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Med 1 UBC Winter 2020 > Week 21: Stroke > Flashcards

Week 21: Stroke Flashcards

1
Q

Ischemia

A

Inadequate blood supply to a tissue or organ

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2
Q

Infarction

A

area of dead tissue resulting from impaired blood supply

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3
Q

Definition of a transient ischemic attack (TIA)

A

Sudden onset of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, *without* acute infarction. Previously only defined by lasting less than 24h, but just because it’s short, doesn’t mean that no damage was sustained.

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4
Q

Ischemic vs hemorrhagic stroke

A

Ischemic - 85% of stroke; results from occlusion of a blood vessel Hemorrhagic - 15% or strokes; Results from rupture of a blood vessel. May be intracerebral or subarachnoid hemorrhage.

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5
Q

Arterial vs venous strokes. Which is more common?

A

arterial strokes are much more common.

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6
Q

Brodmann’s areas

A

Classify regions of the brain based on their microscopic appearance and function. 52 areas distinguished by the relative thickness of each of the 6 cellular layers of the cortex. Thickness of each cell layer correlates to function.

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7
Q

Primary and association areas

A

Primary cortexes are responsible for specific, singular functions (i.e., receiving sensory information or executing motor tasks). Association Cortex receives information from primary areas and is involved in higher-order processing, integration, and interpretation of the information.

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8
Q

Unimodal and heteromodal association cortex

A

Unimodal - areas responsible for higher order processing of single sensory or motor modality. Located adjacent to primary areas. Heteromodal - areas responsible for integration from multiple sensory and/or motor modalities. /.

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9
Q

Lateralization of praxis

A

Praxis = the ability to execute learned purposeful movements. Praxis for both R and L limbs usually programmed by the dominant hemisphere (usually Left).

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10
Q

Lateralization of a complex visuo-spatial skills/attention - implications for lesions

A

The R hemisphere attends to both R and L sides of the body ; L hemisphere only attends to R side. Therefore, lesion in R hemisphere causes inattention to the L side (‘neglect’ syndrome)

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11
Q

Stroke definition

A

Neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, *with* acute infarction or hemorrhage. Don’t use the term cerebrovascular accident ever.

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12
Q

TIA definition

A

brief transient episode of neurological dysfunction caused by focal brain, spinal cord, or tetinal ischemia, without evidence of acute infarction. Typically less than1 hr. Previously less than 24 hr, but that window of time is typically accompanied with damage.

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13
Q

How common is hemorrhagic stroke?

A

15-20% of stroke cases in canada. Includes subarachnoid and intraparenchymal hemorrhage.

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14
Q

Single most important risk factor for stroke?

A

HTN. Accounts for up to 50% of risk.

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15
Q

Praxis

A

The ability to execute learned, purposeful movemens (e.g., brushing teeth, combing hair). A function of the frontal lobe.

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16
Q

Apraxia

A

The loss of praxis. A deficit that usually occurs as a result of a left frontal (or parietal) lesion, often associated with language impairment.

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17
Q

Gerstmann syndrome

A

A rare but localizable syndrome due to lesion to the parietal lobe.

Results in…

  • agraphia (impaired writing)
  • acalculia (impaired calculation ability)
  • right/left disorientation (difficulty distinguishing R vs L side of the body)
  • Finger agnosia (inability to name or identify individual fingers)
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18
Q

Basic Functions of the frontal lobes

A

motor planning and execution, restraint, initiative, order, language production, praxis, eye movements

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19
Q

basic functions of the parietal lobes

A

somatosensory processing, spatial attention, higher-order language and visual processing (spatial localization of objects: “where”)

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20
Q

Temporal lobes

A

auditory processing, language comprehension, higher-order visual processing (object recognition: what is it).

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21
Q

What constitutes spontaneous speech?

A

Fluency of the pt’s speech/smoothness with which they can connect sounds and words. Should be able to form a sentence longer than 5 words with a decent number of function words (prepositions and articles)

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22
Q

Dysarthria

A

impaired articulation of speech that is otherwise linguistically normal. It isn’t a true language problem.

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23
Q

Paraphasic errors

A

inappropriately substituted words or syllables. May be a semantic paraphasia (replace word with another word with a similar meaning) or a phonemic paraphasia (replace word with another word that sounds similar). They may even substitute neologisms (made up words). Pharaphasic errors suggest a deficit in speech spontaneity

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24
Q

Prosody

A

the affective elements of speech, tone of voice. Managed by the non-dominant temporal lobe (parallel to Wernicke’s area)

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25
Q

What constitutes comprehension of speech?

