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Neurophysiology > Neuropathy Common Neurocognitive Disorders > Flashcards

Neuropathy Common Neurocognitive Disorders Flashcards

1
Q

What are disorders called with progressive loss of neurons with associated secondary changes in white matter tracts

A

Neurodegenerative disorders

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2
Q

Are neurodegenerative disorders selective as to which groups of neurons they choose?

A

Yes

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3
Q

What common finding are resistant to degradation through the ubiquitin-proteasome system? What do they form? Give 2 common examples

A

protein aggregates, inclusions with neurons, Parkinson disease, Alzheimer disease

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4
Q

What are the 2 different types of dementia and severity?

A

early – mild neurocognitive disorder
late – major neurocognitive disorder

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5
Q

What is generalized, progressive impairment of cognitive function, accompanied by impairment in ADLS?

A

dementia

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6
Q

Does dementia have impaired level of consciousness?

A

No

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7
Q

With dementia, are executive function, memory, and attention all affected?

A

Yes

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8
Q

Which requires more complex planning and thinking? ADLs or iADLs?

A

IADLs

IADLs: things you do to take care of self and home-telephone, shopping, cooking, housekeeping, laundry, transportation, finances, medications

ADLs: basic self-care tasks- bathing, dressing, toileting, transferring, continence, feeding

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9
Q

Are ADLs significantly impaired with MILD neurocognitive disorder? How many cognitive domains are reduced in function? Is the patient generally aware of deficit?

A

NO
1 or more (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition)
YES

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10
Q

Are ADLs and/or iADLS significantly impaired with MAJOR neurocognitive disorder? How many cognitive domains are reduced in function? Is the patient generally aware of deficit?

A

ADLs and iADLs are affected. iADLS often first!

Larger impairment of 1 or more major cognitive domains

NO

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11
Q

What is the most common cause of dementia in elderly? Prevalence?

A

Alzheimer disease, 1 in 8 in older populations, 40% in 80-90 group, 6th leading cause of death

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12
Q

What are some general pathological findings in Alzheimer disease?

A

1.) neurofibrillary tangles
2.) beta-amyloid plaques
3.) cerebral atrophy
4.) often loss of widely-distributed cholinergic neurons in the nucleus basalis of Meynert

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13
Q

What are focal, spherical collections of dilated, tortuous, neuritic processes (dystrophic neurites)?

A

Neuritic plaques (beta-amyloid)

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14
Q

Where are neuritic plaques often found? What might they be surrounded by?

A

Found around a central amyloid core. In the hippocampus, amygdala, and neocortex

May be surrounded by clear halo

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15
Q

Amyloid core in neuritic plaques contains several abnormal _____________. Examples?

A

PROTEINS

Aβ, a peptide derived through specific processing events from a larger molecule, amyloid precursor protein (APP)

Other proteins are present in plaques in lesser abundance, including components of the complement cascade and pro-inflammatory cytokines

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16
Q

What is the range of size for a neuritic plaque?

A

20-200 um diameter

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17
Q

What is present at the periphery of NPs?

A

microglial cells and reactive astrocytes

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18
Q

Which 2 areas tend to be spared by plaques?

A

primary motor and sensory cortices

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19
Q

What are bundles of filaments in the cytoplasm of the neurons that displace or encircle the nucleus?

A

neurofibrillary tangles

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20
Q

What type of neurons are neurofibrillary tangles typically found? Are they basophilic or acidophilic? What type of staining?

A

cortical neurons (especially in the entorhinal cortex, pyramidal cells of hippocamps, amygdala, basal forebrain), basophilic, H & E staining

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21
Q

What is a major component of many “tangled filaments”? Other components?

A

Abnormally hyperphosphorylated forms of protein TAU.

Tau= axonal microtubule-associated protein that enhances microtubule assembly

MAP2 (microtubule-associated protein)

Ubiquitin

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22
Q

What is APP?

A

Amyloid precursor protein

membrane-associated protein that is thought to be a receptor for an unidentified ligand

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23
Q

What form of APP is thought to be important in the pathogenesis of Alzheimer disease?

A

the insoluble form accumulated in the extracellular space

(APP is cleaved as a part of normal breakdown of cellular proteins. Depending on where it is cut, determines its solubility)

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24
Q

What results in chronic inflammatory injury to neurons? Accumulation of what is responsible for neurofibrillary tangles within neurons?

A

aggregates of beta-amyloid are directly neurotoxic and activate microglia and astrocytes = chronic inflammatory injury.

accumulation of beta-amyloid

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25
Q

REVIEW SLIDE 14 protein aggregation pathway in Alzheimer disease

A
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26
Q

Which cleavage produces Aβ peptides, which form pathogenic aggregates that contribute to the characteristic plaques and tangles of Alzheimer disease?

A.) β-amyloid-converting enzyme (BACE) and γ-secretase
B.) α-secretase and γ-secretase
C.) β-amyloid-converting enzyme (BACE) and α-secretase
D.) Presenilin 1 and α-secretase

A

A.) β-amyloid-converting enzyme (BACE) and γ-secretase

27
Q

Which 2 proteins are associated with severe early-onset of AD? What do they regulate? What else are they involved in?

A

presenilin 1 and presenilin 2

regulate calcium levels associated with LTP (long-term potentiation)

Cleaving APP (similar function as secretase)

28
Q

People that are heterozygous or homozygous for which protein have increased risk of AD? Which has more risk?

A

Apolipoprotein E4 - helps transport cholesterol throughout CNS

Heter- 2x risk (LOAD)
Homo- 16x risk (LOAD)

29
Q

Which is more positively causative? Presenilin or Apo E4?

A

presenilin

30
Q

How does diabetes II (increased blood glucose and FFAs) affect risk of AD?

