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IMC606: Neurology > Dementia > Flashcards

Dementia Flashcards

IMC606

1
Q

Give an example of

Working memory

A

remembering a phone number through rehearsal; doing mental arithmetic

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2
Q

Give an example of

Episodic memory

A

remembering what I ate for dinner last night

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3
Q

Give an example of

Semantic memory

A

knowing what a library is; knowing what a computer is

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4
Q

Give an example of

Procedural memory

A

knowing how to dance, swim, ride a bike

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5
Q

The function of

Amygdala

A

recognizing threatening stimuli and responding to them; attaching emotional responses to life events

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6
Q

The function of

Hippocampus

A

memory consolidation; transferring episodic memories to cortical areas for long term storage.

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7
Q

Cause of Kluver-Bucy

A

bilateral damage to the amygdala

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8
Q

Deficits that occur in Kluver-Bucy

A

loss of aggression/fear, hypo-emotionality, hyperorality, hypersexuality

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9
Q

What is the role of nucleus accumbens in behavior?

A

Nuc Accumbens influences our response to rewarding stimuli. It is involved in our motivation/drive to participate in behaviors that are rewarding/positive/pleasurable.

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10
Q

What transmitter is significant in the nucleus accumbens activation, and how is it related to addiction?

A

It is activated by dopamine. Highly rewarding activities release larger amounts of dopamine in Nuc Accumbens and facilitate reinforcing those activities/behaviors.

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11
Q

Name the structures involved in the Papez circuit and link the structures to show how activity progresses through the circuit.

A

hippocampus -> fornix -> mammillary body -> anterior nucleus of thalamus -> cingulate gyrus -> entorhinal cortex (area around olfactory cortex ) -> hippocampus

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12
Q

Pathological features and proteins in

Alzheimers Disease

A

Senile plaques – b amyloid aggregate, neurofibrillary tangles – hyperphosphorylated t, gliosis, hydrocephalus ex vacuo, brain atrophy

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13
Q

Pathological features and proteins in

Lewy Body dementia

A

Lewy Bodies – a synuclein, neuromelanin inclusions

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14
Q

Pathological features and proteins in

Frontotemporal Lobe Degeneration

A

hyperphosphorylated t inclusions, TDP-43, frontal lobe atrophy

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15
Q

Pathological features and proteins in

Creutzfeldt Jacob Disease

A

prions – misfolded, transmissible proteins, spongiform encephalopathy, amyloid aggregates, MRI: cortical ribbonning, BG/Thalamus intensity; 14-3-3 protein in CSF, sharp waves EEG

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16
Q

Pathological featues and proteins in

Vascular Dementia

A

multiple cortical infarcts

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17
Q

Affected areas in

Alzheimers Disease

A

Cortex, hippocampus, amygdala

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18
Q

Affected areas

Lewy Body Dementia

A

Diffuse cortex

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19
Q

Affected areas in

Frontotemporal Lobe Degeneration

A

Frontal and temporal lobes

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20
Q

Areas affected in

Creutzfeldt Jacob Disease

A

Diffuse Brain

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21
Q

Areas affected in

Vascular Dementia

A

Multiple cortical infarcts

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22
Q

Symptoms of

Alzheimers Disease

A

amnesia (anterograde early, retrograde late)
executive dysfunction
loss of insight
aphasia
visuo-spatial impairment

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23
Q

Symptoms of

Lewy Body Dementia

A

visual hallucinations
fluctuating cognition
PD symptoms
(memory good initially)

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24
Q

Symptoms of

Creutzfeldt Jacob Disease

A

myoclonus
ataxia
rapid progression
cognitive decline

25
Q

Symtpoms of

Frontotemporal Lobe Degeneration

A

Disinhibited behavior
apathy
loss of empathy
overeating sweets
compulsive
aphasia subtypes
(<65 yo, memory good initially)

26
Q

Symptoms of

Vascular Dementia

A

Focal neurological deficits
loss of cognitive abilities

27
Q

Onset of dementia vs delirium

A

Dementia- abrupt onset
Delirium- ongoing condition

28
Q

Reversibility of dementia vs delirium

A

Dementia- irreversible
Delirium- reversible

29
Q

Chronicness of dementia vs delirium

A

Dementia- chronic
Delirium- acute

30
Q

Changing in delirium and dementia

A

Dementia- unchanging mental status
Delirium- waxing and waning mental status

31
Q

Ability to focus in dementia vs delirium

A

Dementia- maintains focus
Delirium- distractible, loss of attention

32
Q

Consciousness in dementia vs delirium

A

Dementia- stable consciousness
Delirium- fluctuating consciousness

33
Q

What is the cause and symptomatic triad of Wernicke Encephalopathy?

A

Thiamine deficiency, a condition often associated with chronic alcohol use, results in hemorrhage of the mammillary bodies.

Symptomatic Triad: confusion, ophthalmoplegias, ataxia.

34
Q

In Wernicke’s Encephalitis What pathological changes occur? How does this disorder fit the definition of encephalopathy?