A

Ability to answer yes/no and multiple choice questions. Pointing to objects and parts of objects. Following simple and complex commands. Able to answer questions phrased with complex syntax (if the lion was killed by the tiger, which animal is dead?)

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26
Q

anomia

A

an impairment in the ability to name objects in the absence of any other language problem. May be a problem with high frequency words or low frequency words.

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27
Q

What is an aphasia, generally?

A

an impairment in langauge caused by brain dysfunction, usually of the dominant (L) cerebral hemisphere; affects both spoken and written language. Many causes! Stroke, tumor, dementia.

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28
Q

What is an ASPECTS score?

A

CT assessment for brain damage after stroke. Scored from 1-10. A high aspects score means there is lots of healthy brain to save.

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29
Q

What is TPA?

A

Tissue plasminogen activator. Busts clots by converting plasminogen to plasmin

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30
Q

Indications for using TPA

A
  1. Stroke was in the last 3 hours (benefit up to 4.5)
  2. age > 18
  3. Disabling stroke
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31
Q

Risks associated with using TPA

A
  • Intracranial hemorrhage (bleeding into stroke area –> deterioration)
  • Systemic hemorrhage
  • Angioedema on the side of weakness (more likely if pt is on an ACE inhibitor).
32
Q

Contraindications for TPA

A

Anything that increases the risk of bleeding:

  • suspected bleed
  • High BP
  • Recent surgery
  • Recent MI
33
Q

Treatment options available for ischemic stroke

A

TPA and EVT

34
Q

Endovascular Therapy (EVT)

A

Interventional radiological procedure for retrieving clots and restoring blood flow.

35
Q

Indications for EVT

A
  • GOod collateral blood flow
  • There is tissue left to save on CT (ASPECTS >6)
  • Disabling stroke (NHHS score > 6)
  • Large vessel involved.

suggested to do it within 6 hrs and up to 24 hours.

36
Q

Two different kinds of EVT

A

Stent retrievers and aspiration devices.

37
Q

Does the stroke have to be recent for TPA to be helpful?

A

tPA is used in wake up or unkown stroke onset patients on a case by case basis because studies show that the agent has benefit even if the patient was last known well more than 4.5 hours ago.

38
Q

What sort of imaging should be done for a stroke patient

A

CT to figure out if it is a hemorrhage; CT angiogram to determine where the clot is if there is one.

39
Q

What labs should be done on a stroke patient

A

INR - how well are they clotting? Before administering warfarin. Blood glucose - rule out hypoglycemia.

40
Q

What is a lacunar stroke

A

An ischemic stroke to any of the small arteries of the brain. The most comm on kind of stroke. The small arteries tend to supply deep tissues of the brain.

41
Q

Intracerebral vs subarachnoid stroke

A

Intracerebral stroke occurs within the brain itself. Usually results from hypertension. Subarachnoid stroke is bleeding between the pia mater and arachnoid mater. Most often caused by ruptured aneurysm.

42
Q

Presentation of stroke to the LEFT middle cerebral artery

A
  • Precentral gyrus –> RIGHT hemiplegia
  • postcentral gyrus –> RIGHT hemianesthesia
  • optic radiations –> right homonymous hemianopsia
  • Wernicke and Broca’s areas –> global aphasia
  • Frontal eye field –> left gaze deviation/preference.
43
Q

What does the frontal eye field do?

A
44
Q

How would stroke to the RIGHT middle cerebral artery present? (5)

A
  • Precentral gyrus –> LEFT hemiplegia
  • Postcentral gyrus –> LEFT hemianesthesia
  • Optic radiations –> LEFT hononymous hemianopsia
  • Parietal cortex –>LEFT hemineglect
  • frontal eye fields –> RIGHT gaze deviation/preference (“look toward the lesion”)
45
Q

How would a left anterior cerebral artery stroke present? (3)

A
  • Precentral gyrus –> leg >arm weakness on right
  • Postcentral gyrus –> leg > arm sensory loss on right
  • Frontal lobe –> behavioural abnormalities

This would be similar on the other side.

46
Q

Presentation of stroke to left posterior cerebral artery

A
  • occipital cortex –> right hononymous hemianopsia
  • This would be the same on the other side
  • (A very early PCA occlusion may lead to hisensory loss and hemiparesis)
47
Q

“top of the basilar” stroke syndrome

A

Small perforating arteries supplying the thalamus and midbrain.

Decreased level of consciousness can sometimes be the only finding. May also find dyarthria, visual field deficit, eye movement abnormalities, weakness, ataxia, numbness.

