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PM&R Recap > Stroke > Flashcards

Stroke Flashcards

1
Q

Most important non-modifiable risk factor for stroke?

Most important modifiable risk factor for stroke?

A

Age

HTN

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2
Q

Common sites of lacunar strokes?

A

putamen, thalamus (pure sensory), internal capsule (pure motor)

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3
Q

What to expect when pt ha suddent onset of “worse HA of my life” during exertion (eg weightlifting)

A

hemorrhagic stroke (berry aneurysm rupture - most commonly Acomm or Pcomm)

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4
Q

term for disturbance of a person’s ability to recognize disability or illness in oneself?

A

Anosognosia

It is thought to be related to hemineglect, a tendency to ignore the contralateral half of one’s body or of external space, that follows damage to the parietal lobe (or rarely, the diencephalon), right more often than left. Patients may not recognize the hemiplegia (anosognosia), their arm (asomatognosia), or any external object to the left of their own midline. These phenomena may occur without sensory defects in patients who are otherwise neurocognitively intact.

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5
Q

Risk factors for developing venous thromboembolic disease in the setting of brain tumor?

A

Risk factors include larger tumors, supratentorial location, presence of intraluminal thrombosis in the tumor pathologic specimen, age older than 60 years, presence of hemiparesis, and use of chemotherapy

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6
Q

Most common site of intracerebral hemorrhage 2/2 HTN?

A

Putamen

*contralateral hemiplegia

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7
Q

Intracranial pressure (ICP) goal in acute stroke management?

What is the cerebral perfusion pressure (CPP) goal?

A

ICP < 20 mmHg
CCP > 60 mmHg (CPP = MAP - ICP)

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8
Q

Time cut offs for tPA and thrombectomy in acute stroke?

A

tPA: 3 - 4.5hrs from onset
Thrombectoy: within 24 hrs

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9
Q

How does acute ischemic stroke appear on MRI?

A

Appears bright on T2

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10
Q

Secondary prevention for thromboembolism 2/2 carotid stenosis?

A

ASA/dipyridamole combination

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11
Q

Majority of recovery following stroke is seen in what time period?

A

3-6 months (especially within first 12 weeks)

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12
Q

Secondary prevention for ischemic stroke 2/2 thromboembolism from carotid stenosis?

A

ASA/dipyradamole combo

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13
Q

Typical deficits seen in ACA strokes?

A

contralateral leg weakness and numbness distal > proximal (leg worse than arm with face/hand spared)
Urinary incontinence

*Can also see abulia (lack of will/initiative)
*If b/l lesion, can see personality deficits/executive function deficits

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14
Q

Transcortical motor aphasia is associated w/ which ischemic stroke distribution?

A

Anterior Cerebral artery (dominant hemisphere ACA lesion)

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15
Q

Paratonic rigidity (Gegehalten) - progressive resistance to passive ROM - is associated w/ which ischemic stroke distribution?

A

Anterior Cerebral artery (ACA)

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16
Q

Superior MCA division lesion typically leads to which deficits?

A

Broca’s aphasia (expressive), and contralateral upper limb weakness

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17
Q

Inferior MCA division lesion typically leads to which type of aphasia?

A

Wernicke’s aphasia (receptive)
*hemineglect if on non-dominant side

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18
Q

contralateral homonymous hemianopia is seen with which type of ischemic stroke lesion?

A

Posterior Cerebral artery (PCA)

Dominant lesions - amnesia, color anomia, alexia without agraphia, simultagnosia (lack of ability to perceive more than a single object at a time)

Non-dominant lesions - prosopagnosia (cannot recognize familiar faces)

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19
Q

Lesions to the optic chiasm cause what type of vision deficit?

A

bitemporal hemianopia

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20
Q

B/l PCA strokes can result in which syndromes?

A

Anton syndrome - cortical blindness, with denial)
Balint syndrome - optic ataxia, loss of voluntary but not reflexive eye movements, inability to understand multiple visual objects

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21
Q

“Pure motor syndrome” is typically seen in which lacunar infarct?

