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B&B Part 2 > B&B Week 8 > Flashcards

B&B Week 8 Flashcards

1
Q

what circuit of structures is responsible for recent memory (aka declarative or episodic memory)?

A

papez circuit

hippocampal formation–> fornix–> mammillary body–> mamillothalamic tract–> anterior group of the thalamus–> cingulate gyrus –> cingulate bundle –> hippocampal formation once again

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2
Q

what is the critical structure in the papez circuit?

A

hippocampus (the most medial part of the temporal lobe)

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3
Q

what type of material specific amnestic syndromes will be produced if there is a lesion in the papez circuit in the dominant hemisphere?

A

verbal memory disturbance

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4
Q

what type of material specific amnestic syndromes will be produced if there is a lesion in the papez circuit in the non-dominant hemisphere?

A

non-verbal memory disturbance

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5
Q

what are the symptoms of an amnestic syndrome?

A
  1. anterograde amnesia
  2. varying degrees of retrograde amnesia
  3. preserved very remote memory (i.e long term, semantic memory)
  4. intact attention
  5. intact non-mnemonic intellectual functions (i.e calculation, visuospatial ability
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6
Q

how do you test cognitive intellectual function?

A
  1. initial assessment–> alert? oriented?
  2. regional cortical function–> assess vision, motor, hearing, sensation, language
  3. complex integrated response–> assess ability to complete 2 and 3 step processes (fist, side, flat hand motions)
  4. CIF–> assess attention (digit span, serial 7s, A test which is raising your hand every time you hear the letter A); assess mnemonic and nonmnemonic cognitive intellectual capacities
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7
Q

doubling/serial 7s…

  1. what neuroanatomical area is being tested with this test?
  2. what cognitive function is being tested with this test?
  3. what hemisphere (dominant or nondominant) is being tested with this test?
A
  1. heteromodal complex
  2. calculation
  3. dominant
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8
Q

3 word repeat…

  1. what neuroanatomical area is being tested with this test?
  2. what cognitive function is being tested with this test?
  3. what hemisphere (dominant or nondominant) is being tested with this test?
A
  1. temporal lobe, recent memory processor
  2. GFK, semantic memory (verbal memory)
  3. dominant hemisphere
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9
Q

3 shape repeat…

  1. what neuroanatomical area is being tested with this test?
  2. what cognitive function is being tested with this test?
  3. what hemisphere (dominant or nondominant) is being tested with this test?
A
  1. temporal lobe, recent memory processor
  2. GFK, non verbal memory
  3. non-dominant
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10
Q

3D cube drawing…

  1. what neuroanatomical area is being tested with this test?
  2. what cognitive function is being tested with this test?
  3. what hemisphere (dominant or nondominant) is being tested with this test?
A
  1. heteromodal complex
  2. visual-spatial processor
  3. non-dominant
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11
Q

in the dominant hemisphere, what does the parietal lobe do in terms of cognitive function? what does the temporal lobe do?

A

dominant hemisphere:
parietal lobe–> calculation
temporal lobe–> GFK/semantic (verbal) memory

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12
Q

in the non-dominant hemisphere, what does the parietal lobe do in terms of cognitive function? what does the temporal lobe do?

A

non-dominant hemisphere:
parietal lobe–> visual spatial
temporal lobe–> nonverbal memory

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13
Q

what are the 3 types of memory based on time?

A
  1. sensory memory–> less than 1 sec
  2. short term memory/working memory–> less than 1 min
  3. long term memory–> lifetime
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14
Q

what are the types of long term memory?

A
  1. EXPLICIT memory (conscious) –> declarative memory (facts, events)–> episodic memory (events ,experiences)//semantic memory (facts, concepts)
  2. IMPLICIT memory (unconscious) –> procedural memory (skills, tasks)
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15
Q

what are the two types of declarative memory (which is a subtype of explicit memory)?

A

episodic (events, experiences)

semantic (facts, concepts)

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16
Q

what are cognitive-intellectual functions?

A

higher levels of information processing (attend, store, retrieve, organize, process)

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17
Q

what are some bedside tests to test cognitive-intellectual function?

A

test attention, orientation, memory, calculation, visuospatial ability, abstraction (similarities and differences) and insight

requires intact lower order systems (motor, sensory, vision, hearing, language)–> i.e regional cortical function

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18
Q

what is a primary cortex? give an example

A

first assessment of input

i.e primary vision cortex

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19
Q

what is a unimodal cortex? give an example

A

association areas, i.e visual association areas

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20
Q

what is a heteromodal cortex? give an example

A

receives input from other heteromodal cortices–> i.e entorhinal cortex (below hippocampus)

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21
Q

what does the orbitofrontal cortex do?

A

inhibits urges, delays gratification

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22
Q

what does the dorsolateral prefrontal cortex do?

A

practice alternatives before making a decision (executive function)

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23
Q

what does the ventromedial cortex do?

A

emotion experience and meaning of events

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24
Q

what does the anterior cingulate gyrus do?

A

attention focusing, tuning into one’s thoughts, apathy

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25
Q

what does CIF stand for?

A

cognitive-intellectual function

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26
Q

what does the MSSE test?

