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8/12/2019 Evaluation of the Patient With Dementia1747
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EVALUATION OF THEPATIENT WITH DEMENTIA
Jonathan T. Stewart, MDProfessor in Psychiatry
University of South Florida College of MedicineChief, Geropsychiatry SectionBay Pines VA Medical Center
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DEMENTIA
A s y n d r o m e characterized by acqui red ,progress ive cognitive impairment
Affects 10% of individuals over 65Caused by at least 80 different diseases,many reversible
Unfortunately, the most common diseases (85
90%) are irreversibleDiagnosis will have prognostic and treatmentimplicationsA ll dem ented p at ien ts n eed a wo rk-up
and its mostly a good history
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PRIMARY SYMPTOMS
ATTENTION
MEMORYPOSTROLANDIC (COGNITION) EXECUTIVE (FRONTAL/SUBCORTICAL)INSIGHT
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PRIMARY SYMPTOMS
ATTENTION: clouded sensorium, delirium
MEMORY: forgetfulnessPOSTROLANDIC: aphasia, apraxia, gettinglostEXECUTIVE: poor judgment, disinhibition,abulia, urge incontinenceINSIGHT: anosognosia, catastrophicreactions
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TWO TYPES OF DEMENTIA
Postrolandic
Frontal/subcortical
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POSTROL NDIC
Memory deficits Aphasia Apraxia Agnosia
Personality more orless preservedMMSE valid
FRONT L SUBCORTIC L
Memory deficitsLoss of behavioral plasticityand adaptability, judgmentPersonality changes
Disinhibition Abulia
Urge incontinenceMMSE useless
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THE REST OF THE
HISTORYTime course
Depressive symptomsPast medical history
Medical and psychiatric conditions
Family HxEtOHMedications (including OTC, OPM)
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THE FOLSTEIN MMSE
Most studied and used of the
standardized examsQuick and easy to administerExcellent inter-rater reliability
Accurately measures the severity andprogression of Alzheimers disease Does n o t detect execut iv e d efic i ts a t
al l
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BEYOND THE MMSE
ATTENTION: digit span or DLROW
MEMORY: 3 word recall, orientationPOSTROLANDIC: naming, praxis,calculations, intersecting pentagons
EXECUTIVE: contrasting programs,Luria figures, go-no go, controlled wordfluency, frontal release signs
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LURIAS RECURSIVEFIGURES
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LURIAS RECURSIVEFIGURES
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LURIAS RECURSIVEFIGURES
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THE GERIATRICDEPRESSION SCALE (GDS)
Good screen for most patients
Easy to administer and scoreFace- valid, so patients can fake goodor fake bad Valid for demented patients with anMMSE above about 12
Use DMAS or Cornell scale for severelydemented patients
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THE REST OF THE WORK-
UPBasic labsThyroid function testsB12 (methylmalonic acid andhomocysteine if borderline)SerologyHIV, drug screen, others, as indicatedNeuroimaging study, usuallyLP or EEG, rarely
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PLEASANT SURPRISES
DepressionIatrogenic (anticholinergics, sedatives,narcotics, H2 blockers, multiple meds)HypothyroidismB12 deficiency
Neurosyphilis Alcoholic dementiaNormal pressure hydrocephalusSubdural hematomaOthers
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POSTROLANDIC
DEMENTIAS Alzheimers disease
Diffuse Lewy body disease
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ALZHEIMERS DISEASE
Slowly, insidiously progressive
postrolandic dementia; executive sxsmuch laterNeurologic exam, labs, neuroimaging
studies unremarkableOften familial, especially in youngerpatients
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ANTI-DEMENTIA DRUGS
May improve cognitive function, ADLs to amodest extent; often ineffective
Dechallenge if no meaningful benefitPossibly delay nursing home placementCholinesterase inhibitors may cause nausea,diarrhea, weight lossMemantine occasionally causes agitationTHESE A GENTS DO NOT SLOW THERA TE OF DECLINE
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BEWARE!
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DIFFUSE LEWY BODY
DISEASESecond most common dementia in
autopsy studiesCharacterized by Lewy bodiesthroughout the cortex
Non-familial2:1 male:female ratio
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CLINICAL FEATURES
Postrolandic dementiaMore rapidly progressive than AD
Fluctuation, episodes of pseudodelirium common Mild parkinsonism
Tremor often absentPoor response to antiparkinsonian medsShy- Drager sxs common
Prominent psychotic sxs, esp visualhallucinations
SEVERE NEUROL EPTIC INTOL ERA NCE
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FRONTAL/SUBCORTICAL
DEMENTIASVascular dementiaFrontotemporal dementia and Picks disease
Alcoholic dementiaHuntingtons disease, Wilsons disease, progressivesupranuclear palsy, late Parkinsons disease
AIDS dementia complex, neurosyphilis, Lyme diseaseNormal pressure hydrocephalus
Most head injuries Anoxia, carbon monoxideMultiple sclerosisTumorsANY ADVANCED DEMENTIA
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TYPES OF VASCULAR
DEMENTIAMulti-infarct dementia
Small vessel diseaseLacunar state (gray > white)Binswangers disease (white)
Hemorrhagic vascular dementiaStrategic infarct dementiaDementia due to hypoperfusion
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SMALL VESSEL DISEASE
At least 50% of all vascular dementia
Often coexists with MIDUsual vascular risk factors, especiallyHPT
Steady, not step-wise deteriorationRelatively more abulia than disinhibition
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FRONTOTEMPORAL DEMENTIA
Relatively uncommon, non-familial
illnessProminent (macroscopic) atrophy offrontal and anterior temporal cortex
Symptoms include executive deficits,Klver-Bucy syndrome About 25% of pts have Pick bodies
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BEHAVIORAL PROBLEMS INDEMENTIA
Present in 80% of cases
Major source of caregiver stress,institutionalizationCommon at all stages of the disease
Much more treatable than theunderlying dementiaPoorly described in the literature
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WOOF.
MEDS OTHER
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THREE BASIC PRINCIPLES
Simplicity
Limited goalsThe no -fail environment
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THE CUSTOMERIS ALWAYS
RIGHT!
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DEPRESSION
20- 30% incidence in Alzheimers
disease, often early in the course of theillnessMos t im po rtan t t reatab le caus e ofexc ess d isabi l i ty
Responds very well to treatment
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ACUTE BEHAVIOR CHANGE
I atrogenic
I nfection I llness I njury I mpaction I nconsistency I s the patient depressed?
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AGITATION
Present in up to 80% of patients
Up to 34% of patients are combativeFew predictorsProbably a very heterogeneous problem
Cornerstone of treatment isnonpharmacologic
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EMPIRICALLY EFFECTIVEMEDS FOR AGITATION
Atypical neuroleptics (best when agitation isclearly related to delusions or hallucinations)
AnticonvulsantsTrazodoneBeta-blockersBuspironeBenzodiazepinesOthers
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THE BEST NUMBER OFMEDICATIONS TO USE ISZERO (or sometimes one)
WHEN IN DOUBT, GET RID OFMEDICATIONS!
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DONT FORGET SAFETYISSUES!
DRIVING
FIREARMSPOWER TOOLS
SMOKING IN BED
POISONS, MEDICATIONSFALL RISK
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WOOF!
MEDS OTHER
GOOD LUCK!