Beruflich Dokumente
Kultur Dokumente
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
Diagnosis will have prognostic and treatment implications All demented patients need a work-up
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
POSTROLANDIC
FRONTAL/SUBCORTICAL
Memory deficits Aphasia Apraxia Agnosia Personality more or less preserved MMSE valid
Memory deficits Loss of behavioral plasticity and adaptability, judgment Personality changes Disinhibition Abulia Urge incontinence MMSE useless
studied and used of the standardized exams Quick and easy to administer Excellent inter-rater reliability Accurately measures the severity and progression of Alzheimers disease Does not detect executive deficits at all
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
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
Alzheimers
ALZHEIMERS DISEASE
Slowly,
insidiously progressive postrolandic dementia; executive sxs much later Neurologic exam, labs, neuroimaging studies unremarkable Often familial, especially in younger patients
ANTI-DEMENTIA DRUGS
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!
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 sxs common
FRONTAL/SUBCORTICAL DEMENTIAS
Vascular dementia Frontotemporal dementia and Picks disease Alcoholic dementia Huntingtons disease, Wilsons disease, progressive supranuclear palsy, late Parkinsons disease AIDS dementia complex, neurosyphilis, Lyme disease Normal pressure hydrocephalus Most head injuries Anoxia, carbon monoxide Multiple sclerosis Tumors ANY ADVANCED DEMENTIA
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, Klver-Bucy syndrome About 25% of pts have Pick bodies
MANAGEMENT
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
MEDS
OTHER
WOOF.
DEPRESSION
20-30%
incidence in Alzheimers disease, often early in the course of the illness Most important treatable cause of excess disability Responds very well to treatment
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
POWER
GOOD LUCK!
MEDS OTHER
WOOF!