A
  1. orientation (recent memory)
  2. naming (memory and language)
  3. serial 7s/world backwards (attention and calculation)
  4. recall (memory)
  5. naming (memory and language)
  6. repetition (language)
  7. 3 step command (language, memory, sequencing)
  8. read (language)
  9. write (language)
  10. copy (2-D visuospatial)
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27
Q

what neuroanatomical structures are association with attention?

A

arousal starts in the RAF and thalamus –> goes to right heteromodal cortices (especially the prefrontal and posterior parietal cortices)

limbic system adds mood and motivation

**in impairment of attention, delirium represents global failure of CIF (attention, recent and remote memory, calculation and visuospatial)

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28
Q

what 4 bedside tests assess attention?

A
  1. digit span (repeat 7 numbers forward, 5 backwards)
  2. A test (raise hand every time you hear the letter A)
  3. serial 7s (not a good attention task as it involves calculation as well)
  4. world backwards (working memory)
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29
Q

what are 4 bedside tests for recent/episodic memory?

A
  1. 3 word test
  2. 3 shape test

these test attention, encoding and retrieval

if have 2/3, encoded but no retrieval (forgetful)
if 0/3 there is no encoding (amnesia)

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30
Q

what function is missing in amnesia?

A

encoding

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31
Q

what is remote/semantic memory?

A

recall of learned material

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32
Q

what neuroanatomical structures are involved in remote/semantic memory?

A

inferolateral cortex and pole of temporal lobes, LEFT (dominant?) side only

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33
Q

what bedside test assesses remote/semantic memory?

A

animal fluency test (less than 15 in 1 minute is impaired)

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34
Q

what is the clinical presentation of someone with a semantic memory problem?

A

i.e semantic amnesic syndrome

impaired remote memory, anomia, preserved recent memory, intact attention and intellect, impaired comprehension of common concepts

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35
Q

what is the anatomy of calculation?

A

DOMINANT parietal cortex –> heteromodal

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36
Q

what is the anatomy of visuospatial ability?

A

NON-dominant parietal cortex

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37
Q

what are the non-memory CIFs?

A

calculation and visuospatial

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38
Q

what is a mnemonic to remember TREATABLE causes of dementia?

A

DEMENTIA (these causes are treatable)

Drugs (too many, too few, wrong ones)
Emotional problems (depressions, psychosis)
Metabolic disturbances (hyponatremia, alkalosis etc)
Endocrine disturbances (hypo or hyperglycemia, hypo or hyperthyroid, hypercalcemia etc)
Nutritional problems (B12, folate)
Trauma (i.e subdural hematoma)//Tumor (including paraneoplastic syndromes)
Infections (neurosyphilis)
Anemia//Alcohol

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39
Q

what are the most common causes of dementia?

A

alzheimer’s disease –> gradual onset and progression, prominent amnesia

vascular dementia–> encompasses multi-infarct dementia, white matter disease, and (less commonly) single large CVAs–> often stepwise in progression and having focal neurological symptoms and signs

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40
Q

other than alzheimer’s and vascular dementia, what are 7 other neurodegenerative causes of dementia?

A
  1. dementia with lewy bodies (DLB)
  2. parkinson’s disease and parkinson’s plus syndromes
  3. frontotemporal dementia
  4. normal pressure hydrocephalus
  5. huntington’s disease
  6. HIV
  7. cruetzfeld-jacob disease (prion)
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41
Q

what is dementia with lewy bodies?

A

criteria include fluctuations in course, hallucinations, sensitivity to antipsychotics, prone to falls and extrapyramidal signs

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42
Q

how is parkinson’s disease/parkinson’s plus syndromes related to dementia?

A

a neurodegenerative cause of dementia

i.e progressive supranuclear palsy–> presence of extramyramidal symptoms and signs as well as cortical and subcortical features

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43
Q

what is frontotemporal dementia?

A

YOUNGER age of onset than alzheimer’s disease

prominent behavioral changes including social conduct dysregulation, disinhibitions and emotional blunting OR prominent language impairment (i.e progressive NON-fluent aphasia or semantic problems, with breakdown of words meaning and knowledge)

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44
Q

what are symptoms of normal pressure hydrocephalus?

A

ataxia, urinary incontinence

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45
Q

what % of dementias have a known genetic cause?

A

only a fraction

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46
Q

what is the abnormality (mutation) associated with most types of genetically related dementia?

A

missense mutations

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47
Q

what genes are involved in alzheimer’s disease?

A

APP

PS-1

PS-2

ApoE is a susceptibility gene only

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48
Q

what genes are involved in frontotemporal dementia?

A

MAPT

PRGN

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49
Q

what genes are involved in CADASIL (a type of vascular dementia)?

A

NOTCH 3

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50
Q

when are patients tested for genetically-related dementia?

A

there exists strict guidelines for predictive genetic testing of asymptomatic “at risk” individuals–> patients are typically not tested unless there is a strong genetic background

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51
Q

what are the patterns of inheritance associated with dementia?

A

include sporadic and autosomal dominant

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52
Q

what is the believed cause of alzheimer’s disease?

A

thought to be caused by pathology in proteins A-beta and tau

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53
Q

what is amyloid precursor protein (APP)? how is it processed by the body, and how does this relate to alzheimer’s?

