementia of the Alzheimer’s Type Disorders: disorders: ƒ Vascular dementia (Multi-infarct – Parkinson’s disease – Leukodystrophies dementia) – Huntington’s dz – Dialysis dementias ƒ Dementia due to a general medical – progressive – Renal insufficiency supranuclear palsy – Hepatic insufficiency condition – Pick’s disease – Hypo- and hyper- ƒ Substance-induced persisting – Wilson’s disease thyroidism dementia – Cushing’s syndrome ƒ Dementia due to multiple etiologies ƒ Dementia not otherwise specified 31 32

DSM-IV-TR Criterion DSM-IV-TR Criterion

ƒ The development of multiple – One (or more) of the following cognitive cognitive deficits manifested by disturbances: • aphasia (language disturbance) both: • apraxia (impaired ability to carry out motor – Memory impairment (impaired ability to activities despite intact motor function learn new information or to recall • agnosia (failure to recognize or identify objects previously learned information) despite intact sensory function) • disturbance in executive functioning (ie, planning, organizing, sequencing, abstracting)

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DSM-IV-TR Criterion Diagnosis ƒ Clinical examination: mental status and physical exam ƒ The cognitive defects in Criteria A1 ƒ Comprehensive history from pt, family and A2 each cause significant ƒ Memory, problems with behavior and impairment in social or occupational functioning, mood and personality functioning and represent a changes significant decline from a previous ƒ Mini-mental status exam (Folstein’s) level of functioning. ƒ Need a baseline score ƒ The deficits do not occur exclusively ƒ Widely used, can compare between during the course of a delirium. different clinicians, and as illness progresses 35 36

6 Laboratory Work-Up Psychiatric Symptoms

ƒ Personality changes ƒ CBC ƒ Chest X-ray ƒ Hallucinations and delusions ƒ Chemistries: ƒ EKG ƒ Mood changes: anxiety and Electrolytes, renal ƒ CT or MRI of brain and liver function depression ƒ SPECT or PET of ƒ “Pseudodementia” ƒ B12, folate brain ƒ Dementia can co-exist with ƒ Urinalysis ƒ Neuropsychologic ƒ RPR (syphilis) al testing depression ƒ HIV ƒ Dementia is a risk factor for depression

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Alzheimer’s Dementia Alzheimer’s Dementia

ƒ Continuing and gradual decline ƒ ƒ Onset: ages 40-90 Definitive diagnosis: brain autopsy ƒ ƒ Early onset < age 65 Senile plaques (amyloid) ƒ ƒ Late onset > age 65 Neurofibrillary tangles ƒ Apolipoprotein E (APOE) 4 allele: ƒ Early onset linked to chromosome increased risk mutations 1, 14, 21 ƒ ƒ Systemic and other brain diseases Confirmatory testing: SPECT or PET need to be ruled out scan, APOE-4, presenilin

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Vascular Dementia Lewy Body Disease

ƒ Associated with arteriosclerosis ƒ Clinical features similar to ƒ Cannot make diagnosis without Alzheimer’s clinical evidence (focal neurological ƒ Early onset visual hallucinations and signs) or evidence from brain parkinsonism imaging ƒ Lewy bodies: eosinophilic inclusions ƒ Often abrupt deterioration in neurons throughout the cortex ƒ Fluctuating, step-wise progression ƒ Patients very sensitive to typical ƒ Associated with HTN, diabetes, antipsychotics stroke 41 42

7 Fronto-Temporal Dementia Pharmocologic Treatment (Pick’s Disease) ƒ Medications used in Alzheimer’s ƒ Insidious onset, gradual progression dementia: – Acetylcholinesterase inhibitors: ƒ Early decline in social conduct, tacrine, donepazil, rivastigmine, and personality changes, disinhibition galantamine ƒ Brain biopsy: fronto-temporal • Improve cognition, best in early atrophy and Pick’s bodies in the dementia – Memantine, NMDA antagonist, used in neurons severe dementia, can be used in ƒ Pick’s bodies contain antibodies to combination neurofilaments and neurotubules – Vascular dementia: anticoagulants, ASA to prevent myocardial infarction, stroke 43 44

Treatment of Psychiatric Somatoform Disorders Symptoms

ƒ Depression: Selective Seratonin Reuptake ƒ Physical symptoms which cannot be Inhibitors explained by a medical, another ƒ Psychosis: atypical antipsychotics, haldol psychiatric or substance abuse only for acute agitation disorder ƒ Clozaril useful with Parkinson’s disease ƒ Patients do not voluntary feign ƒ Avoid routine use of benzodiazepines symptoms ƒ Reminiscent, music, exercise therapies ƒ Symptoms cause distress and ƒ Self-help groups for family members decreased functioning

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Somatoform Disorders Somatization Disorder

ƒ Somatization disorder ƒ Multiple somatic ƒ Symptoms not symptoms: correlated with ƒ Hypochondriasis – 4 pain symptoms tests ƒ Conversion disorder –2 GI symptoms ƒ Begins < age 30 ƒ Pain disorder – 1 sexual symptom ƒ Mostly female – 1 pseudoneurologic ƒ Body dysmorphic disorder symptom ƒ Genetic/cultural/en -vironmental ƒ Undifferentiated somatoform ƒ Not voluntarily factors feigned disorder ƒ Rural, low socio- ƒ Somatoform disorder not otherwise economic status specified ƒ Hysteria, Briquet’s 47 48

8 Hypochondriasis Conversion Disorder

ƒ One or more ƒ History of trauma ƒ Preoccupation with ƒ 1-5% of population symptoms or ƒ Primary gain, fears of having or the ƒ Men and women deficits affecting secondary gain idea that one has a equally affected voluntary motor or serious illness ƒ Rural, lower socio- sensory fx economic status ƒ 6 mo/more duration ƒ Occurs at any age ƒ Psychological ƒ Good remission ƒ distress, decreased ƒ Amplify vague factors functioning bodily sensations ƒ Good prognosis: ƒ Not purposefully acute, clear ƒ Chronic or life-long ƒ Unnecessary tests, feigned stressor, no co- doctor shopping ƒ Diagnostic tests morbid disease neg.

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Pain Disorder Body Dysmorphic Disorder

ƒ Pain is major focus ƒ More common in ƒ Preoccupation with imagined defect and severe women in appearance ƒ Causes stress and ƒ Genetic and ƒ Distress, shame dysfunction environmental ƒ Psychological factors ƒ Early onset factors ƒ Related to ƒ Women more affected ƒ Does not match stressors ƒ High co-morbidity with depression physical pathology ƒ Primary, secondary gain

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Treatment

ƒ Identify the disorder ƒ See patient ƒ Empathize with the frequently, regular patient’s symptoms intervals, briefly ƒ Goal is management ƒ Psychotherapy for not cure hypochondriasis, ƒ Avoid unnecessary body dysmorphic procedures disorder, conversion ƒ SSRIs for BDD

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