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Neurology > TN Stroke > Flashcards

TN Stroke Flashcards

1
Q

What is infarction?

A

permanent tissue injury, confirmed by neuroimaging (vascular etiology)

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2
Q

What is stroke?

A

sudden onset of neuro deficits of a vascular etiology with infarction of CNS tissue

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3
Q

What is TIA?

A

sudden onset of neuro deficits of a vascular etiology without infarction of CNS tissue (no imaging evidence of stroke)

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4
Q

What is amaurosis fugax?

A

transient monocular painless vision loss (can be presentation of TIA)

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5
Q

What is hypertension encephalopathy?

A

Encephalopathy caused by acute severe HTN (typically dBP>130 of sBP>200)

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6
Q

What are the clinical findings of hypertension encephalopathy?

A
  • abn fundoscopy (papilledema, hemorrhages, exudates, cotton-wool spots)
  • focal neuro Sx
  • N/V
  • visual disturbances
  • change in LOC
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7
Q

What are the two major types of stroke, and what is the proportion of each?

A

Ischemic (80%) and hemorrhagic (20%)

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8
Q

What are the three major etiologies/pathophys of ischemic stroke?

A

arterial thrombosis (large or small vessel)
cardioembolic
systemic hypoperfusion

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9
Q

What is the mechanism of large vessel thrombotic stroke, and which are considered “large”?

A

stenosis or occlusion –> insufficient blood flow beyond lesion (hemodynamic stroke)
Internal carotid artery, vertebral, or intracranial arteries

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10
Q

What are the etiologies/pathophys of large vessel stroke?

A

atherosclerosis (most common cause)
dissection
vasculitis

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11
Q

What is the mechanism of large vessel thrombotic stroke, and which are considered “small”?

A

chronic HTN and DM cause vessel wall thickening and decreased luminal diameter
affects mainly small penetrating arteries (primarily basal ganglia, internal capsule, and thalamus)

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12
Q

What is the mechanism of cardioembolic stroke?

A

blockage of cerebral arterial blood flow due to particles originating from a cardiac source

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13
Q

What conditions can cause cardioembolic stroke?

A 
atrial fibrillation (most common)
rheumatic valve disease
prosthetic heart valves
recent MI
fibrous and infectious endocarditis
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14
Q

What is the mechanism of stroke due to systemic hypoperfusion?

A

inadequate blood flow to brain, usually secondary to cardiac pump failure (e.g. cardiac arrest,
arrhythmia, or MI)

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15
Q

What areas are affected in stroke due to systemic hypoperfusion?

A

There is global cerebral ischemia; primarily affects watershed areas

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16
Q

What are the main types of hemorrhagic stroke?

A

intracerebral hemorrhage

subarachnoid hemorrhage

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17
Q

What are the mechanisms of intracerebral hemorrhage?

A 
hypertensive (most common)
trauma
amyloid angiopathy (associated with lobar hemorrhage)
vascular malformations
vasculitis
drug use (cocaine or amphetamines)
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18
Q

What is the difference between the aneurysms that cause intracerebral vs other intracranial hemorrhage?

A

Intracerebral hemorrhage: smaller microaneurysm in penetrating vessels
other: on larger vessels
[this is my interpretation, would be worth double checking]

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19
Q

What is a subarachnoid hemorrhage?

A

bleeding into subarachnoid space (intracranial vessel between arachnoid and pia)

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20
Q

What are the main causes of SAH?

A 
trauma (most common) 
spontaneous: ruptured aneurysms (75-80%), idiopathic (14-22%), AVMs (4-5%)
other:
coagulopathies (iatrogenicorprimary)
vasculitides
tumours
cerebral artery dissections
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21
Q

What are the clinical features of SAH?

A

• sudden onset (seconds) of severe “thunderclap” H/A usually following exertion and described as the “worst headache of my life” (up to 97% sensitive, 12-25% specific)
• N/V, photophobia
• meningismus (neck pain/stiffness, positive Kernig’s and Brudzinski’s sign)
• decreased LOC (due to any of: raised ICP, ischemia, seizure)
• focal deficits: cranial nerve palsies (CN III, IV), hemiparesis
• ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein)
• reactive HTN
also, Hx of sentinel bleed

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22
Q

What is a sentinel bleed (in context of SAH)?

A

■ represents undiagnosed SAH
■ SAH-like symptoms lasting <1 d (“thunderclap H/A”)
■ may have blood on CT or LP
■ ~30-60% of patients with full blown SAH give history suggestive of sentinel bleed within past 3 wk

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23
Q

What Ix should be done to assess for SAH?