A

belongs to a family of membrane inserted glycoproteins expressed by neurons and other cells

majority of APP is normally broken down by alpha and gamma secretase generating p3

minority of APP is processed y beta and gamma secretase generating A-beta, an amylogenic product

A-beta protein is amylogenic in vitro and is a major constituent of senile plaques and congophilic angiopathy–> it varies in amino acid length from 39-43 and is an abnormal/minor metabolite of APP

**amyloid/senile plaques are also present in normal aging (but more in alzheimer’s)

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54
Q

what is A-beta protein?

A

produced by conversion of APP by beta and gamma secretase

A-beta protein is amylogenic in vitro and is a major constituent of senile plaques and congophilic angiopathy–> it varies in amino acid length from 39-43 and is an abnormal/minor metabolite of APP

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55
Q

describe the pathophysiology of early-onset familial alzheimer’s

A

APP mutation near enzymatic cleavage site results in increased production of A-beta protein

mutations in PS-1 and PS-2 (components of gamma secretase) results in increased production of A-beta42

APP, PS-1 and PS-2 are therefore the causative genes of alzheimer’s disease

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56
Q

describe the pathophysiology of late onset familial alzheimer’s

A

carriers of E4 allele of ApoE gene are associated with higher risk of sporadic alzheimer’s

E4 protein isoform binds A-beta protein with high avidity, thereby increasing its amylogenic potential

E4 allele of ApoE is therefore the susceptibility gene of alzheimer’s

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57
Q

what is tau protein?

A

microtubule-associated protein

different neurons express different isoforms of tau

hyperphosphorylation of tau results in the formation of paired helical filaments (PHF) and straight filaments

PHFs are the major constituent of NEUROFIBRILLARY TANGLES, plaque associated neuritis and neuropil threads

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58
Q

how is inflammation related to alzheimer’s pathophysiology?

A

thought to play a key role in accelerating the progression of alzheimer’s by causing further neuronal damage as amyloid genesis occurs

however, there is no evidence that supports tx with anti-inflammatory drugs

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59
Q

what are the diagnostic criteria for dementia?

A

the presence of an acquired impairment in memory, associated with an impairment in one or more cognitive domains including:

  1. executive function (abstract thinking, reasoning, judgement)
  2. language (expressive or receptive)
  3. praxis (learned motor sequences)
  4. gnosis (ability to recognize objects, faces or other sensory information)

impairments in cognition must be severe enough to interfere with work, usual social activities or relationships with others

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60
Q

what is the diagnostic criteria for alzheimers?

A
  1. dementia established by means of clinical diagnosis and cognitive testing
  2. progressive worsening of memory and other cognitive functions
  3. no disturbance on consciousness
  4. absence of systemic disorders or other brain diseases that could account for the progressive cognitive decline
  5. supportive features include:
    - altered behavioural patterns
    - family history of similar disorders, particularly if have confirmed neuropathology
  6. features that make a diagnosis of alzheimer’s uncertain or unlikely:
    - sudden onset
    - focal neurological findings, including hemiparesis, sensory loss, visual field deficits or incoordination
    - early presence of a gait disorder ot seizure
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61
Q

what are important things to note on the history and physical exam in someone with suspected dementia/alzheimers?

A

inquire about onset, duration, and evolution

substance abuse

metabolis disorders

systemic illnesses

depression

stroke

family history

physical exam should be NORMAL in alzheimer’s disease

should expect focal neurological deficits for vascular dementia and parkinson’s symptoms with dementia with lewy bodies or parkinson’s dementia

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62
Q

list the psychometric/cognitive screening tests that can be useful in assessing/making the diagnosis of dementia

A
  1. MSSE
  2. MoCA
  3. clock drawing test
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63
Q

how is the MSSE scored?

A

out of 30

mild is 18-16

moderate is 10-18

severe is less than 10

widely used in research and clinical settings but lacks sensitivity to detect mild cognitive impairment levels

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64
Q

how is the MoCA scored? what is an advantage of the MoCA over the MSSE?

A

scored out of 30, cut off score is less than 26

more sensitive than the MSSE in detecting alzheimer’s and mild cognitive impairment

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65
Q

what is the clock drawing test?

A

score range is varied

test for dementia

widely used in research and clinic setting but lacks sensitivity to detect mild cognitive impairment levels

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66
Q

what is the primary role of lab tests and CT/MRIs in the assessment and diagnosis of dementia/alzheimers?

A

primary role is to rule out the rare presence of a treatable disorder presenting as memory loss such as renal failure, brain tumour, normal pressure hydrocephalus and subdural hemorrhage

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67
Q

what are the basic lab investigations for dementia?

A

CBC

TSH

serum calcium

electrolytes and fasting glucose

renal function

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68
Q

what are the selective lab tests for dementia?

A

B12

rapid plasma regain (RPR) for syphilis

HIV antibodies

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69
Q

what are you looking for on CT/MRI in the case of dementia/alzheimer’s?

A

CT/MRI imaging permits assessment of early atrophy in medial temporal lobe suggestive of alzheimer’s

also, imaging allows exclusion of neurosurgical lesions including tumours, subdural hematomas and hydrocephalus

**brain atrophy does NOT correlate well with clinical signs and symptoms of alzheimer’s disease

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70
Q

what are the criteria for neuroimaging in suspected dementia/alzheimers?

A

young patient

short duration

unusual course

unexplained neurological signs and symptoms including gait disorder

history of head trauma

anticoagulant usage

malignancy

71
Q

what is the use of neuropsychological testing in dementia/alzheimers?

