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Physio > physio final lecture 6/microbiome/TBI/stroke syndrome > Flashcards

physio final lecture 6/microbiome/TBI/stroke syndrome Flashcards

1
Q

Broca’s Area

A

“non-fluent” “Broca’s broken words”
motor frontal lobe
speech is slow and broken
known

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2
Q

Wernicke’s area

A

“fluent”
sensory, temporal lobe
speech is normal and excessive

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3
Q

Learning

A

acquisition of new information
process by which experiences change our nervous system and our behaviors

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4
Q

stage 1 of learning

A

sensory information;
first processed through out senses
“echoic memory”
< 1 second

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5
Q

Stage 2 of learning

A

short term memory
meaningful/salient information
< 1 minute
can support via repetition or chunking (7 +/- 2 rule)

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6
Q

stage 3 of learning

A

long term memory
short term memories are converted into long term memories (consolidation “made solid”)
can be retrieved across lifetime
increased retrieval “rehearsal” = strengthening of memory
hippocampus

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7
Q

Observational learning

A

“social learning theory”
process of learning by watching the behaviors of models
occurs via operant conditioning and vicarious conditioning (can be positive or negative)
pro social and antisocial modeling

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8
Q

pro social modeling

A

prompts engagement in helpful and healthy bxs

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9
Q

antisocial modeling

A

prompts others to engage in aggressive/unhealthy bx

Bandura and BoBo doll - physical aggression

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10
Q

we are more likely to mimic models who:

A

positive perception (like or high status)
shared traits
stand out
familiarity
self-efficacy in mimicry
social media - influencers
violence in games and entertainment

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11
Q

social learning theory order:

A

attention > retention > production > motivation (positive or negative)

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12
Q

Middle cerebral artery (MCA) stroke

A

90% of strokes
largest of the brain arteries
supplies most of the outer surface of the frontal, parietal, temporal, and basal g

includes: pre-central (sensory) and post-central (motor) gyrus

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13
Q

MCA stroke symptoms

A

contralateral weakness and sensory loss in upper extremities
loss of visual field
left MCA stroke = speech deficits (Broca’s and Wernicke’s aphasia)
Right MCA stroke = neglect and poor motivation (flat prosody)

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14
Q

Anterior cerebral artery (ACA) stroke

A

less common
Left ACA > R ACA
feeds deep structures in the brain: frontal, parietal, corpus callosum and bottom of cerebrum

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15
Q

ACA stroke symptoms

A

contralateral motor and sensory loss in lower extremities
poor gait and coordination (clumsy)
slowed initiation (abulia)
flat affect
urinary incontinence

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16
Q

Post-stroke depression tx =

A

early psychopharmacological tx is KEY

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17
Q

Depression and post-stroke considerations

A

1/3 survivors
6x increased risk of depression 2-3 years post stroke
more common in Left frontal and BG stroke
adversely effects fxal recovery
increased risk factors = premorbid depression and social isolation post stroke

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18
Q

Anxiety and post-stroke considerations

A

1/4 meet GAD criteria post stroke
less common

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19
Q

Psychosis and post-stroke considerations

A

more common in right-temporo-parietal-occipito area lesions, seizures and subcortical atrophy
pseudobulbar affect = 10-15% post-stroke patients
hypomanic symptoms = 1%

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20
Q

BE FAST (strokes)

A

Balance - have they lost balance
Eyes - have they lost vision in one/both eyes
Face - does the persons face look droopy
Arms - can they raise both arms for 10 secs
Speech - do they have slurred speech
Time - “time is brain” call 911

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21
Q

tissue plasminogen (tPA)

A

can be administered within 4.5 hours
helps restore blood flow to brain regions affected by stroke
after time limit = hemorrhagic effect

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22
Q

deficiency of vitamin D

A

depression/negative emotions
nearly 40-50% of men and women in Denver metro are deficient in vitamin D
more melanin in skin = harder to synthesize vitamin D
concurrent use with anti-depressants = supported

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23
Q

magnesium deficiency

A

w/stress = increased agitation, anxiety, sleeplessness, headaches, and apathy
can tx restless leg syndrome
slow response time to reach steady state via oral supplements (~30 weeks)

24
Q

omega-3 fatty oils

A

add on tx for depression = strong evidence
add on tx for ADHD = some evidence

25
Q

Anorexia

A

twin studies = 58-76% hereditary
risk increases with premature birth or birth trauma
associated with:
- loss of gray and white matter in the brain
- enlarged ventricles and widened sulci (shrinkage of brain tissue)
inhibited emotional facial expression despite reporting similar or more intense emotions
tissue loss can be reversed with successful eating disorder tx

26
Q

starvation study

A

6 months ate at 50% of baseline
loss 25% of body weight
demonstrated preoccupation w/food, ritualistic eating, erratic mood, impaired cognition, slowed eating/lingering
post-study: complained of fat on their abdomens and legs

27
Q

excessive exercise

A

starved mice will still run on their wheel all day = looking for food?

