EVALUATION OF THE PATIENT WITH DEMENTIA Jonathan T. Stewart, MD Professor in Psychiatry University of South Florida College of Medicine Chief, Geropsychiatry Section Bay Pines VA Medical Center DEMENTIA A syndrome characterized by acquired, progressive cognitive impairment Affects 10% of individuals over 65 Caused by at least 80 different diseases, many reversible Unfortunately, the most common diseases (85 – 90%) are irreversible Diagnosis will have prognostic and treatment implications All demented patients need a work-up …and it’s mostly a good history PRIMARY SYMPTOMS ATTENTION MEMORY POSTROLANDIC (“COGNITION”) EXECUTIVE (FRONTAL/SUBCORTICAL) INSIGHT PRIMARY SYMPTOMS ATTENTION: clouded sensorium, delirium MEMORY: forgetfulness POSTROLANDIC: aphasia, apraxia, getting lost EXECUTIVE: poor judgment, disinhibition, abulia, urge incontinence INSIGHT: anosognosia, catastrophic reactions TWO TYPES OF DEMENTIA Postrolandic Frontal/subcortical POSTROLANDIC Memory deficits Aphasia Apraxia Agnosia Personality more or less preserved MMSE valid FRONTAL/SUBCORTICAL Memory deficits Loss of behavioral plasticity and adaptability, judgment Personality changes Disinhibition Abulia Urge incontinence MMSE useless THE REST OF THE HISTORY Time course Depressive symptoms Past medical history Medical and psychiatric conditions Family Hx EtOH Medications (including OTC, OPM) THE REST OF THE EXAM Physical exam Neurologic exam Mental status exam THE FOLSTEIN MMSE Most studied and used of the standardized exams Quick and easy to administer Excellent inter-rater reliability Accurately measures the severity and progression of Alzheimer’s disease Does not detect executive deficits at all BEYOND THE MMSE digit span or “DLROW” MEMORY: 3 word recall, orientation POSTROLANDIC: naming, praxis, calculations, intersecting pentagons EXECUTIVE: contrasting programs, Luria figures, go-no go, controlled word fluency, frontal release signs ATTENTION: LURIA’S RECURSIVE FIGURES LURIA’S RECURSIVE FIGURES LURIA’S RECURSIVE FIGURES THE GERIATRIC DEPRESSION SCALE (GDS) Good screen for most patients Easy to administer and score Face-valid, so patients can “fake good” or “fake bad” Valid for demented patients with an MMSE above about 12 Use DMAS or Cornell scale for severely demented patients THE REST OF THE WORKUP Basic labs Thyroid function tests B12 (methylmalonic acid and homocysteine if borderline) Serology HIV, drug screen, others, as indicated Neuroimaging study, usually LP or EEG, rarely PLEASANT SURPRISES Depression Iatrogenic (anticholinergics, sedatives, narcotics, H2 blockers, multiple meds) Hypothyroidism B12 deficiency Neurosyphilis Alcoholic dementia Normal pressure hydrocephalus Subdural hematoma Others POSTROLANDIC DEMENTIAS Alzheimer’s disease Diffuse Lewy body disease ALZHEIMER’S DISEASE Slowly, insidiously progressive postrolandic dementia; executive sx’s much later Neurologic exam, labs, neuroimaging studies unremarkable Often familial, especially in younger patients ANTI-DEMENTIA DRUGS May improve cognitive function, ADL’s to a modest extent; often ineffective Dechallenge if no meaningful benefit Possibly delay nursing home placement Cholinesterase inhibitors may cause nausea, diarrhea, weight loss Memantine occasionally causes agitation THESE AGENTS DO NOT SLOW THE RATE OF DECLINE A TYPICAL STUDY BEWARE! DIFFUSE LEWY BODY DISEASE Second most common dementia in autopsy studies Characterized by Lewy bodies throughout the cortex Non-familial 2:1 male:female ratio CLINICAL FEATURES Postrolandic dementia More rapidly progressive than AD Fluctuation, episodes of “pseudodelirium” common Mild parkinsonism Tremor often absent Poor response to antiparkinsonian meds Shy-Drager sx’s common Prominent psychotic sx’s, esp visual hallucinations SEVERE NEUROLEPTIC INTOLERANCE FRONTAL/SUBCORTICAL DEMENTIAS Vascular dementia Frontotemporal dementia and Pick’s disease Alcoholic dementia Huntington’s disease, Wilson’s disease, progressive supranuclear palsy, late Parkinson’s disease AIDS dementia complex, neurosyphilis, Lyme disease Normal pressure hydrocephalus Most head injuries Anoxia, carbon monoxide Multiple sclerosis Tumors ANY ADVANCED DEMENTIA TYPES OF VASCULAR DEMENTIA Multi-infarct dementia Small vessel disease Lacunar state (gray > white) Binswanger’s disease (white) Hemorrhagic vascular dementia Strategic infarct dementia Dementia due to hypoperfusion SMALL VESSEL DISEASE At least 50% of all vascular dementia Often coexists with MID Usual vascular risk factors, especially HPT Steady, not step-wise deterioration Relatively more abulia than disinhibition FRONTOTEMPORAL DEMENTIA Relatively uncommon, non-familial illness Prominent (macroscopic) atrophy of frontal and anterior temporal cortex Symptoms include executive deficits, Klüver-Bucy syndrome About 25% of pts have Pick bodies MANAGEMENT BEHAVIORAL PROBLEMS IN DEMENTIA Present in 80% of cases Major source of caregiver stress, institutionalization Common at all stages of the disease Much more treatable than the underlying dementia Poorly described in the literature OTHER MEDS WOOF. THREE BASIC PRINCIPLES Simplicity Limited goals The “no-fail” environment “THE CUSTOMER IS ALWAYS RIGHT!” DEPRESSION incidence in Alzheimer’s disease, often early in the course of the illness Most important treatable cause of excess disability Responds very well to treatment 20-30% ACUTE BEHAVIOR CHANGE I atrogenic I nfection I llness I njury I mpaction I nconsistency I s the patient depressed? AGITATION Present in up to 80% of patients Up to 34% of patients are combative Few predictors Probably a very heterogeneous problem Cornerstone of treatment is nonpharmacologic EMPIRICALLY EFFECTIVE MEDS FOR AGITATION Atypical neuroleptics (best when agitation is clearly related to delusions or hallucinations) Anticonvulsants Trazodone Beta-blockers Buspirone Benzodiazepines Others THE BEST NUMBER OF MEDICATIONS TO USE IS ZERO (or sometimes one) WHEN IN DOUBT, GET RID OF MEDICATIONS! DON’T FORGET SAFETY ISSUES! DRIVING FIREARMS POWER TOOLS SMOKING IN BED POISONS, MEDICATIONS FALL RISK GOOD LUCK! MEDS OTHER WOOF!