A

shown utility in distinguishing early or mild dementia from mild cognitive impairment or cognitive impairment without dementia and from normal cognitive function (i.e utility in distinguishing between dementia subtypes)

have a greater sensitivity than brief cognitive tests in documenting clear cognitive abnormalities across a range of cognitive domains

72
Q

what are some drawbacks to neuropsychological testing?

A

costly ($600-1500) and often not covered by MSP

requires 2-4 hours of time

long wait times due to limited resources

73
Q

what is the gross pathology associated with alzheimer’s disease?

A
  1. diffuse cortical atrophy (widened sulci, gyri) especially in the frontal, parietal and temporal lobes
  2. decreased cerebral volume
  3. enlarged ventricles
74
Q

what is the neuropathology seen in alzheimer’s disease?

A
  1. neurofibrillary tangles
  2. senile plaques
  3. neuronal loss
75
Q

what is a neurofibrillary tangle?

A

neuropathology associated with alzheimer’s disease

INTRACYTOPLASMIC paired helical filaments with beta-amyloid and hyperphosphorylated Tau protein composed of helical and straight filaments –> helical have abnormal hyperphosphorylated tau

initially most abundant in the ENTORHINAL COMPLEX and HIPPOCAMPUS

number of neurofibrillary tangles correlates better with clinical impairment in alzheimer’s than does number of neuritic plaques

76
Q

what are senile/neuritic plaques?

A

neuropathology seen in alzheimer’s disease (also in normal aging)

EXTRACELLULAR deposits of amyloid in the GRAY matter of the brain

focal spherical collections of dilated, tortuous neuritic processes around a central amyloid core

microglia and astrocytes at periphery

result from accumulation of several proteins (beta-amyloid, tau, ubiquitin, alpha1-antichymotripsin, ApeE, PS-1, PS-2, alpha2-macroglobulin and an inflammatory reaction around deposits of beta-amyloid

degenerating nerve terminals also contain tau

77
Q

where are neurons lost in alzheimer’s neuropathology?

A

as cellular changes progress, neurons are lost in the hippocampus, entorhinal complex, and association areas of the cortex

78
Q

what neurotransmitter changes happen in alzheimer’s?

A

ACETYLCHOLINE DEFICIENCY

substantial loss of ACh content in cerebral cortex

progressive decline (50-90%) in cortical levels of choline transferase (CAT) which is required for synthesis of ACh

loss of neurons in the subcortical cholinergic nuclei that project to the cerebral neocortex and hippocampus

loss of cortical CAT and decline in Ach synthesis in biopsy specimens have been found to correlate with cognitive impairment to and reaction time performance–> because cholinergic dysfunction may contribute to the symptoms of patients with alzheimer’s, enhancing cholinergic neurotransmission constitutes a rational basis for symptomatic treatment

**also decreased DOPAMINE, NE and SEROTONIN activity

79
Q

what are the major DDXs for dementia?

A
  1. alzheimer’s –> most common cause; insidious onset, gradual decline; memory impairment and one or more areas of cognitive deficit
  2. lewy body dementia–> second most common cause; gradual decline, fluctuating course; associated with visual hallucinations, parkinsonian motor features, recurrent falls and syncope, delusions and neuroleptic sensitivity
  3. vascular dementia–> 3rd most common cause; stepwise declining course; focal neurological signs and evidence of relevant cerebrovascular disease by brain imaging
  4. frontotemporal dementia–> insidious onset and gradual progression; impaired social interpersonal conduct, emotional blunting, loss of insight; may not have memory impairment until late
  5. huntingtons
  6. HIV
  7. creutzfeld-jacob
**rare but important reversible causes of dementia:
normal pressure hydrocephalus
intracranial mass lesion
vitmain B12 deficiency
hypothyroidism
neurosyphilis
80
Q

what % of dementia is caused by:

  1. alzheimer’s
  2. lewy body dementia
  3. vascular dementia
A
  1. 64%
  2. 15-30%
  3. 5-20%
81
Q

list acute confusional states associated with drugs

A

ethanol intoxication/withdrawal

sedative drug intoxication/withdrawal

opioids

anticholinergic drugs

82
Q

list acute confusional states associated with endocrine disturbances

A

hypothyroidism

hyperthyroidism

hypoglycemia

hyperglycemia

83
Q

list acute confusional states associated with electrolyte disturbances

A

hyponatremia

hypercalcemia

hypocalcemia

84
Q

list acute confusional states associated with nutritional disorders

A

wernicke’s encephalopathy

vitamin B12 deficiency

85
Q

list acute confusional states associated with organ system failure

A

hepatic encephalopathy

reye syndrome

uremia

pulmonary encephalopathy

organ transplantation

86
Q

list acute confusional states associated with infectious disease

A

meningitis

encaphalitis

sepsis

87
Q

list acute confusional states associated with vascular disorders

A

strokes

hemorhhages

88
Q

list acute confusional states associated with head trauma

A

head trauma

89
Q

list acute confusional states associated with seizures

A

post ictal states

complex partial seizures

90
Q

list the primary sleep disorders

A
  1. primary insomnia (sleepless)
  2. primary hypersomnia (sleepy)
  3. narcolepsy (sleepy)
  4. breathing-related sleep disorder (sleepy)–> i.e obstructive sleep apnea
  5. circadian rhythm sleep disorder (mixed)
  6. parasomnnias (behavior during sleep)
91
Q

list the secondary sleep disorders

A
  1. general medical conditions (i.e due to pain, physical distress most commonly)
  2. psychiatric disorder (mood disorder, anxiety disorder)
  3. substance abuse
92
Q

what is polysomnography?