48
Q

How does pontine “locked in” syndrome occur and what does it include?

A

The result of a mid basilar occlusion.

Results in bilateral horizontal gaze palsy, bifacial weakness, anarthria, quadriplegia (corticospinla tracts).

49
Q

How may a cerebellar stroke present?

A

Main finding is usually ataxia on the ipsilateral side.

May also find nystagmus (toward the lesion), dysarthria, vertigo, nausea, vomiting.

50
Q

Amaurosis Fugax

A
  • Painless ransient vision loss. Either monocular or binocular.
  • Cuased by ischemia to the ipsilateral carotid artery
  • ichemia anterior to optic chiasm will lead to monocular vision loss and ischemia posterior to optic chiasm will lead to binocular vision loss.
51
Q

Causes of monocular vision loss (6)

A

**Carotid artery stenosis (amaurosis fugax)

** Giant cell arteritis

Nonarteric AION (small vessel disease)

retinal vasospasm

Papilledema

Ocular disease

52
Q

Causes of binocular transient vision loss

A

Vertebrobasilar ischemia (PCA)

Migraine

Seizure

53
Q

What is small vessel disease and what causes it?

A

Small arteries in the brain can be dmaaged by HTN, hyperlipidemia, diabetes, and smoking.

Cumulative damage leads to small subcortical strokes in the corona radiata, gasal ganglia, internal capsule, thalamus, and pons.

54
Q

How is atrial fibrillatio nimplicated in stroke?

A

It’s the most common cause of a carbioembolic stroke. The fluttery heart contractions allow thrombi to form in the heart, that may travel in the blod stream to the brain.

55
Q

Three common ischemic stroke mechanisms

A

Large vessel atherosclerotic disease;

Small vessel disease

Atrial fibrillation/cardioembolism

56
Q

Carotid endarterectomy vs stenting

A

Carotid endarteractomy: Clearing out atherosclerotic plaque from the internal carotid artery to prevent recurrent ischemia and stroke.

  • First line for moderate-to-severe symptomatic carotid stenosis
  • Indicated when…
    • Patient is symptomatic
    • 50-99% blockage
    • Patient is > 70 years old

Carotid artery stenting comes with less risk of MI, but more periprocedural risk (stroke). May be preferable if…

  • high perioperative cardiac risk
  • Previous carotid endarterectomy
  • The patient is younger
57
Q

What are some modifiable risk factors for stroke?

A
  1. Hypertension
  2. hyperlipidemia
  3. diabetes
  4. cardiac disease (atrial fibrillation)
  5. large vessel intra/extracranial atherosclerotic disease
  6. wait-to-hip ratio
  7. smoking (current)
  8. Alcohol use
  9. Diet and physical inactivity
  10. psychosocial stress/depression
58
Q

Non-modifiable risk factors for stroke (4)

A

age

low birthweight

race/ethinicity (being black in america; being asian in asia for hemorrhagic)

genetics (family history and rare monogenic conditions)

59
Q

What is the most important risk factor for stroke? Why?

A

Hypertension! Direct relationship with causing stroke and reducing risk of stroke. Accounts for 30-50% of stroke.

This is because HTN causes brain disease, especially intracerebral hemorrhage.

60
Q

How to lipids impact stroke risk?

A
  • HIgh levels LDL increase risk of ischemic stroke. Low levels LDL increase risk of hemorrhagic stroke. Aim for LDL < 2.0.
  • High HDL is protective against cardiac disease, but not known for stroke.
  • Statins have benefit for preventing vascular disease and therefore ischemic stroke.
61
Q

Impact of diabetes on stroke risk

A
  • Nearly doubles stroke risk.
  • Glycemic control is key - A1C < 7.0
62
Q

Impact of BMI on stroke risk

A

BMI ipmarts risk for stroke. Weight reduction helps lower BP and prevent stroke.

63
Q

Stroke prevention approaches:

A
  1. Lifestyle modification
    • Physical activity
    • Diet high in fruits, DASH diet, mediterranean diet
  2. Stop smoking and minimize drinking
  3. Glycemic control
  4. Weight loss
  5. Lipid control (statins)
  6. BP control
  7. Treat cardiac disease
64
Q

Primary prevention of stroke

A

Prevent a stroke from ever happening!

  • Screen for vascular risk factors
  • Treat HTN
  • Identify and treat other risk factors (i.e., diabetes, dyslipidemia)
  • Promote healthy lifestyle (no smoking, limit alcohol, exercise, diet)
65
Q

Should old people take aspirin to prevent stroke?