A

This is a metabolic/nutritional disorder that results in an acute state of confusion. A patient with WE presenting to the ED in a state of confusion would be exhibiting delirium or the effects of an encephalopathy.

35
Q

How is the memory deficit in Korsakoff Syndrome related to the memory structures in Papez’s circuit?

A

Korsakoff syndrome is associated with late stages of Wernicke encephalopathy. KS causes anterograde amnesia and confabulation (fabricating stories to explain unremembered events). It is a consequence of damage to the mammillary bodies, which are connected to the hippocampus via the fornix as part of Papez’s circuit.

36
Q

How are focal neurological deficits associated with vascular dementia? What about Alzheimer D, LBD, FTLD?

A

These are deficits that can be attributed to a lesion at a specific location in the central nervous system. Vascular dementia results from strokes that affect specific locations of the cerebral cortex. Damage to specific areas will result in specific deficits associated with those functional areas. In contrast, AD, LBD, FTLD result in diffuse damage to cortical areas that cause a more general loss of cognitive function. However, the restricted areas of frontal and temporal damage and their related symptoms in FTLD could be considered focal deficits.

37
Q

What score on the MMSE indicates mild cognitive impairment?

A

26-21

38
Q

Which disorders (AlzheimerD, LewyBodyD, FTLD) are associated with anterograde amnesia?

A

Anterograde amnesia is a feature of Alzheimer D due to atrophy of the hippocampus. LBD and FTLD do not affect the hippocampus.

39
Q

Formation of protein aggregates is one of the mechanisms underlying neurodegenerative diseases. Describe how amyloid and tau proteins are involved in this process: what leads to aggregate formation, where are the aggregates deposited.

A

Improper cleavage of APP by secretase molecules results in longer b-amyloid fragments that aggregate as they accumulate. These aggregates form insoluble, extracellular deposits in the cortex. They appear either as separate deposits (b-amyloid plaques) or they become surrounded by degenerating neurites (neuritic plaques). (neurite=unidentified axon or dendrite)
In AD, the microtubule associated protein, tau, becomes hyperphosphorylated. This causes it to form insoluble, intracellular aggregates that accumulate as twisted filaments (neurofibrillary tangles) in the cell body, axons, and dendrites.

40
Q

Disorder associated with image A

A

Lewy Body Dementia

41
Q

Disorder associated with image B

A

Neuritic Plaques

42
Q

Disorder associated with image c

A

Creutzfeldt Jacob Disease

43
Q

Disorder associated with image D

A

Neurofibrillary tangles

44
Q

Disorder associated with image E

A

Frontotemporal Lobe Degeneration

45
Q

How can Down’s syndrome provide insight into the role of b-amyloid in AD?

A

In Down’s syndrome there are 3 copies of chromosome 21. This chromosome contains the gene for APP, increasing the expression of amyloid compared to normal. Most individuals with Down’s syndrome develop b-amyloid plaques and AD by their 50s.

46
Q

Is hydrocephalus ex vacuo a feature of Alzheimer Disease? Explain your answer.

A

YES! Cortical atrophy that occurs in AD is accompanied by expansion of the lateral ventricles. The volume of CSF in the lateral ventricles expands to fill the space in the cranial cavity vacated by cortical tissue.

47
Q

How do the areas of degeneration in FTLD correlate with the clinical subtypes of FTLD?
Frontal lobe -

A

impaired executive functions (judgment, impulse control, social behavior, personality) correlates with bv-FTLD and damage to Broca area correlates with PPA type where speech is affected.

48
Q

How do the areas of degeneration in FTLD correlate with the clinical subtypes of FTLD?
Temporal lobe

A

Wernicke language area correlates with PPA type where language comprehension is impaired.

49
Q

Which cholinesterase inhibitors are used to treat AD and what is the rationale for their use?

A

Donepezil, rivastigmine, galantamine. Circuits involved in memory function depend on acetylcholine as an important transmitter. As neurodegeneration progresses and neurons become impaired, transmitter levels decrease, which can be compensated by inhibiting breakdown of acetylcholine in the brain.

50
Q

Disorders that affect the Loop of Meyer

A

HSV1
Stroke

51
Q

Deficits that affect the Loop of Meyer

A

Contralateral superior quadrantanopia

52
Q

Disorders that affect the Olfactory Cortex Uncus

A

Uncinate seizures
HSV1

53
Q

Deficits that occur in the Hippocampus

A

Inability to remember recent events

54
Q

Disorders that affect the hippocampus

A

HSV1
Seizure
Alzheimers Disorder
Kluver-Bucy

55
Q

Deficits in the Olfactory Cortex Uncus

A

Olfactory hallucination
Anosmia

56
Q

Disorders that affect the amygdala

A

HSV1
Seizure
Kluver-Bucy

57
Q

Disorders that affect Wernickes Area

A

HSV1
Stroke
Tumor
Seizure
FTLD
Alzheimer Disease

58
Q

Deficits in the Amygdala

A

Loss of fear and awareness of threat to self

59
Q

Deficits in Wernickes Area

A

Impaired ability to comprehend language

IMC606: Neurology (11 decks)

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