A

Posterior limb of internal capsule - also causes ataxic hemiparesis

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22
Q

“Pure sensory Syndrome” is typically seen in which lacunar infarct?

A

Thalamic - central post-stroke pain
Thalamogeniculate branch off of PCA

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23
Q

Dysarthria - Clumsy Hand syndrome is seen in which lacunar infarct?

A

pontine lesion (basis pontis; anterior limb of internal capsule)

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24
Q

Which lacunar infarct presents w/ contralateral hemiballismus?

A

subthalamic nucleus

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25
Q

Which lacunar infarct presents w/ contralateral hemichorea?

A

caudate nucleus

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26
Q

Which lacunar infarct presents w/ hemiparesis-hemiataxia syndrome?

A

pons, midbrain, internal capsule, or parietal white matter

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27
Q

Pseudobulbar palsy (loss of volitional bulbar control, but involuntary motor control of same muscles is intact - e.g. can yawn or cough) is seen in which lacunar infarct?

A

Anterior internal capsule and corticobulbar pathways

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28
Q

Pt w/ vertigo, nystagmus, dysphagia, dysarthria, ipsilateral Horner syndrome, ipsilateral facial pain/numbness has which brainstem lesion?

A

Lateral medullary syndrome (Wallenberg)

PICA lesion - “Dr. Horner Wallenberg at the VA says don’t PICA horse that can’t eat”

*Hoarseness/dysphagia - CN 9, 10 - help to distinguish from lateral pontine syndrome

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29
Q

Contralateral hemiparesis w/ ipsilateral CN3 palsy?

A

Medial Midbrain (Weber) Syndrome

PCA stroke

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30
Q

Contralateral hemiparesis w/ contralateral numbness and tongue deviating towards side of lesion?

A

Medial Medullary Syndrome

Anterior Spinal Artery Stroke (affects corticospinal tract, medial lemniscus, CN12)

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31
Q

Pt paralyzed w/ voluntary blinking and vertical gaze intact?

A

“Locked in” syndrome/ basilar artery occlusion

Reticular activating system is spared (midbrain) - pt fully conscious

32
Q

Pt w/ contralateral hemiplegia, ipsilateral lateral rectus palsy (abducens), and ipsilateral facial paresis?

A

Millard-Gluber Syndrome - unilateral lesion to ventrocaudal pons that may involve basis of pontis and fascicles of CN VI and VII

33
Q

When does peak spasticity occur in stroke recovery (stages of hemiparesis?)

A

Stage 3

(1 = totally flaccid
2 = spasticity, hyperreflexia, UE flexor synergy pattern, LE extensor synergy pattern)
3 = spasticity peak, control over synergy patterns begin
4 = spasticity decreases; control is maximized
5 = complex voluntary movements
6 = spasticity gone
7 = normal
*pts can plateau at any stage

34
Q

Pattern of motor recovery in stroke (prox vs. distal, UE vs. LE?)

A

motor control returns proximally before distally; lower limb function recovers earlier and more completely than upper limb function

35
Q

Motor recovery from stroke typically occurs over what time frame (# of weeks)?

A

12 weeks
(best neurologic recovery is seen at 11 weeks in 95% of patients; most ADL recoveries are by 12.5 weeks)

most function recovered in 3-6 months, although improvement can continue up to 18 months

36
Q

Rehab approach that seeks to eliminate all primitive reflexes and flexor synergy patterns?

A

Bobath/Neurodevelopmental Technique

eliminate primitive reflexes such as babinski, palmomental (stroke thenar eminence -> chin twitch)

Inhibit spastic tone w/ therapy and orthoses, facilitate automatic reactions.

Don’t allow pts to use flexor synergy or extensor synergy patterns to perform tasks (don’t want to reinforce primitive pathways)

37
Q

Rehab approach that seeks to “use what you’ve got” and embraces primitive synergistic patterns?