A

• non-contrast CT – for diagnosis of SAH
• lumbar puncture (highly sensitive) – for diagnosis of SAH if CT negative but high suspicion
• four vessel cerebral angiography (“gold standard” for aneurysms)
• MRA and CTA: sensitivity upto 95% for aneurysms, CTA>MRA for smaller aneurysms and delineating adjacent bony anatomy
[see TN for more details on findings for each]

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24
Q

What particular features should be assessed in neurological exam of suspected SAH?

A 
BP
LOC
Limb movements
Stiff neck
Fundi
[this is from the neurosurgery section, so, sparse]
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25
Q

What is the syndrome of an ACA stroke?

A

contralateral leg paresis, sensory loss, cognitive deficits (e.g. apathy, confusion, and poor judgment)

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26
Q

What is the syndrome of an MCA stroke?

A

proximalocclusioninvolves:

  1. contralateral weakness and sensory loss of face and arm
  2. cortical sensory loss
  3. may have contralateral homonymous hemianopia or quadrantanopia
  4. if dominant (usually left) hemisphere: aphasia
  5. if non-dominant (usually right) hemisphere: neglect
  6. eye deviation towards the side of the lesion and away from the weak side
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27
Q

What is the syndrome of a PCA stroke?

A
  1. contralateral hemianopia or quadrantanopia
  2. midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis
  3. thalamic findings: sensory loss, amnesia, decreased level of consciousness 4. if bilateral: cortical blindness or prosopagnosia
  4. hemiballismus
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28
Q

What is the syndrome of a proximal basilar artery stroke?

A

proximal (usually thrombosis): impaired EOM, vertical nystagmus, reactive miosis, hemi- or
quadriplegia, dysarthria, locked-in syndrome, coma

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29
Q

What is the syndrome of a distal basilar artery stroke?

A

distal (usually embolic, i.e. top of the basilar sydrome): somnolence, memory and behaviour
abnormalities, oculomotor deficit

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30
Q

What is the syndrome of a PICA stroke?

A

ipsilatera lataxia, ipsilateral Horner’s, ipsilateral facial sensory loss;
contralateral limb impairment of pain and temperature sensation;
nystagmus, vertigo, nausea/vomiting;
dysphagia, dysarthria, hiccups

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31
Q

What are other names for the PICA stroke syndrome?

A

lateral medullary or Wallenberg syndrome

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32
Q

What is the syndrome of a medial medullary stroke, and what artery is involed?

A 
contralateral hemiparesis (facial sparing), contralateral impaired proprioception and vibration
sensation, ipsilateral tongue weakness

(anterior spinal artery, which can be associated with anterior cord infarct)

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33
Q

What structures are involved in lacunar infarcts?

A

Deep hemispheric white matter; involving deep penetrating arteries of MCA, circle of Willis, basilar, and vertebral arteries

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34
Q

Describe the four syndromes seen in lacunar stroke

A

■ pure motor hemiparesis (posterior limb of internal capsule): contralateral arm, leg, and face
■ pure sensory loss (ventral thalamic): hemisensory loss
■ ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia and leg paresis
■ dysarthria-clumsy hand syndrome (ventral pons or genu of internal capsule): dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness

35
Q

What proportion of patients with ICH have early seizure activity?

A

5-25%

36
Q

What uncommon condition should be considered in DDx of stroke and headache?

A

Cerebral venous sinus thrombosis

It is an uncommon cause of either, but is associated with high morbidity and mortality. Patients often present with headache alone, but can also have seizures, focal neurological deficits, or cranial nerve palsies.

This is diagnosed with MRV or CTV. Treatment is typically anticoagulation with heparin initially, then transition to warfarin

37
Q

What percentage of patients with ischemic stroke may develop hemorrhagic transformation within 1w after initial infarction?

A

20-40%

38
Q

Why would bloodwork delay treatment of stroke?

A

patient is on anticoagulants

or suspicion of low platelet count, abnormal electrolytes, or any bleeding abnormality

39
Q

Name 6 stroke mimics

A

drug intoxication, infections, migraines, metabolic, seizures, tumours

40
Q

What SSx should raise suspicion of an alternate diagnosis, instead of stroke?

A

fever, decreased LOC, fluctuating symptoms, gradual onset, no focal neurological symptoms, and/or positive symptoms

41
Q

What is the Aspect score?

A

10-point quantitative score to assess ischemic changes on CT scan
10/10 is normal and <4/10 signifies high risk of bleed with rtPA; points are subtracted for each of 10 structures with potential abnormalities

42
Q

What are the absolute contraindiations to rtPA on history?

A

improving sx, minor sx,
seizure at stroke onset,
recent major surgery (within 14 d) or trauma, recent GI or urinary hemorrhage (within 21 d),
recent LP or arterial puncture at noncompressible site,
PMHx ICH, sx of SAH/ pericarditis/MI,
pregnancy

43
Q

What are the absolute contraindiations to rtPA on exam?

