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Neuro II > Degenerative Disease/Dementia > Flashcards

Degenerative Disease/Dementia Flashcards

1
Q

What are the 5 cognitive domains?

A
  1. Memory
  2. Language
  3. Visual-Perceptual-Spatial
  4. Executive Function
  5. Social Function / behavior
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2
Q

What are the subcomponents of the memory domain?

A
  • Short term / working
    • abmility to maintain material in active form
  • Long term
    • declarative - conscious acquisition, retention & retrieval of knowledge
      • episodic- dependent on personal experience
      • semantic- factual, non-personal
    • non-declarative - unconscious experience-induced changes in performance
      • procedual memory - acquisition of sklls/habits from repeated practice
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3
Q

What is the differential for an acute (minutes) cognitive decline?

A

delirium

stroke

head injury

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4
Q

What is the differential for as subacute cognitive decline?

A
  • hours/days
    • infection/metabolic dereangement
  • weeks/months
    • mass effect from neoplasm or rapidly progressive dementia
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5
Q

What is the differential for a chronic cognitive decline?

A

classic neurodegeneration

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6
Q

What is the difference between delirium & dementia?

A
  • delirium is fluctuant
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7
Q

What are the criteria for delirium

A
  1. acute change in baseline mental status in 24 hr period that may be fluctuant
  2. difficulty sustaining attention
  3. may have altered consciousness OR difficult answering simple quesitons
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8
Q

What is reaplidly progressive dementia?

A
  • weeks to months of progressive cognitive decline
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9
Q

What is the work-up if you suspect a patient has rapidly progressinve dementia?

A
  • Exclude metabolic/infectious/toxic causes
    • TSH, RPR, B1, B12, HIV, Lyme
  • Exclude structural cause
  • Exclude infection/autoimmunity
  • Exclude seizure
    • EEG to exclude seizure activity
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10
Q

You use a MRI, CTA & MRV to look for what specific structural problems?

A
  • MRI brain w/ w/o contrast to exclude carcinomatous process
  • CTA to exclude dural arteriovenous fistul
  • MRV to exclude venous sinus thrombosis
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11
Q

What are the main cuases of rapidly progressive dementia?

A
  • non-prion neurodegeneration
  • prion diseases (jakon-Creutzfeldt disease)
  • Antibody-mediated encephalopathies
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12
Q

What is Limbic encephalitis?

It is associated with what other conditions?

Lab findings on lumbar puncture / MRI?

A
  • Autoimmune Encephalopathy - altered sensorium, rapid cognitive decline, altered mood/personality, seizures
  • Associated
    • autoimmunity
    • cancers
  • Tests
    • lumbar - elevate proteins, elevated IgG index, oligoclonal bands, (+) Ab VGKC or NMDA
    • MRI - normla or mesial temporal T2 hypersensitivity
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13
Q

What is the treatment for autoimmune encephalopathy?

A

Limbic encephalitis

high dose pulse IV steroids, IVIG, PLEX rituximab, cyclophosphamide

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14
Q

The provided MRI is indicative of what condition?

A

Limbic encephalitis

mesial temporal T2 hyperintensity

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15
Q

What is the cause of Jakob-Creutzfeldt disease?

symptoms?

prognosis?

A

abnormally shaped, deviant protein (prion)rapidly

progressive dementia with behavioral disturbance, ataxia & eventually myoclonus, visual/cerebellar dysfunction

months - year

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16
Q

What laboratory findings are indicative of Jakob-Creutzfeldt disease?

A

lumbar puncture: 14-3-3, RT-QUIC (+)

MRI w/ cortical ribboning on diffusion weighted imaging and EEG w/ 1 to 2 Hz periodic sharp wave complex (sensitive/specific)

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17
Q

What is the most common form of human prion disease?

A

Jakob-Creutzfeldt Disease

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18
Q

The provided MRI is indicative of what condition?

A

cortical riboning (white along outside)

Jakob-Creutzfeldt Disease

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19
Q

What are the 5 criteria for dementia?

A
  1. Interfere with ability to function (work or social)
  2. Represents a decline from prior levels
  3. Not explained by delirium or anothe rmedical, neurological or psychiatric disorder
  4. Cognitive impairment is detected/diagnosed
  5. Cognitive / bejavioral impairment involveds at least TWO cognitive domains
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20
Q

How can you establish that cognitive impairment in the criteria for dementia?

A

history from patient & informant

objective cognitive assessment (MMSE, MoCA, etc)

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21
Q

What is mild cognitive impairment?

A

impairment in one or more cognitive domians but daily function is preserved

border btw cognitive changes related to aging & very early dementia

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22
Q

What is the most common prodromal state of Alzheimer Disease?

A

mild cognitive impairment

but NOT ALL MCI is early Alzheimer

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23
Q

What are the risk factors for mild cognitive impairment to rapidly progress to Alzheimer?