A

Brunnstrom Technique

Use what you’ve got, no guarantee anything else will come back; synergies can be used for ADLs, mobility, muscle conditioning

38
Q

Rehab approach that uses cutaneous stimuli to enhance motor control and activity?

A

Rood Technique (“rude” to touch me)

Stretching, heat/ice, stroking, pushing, tapping, vibrating, etc are all used to facilitate recovery

39
Q

2016 AHA/ASA Guidelines for Adult Stroke Rehab advocate for intensive, repetitive ____________ training?

A

task-specific training

40
Q

Improvement in cardiorespiratory fitness following stroke can be seen with what type of exercise training?

A

High-intensity interval training (HIIT)

41
Q

Rehab approach that challenges patient’s proprioceptive abilities by performing diagonal movements?

A

Proprioceptive Neuromuscular Facilitation (PNF)

42
Q

Rehab approach that inhibits good/strong side to force paretic side to do work?

Special considerations for pt population?

A

Constraint-Induced Movement Therapy (CIMT)

Don’t do w/ hemineglect (won’t work)

43
Q

Minimal movement requirement in paretic arm for constraint-induced movement therapy?

A

must have at least 10 degreees of active wrist extension

44
Q

% of stroke pt walking 1 year later?
% of stroke pts w/ normal swallow 1 yr later?
% of stroke pts returned to work 1 yr later?
% of pts that return home after stroke?

A

80% of stroke pt walking 1 year later?
85% of stroke pts w/ normal swallow 1 yr later?
40% of stroke pts returned to work 1 yr later?
90% of pts that return home after stroke?

45
Q

Modified Rankin Scale measures what outcome?

A

functional outcome

0-6 scale, study of stroke pts 5 years out showed 2/3 had good functional outcomes (MRS scores < 3)

46
Q

Initial NIHSS score equal/greater than _____ forecasts high probability of death or severe disability

initial HIHSS score equal/less than ______ forecasts good recovery?

A

Initial NIHSS score equal/greater than 16 forecasts high probability of death or severe disability

initial HIHSS score equal/less than 6 forecasts good recovery

47
Q

Which has better prognosis? Hemorrhagic or ischemic stroke?

A

Hemorrhagic stroke has better functional prognosis

48
Q

4 phases of swallow?
Which are voluntary?

A

Oral prepratory phase - voluntary
Oral phase - voluntary
Pharyngeal phase - involuntary aspiration most likely
Esophageal phase - involuntary

49
Q

Signs/symptoms of dysphagia on bedside swallow?

A

cough, wet voice, altered vocal quality (silent aspiration still possible)

50
Q

Gold standard for evaluating swallow function?

A

Modified barium swallow study

51
Q

which study allows direct visualization of secretions in context of swallow function?

A

FEES (fiberoptic endoscopic evaluation of swallowing)

52
Q

Compensatory strategy for dysphagia: chin tuck function?

A

Pushes larynx away from pharynx; constricts posterior pharynx to squeeze bolus through and into esophagus

53
Q

Compensatory strategy for dysphagia: head rotation towards which side?

Function of head rotation?

A

rotate towards paretic side - closes off paretic side to push bolus towards strong side to facilitate normal swallow

Rotating the head toward the affected side decreases, the anatomical space of the pyriform sinus, and food residue can be sent down the healthy side

54
Q

Compensatory strategy for dysphagia: head tilt towards which side?

Function of head tilt?

A

tilt towards strong side - Tilting the head towards the healthy side, a bolus can flow along the healthy side pharyngeal wall

55
Q

Treatment for DVT in rehab phase?

A

heparin drip vs. increased enoxaparin dosage (1mg/kg BID)

56
Q

Increased neuropathic pain, hypersensitivity, allodynia, skin and vasomotor changes over affected area of body WITHOUT a known peripheral nerve injury?

A

CRPS type 1

57
Q

Increased neuropathic pain, hypersensitivity, allodynia, skin and vasomotor changes over affected area of body WITH a known peripheral nerve injury?

