Download Dementia

Dementia
Prof AK Daif
WHAT IS DEMENTIA?
• An acquired syndrome of decline in memory and other
cognitive functions sufficient to affect daily life in an alert
patient
• Progressive and disabling
• NOT an inherent aspect of aging
• Different from normal cognitive lapses
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Dementias – classification
Based on site
DSM-IV DIAGNOSTIC CRITERIA FOR
AD
• Development of cognitive deficits manifested by both
• impaired memory
• aphasia, apraxia, agnosia, disturbed executive function
• Significantly impaired social, occupational function
• Gradual onset, continuing decline
• Not due to CNS or other physical conditions
(e.g., PD,
delirium)
• Not due to an Axis I disorder (e.g., schizophrenia)
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NORMAL LAPSES
vs
DEMENTIA
• Forgetting a name
• Leaving kettle on
• Finding right word
• Forgetting date or day
• Not recognizing family
member
• Forgetting to serve
meal just prepared
• Substituting
inappropriate words
• Getting lost in own
neighborhood
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Mild Cognitive
Impairment
“Mild Cognitive Impairment (MCI) is a state between normal
cognition and dementia, characterized by deficits not
explainable by age, educational background, or medical
illness.”
Kryscio RJ, Schmitt FA, et al. Risk factors for transitions from normal to mild cognitive impairment and dementia. Neurology
2006; 66: 828-32.
• MCI is common (5-25%)
• MCI carries an increased risk of dementia and of death
– If the deficits exist primarily in memory and executive function, risk of
progression to dementia is higher
• 10-15% per yr rate of development of dementia and AD compared to 1-7% per yr
for those without MCI
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DIFFERENTIAL DIAGNOSIS
FOR DEMENTIA
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Alzheimer’s disease
Vascular (multi-infarct) dementia
Dementia associated with Lewy bodies
Delirium
Depression
Other (alcohol, Parkinson's disease [PD], Pick’s
disease, frontal lobe dementia, neurosyphilis)
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ASSESSMENT:
HISTORY/PHYSICAL
• Ask both the patient & a
reliable informant
• Current condition
• Medical history
• Current medications
• Patterns of alcohol use or
abuse
• Living arrangements
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Neurologic status
Functional Status
Mental Status
ie. Folstein, MiniCog,
Neuropsych testing
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Evaluation of Dementia
• Standard laboratory studies
– Complete blood count
• Anemia, infection
– Comprehensive metabolic panel
• Glucose, electrolytes, renal or hepatic failure
– Thyroid function tests
• Studies done in suspect cases
– Estimated sedimentation rate
– Serology for syphilis, HIV, lyme disease
– Screen for heavy metals
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ASSESSMENT: BRAIN IMAGING
• Use imaging when:
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Onset occurs at age < 65 years
Symptoms have occurred for < 2 years
Neurologic signs are asymmetric
Clinical picture suggests normal-pressure hydrocephalus
• Consider:
– Noncontrast computed topography head scan
– Magnetic resonance imaging
– Positron emission tomography
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Evaluation of Dementia
• Radiologic/Neuro-Imaging studies
• Carotid dopplers
• CT Scan, MRI of Brain
– Linear/volumetric measurement is not recommended
• PET and SPECT imaging not recommended for routine
use in the diagnosis of dementia
– “Little evidence to support the routine use of PET in pts with
suspected or established dementia” JAGs 51: 2003 Clinical criteria
accurate in 90%
*PET scan may help clarify Alzheimer’s vs. other types dementias in those
already fully evaluated
*SPECT scan may help identify early dementia but studies are limited
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Potential Reversible Causes
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Neoplasms
Metabolic disorders
Trauma
Toxins
Infections
Autoimmune
disorders
• Drugs
• Nutritional disorders
• Psychiatric disorders
• Normo-pressure
Hydrocephalius
(NPH)
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Distinguishing Dementia
• Delirium versus Dementia
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Acute onset
Cognitive fluctuations over hours or days
Impaired consciousness and attention
Altered sleep cycles
• Depression versus Dementia
– Demonstrate  motivation during cognitive testing
– Express cognitive complaints that exceed measured
deficits
– Maintain language and motor skills
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SPECIFIC
DEMENTIAS…
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Alzheimer’s Dementia
• Dementia NOT caused by other medical/mood or CNS
disorder
– Definitive diagnosis is on brain biopsy/autopsy
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Neurofibrillary tangles and senile plaques
Reduced cerebral production of choline acetyl transferase
Decreased Acetylcholine synthesis
Marked cholinergic deficit
– DSM-IV criteria
• Cognitive deficits including impaired memory, executive function and
aphasia/apraxia/agnosia
• Gradual onset, continuing decline; impaired social/occupational
function
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SYMPTOMS & SIGNS OF AD
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Memory impairment
Gradual onset, progressive cognitive decline
Behavior and mood changes
Difficulty learning, retaining new information
Aphasia, apraxia, disorientation, visuospatial dysfunction
Impaired executive function, judgment
Delusions, hallucinations, aggression, wandering
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Alzheimer's disease
• CT scanning aids diagnosis by excluding
multiple infarction or a mass lesion.