A

decreased sleep efficiency

93
Q

what are the clinical features of a sleep disorder?

A
  1. polysomnography
  2. staying longer in bed to get fewer hours of sleep (i.e elderly)
  3. increased risk for falls
  4. symptoms of depression and anxiety
  5. slower reaction times
  6. cognitive dysfunction–> attention, memory
  7. obstructive sleep apnea–> obesity, high neck circumference (more than 40 cm), deviated nasal septum, macroglossia
  8. restless leg syndrome (urge to move legs with unpleasant sensations, worse at night)
94
Q

what class do most sedative/hypnotic drugs belong to?

A

benzodiazepines

95
Q

list 4 benzodiazepine sedative/hyponotic drugs

A
  1. temazepam–> short acting
  2. triazolam–> short acting
  3. oxazepam–> short acting
  4. lorazepam–> short to intermediate acting
96
Q

what is a non-benzodiazepine sedative/hypnotic drug?

A

zopliclone

97
Q

what is the current trend regarding sedative/hypnotic drug use?

A

anything but a benzodiazepine

off label use of other drugs which have sedative effects is becoming popular

i.e trazodone, gabapentin, quietiapine, olanzapine

**because of significant safety concerns and a lack of efficacy data their use is NOT advised in the elderly

98
Q

what is melatonin?

A

hormone secreted by the pineal gland

under circadian influence and is inhibited by bright light

amount produced decreases with age

in canada, specific melatonin receptor agonists are NOT available and pharmaceutical grade melatonin is used

dosing: standard dose is 3mg
available in regular and slow release (increasing evidence shows that slow release is helpful in the elderly but its still controversial

99
Q

what effect does normal ageing have on crystallized abilities (i.e information and skills gained from experience)?

A

remain relatively intact with age

i.e attention, real world executive functions, remote memory (when i was a kid…), procedural memory, semantic recall, comprehension of language, vocabulary and syntactic abilities, construction and simple copy (visuospatial)

100
Q

what effect does normal ageing have on fluid intelligence (i.e flexible reasoning, problem solving)?

A

declines with age

i.e possible divided attention, novel executive tasks more difficult, learning and recall of new information is more challenging, spontaneous word finding, verbal fluency decline, reaction time decreases (due to psychomotor slowing)

101
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
alzheimers, vascular dementia

A

depression

102
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
frontotemporal dementia

A

apathy, blunting disinhibition, lack of insight

103
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
parkinson’s dementia, dementia with lewy bodies

A

depression is common

may exhibit hallucinations, delusions

104
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
persistent alcohol dementia

A

apathy, depression

105
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
wernicke-korsakoff syndrome

A

personality changes, inappropriate behavior

106
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
prion diseases

A

apathy, emotional lability, impaired sleep, appetite loss

107
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
HIV

A

depression

108
Q

what behavioural changes might be expected in the following neurodegenerative diseases?
neurosyphilis

A

hallucinations, delusions, personality changes, mood disturbances

109
Q

define “poor judgement”

A

the lack of the operation of the mind, involving comparison and discrimination, by which knowledge of the values and relations of things, whether of moral qualities, intellectual concepts, logical propositions or material facts, is obtained

there are many diseases that may result in the concept of “poor judgement”–> with specific reference to the cognitive intellectual functions (CIFs) there may be many different etiologies behind this concept and many different causes for it

110
Q

from a neuroanatomical point of view, where does “poor judgement” likely arise from?

A

most likely to arise from lesions in the frontal cortex, as this is the cortex responsible for specific personality traits, reasoning and judgement

*not always the case

111
Q

what are some diseases that may result in poor judgement, and why they do?

A
  1. alzheimer’s–> prototypical example of a neurodegenerative disease that results in lesions found within the frontal cortex that seem to be responsible for a number of different effects, including those of poor judgement
  2. mood disorders (mainly BP1 and 2)–> manic patients have been known to seek out high risk activities with disregard to their consequences; there is a belief that this is a direct result of increased DOPAMINE transmission within the frontal cortex leading to deficiencies in judgement and changes in personality
  3. orbitofrontal syndrome–> commonly known as “disinhibited syndrome” this disease state results from a clinical diagnosis and a collection of symptoms; common symptoms may include poor insight and judgement, disinhibition, impulsive behavior, inane euphoria and sexual preoccupation; thought to result from lesions from dementia or physical trauma to the frontal lobe
  4. schizophrenia–> this is another common cause of poor judgement; exact reason remains controversial, but it is thought to result from increased DOPAMINE transmission in the frontal cortex, similar to bipolar disorder
  5. delirium–> thought to be mainly a problem with impaired attention; attention, being the bedrock of cognition, will disrupt all intellectual functions if disrupted itself, including judgement; exact reason remains unclear
  6. frontal convexity syndrome
  7. medial frontal syndrome
  8. physical injury (stroke, epileptic event, neoplasm, inflammation)
112
Q

define delirium

A
  1. reduced ability to focus, sustain, or shift attention
  2. a change in cognition (memory orientation, language) or perceptual disturbance
  3. ABRUPT onset and FLUCTUATING course
  4. NOT caused by a general medical condition

**patient can be hyper or hypoactive

113
Q

define dementia

A

development of MULTIPLE cognitive deficits manifested by both

  1. memory impairment
  2. one or more of: aphasia, apraxia, agnosia, disturbance in executive function

deficits must be SIGNIFICANT to impair function and must NOT occur exclusively during the course of delirium

114
Q

what is a mnemonic for the DDx of delirium?