A

Insulin resistance likely reduces synaptogenesis

As resistance to insulin builds due to long-term hyperglycemia, then the intracellular signaling cascades are down-regulated –> decreased plasticity

Insulin resistance increases the levels of circulating pro-inflammatory cytokines

May lead to glial activation –> neuronal damage

31
Q

What is the relationship between an increase in blood glucose and leaky BBB?

A

As blood glucose increases, it becomes non-enzymatically linked to the basement membrane of brain capillaries –> a “leaky” blood-brain barrier

Systemic pro-inflammatory cytokines can then leak through into the brain –> maladaptive glial activation and neuronal damage

32
Q

When glucose becomes non-enzymatically bound to an extracellular protein it’s known as what?

A

AGE (advanced glycation end-product)

33
Q

What kind of pathways do rAGEs often activate?

A

Pro-inflammatory pathways

34
Q

Which cognitive impairment happens relatively early in AD?

A

short-term memory and executive functions (planning, logic) impaired

personality changes and loss of normal inhibitions can follow some time after

35
Q

Which cognitive impairment happens in more advanced AD?

A

language deficits and loss of learned motor skills

36
Q

Which cognitive impairment happens in severe AD?

A

incontinence and impaired ambulation

impaired mobility related to development of pneumonia and sepsis

37
Q

Clinical features of AD? (the 4 A’s and 1 D)

A

1.) anterograde amnesia
2.) aphasia
3.) Apraxia – difficulty with motor planning to perform tasks or movements
4.) Agnosia – difficulty recognizing/identifying objects, persons, or sounds although sensation is intact
4.) disturbance in executive function

38
Q

Which one of the A’s is used to make the diagnosis?

A

Anterograde amnesia PLUS at least 1 other

39
Q

What protein is mutated in dementia with Lewy bodies? What does this result in?

A

tau proteins

aggregation of tau protein, or alteration of how tau interacts with microtubules

40
Q

Which lobes of the brain show more marked atrophy in Dementia with Lewy bodies?

A

frontal and temporal lobes

41
Q

Which type of dementia has Parkinsons-like movements? What movements are these? Are these movements before or after the dementia?

A

Dementia with Lewy bodies

tremor, rigidity, bradykinesia

after

42
Q

Dementia with Lewy Bodies usually predates or follows the diagnoses of Parkinson’s?

A

predates

43
Q

Presence of Lewy bodies in neurons – likely aggregates of misfolded what?

A

alpha-synuclein

44
Q

What percent of general elderly population have dementia with Lewy Bodies?

A

0.1-5%

45
Q

AD or Lewy?
1.) Fluctuations in cognitive function with varying levels of alertness and attention
2.) Visual hallucinations that are vivid
3.) incontinence
4.) Prominent anterograde memory loss
5.) Executive function deficits

A

1.) Lewy
2.) Lewy
3.) AD
4.) AD
5.) Lewy

46
Q

What is an impairment in reality testing, characterized by delusions and hallucinations

A

psychosis

47
Q

What are beliefs that are not compatible with reality and are not normal beliefs for a culture?

A

delusions

48
Q

What is the perception of a stimulus that isn’t there?

A

hallucination (can be audible or visual)

49
Q

Which type of hallucination is more common in dementia? Audible or visual?

A

audible

50
Q

Where are executive functions orchestrated from?

A

prefrontal cortex

51
Q

True or False.
Executive functions often rely on memory and verbal fluency and therefore are always lost along with memory and verbal fluency.

A

FALSE.

Executive functions often rely on memory and verbal fluency, but can be lost even when memory and verbal fluency are not that impaired

52
Q

What is your brain’s “taskmaster” to keep you doing things effectively and appropriately, either in a social or job or school context?

A

executive functions

53
Q

Shifting effectively between tasks
Inhibiting unwanted or inappropriate behaviours or responses
Selecting and paying attention to information that applies to a particular task
Using working memory to accomplish tasks
Planning tasks

These are all examples of what?

A

executive functions

54
Q

Patients with long-standing PD without cognitive impairment who slowly develop a dementia have what?

A

PD dementia

55
Q

Which kind of dementia is associated with visual hallucinations and fluctuating alertness?

A

PD dementia

56
Q

True or False. Lewy bodies are only found in Dementia with Lewy bodies.

A

FALSE. They are also found in PD dementia

57
Q

Which type of dementia is a large group with diverse nomenclature and characterized by deficits in executive function, poor mental flexibility and abstract reasoning, response inhibition, planning/organization, and increased distractibility?

A

frontotemporal dementias

58
Q

What are the most common behavioral variants in frontotemporal dementias?

A

behavioural disinhibition (socially inappropriate behaviour, impulsive, careless)
apathy or inertia
loss of sympathy or empathy
Perseverative, stereotyped, or compulsive/ritualistic behaviour
hyperorality and dietary changes

59
Q

FTD OR AD?
1.) more prominent memory deficits
2.) progressive inability to form words or use language
3) rapid decline
4.) common in older patients

A

1.) AD
2.) FTD
3.) FTD
4.) AD

60
Q

What is 2nd most common cause of dementia after AD, with multiple small infarcts (often affecting gray matter of the cortices) or hypertension (often affecting white matter)?

A

vascular dementia

61
Q

Depression and psychosis can be common in which type of dementia?

A

vascular

62
Q

Which type of dementia has psychosis will frequently include delusions and hallucinations; agitation can be dangerous to both the patient and the caregiver?

A

vascular

63
Q

True or False. Gait abnormalities are common (gait apraxia), and lateralizing signs (increased tone/reflexes) often present in VD?

A

True.

64
Q

Which type of dementia progresses in a step-wise fashion?

A

VD

Neurophysiology (9 decks)

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