A

CRPS type 2

58
Q

Most common subtype of CRPS in stroke patients?

A

shoulder-hand syndrome (CRPS type 1)

CRPS reported in 12-25% of hemiplegic stroke patients

59
Q

stage of CRPS? Duration of stage?

Increased pain (burning/shooting), sweating (hyperhidrosis), swelling/edema, allodynia, vasomotor changes, hyperalgesia, increased hair growth

A

Sage 1 (acute), lasts 3-6 months

60
Q

stage of CRPS? Duration of stage?

Pain spreads proximally, skin/muscle atrophy, brawny edema, cold insensitivity, brittle nails/nail atrophy, osteopenia (late)

A

Stage 2 (dystrophic), lasts 3-6 months

61
Q

stage of CRPS? Duration of stage?

Decreased pain, cool and shiny skin, skin/nail atrophy, muscle atrophy, hairlessness, lack of sweating, no edema, osteopenia (bone demineralization progresses), contractures

A

Stage 3 (atrophic), chronic after 6-12 months

62
Q

When is a stellate ganglion block considered successful?

A

when pt develops ipsilateral Horner syndrome

63
Q

Is routine use of sling for subluxed shoulder in stroke pts recommended?

A

No - slings to do not prevent/correct subluxation; no appreciable difference in shoulder ROM, subluxation or pain in pts with and without slings

64
Q

Major risk factors for not returning to work following stroke?

A

prolonged IPR stay, aphasia

65
Q

What causes nasal speech?

A

partial or complete failure of soft palate to close off nasal cavity from oral cavity; or by incomplete closure of the hard palate

*Uplifting the soft palate prevents nasal speech

66
Q

Type of aphasia? Location?

Fluent, can comprehend, can repeat, CANNOT name things

A

Anomnic aphasia

Temporo-parietal injury, angular gyrus

67
Q

Type of aphasia? Location?

Fluent, can comprehend, CANNOT repeat

A

Conduction aphasia

Parietal operculum (arcuate fasciculus) or insula or deep to supramarginal gyrus (usually left side)

68
Q

Type of aphasia? Location?

Fluent, CANNOT comprehend, can repeat

A

Transcortical sensory aphasia

Watershed lesion isolating perisylvian speech structures (Broca’s and Wernicke’s areas) from the posterior brain; angular gyrus or posterior/inferior temporal lobe

69
Q

Type of aphasia? Location?

Fluent, CANNOT comprehend, CANNOT repeat

A

Wernicke’s aphasia

Posterior part of superior (first) temporal gyrus of dominant hemisphere (usually left)

70
Q

Type of aphasia? Location?

Nonfluent, can comprehend, can repeat

A

Transcortical Motor aphasia

Frontal lobe, anterior/superior to Broca’s area; or in the subcortical region deep to Broca’s area

71
Q

Type of aphasia? Location?

Nonfluent, can comprehend, CANNOT repeat

A

Broca’s aphasia

Posterior-inferior frontal lobe (third frontal convolution) of dominant hemisphere (usually left)

72
Q

Type of aphasia? Location?

Nonfluent, CANNOT comprehend, can repeat

A

Mixed transcortical aphasia

(ACA/PCA, watershed zone)

73
Q

Type of aphasia? Location?

Nonfluent, CANNOT comprehend, CANNOT repeat

A

Global aphasia

Usually involves distribution of L mCA (entire perisylvian region), can vary in size and location

74
Q

Melodic intonation therapy is indicated for which type of aphasia?

A

Nonfluent (Broca’s) aphasia

Melodic intonation therapy recruits the right hemisphere for communication by incorporating melodies of rhythms with simple statements

75
Q

Greatest improvements in aphasia recovery occur in what timeframe?

A

first 2-3 months

After 6 months there is a significant drop in rate of recovery

76
Q

Which scale/index is correlated w/ not returning to work following stroke when score is low at time of rehabilitation discharge?

A

Barthel Index

Scored 0-100; functional assessment tool that measures independence in ADLs

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