28
Q

gender differences in anorexia

A

women at less post-fast than men

29
Q

anorexia tx

A

CBT, increasing eating speed, stimulation of ACC

30
Q

restricted food access =

A

starvation = anorexia

31
Q

alpha diversity

A

a measure of microbial ecology of “species” diversity within a sample; species in my mouth

32
Q

beta diversity

A

a measure of microbial ecology of species diversity between samples: difference in species in my mouth compared to someone else’s mouth

33
Q

dysbiosis

A

disruption of the gut microbial diversity and community structure; due to reduction in beneficial bacteria and overgrowth of harmful bacteria, yeast, and/or parasites

34
Q

alpha diversity, beta diversity, dysbiosis

A

“health promoting”
“disease predisposing”

35
Q

one factor contributing to increase in chronic inflammatory d/o in high income countries =

A

failing immunoregulation attributable to reduced exposure to the microbial environment within which the mammalian immune system co-evolved

“old friends” and a Failure of immunoregulation

36
Q

“old friends” and psychiatric d/o

A

some psychiatric d/o in developed countries might be attributable to failure of immunoregulatory circuits to terminate ongoing inflammatory response

37
Q

sex/age breakdown of TBI

A

highest:
- males 15-24 yrs (400,000)
- females 75+ yrs (100,000)
- total: people 15-24 years (250,000)

lowest:
- males: 45-54 and 65-74 years
- females: 35-44 and 55-64 years
- total: people:

38
Q

Diffuse axonal injury (DAI)

A

shearing/tearing of the brain’s long connecting nerve fibers (axons) that happen when the brain is injured as it shifts and rotates inside the skull

damage to white matter
changes are microscopic
can lead to disorders of consciousness (persistent vegetative state, coma)
difficult to see on CT or MRI
can occur without other visible damages

39
Q

grade 1 DAI

A

mildest form of DAI
microscopic changes in the white matter of the cerebral cortex, corpus callosum, brain stem and cerebellum

40
Q

grade 2 DAI

A

moderate form of DAI
grossly evident focal lesions isolated to the corpus callosum

41
Q

grade 3 DAI

A

severe form of DAI
additional and severe focal lesions on the brainstem itself

42
Q

classification system for TBI

A

duration of unconsciousness
Glasgow coma scale
post-traumatic amnesia

43
Q

classification system for TBI: mild

A

duration of unconsciousness: <30 mins
Glasgow Coma scale: 13-15
PTA: <24 hours

44
Q

classification system for TBI: moderate

A

duration of unconsciousness: 30 min-24 hours
Glasgow Coma scale: 9-12
PTA: 1-7 days

45
Q

Classification system for TBI: severe

A

duration of unconsciousness: >24 hours
glasgow coma scale: 3-8
PTA: >7 days

46
Q

Glasgow coma scale

A

eye opening
best motor response
verbal response

47
Q

Glasgow coma scale limitations

A

substance use
administered drugs
intubation - no verbal response
injury to eye - no eye opening
hemiplegia - no motor response
language - verbal response

48
Q

non-injury risk factors that can influence TBI outcomes

A

pre-injury psychiatric status and conduct issues/incarceration = negatively effect outcome, can prolong symptoms
age at injury - older = longer recovery
level of education
stable employment 6 months pre-injury = best predictor of return to employment post-injury
marital status = proxy for perceived social support
other non-neurological injuries sustained = physical injuries can prevent return to meaningful activities

49
Q

why loss of consciousness in subarachnoid hemorrhage

A

“transient intracranial circulatory arrest”

“percussive” blood pressure impact of the hemorrhage increases ICP (intracranial pressure) = reduced CPP (cerebral perfusion pressure)

50
Q

Hunt-Hess and Fisher Scale grade I

A

HH: asymptomatic or minimal headache and slight nuchal rigidity

Fisher: no blood visualized

51
Q

Hunt-Hess and Fisher scale grade V

A

HH: deep coma, decerebrate rigidity, moribund appearance

52
Q

hemiplegia

A

paralysis affecting one side of the body (face arm trunk leg)

53
Q

hemiparesis

A

implies a lesser degree of weakness than hemiplegia

54
Q

neglect

A

failure to attend to, respond to, and/or report stimulation that is introduced contralateral to the lesion
- most often seen with non-dominant parietal association area lesions
- affects contralesional side

persistent neglect is a negative fxal outcome predictor

55
Q

Agnosia

A

acquired inability to associate a perceived unimodal stimulus (visual, auditory, tactile) with meaning
disorder of recognition NOT NAMING

56
Q

anosagnosia

A

denial of deficit

57
Q

prosopagnosia

A

impaired ability to recognize faces

Physio (11 decks)

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