EVALUATION OF THE PATIENT WITH DEMENTIA
Jonathan T. Stewart, MDProfessor 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 conditionsFamily HxEtOHMedications (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
ATTENTION: 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
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 12Use DMAS or Cornell scale for severely
demented patients
THE REST OF THE WORK-UP
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
WOOF.
MEDS OTHER
THREE BASIC PRINCIPLES
Simplicity Limited goals The “no-fail” environment
“THE CUSTOMER IS ALWAYS
RIGHT!”
DEPRESSION
20-30% 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
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
WOOF!
MEDS OTHER
GOOD LUCK!
Top Related