A
  • apolipoprotein E4
  • abnormal tau PET scan
  • low CSF aB42
  • elevated CSF tau
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24
Q

What is the most preventable cause of dementia?

A

vascular cognitive impairment

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25
Q

What are the criteria for vasclar cognitive impairment?

A
  1. imaging evidence of cerebrovascular disease
  2. Temporal relationship between a _vascular event & onset of cognitive deficit_s OR clear relationship between severity of / pattern of cognitive impairment & presence of subcortical cerebrovascular disease
  3. no history of gradually progressive cognitive deficitys before / after stroke to suggest another cognitive disorder
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26
Q

What type of memory is most affected in vascular cognitive impairment?

A

deficitys in executive function/processing speed > episodic memory

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27
Q

What form of VCI is seen in the provided image?

This is indicative of what type of disease course?

A

multiple infarcts

step-wise course

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28
Q

What form of VCI is seen in the provided image?

This is indicative of what type of disease course?

A

Lacunar infarcts & single strategic infarcts

small stokes - likely to impair cognition

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29
Q

What is Binswanger Disease?

A

nonstroke vascular cognitive impairment caused by subcortical ischemic cerebral small vessel disease

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30
Q

What is CADASIL?

Symptoms?

A

cerebral autosomal dominant arteriopathy with subcortical infarcts & leukoencephalopathy

genetic small vessel disease w/ vessel smooth muscle NOTCH3 accumulation

migraines, MS, dementia

31
Q

What is the autosomal recessive form of CADASIL?

What substance is accumulated in this condition?

A

CARASIL

NOTCH3 (in vessels of SM)

32
Q

What aspect of this MRI is indicative of CADASIL?

A

anterior temporal love involvement

33
Q

Is cerebral amyoid angiopathy related to atherosclerosis?

34
Q

What is cerebral amyloid angiopathy?

treatment?

A
  • vascular B-amyloid deposition in the cerebral cortex & leptomeninges
    • vessels become fragile & rupture
    • intracranial bleeding (superficial & lobar)
  • No treatment
35
Q

The provided image is from a patient with what condition?

A

Cerebral amyloid angiopathy

all they hyperdense areas are hemorrhages

36
Q

What is the clinical picutre of a patiet with Alzheimer disease?

A
  • F ; 65+
  • short-term memory impairment > executive > visuospatial
  • apathy, anxiety, irritability, depression, hallucinations, delusions
  • anosognosia
37
Q

Describe the pathophysiology of Alzheimer disease

A

starts years prior to clinical symptomatology

  • Tau hyperphosphorylation
    • intraneuronal neurofibrillary tangles
  • overproduction / impaired clearnce of B-amyloid
    • neuritic plaques
    • B-amyloid deposits in cerebral blood vessels
  • mesial temporal
    • global atrophy
38
Q

What components of Alzheimers pathology are shown in the provided samples?

A
  1. Left
    1. neurofibrillary tangles (silver stain)
  2. Right
    1. Amyloid in plaques & vessels of cerebral cortex (beta amyloid immunostain)
39
Q

What components of Alzheimers pathology are shown in the provided samples?

A
  1. Neurofibrillary tanglees & Neuritic Plaque (silver stain)
  2. Global brain atrophy in advanced AD
40
Q

What allele is associated with increased risk for developing Alzheimer Disease?

A
  • APOE4 allele
41
Q

What modifiable risk factor is an imporant in Alzheimer Disease?

A

midlife metabolic profile

(low polyphenol dietary intake)

42
Q

What are the 5 ways we can clinically test for Alzheimer Disease?

A
  1. Neuropsychological testing
  2. MRI to look for mesial temporal lobe atrophy
  3. Lumbar Puncture: elevated CSF tau & reduced CSF AB142
  4. FDG-PET & SECT imaging to differentiate AD from FTD
  5. Abnormal plasma P-tau
43
Q

When looking at an MRI in the process of diagnosing Alzheimer Disease, what pathology are you looking to exclude?

A
  • exclude
    • mass
    • subdural hematoma
    • features of normal presure hydrocephalus
44
Q

What are the treatments for Alzheimer Disease?

A
  • Moderate to severe AD
    • Donepezil & Rivastigmine
    • Mematine
  • Depression & Agitation can be treated with SSRI
45
Q

What is the progression of Dementia with Lewy Bodies?

A

Ascending Spread of Lewy Body Pathology

  1. Brainstem
    1. anosmia, depression, REM sleep disorders, arousal/attention, autonomic, movement
  2. Limbic
    1. amnesia/psychosis
  3. Cortical
    1. multidomain dementia
46
Q

What is the mean age of onset of Dementia with Lewy bodies?

47
Q

What are the 4 clinical features of Dementia with Lewy Bodies?

A
  1. Fluctuating Cognition
  2. Visual Hallucinations
  3. REM Sleep Behavior Disorder
  4. Motor Parkinsonism
48
Q

What are the characteristics of the visual hallucinations seen in patients with DLB?