A

DELIRIUMS

Drugs (narcotics, anticholinergics, withdrawal from EtOH and benzos)
Endocrine (hypo or hyperglycemia, hypo or hyperthyroid, hypercalcemia etc...) 
Low oxygen
Infection
Retention (urinary)
Inflammation/Intoxication
Underperfused 
Metabolic (sodium, potassium, azotemia)
Stool impaction
115
Q

what is a mnemonic for the DDx of dementia?

A

DEMENTIA (treatable)

Drugs (too few, too many, wrong ones)
Emotional problems (depressions, psychosis)
Metabolic disturbances (hyponatremia, alkalosis)
Endocrine disturbances (hypo or hyperglycemia, hypo or hyperthyroid, hypercalcemia etc)
Nutritional problems (low B12, folate)
Trauma (subdural hematoma) / Tumor (including paraneoplastic syndromes)
Infections (neurosyphilis)
Anemia/Alcohol

116
Q

what clinical aspects would support a diagnosis of delirium? how about dementia?

A

delirium:

  • mild dehydration
  • misuse of medication (short acting benzos without sleep hygiene)

dementia:

  • difficulty with memory and finding names for common objects starting 4 years ago
  • unable to care for household, organize appointments, pay bills
  • normal blood work and lab studies
117
Q

what are the appropriate clinical investigations for a patient with a change in mental status?

A
  1. mental status exam (MSE)
  2. MMSE

for delirium:
standard –> CBC, electrolytes, calcium phosphate, magnesium, glucose, ESR, LFTs, Creatinine, BUN, TSH, cobalamin, folate, albumin, urine C&S

as indicated–> ECG, CXR, CT head, toxicology/heavy metal screen, VDRL (syphilis), HIV, EEG (typically abnormal…generalized slowing or fast activity), blood cultures

for dementia:
standard–> same as for delirium

as indicated–> VDRL (syphilis), HIV, SPECT (hypometabolism in temporal and parietal lobes), CT head in dementia (dilation of lateral ventricles, widening of cotical sulci)

indications for CT head–> same as above, plus age less than 60, rapid onset (unexplained decline in cognition or function over 1-2 months), dementia of relatively short duration (less than 2 years), recent significant head trauma, unexplained neurological symptoms (new onset of severe headache/seizures)

118
Q

how do sleep patterns change in normal aging?

A
  1. stay longer in bed to get fewer hours of sleep
  2. relative advance of sleep phase
  3. shallow sleep–> more awakenings, less restorative (less slow wave sleep from age 20 or so onwards)
  4. dream content is often unpleasant
  5. daytime sleepiness
119
Q

how do sleep patterns change in alzheimer’s?

A
  1. similar to but WORSE than disturbances seen in non-demented elderly
  2. increased frequency of awakenings
  3. increased duration of awakenings
  4. increased stage 1
  5. decreased slow wave sleep
  6. decreased REM sleep
  7. increased daytime napping
120
Q

what are the non-pharmacological treatments for managing alzheimer’s disease?

A
  1. assess the abilities and needs of the partner (if present) as a caregiver, look for safety concerns (i.e medication management, driving), address advance planning needs, agree on treatment goals
  2. monitor for increasing cognitive, functional, and behavioral challenges, in addition to response to treatment interventions
  3. monitor nutritional status and deal with other ongoing medical conditions
  4. consider referral to neurology, psychiatry, geriatrics/geriatric psychiatry or long term care facility
  5. regular toileting for urinary frequency, sleep hygiene and daily walking for insomnia
  6. alzheimer’s support groups
  7. psychotherapy, pet therapy, music and art therapy
121
Q

is there a treatment available thats been shown to cure the underlying pathology behind alzheimer’s?

A

no

122
Q

what are some pharmacological treatments for alzheimers?

A
  1. acetylcholinesterase inhibitors –> FIRST LINE for mild to moderate alzheimer’s (donepezil, rivastigmine, galantamine)
  2. memantine (Nameda)–> an NMDA receptor antagonist–> useful for moderate to severe alzheimer’s, plus a cholinesterase inhibitor
123
Q

what is the goal of pharmacological tx of alzheimers?

A

manage cognitive symptoms and behavioural manifestations and ameliorate progression

124
Q

name an NMDA receptor antagonist used in the tx of alzheimers

A

memantine (nameda)

125
Q

name 3 acetylcholinesterase inhibitors used in the treatment of alzheimer’s

A

donepezi

rivastigmine

galantamine

126
Q

how to cholinesterase inhibitors work in treating alzheimers?

