Non-Ad Dementia

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frontotemporal degeneration

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45-65 yrs; spares memory usually; major subtypes: behavioral variant FTD, progressive nonfluent aphasia, semantic dementia

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orbitofrontal cx/anterior cingulate functions

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emotional valence (esp right frontal lobe), behavioral control and inhibition

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dorsolateral prefrontal cx function

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organization, executive function

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temporal lobes (anterior and inferior) function

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semantic knowledge

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bv-FTD affects what?

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prefrontal cortex (including orbitofrontal and dorsolateral prefrontal cx) with right-sided predominance

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PNFA affects what?

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left fronto-insular lobe (Broca's)

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SD affects what?

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temporal lobe (anterior, inferior) -> left temporal lobe associated with profound anomia and loss of conceptual knowledge of words while right temporal lobe associated with deficits in knowledge about emotions and ability to recognize emotions in others

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bv-FTD characteristics (4)

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personality change (with loss of insight into behavior), emotional blunting and inappropriate emotional reactions, disinhibition (incl. overeating, perseveration), dysexecutive function (inflexible behavior, inefficient learning, poor working memory)

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PNFA characteristics (4)

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effortful, non-fluent speech; insight into impairment; agrammatism; phonological (pronunciation) errors but not semantic (naming) errors

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semantic dementia characteristcs (6)

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loss of concepts, poor comprehension, anomia (can't name), associative agnosia (don't understand meaning of objects), surface dyslexia (sound out letters rather than understanding word); but still fluent!

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FTD pathology

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50% have intracellular tau inclusions at autopsy while 50% have intracellular pathology immunoreactive to TDP-43

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Pick bodies

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intracellular inclusion bodies composed of randomly arranged filaments of tau protein

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tauopathies (3)

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FTLD (about half), progressive supranuclear palsey (PSP), corticobasilar degeneration (CBD) -> PSP and CBD are parkinsonian disorders

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FTD-ALS

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ALS occurs in 15% of pts with FTD - almost all these cases have TDP-43 pathology in this case

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FTD with parkinsonism

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occur together due to mutations in tau gene (chr 17) - the FTD is always tauopathy in this case (FTLDP-17)

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dementia with Lewy bodies

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very common (20% of dementia, 5% of ppl over 85 -> likely underdiagnosed or misdiagnosed as PD or AD); us. onset between 60-90 yo; significant overlap with PD (may be different versions of the same disease)

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dementia with Lewy bodies central feature (1) and core features (3) and suggestive features (3)

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central feature: progressive dementia -> deficits in attention, executive function, memory, visuospatial deficits; core features: visual hallucinations, fluctuating cognition (variations in attention and alertness), parkinsonism (however, no resting tremor and less response to L-dopa); suggestive features: REM sleep behavior disorder (RBD), hypersensitivity to neuroleptic and antiemetic meds that affect DA and ACh, autonomic dysfunction

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DLB pathology

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Lewy bodies: large cytoplasmic inclusions containing ubiquitin and alpha-synuclein; LB are in SN for PD and in neocortex (mainly cingulate cortex) for DLB; can also see AD-like plaques and tangles

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DLB tx (5)

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low doses of L-dopa to tx parkinsonism, but this can exacerbate hallucinations and confusion; acetocholinesterase inhibitors to benefit cognition; avoid neuroleptics (block DA); SSRIs for depression/anxiety, clonazepam for RBD

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vascular dementia subtypes

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multi-infact dementia, subcortical vascular dementia, strategic infact dementia

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multi-infarct dementia types

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symptomatic large vessel stroke; vessel obstructed determines symptoms: MCA (left) = aphasia, MCA (right) = neglect, ACA: apathy, loss of initiative, akinetic mutism; PCA: amensia, agnosia, anomia

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multi-infarct dementia history

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stepwise abrupt decline and vascular risk factors

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subcortical vascular dementia causes

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extensive small vessel lesions of white matter OR other conditions: HIV, hydrocephalus, vasculitis

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subcortical vascular dementia features (5)

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psychomotor slowing, impaired concentration, impaired reading, forgetfulness -- absence of focal cortical deficits (aphasia, agnosia, apraxia, etc.)

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multi-infarct dementia cause

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symptomatic large vessel stroke; vessel obstructed determines symptoms

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strategic infarct dementia cause

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lesion interrupting critical frontal-subcortical connections (anterior and dorsomedial thalamus, genu of internal capsule) -> single small infarcts that can result in broad deficits in cognition with prominent subcortical symptoms

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tx of vascular dementia (3)

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primary (prevention): managing risk factors (hypertension); secondary (prevention): manage stroke risk factors after initial episode of stroke; tertiary (amelioration of symptoms): Alzheimer's agents, neurostimulants, antidepressants, antipsychotics