A

Aspirin does not help prevent the first stroke

ALl patients who have already had a TIA/stroke should take an antiplatelet agent (aspirin), unless there is an indication for anticoagulation (all afib pts get anticoahulants).

66
Q

ABCD2 score

A

To assess increased risk for stroke after a TIA

Age (>60 years = 1 pt)

BP (>14/90 at time of event = 1 pt)

Clinical features

  • Isloated speech = 1 pt
  • unilateral weakness = 2 pt

Diabetes = 1 pt

Duration of TIA sx

  • 10-59 mins = 1 pt
  • >60 mins = 2 pt
67
Q

What is a low, moderate, high risk ABCD2 score?

A

Score 0-3 = low risk (2 day storke risk of 1%)

Score 4-5 = moderate risk (2 day stroke risk of 4%)

Score 6-7 = high risk (2 day stroke risk of 8%)

68
Q
A
69
Q

Secondary Stroke Prevention

A

ABCDE

Antithrombotic: Anticoagulation for afib pts. Everyone else should take an antiplatet agent (aspirin).

Blood Pressure: Keep it under 140/90

Cholesterol: Statin to reach LDL < 2.0 target

DIabetes and Diet: A1C < 7%; diet with low salt, fresh fruit and vegetables, nuts, etc

Exercise and lifestyle: counsel about smoking, alcohol, stress, and exercise

70
Q

Medications for after stroke

A

Aspirin, anticoagulation (afib pts), clopidogrel for 3 wks (longer than that may lead to hemorrhage).

71
Q

CHADS2VaSc

A

Stroke risk assessment for patients with atrial fibrillation. Increasing risk of stroke with higher CHADS2VaSc score. THe score tells you how high your risk of getting a stroke this year is.

This was developed out of the CHAD score to accont better for younger age, being female and having vascular disease.

Congestive heart failure + 1

Hyptertension + 1

Age > 75 +2; 65-75 +1

Diabetes + 1

Stroke/TIA +2

VAscular disease (CAD, PAD) + 1

Sex - female +1

72
Q

According to the CHAD guidelines, when should you give oral anticoagulants (warfarin or DOAC) or antiplatelet therapy (aspirin) in atrial fibrillation?

A
  • Oral anticoagulants (warfarin)
    • Patient > 65
    • prior stroke, HTN, heart failure, diabetes (CHAD risk factors)
  • Antiplatelet therapy (aspirin)
    • Patient has coranary artery disease or peripheral artery disease
  • No antithrombotic if the patient doesn’t have any of these risk factors, even if they have atrial fibrillation.

warfarin is better than aspirin at preventing strokes.

73
Q

Warfarin versus direct oral anticoagulants

A

Warfarin

  • way cheaper
  • narrow therapeutic dose window
  • REversible
  • Processed in liver
  • multiple drug interactions
  • INR monitoring required
  • More change of intracranial hemorrhage

Direct oral anticoagulants (rivaroxaban, dabigatran, apixaban, edoxaban)

  • Very expensive
  • Dose dependent on age and renal function
  • Not reversible (at least for now)
  • Excreted renally
  • No need for monitoring
  • Less drug interactions - but there are still some!
  • Less chance of intracranial hemorrhage
74
Q

When is warfarin defos a better choice than a direct oral anticoagulant (DOAC)?

A
  • Mechanical heart valve (+/- Afib)
  • LV thrombus
  • Severe cardiomyopathy with reduced ejection fraction
  • Rheumatic mitral stenosis/valvular Afib
75
Q

What are two mechanisms for stroke that you never want to miss? Why is this?

A

These are mechanisms of stroke that have specific and effective interventions!

Symptomatic carotid artery stenosis - carotid endarterectomy or stent

Atrial fibrillation - CHADS2 guides treatment with anticoagulants

76
Q

Name all of the aphasias from least to most impaired. What areas are involved?

A
  1. Anomia - unclear
  2. conduction aphasia - arcuate fasciculus
  3. transcortical sensory aphasia - wernicke’s + association areas
  4. wernicke’s aphasia - wenicke’s (temporal)
  5. transcortical motor aphasia - broca’s + association areas
  6. broca’s aphasia - broca’s (frontal lobes)
  7. mixed transcortical aphasia - broca’s and wernicke’s
  8. global aphasia - areas in frontal, parietal and temporal lobe
77
Q

.
Endovascular thrombectomy is the standard of care for appropriate patients with

A

proximal clot, low burden of early infarct signs, good collaterals.

Med 1 UBC Winter 2020 (14 decks)

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