A

patients demonstrate cholinergic deficits in the neurotransmission of presynaptic excitatory amino acids in attentional circuits relating to the hippocampus which is a main centre for memory

cholinesterase inhibitors work to minimize this cholinergic deficit

127
Q

how do NMDA receptor antagonists work in treating alzheimers?

A

glutamate activation at the NMDA receptor is required for learning and memory processes in the brain (it is the dominant excitatory NT in the brain)

in alzheimer’s, there is chronic excitatory action of glutamate–> excess intraneural accumulation of calcium–> neural damage

magnesium normally blocks NMDA receptors and thus normally prevents excess influx of calcium, but depolarization removes the magnesium

memantine has a low to moderate affinity for the NMDA receptor–> this attenuates the calcium influx and prevents excess excitatory amino acid neurotoxicity while not preventing the necessary actions of glutamate at the NMDA receptor

128
Q

in imaging a patient with dementia, what MRI finding is particularly important?

A

medial temporal lobe atrophy

coronal MRI can demonstrate progressive medial temporal and generalized atrophy in patients with alzheimers

129
Q

what imaging modality should you use in a patient with dementia to check for vascular disease?

A

CT

vascular diseases also coexist with alzheimer’s

130
Q

what is SPECT?

A

nuclear medicine scan that looks at brain function (rather than just structure)

it is “like a bone scan” –> give injection of radioactive nucleotide and then look at where the blood flows in brain

if theres no structural abnormality on the CT, then low perfusion to a certain area may suggest decreased function in that area and thus decreased demand–> in alzheimers we look for temporoparietal hypoperfusion

when there is bilateral hypoperfusion in this area, its 80% specific for alzheimers

131
Q

on a perfusion scan of the brain (SPECT) where do we expect to see hypoperfusion in alzheimers?

A

temporoparietal region

*decreased perfusion is not definitive but may make you more confident of a diagnosis if it is consistent with the clinical picture of alzheimers

132
Q

when assessing alzheimer’s using a PET scan, are you looking for hyper or hypometabolism?

A

hypometabolism (unlike in cancer, where you are looking for hypermetabolism)

in dementia, there is profoundly diminished uptake in temporoparietal and parietal regions bilaterally

133
Q

in what populations would amyloid imaging be the most useful and why?

A

in young populations, as many normal elderly have some amyloid deposits despite being cognitively normal

134
Q

which correlates most strongly to neurodegeneration and cognitive deficits: A-beta burden (as shown by PET) or neurofibrillary tangles (tau proteins–shown on human post mortem studies)?

A

NFTs–> A-beta burden does not strongly correlate with cognitive impairment in alzheimer’s patients

135
Q

what is a mnemonic to remember the geriatric evaluation?

A

GRANDMA

Gait–> gait, get up and go, falls history

Residence–> where? with whom? what supports?

Activities of daily living–> basics

Nutrition–> appetite, weight, diet

Drugs–> compliance? adverse reaction? OTC?

Memory–> MMSE at least for screening

Advance directives–> goals of care? proxy? DNR?

136
Q

what neural structures must be intact to have alertness/attention?

A
  1. brainstem (ARAS)
  2. bilateral thalami
  3. bilateral cortices (especially dorsolateral prefrontal cortex)
137
Q

what are the two types of explicit memory?

A

semantic and episodic

138
Q

what are the four types of implicit memory?

A

procedural
emotional
conditional
priming

139
Q

what neural structures are involved in executive function?

A

frontal lobe (dorsolateral prefrontal cortex, ventromedial and orbitofrontal)

anterior cingulate

posterior parietal

basal ganglia connections

140
Q

what neural structures are involved in visuospatial function?

A

parietal lobe

occipital lobe

inferior temporal lobe (fusiform gyrus)

141
Q

what aspects of movement are controlled by the cerebellum? by the basal ganglia?

A

cerebellum controls proprioception, vestibular information and environmental cues

basal ganglia control decision to move, direction of movement, amplitude of movement, emotional body language

142
Q

what does the cerebellum do?

A

Coordinator and predictor of cortical output related to movement and cognition

receives and interprets proprioceptive information

coordinates BALANCE–> tightly linked to the vestibular nuclei

coordinates fine movement and eye-hand coordination

predicts the sensory consequences of movement (i.e how much harder is it to go up old, even stairs rather than regular flat stairs?)

info sent to the cerebellum can be used for the skilled manipulation of muscles or the skilled manipulation of mental concepts

143
Q

what does the vestibulocerebellum control?

A

flocculonodular lobe and vermis

TRUNK control

144
Q

what does the spinocerebellum control?

A

vermis and anterior lobe

SYNERGISTIC movements of the EXTREMITIES

145
Q

what does the cerebrocerebellum control?

A

posterior lobe

topographical representation of the extremities, areas for eye movement and speech, coordination of intricate and complex movements

146
Q

how does the cerebellum coordinate with and use vestibular information?

A

afferents from the vestibular nuclei project into the paravermis and flocculonodular lobes

provide information on the position of the head and body in space

helps orient eyes movements during locomotion

147
Q

describe the vestibulocerebellar loop

A

info from the vestibular nuclei goes to the paravermal area and the flocculonodular lobe in the cerebellum

this information goes via the FASTIGIAL nucleus back to both the reticular formation and back to the vestibular nuclei

information flows from the reticular formation and vestibular nuclei down to the spinal cord, resulting in truncal stability and balance

148
Q

where does the cerebellum receive proprioceptive information from?

