Dementia

Thomas Horton

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Background

• Alzheimer’s Disease (AD): short-term memory deficits prominent
• Vascular Dementia: “Stepwise decline” in memory and functional status
• Lewy Body Dementia: hallucinations, memory difficulties with atypical Parkinsonism early
• Frontotemporal Dementia: behavioral (aggressive or disinhibited), language (primary progressive aphasias) or memory (Alzheimer’s/FTD overlap) variants
• Posterior Cortical Atrophy: visual difficulties and ocular apraxia preceding memory problems
• Creutzfeldt-Jakob Disease (CJD): manifests with subacute cognitive decline, seizures, vision loss, personality changes. Can develop startle myoclonus
• Corticobasal degeneration: focal neurologic changes with parkinsonism
• Neurosyphilis: rare, but treatable, present with a range of cognitive changes. Develop meningovascular encephalitis. Pts can develop an arteritis, headache, and hydrocephalus.
• Normal Pressure Hydrocephalus (NPH): “wet, wacky and wobbly” meaning incontinence, gait apraxia and cognitive changes (usually frontal symptoms)
• Autoimmune Dementias: includes limbic encephalitis (like NMDA) where there are memory and personality changes, autonomic changes, hallucinations, and seizures

Normal Aging	Mild Cognitive Impairment	Alzheimer’s Dementia (DSM V Diagnostic Crit.)
Mild decline in working memory More effort/time needed to recall new info New learning slowed but well compensated by lists, calendars, etc. + No impairment in social & occupation functioning	Subjective complaint of cognitive decline in at least one domain + Cognitive decline is noticeable and measurable + No impairment in social & occupation functioning	Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains + Causes significant impairment in social & occupation functioning + Other medical & psychiatric conditions, including delirium, have been excluded + Insidious onset and gradual progression of impairment in at least two cognitive domains
Cognitive domains: learning/memory, language, executive function, complex attention, perceptual motor, social cognition

	Alzheimer’s Disease	Vascular Dementia	Lewy Body Dementia	Frontotemporal Dementia
Onset	Gradual	Sudden or stepwise	Gradual	Gradual (age < 60)
Cognitive Domains & Symptoms	Memory, language, visuospatial	Depends on location of ischemia	Memory, visuospatial	Executive dysfunction, personality changes, disinhibition, language, +/- memory
Motor Symptoms	Rare early Apraxia later	Correlates with ischemia	Parkinsonism	None
Progression	Gradual (over 8-10 years)	Gradual or stepwise with further ischemia	Gradual, but faster than Alzheimer’s disease	Gradual, but faster than Alzheimer’s disease
Imaging	Possible global atrophy	Cortical or subcortical on MRI	Possible global atrophy	Atrophy in frontal & temporal lobes

Evaluation

• MINI-COG: Screening test for cognitive impairment (highly sensitive)
  • Ask pt to remember three words (banana, sunrise, chair). Ask pt to repeat immediately
  • Ask pt to draw clock. After numbers are on the face, ask pt to “set hands to 10 past 11”
    • Correct is all numbers in right position AND hands pointing to the 11 and the 2
• Ask pt to recall the three words

MINI-COG Flowchart

• MOCA: Montreal Cognitive Assessment

  • Lengthier test of cognition (but highly specific for cognitive impairment)
  • Useful for detecting subtle deficits as in Mild Cognitive Impairment (MCI)
  • Scores:
    • 18-25: Mild cognitive impairment
    • 10-17: Moderate cognitive impairment
    • <10: Severe cognitive impairment

• Rule out reversible causes of dementia-like symptoms: DEMENTIA

  • Drugs
  • Emotional (depression)
  • Metabolic (CHF, COPD, CKD, OSA)
  • Endocrine (hypothyroidism, hyperparathyroidism, hyponatremia)
  • Nutrition (B12 deficiency)
  • Trauma (chronic SDH)
  • Infection
  • Arterial (vascular)
• B12, thyroid studies
• RPR, HIV testing in at-risk patient groups
• Neuropsych testing can be done for more clear patterns of dysfunction
• MRI brain with contrast if concerned for inflammatory or infectious causes
  • CJD: cortical ribboning on DWI with T2 hyperintensity in the thalamus and basal ganglia
  • Sulcal crowding and bowing of the corpus callosum can be seen in NPH on imaging

Management

• Targeting Cognitive Impairment
  • Cholinesterase Inhibitors: Donepezil, rivastigmine
    • Indicated for any stage (except FTD)
    • SE: GI (nausea, diarrhea), bradycardia, orthostasis
  • NMDA antagonists: Memantine
    • Indicated in moderate to severe AD in combination with cholinesterase inhibitors
    • Fewer SE than cholinergic medications
• Vitamin supplementation (i.e. Vitamin E)
  • Unclear benefit in delaying progression of dementia
• Targeting Behaviors
  • Non-pharmacologic management has the best evidence of effectiveness
  • Depression: Treat with antidepressants (SSRI’s)
  • Sleep Disturbance: Mirtazapine (7.5 mg nightly) or Trazodone (25 mg nightly)
  • Agitation: Try SSRI (citalopram, sertraline)
    • Consider antipsychotics (black box warning increased risk of death in elderly)

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Last update: 2022-07-05 14:41:01