A

sBP≥185, dBP≥110, aggressive treatment to decrease BP, uncontrolled serum glucose, thrombocytopenia

44
Q

What are the absolute contraindiations to rtPA on investigations?

A

hemorrhage or mass on CT, high INR or aPTT

45
Q

What should be assessed on exam for a new patient with ?stroke?

A
  • ABCs, full vital sign monitoring, capillary glucose(Accu-Chek®), urgent CODESTROKE if <4.5h from symptom onset (for possible thrombolysis)
  • level of consciousness (knows age, month, obeys commands), dysarthria, dysnomia (cannot name objects)
  • gaze preference, visual fields, facial palsy
  • arm drift, leg weakness, ataxia
  • sensation to pinprick, extinction/neglect
46
Q

What should be assessed on history for a new patient with ?stroke?

A

■ onset: time when last known to be awake and symptom free

■ mimics to rule out: seizure/post-ictal, hypoglycemia, migraine, conversion disorder

47
Q

What investigations should be done for a patient with new ?stroke ?

A

■ non-contrast CT head (STAT): to rule out hemorrhage and assess extent of infarct ■ ECG: to rule out atrial fibrillation (cardioembolic cause)
■ carotid dopplers, echocardiogram
■ CBC, electrolytes, creatinine, PTT/INR, blood glucose, lipid profile

48
Q

What are the signs of stroke on imaging?

A

■ loss of cortical white-grey differentiation
■ sulcal effacement (i.e. mass effect decreases visualization of sulci)
■ hypodensity of parenchyma
■ insular ribbon sign
■ hyperdense MCA sign

49
Q

What are the three main options for treatment of acute stroke?

A

Thrombectomy
Thrombolysis
Anti-platelet (eg ASA) + if afib, Acute anti-coagulant (eg heparin)

50
Q

What is rtPA?

A

recombinant tissue plasminogen activator

51
Q

What is the time window for rtPA?

A

4.5h of acute ischemic stroke onset (last seen normal)

52
Q

What is the threshold of NIHSS above which rtPA is typically offered?

A

≥6
Some stroke neuro may offer at lower level
(eg Giilck: if you have total aphasia that’s only a 3 … but … … might still be worth the tPA)

53
Q

What is the recommended antiplatelet therapy at presentation of acute stroke?

A

81mg ASA chewed
if patient intolerant to ASA, use other antiplatelet agent (i.e. clopidogrel)

Only if not getting tPA [though, check this]

54
Q

What is considered in the initiation of acute anticoagulation in stroke?

A
  • only done to manage afib
    ■ recommend IV heparin (or ensuring INR between 2-3 if already anticoagulated on warfarin)
    ■ may delay initiation of oral anticoagulation depending on size of infarct and presence of petechial/
    frank hemorrhage
55
Q

What should be done about blood sugar in the acute stroke period?

A

Keep it in range: hyperglycemia can increase infarct size

56
Q

What should be done about fever in the acute stroke period?

A

Lower temperature

Consider endocarditis leading to septic emboli

57
Q

What non-pharm measures should be done in acute stroke pt to prevent complications?

A

■ NPO if dysphagia (to be reassessed by SLP)
■ exercise, or, DVT prophylaxis if bed-bound
■ initiate rehabilitation early

58
Q

How should BP be managed in the acute stroke period?

A

• do NOT lower the blood pressure unless the HTN is severe
• antihypertensive therapy is withheld for 48-72 hr (permissive hypertension) after thromboembolic
stroke unless sBP >220 mmHg or dBP >120 mmHg, or in the setting of acute MI, renal failure, aortic
dissection

59
Q

Why don’t we manage HTN after stroke?

A

• acutely elevated BP is necessary to maintain brain perfusion to the ischemic penumbra
• most patients with an acute cerebral infarct are initially hypertensive and their BP will fall spontaneously
within 1-2 d

60
Q

What is first-line for management of HTN post-stroke?

A

[this was unclear, if it was the case genearlly or just for … aortic dissection? but looks like it’s: ]
IV labetalol first-line if needed

61
Q

What Ix do we do after stroke to assess etiology?

A

■ additional neuroimaging (MRI)
■ vascular imaging: CTA/MRA/carotid dopplers
■ cardiac tests: echocardiogram, Holter monitoring

62
Q

Why do we do additional Ix to assess etiology?

A

Correct etiological diagnosis is critical for appropriate secondary prevention strategies

63
Q

What is the role of anti-platelet therapy in primary prevention of stroke?