• MRI shows bilateral temporal lobe atrophy.
• SPECT usually shows temporoparietal
hypoperfusion.
The brain in AD
microscopic
view:
neurofibrillary
tangles and
protein deposits
macroscopic
view:
neuronal loss
appears as
atrophy
PET scan in Alzheimer’s disease
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PROGRESSION OF AD
Mild Impairment
• Disorientation for date
• Naming difficulties
• Recent recall problems
• Mild difficulty copying
figures
• Decreased insight
• Social withdrawal
• Irritability
• Mood change
• Problems managing
finances
Moderate
• Disorientation for date and
place
• Comprehension difficulties
• Impaired new learning,
calculating skills
• Getting lost in familiar areas,
wandering
• Not cooking, shopping, banking
• Delusions, hallucinations
• Agitation, restlessness, anxiety,
aggression
• Depression
• Problems with dressing and
grooming
• Aphasia and apraxia
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PROGRESSION OF AD
Severe Impairment
• Nearly unintelligible verbal output
• Remote memory gone
• Unable to copy or write
• Unable to feed*
• No longer grooming or dressing
• Incontinent
• Unable to Walk
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Other Dementias……..
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DSM-IV DIAGNOSTIC CRITERIA
FOR VASCULAR DEMENTIA
• Development of cognitive deficits manifested by
both
• impaired memory
• aphasia, apraxia, agnosia, disturbed executive function
• Significantly impaired social, occupational function
• Focal neurologic symptoms & signs or evidence of
cerebrovascular disease
• Stepwise Deterioration (after each event)
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Multi-infarct dementia (MID)
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This is an overdiagnosed condition which accounts for less than
10% of cases of dementia.
MID is caused by multiple strokes - SILENT STROKES
Dementia occurs ’stroke by stroke‘, with progressive focal loss
of function.
Clinical features of stroke profile – hypertension, diabetes, etc.
– are present. More often in males.
Diagnosis is obtained from the history
and confirmed by CT or MRI scan
(the presence of multiple areas of
infarction).
Treatment: Maintain adequate blood
pressure control, anti-platelet
aggregants (aspirin).
DEMENTIA ASSOCIATED WITH
LEWY BODIES
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Dementia
Visual hallucinations
Parkinsonian signs
Alterations of alertness or attention
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DLB-Other Features
• Neuroleptic Sensitivity (ie Olanzapine)
• Falls
• Early incontinence
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OTHER DEMENTIAS
• Alcoholic Dementia
– Direct effects of alcohol, Secondary effects of
alcohol,Wernicke-korsakoff syndrome
• Toxic Metal and Gas Exposure
– Common exposures: lead, mercury, manganese, arsenic,
carbon monoxide & carbon disulfide
• Vitamin Deficiencies
– Vitamins B12, folate, niacin, and thiamine
– More severe B12 deficiency: subacute combined degeneration
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Organic causes of dementia
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Organ Failure (liver, kidneys)
Endocrine (hypothyroidism, diabetes)
Inflammatory (Lupus)
Neurodegenerative causes (multiple
sclerosis & Huntington’s Chorea)
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Normal-Pressure
Hydrocephalus
• May appear similar to Alzheimer’s…..
• Early treatment may reverse cognitive
changes before they become permanent
• Triad of symptoms: gait instability, urinary
incontinence and dementia
– Wide-based, shuffling gait with poor coordination
– Incontinence follows gait change, includes urgency
– Slow thinking/response, decreased spontaneity
• Enlarged ventricles on MRI
– But no evidence of atrophy: Alzheimer’s shows large
ventricles due to brain atrophy
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Parkinson Dementia
• Age Onset: 50 to 80; survival 8-15 yrs
• Dementia occurs later in the disease, mild to
mod.