A
  • Early
    • visual misperceptions (mistake stick for animal)
  • Later (common)
    • visual hallucinations
    • recurrent, complex, usually not persecutory
  • Late
    • delusions (paranoid, intrusion, infidelity)
    • depression/anxiety
49
Q

What is Capgras syndrome? It is seen in what condition?

A

when the person is having a delusion that their spouse has been replaced by an imposter

seen in late DLB

50
Q

What type of REM sleep behavior disorders are seen in DLB?

A

parasomnia; recurrent enactment of dreams

chasing/attacking themes of dream

(precede cognitive decline)

51
Q

What polysomnogram result is suggestive of synucleinopathy?

A

REM sleep without atonia ina person with dmentia & history or RBD

52
Q

When does the motor parkinsonism in DLB develop?

Characteristics?

A

with or after the onset of the 3 core features

motor signs are often symmetric

generalized myoclonus

53
Q

How can you differentiate Motor Parkinsonism in DLB from Parkinson disease?

A
  • Motor Parkinsonism
    • motor usually symmetric
    • generalized myoclonus
    • limited response to carbidopa/levodopa
    • dementia precedes or occurs within 1 year
  • Parkinson
    • usually unilateral
    • usually response to carbidopa/levodopa
    • motor features precede dementa by at least 1 year
54
Q

What type of dementia is seen in synucleinopathies?

A

Visual-spatial function

  • Difficulty multitasking, following conversation
  • getting lost when driving; relying more on GPS devices
55
Q

Fill out the provided table

56
Q

Where do you see decrease in metabolic activity in Alzheimer & DLB?

A
  • AD: temporal lobe
  • DLB: parietal lobe
57
Q

Which of the provided scans is a patient with Alzheimer Disease & which is a patient with DLB?

A

Left: AD (notice severe hippocampal degeneration)

Right: DLB (less hippocampal degeneration)

58
Q

What medications should be avoided in patients with DLB?

A
  • Typical antipsychotics
    • haloperidol, thioridazine, fluphenazine
  • Benzodiasepines
  • Anticholinergic medications
    • tricyclic antidepresants
  • Dopamine agonists
    • pramipexole, ropinirole
59
Q

What symptoms of dysautonomia are seen in patients with DLB?

Treatment?

A

nocturnal hypotension, orthostatic hypotension, sensitivity to head or cold, sexual dysfunction

Treatment: compression stockings, abdominal binders, salt tablets, midodrine; fludrocortisone

60
Q

What is the clinical picture of a patient with Multiple System Atrophy?

A
  • >30
  • Symptoms
    • autonomic failure
    • atypical tremor
    • hypokinetic dysarthria
    • jaw opening dystonia
61
Q

What type of tremor is seen in multiple system atrophy?

A

atypical tremor

high frequency, low amplitude, jerky, stimulus sensitive, myoclonic

62
Q

What is another name for multiple system atrophy?

A

alpha synucleinopathy

63
Q

Howo does multiple systme atrophy respond to L-Dopa?

A

poor response

64
Q

What ar the other terms for frontotemporal dementias?

A

tauopathy / TDP-43

65
Q

What is the primary presentation of a patient with frontotemoral dementia?

A

behavioral/personality changes

disinhibition, impulsivity, apathy, hyperorality, hyperfixation, odd collections

66
Q

What are the are the two variants of frontotemporal dementia?

They are associated with which specific parts of the brain?

A
  • Behavior variant (Pick Disease) >50%
    • right frontal / temporal lobe atrophy
  • Primary progressive aphasia
    • semanitc variant - loss of word meaning; speech is fluent & gramatically correct
      • anterior trmporal atrophy
    • nonfluent agrammatic variant
      • speech is effortful & halted
67
Q

What is the clinical presentation of a patient with progressive supranuclear palsy?

A
  • onset ~65
  • Symptoms
    • early falls
    • vertical supranuclear palsy: downgase more sensitive
    • frontal dementia w/ pseudobulbar affect
      • “applause sign”
    • worried / astonished look
    • axial rigidity
68
Q

Do patients with progressive supranuclear palsy respond to L-dopa?

69
Q

What is the name of the sign shown in the provided MRI?

It is indicative of what pathology?

A

Hummingid sign - midbrain is atrophied making the “beak” of the hummingbird

progressive supranuclear palsy (PSP)

70
Q

What cellular abnormality is seen in patients with progressive supranuclear palsy?

A

Tufted Astrocyte

71
Q

What type of degeneration is seen in corticobasal degeneration?

A

asymmetric frontoparietal atrophy

72
Q

Corticobasal Degeneration is what kind of pathology?

73
Q

What is the presentation of a patient with corticobasal degeneration?

A

asymmetric rigidity with dystonia & ideomotor apraxia (Alien Limb phenomenon)

course rest/action tremor

myoclonus

cortical sensory loss

74
Q

Does corticobasal degeneration respond to L-dopa?

Neuro II (30 decks)

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