A

No firm evidence for a protective role for antiplatelet agents for low-risk patients without prior stroke/TIA

64
Q

What is the role of anti-platelet therapy in secondary prevention of stroke?

A

Initial choice: ASA
If cerebrovascular symptoms while on ASA or if unable to tolerate ASA: Aggrenox® (ESPRITtrial), clopidogrel (CAPRIE trial)

65
Q

What is the role of carotid endarterectomy in primary prevention of stroke?

A

controversial: if stenosis >60%, risk of stroke is 2% per yr; carotid endarterectomy reduces the risk of stroke by 1% per yr (but 5% risk of complications)

66
Q

What is the role of carotid endarterectomy in secondary prevention of stroke?

A

carotid endarterectomy clearly benefits those with symptomatic severe stenosis (70-99%), and is less beneficial for those with symptomatic moderate stenosis (50-69%) (NASCET trial)

67
Q

Compare endarterectomy and carotid stenting

A

according to the CREST trial, endarterectomy and carotid stenting have similar benefits in a composite endpoint of reduction of stroke, MI, and death;
However, in the periprocedural period, stenting results in a higher rate of stroke, while endarterectomy results in a higher rate of MI

68
Q

How should atrial fibrillation be managed for prevention of stroke?

A

Same for primary and secondary prevention: classify risk based on CHADS2, then antiplatelet vs anticoagulation accordingly

69
Q

How do you decide between anticoagulation and antiplatelet therapy for a patient with afib?

A

Stroke 2014 guidelines recommend that virtually all pt with afib without contraindication be anticoagulated

Traditionally, Based on Chads2 score:
◆ 0 (low risk, 1.9% annual stroke risk): antiplatelet
◆ 1 (intermediate risk, 2.8% annual stroke risk): anticoagulant or antiplatelet – patient specific
decision
◆ >2 (high risk, 4-18.2% annual stroke risk): anticoagulant

70
Q

What are the anticoagulation options?

A

◆ warfarin (titrate to INR 2-3)
◆ dabigatran (110 or 150 mg PO bid), apixaban (2.5 or 5 mg PO bid) or rivaroxaban (15 or 20 mg
PO daily) may be alternatives to warfarin, but should be used cautiously; Praxbind reversal agent for dagibatran if necessary

71
Q

How should hypertension be managed in primary prevention of stroke?

A

■ targets: BP<140/90 (or <130/80 for diabetics or renal disease); high risk but without diabetes, target sBP < 120 (SPRINT trial)
■ ACEI: ramipril 10mg PO OD is effective in patients at high risk for cardiovascular disease (HOPE trial)

72
Q

How should hypertension be managed in secondary prevention of stroke?

A

ACEi and thiazide diuretics are recommended in pt with previous stroke/TIA (PROGRESS trial)

73
Q

How should hypercholesterolemia be managed in primary prevention of stroke?

A

Statins in pt with CAD or at high risk of CV events, even with normal cholesterol (CARE trial)

74
Q

How should hypercholesterolemia be managed in secondary prevention of stroke?

A

Statins: high dose atorvastatin (SPARCL trial) but lower doses may be appropriate if pt cannot tolerate high dose

75
Q

How should diabetes be managed for prevention of stroke?

A

Ideal management: HbA1c <7%, fasting BG between 4-7

76
Q

How does smoking relate to stroke risk?

A

Smoking increases risk of stroke in a dose-dependent manner; after cessation, risk of stroke decreases to baseline within 2-5y (noted in 2y, so might just be baseline for stroke recurrence)

77
Q

How does physical activity relate to stroke risk?

A

Beneficial effect of regular physical activity has a dose-related response in terms of intensity and duration of activity

78
Q

What are the features of a multidisciplinary approach to stroke rehab?

A

Dysphagia assessment and dietary modifications
communication rehabilitation
cognitive and psychological assessments including screen for depression
therapeutic exercise programs
assessment of ambulation and evaluation of need for assistive devices, splints or braces
vocational rehabilitation

79
Q

What is the definition of a cerebral hemorrhage?

A

Intracranial bleeding into brain tissue

80
Q

What are the most common etiologies of cerebral hemorrhage?

A

head trauma, hemorrhagic stroke (…)

81
Q

What are the investigations for cerebral hemorrhage?

A

General Ix for stroke
and:
- consider LP if ?SAH
- consider angiogram if ?aneurysm, ?AVM

82
Q

What test should be repeated 4-6w after hemorrhage resolution, and why?

A

CT head: rule out underlying lesion

83
Q

What is the treatment of cerebral hemorrhage?

A

… realistically, NSx consult.
Medical: consider BP management (no conclusive guidelines, suggest 140-160 sBP), consider medically lowering ICP [notes to see NSx]

Neurology (2 decks)

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