• Slowness of thought
• Neuropsychiatric symptoms common
• Dysphagia, dysphonia
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Frontotemporal Dementia
• Diagnostic criteria similar to Alzheimer’s
BUT
• Onset typically younger (less than 65 years)
• Predominant changes/disturbances in behavior
– Personality change is a hallmark
– Changes occur early and progress
• Non-fluent, expressive aphasia common
– Words remain but are presented in nonsensical format
• Frontal and/or temporal atrophy on MRI
• Early absence of neurologic signs, neurologic signs occur
with progression
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Structural
Changes in
MRI:
Frontotemporal
dementias
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Parkinson Plus Dementias
• Dementia occurs early
Additional physical symptoms
• More frontal lobe features
• Earlier onset, more rapid course
• Frontal lobe features
• Poor response to levodopa
• Rapidly accelerates
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Multisystem Atrophy
• Onset 55; survival 6-7 years
• Autonomic dysfunction (incontinence,
impotence, orthostasis)
• Ataxia, dysarthria, contractures, dystonia
• Mild to moderate dementia
• Less tremor
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Progressive Supranuclear Palsy:
Dudley Moore (1935-2002)
• Initially presents similar to
Parkinsons (earlier age)
• Difficulty with vision
• Falls
• Unable to look down
• Dysarthria/dysphagia
• Lifespan 6 years
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Progressive Supranuclear Palsy
• Onset: late 50 to mid 60, survival 10 years
• Mental slowness, frontal lobe dysfunction,
pseudobulbar symptoms
• “surprised look”
• Dysarthria, dysphagia
• Often misdiagnosed:late onset of eye sx, missed
gait and posture instability
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AIDS dementia complex
• Approximately two-thirds of persons with AIDS
develop dementia, mostly due to AIDS dementia
complex.
• In some patients HIV is found in the CNS at
postmortem. In others an immune mechanism or an
unidentified pathogen is blamed.
• Dementia is initially of a "subcortical " type.
• CT - atrophy; MRI - increased T2 signal from
white matter.
• Treatment with Zidovudine (AZT) halts and
partially revers neuropsychological deficit.
Dementia – diagnostic approach
MANAGEMENT……….
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SYMPTOM MANAGEMENT
• Sundowning
• Psychoses (delusions, hallucinations)
• Sleep disturbances
• Aggression, agitation
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NONPHARMACOLOGIC
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Cognitive enhancement
Individual and group therapy
Regular appointments
Communication with family, caregivers
Environmental modification
Attention to safety
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PHARMACOLOGIC
• Cholinesterase inhibitors:
Inhibit cholinesterase at the
synaptic cleft
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Offer a small improvement :
cognition and activities of daily
living
Examples:
donepezil, rivastigmine,
galantamine
• Memantine: (Namenda): NMethyl-D-Aspartate
• Antagonist: A receptor
• excessive nmda:
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excitotoxicity and neurotransmittter
damage
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Memantine is neuroprotective &
disease modifying;
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for moderate to severe
dementia
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alone or in combination
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Other cognitive enhancers:
estrogen, NSAIDs, ginkgo, vit. E
activated by glutamate: decr
nmda
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IMPROVEMENT w/ NAMENDA
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TREATING PSYCHOSIS IN
DEMENTIA
Antipsychotic medications (side effects):
• Higher potency: haloperidol (extrapyramidal symptoms)
• Lower potency: thioridazine (anticholinergic effects,
sedation, hypotension, constipation, urine retention)
• Atypical antipsychotics: clozapine, risperidone, olanzapine
 Beware new prescribing information on some of the atypical
antipsychotics!
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ANTIPSYCHOTICS USED IN
DEMENTIA
Drug
Starting Dose
Peak Effective
Dose
12.5-25 mg twice daily
100 mg daily
Haloperidol
0.25 at bedtime
3-5 mg daily
Olanzapine
1.25-2.5 mg at bedtime
5 mg daily
Risperidone
0.25-0.5 mg at bedtime
1-1.5 mg daily
Clozapine
Note: Start low, go slow.
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MANAGING SLEEP
DISTURBANCES
• Improve sleep hygiene (e.g, consistent bedtime,
comfortable setting)
• Provide daytime activity, prevent daytime sleeping
• Use bright-light therapy
• Treat associated depression, delusions
• If the above do not succeed, consider:
• trazodone 25-150 mg
• nefazodone 100-500 mg
• zolpidem 5-10 mg
• Avoid benzodiazepines or antihistamines
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MANAGING AGITATION
• Behavioral interventions: distraction,
supervision, routine, structure
• Behavior modification using rewards
• Pharmacologic interventions:
antipsychotics, antidepressants, mood
stabilizers, buspirone, -blockers
• Avoid physical restraints
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RESOURCES
FOR MANAGEMENT
• Specialist referral to:
• geriatric
psychiatrist
• Neuropsychologi
st
• Social worker
• Attorney
• Day Care, Respite
Care
• Alzheimer’s
Association
• Meals on Wheels
• Physical therapist
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