A

from muscle spindles and golgi tendon organs that indicate where and how the limbs are positioned–> flows through POSTERIOR spinocerebellar tract through ICP

from spinal border cells which have a copy of the movement command that went to the LMNs–> flows through ANTERIOR spinocerebellar tract through the SCP

terminates in ANTERIOR lobe for limb info and VERMIS for trunk info

149
Q

describe the spinocerebellar loop

A

spinocerebellar tracts from trunk and limbs go to cerebellum (anterior lobe and vermis)

info goes from there to the EGF

from the EGF, info goes to the red nucleus, the vestibular nuclei and the thalamus

  1. from the thalamus–> motor cortex–> spinal cord (for LIMBS)
  2. from the red nucleus–> spinal cord (for TRUNK and axial musculature)
  3. from vestibular nuclei–> spinal cord (for TRUNK and axial musculature)
150
Q

how does the cortex communicate with the cerebellum?

A

the cortex projects to the PONTINE NUCLEI which project to the cerebellar hemispheres

PONTOCEREBELLAR tract through the MCP

fine motor control of upper extremity, dextrous hand movement, hand-eye coordination

151
Q

describe the cerebrocerebellar loop

A

motor cortex (and other cortical areas) sends info to spinal cord AND to to pontine nuclei

pontine nuclei communicates with posterior lobe of cerebellum –> contralateral

cerebellum sends info to DENTATE nucleus–> red nucleus and thalamus–> motor cortex

152
Q

what are symptoms of midline cerebellar disease?

A

gait difficulty

truncal imbalance (wide based irregular steps, veers to one side)

abnormal head postures (i.e head tilt)

occulomotor dysfunction (i.e nystagmus)

153
Q

what are symptoms of a lesion to the flocculonodular node?

A

truncal ataxia

nystagmus

154
Q

what are symptoms of lateral cerebellar disease?

A

hypotonia
(decreased resistance to passive movement)

dysarthria
(slow laboured speech, garbled words but comprehension and grammar intact… i.e not an aphasia)

limb ataxia

intention tremor 
(increases as patient approaches a target)
impaired check
(difficulty putting a limb back into position after it has been displaced)

oculomotor disorders
(i.e gaze disorder, clonus, nystagmus)

155
Q

what are symptoms of a lesion to the anterior lobe of the cerebellum?

A

affects spinocerebellar input

mostly LOWER LIMB coordination affected

gait ataxia

i.e ethanol is toxic to purkinje cells in the cerebellar cortex and the anterior lobe is most affected–> get permanent damage in chronic alcoholics

156
Q

what afferents flow through teh superior cerebellar peduncle?

A

anterior spinocerebellar tract

acoustic and optic info

157
Q

what efferents flow from the superior cerebellar peduncle?

A

dentarubrothalamic tract

158
Q

what afferents flow through the middle cerebellar peduncle?

A

pontocerebellar tract

159
Q

what afferents flow through the inferior cerebellar peduncle?

A

vestibulocerebellar tract

olivocerebellar tract

posterior spinocerebellar tract

160
Q

what efferents flow out of the inferior cerebellar peduncle?

A

cerebello-vestibular tract

cerebello-olivary tract

161
Q

what age is considered early onset alzheimers?

A

before age 65

162
Q

what are the 4 most common causes of dementia?

A
  1. alzheimers (66%)
  2. vascular dementia (10-20%)
  3. lewy body dementia (10-20%)
  4. frontotemporal dementia (5-15%)
163
Q

how often is a clinical diagnosis of alzheimer’s correct on autopsy?

A

90% of the time

164
Q

what % of alzheimer’s is sporadic?

A

75-95%

165
Q

what is the greatest risk factor for alzheimers?

A

aging

166
Q

what is the population risk of alzheimers? what is the risk if you have a first degree relative with alzheimers?

A

population–> 6-8%

first degree relative–> 15-50% recurrence risk

167
Q

does age of onset of alzheimers suggest genetic etiology?

A

NO

only 13% of early onset alzheimer’s cases display familial pattern of inheritance

168
Q

how is familial alzheimer’s inherited?

A

autosomal dominant

causative genes display almost complete inheritance

affected first degree relative –> 50% recurrence risk

3 causative alzheimer’s genes ID-ed–> PS1, PS2, APP

mutations in these genes affect processing of amyloid precursor protein and an increase in beta-amyloid peptide

169
Q

what % of nursing home residents have dementia?

A

over 60%

170
Q

how much of total sleep time is usually stage 1? what does an increased % of stage 1 sleep indicate?

A

usually about 5% of total sleep time

increased indicates sleep disruption

*stage 1 is light sleep, the transitional stage passed through from wake to sleep and sleep to wake

171
Q

in what stage of sleep do you spend most of the night?

A

stage II

172
Q

what is the “deepest” stage of sleep?

A

stage III

hard to awaken

sleep drunkenness/”sleep inertia” when awakened

parasomnias (confused arousals) occur from this stage

often restorative

often REDUCED by benzodiazepines

maintained by zopiclone zalepon, zolpidem

173
Q

what phase of sleep is dream sleep?

A

REM

tonic and phasic stages

i.e voluntary muscle atonia (tonic) and movements (phasic)

B&B Part 2 (5 decks)

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