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Flashcards in Cerebrovascular Disease Deck (30)
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3 different stroke etiologies

1) Embolic - thrombus somewhere else, flicks off and happens to go to brain - consider AFib or valve disease, arterial dissection elsewhere or carotid artery stenosis

2) Thrombotic - cerebrovascular disease in artery to brain - plaque ruptures - distal tissue poorly perfused. AS, HTN, DM, CAD, PVD

3) Hemorrhagic - blood is an irritant to brain. If you have brain bleed you can lose brain parenchyma
- Sub-arachnoid or IPH


Various patient presentations in stroke

FND!!! plus

1) HTN diabetic smoker with bad cholesterol and is old (for CAD old is 45F, 55M)

2) AFib, prosthetic valve off anticoagulation

3) Young woman with neck pain

4) Thunderclap HA (prob proceeded by sentinel HA 1-2w before)


Various infarct locations and body areas involved

ACA - Feet, legs

MCA - arms, hands, face, speech - broca's is in superior division, wernicke in inferior

PCA - vision changes, homonymous hemianopsia

Basilar and vert - locked in, syncope

Cerebellum - ataxia, disdiatokinesia, coordination


Basic treatment for hemorrhagic stroke

Lower BP
Neurosurg - clip, coil, craniotomy
FFP (reverses risk of bleeding)


Basic treatment of ischemic stroke


Then next day get EKG*, Echo*, Carotid US*, maybe MRI, MRA

If EKG shows AFib - anticoagulation

If Echo shows thrombus - anticoagulation - hep-warf bridge

If patient is ASx and Carotid US shows more than 80% stenosis OR if patient is Sx and shows 70% then consider CEA or stent. CEA is better. Wait 2w for the surgery.

If patient is Asx OR less than 70% stenosis then medical management

TIA is when symptoms resolve on own and improve within 24h. MRI without evidence of stroke.


Management of acute stroke

1) tPA? Yes if less than 4.5 hrs from LKN. Avoid if previous ICH, risk of current bleeding like GI bleed or recent surgery

2) Heparin? No

3) Warfarin? No

4) Anti-platelets? ASA 325

5) BP? Permissive HTN less than 220/120. This is to preserve the penumbra

6) DM? Gluc less than 140

7) Statins? Start high-potency statin since they will go home on it anyway. Atorva 80


Management of stroke chronically

1) tPA? no

2) Heparin? No

3) Warfarin? Afib or CHADS2 at or higher than 2 (must be anticoagulated). CHF, HTN, Age over 75, DM, stroke, stroke

4) Anti-platelets? ASA 81, stroke on ASA then ASA + dipyridamole. If can't tolerate ASA then clopidogrel

5) BP? ACEi, diuretics, BP less than 140/90

6) DM? A1C less than 7

7) Statins? High dose statin like atorva 40/80 or rituvastatin 20/40


What are the 5 lacunar syndromes?

1) Pure motor - internal capsule
2) Pure sensory - thalamus
3) sensorimotor - both
4) Ataxic hemiparesis
5) Dysarthria clumsy hand - subcortical white matter



Left - aphasia (brocas and wernickes are on the left if you are R dominant)

Right - neglect, apraxia


Contraindications to tPA

1) not a candidate - greater than 4.5 hrs, rapidly resolving symptoms, GI bleed, low platelets

2) Large hypodensity on CT (too late! it's stroked out and we don't want to bleed into it)

3) BG less than 50 or higher than 400

4) Stroke within 3 months (high risk of hemorrhagic conversion)

5) Prior ICH

6) Recent major surgery last 2w

7) Catheter in non-compressible site

8) Oral anticoagulation (ASA is ok). INR less than 1.7 is ok or if they haven't taken in a few days is ok.

9) recent GI bleed

10) SBP higher than 185 or DBP higher than 110

11) High PT or PTT


How long can you do an INR procedure?

less than 6hrs


Management after tPA

Before: BP less than 185/110
After: BP less than 185/105

Labetalol 10-20IV, Nicardipine drip

BP monitoring q15m for 2h. q30 for 4h. q1h for 16h

Neuro exams at same intervals

Stability CT at 24h (r/o hemorrhage from tpa)

No ASA, heparin, lovenox until that stability CT


Management of inpatient stroke - couldn't get TPA

Permissive HTN less than 220/120

Dysphagia screen or NPO


Resume home B blockers, hold anti-hypertensives

DVT ppx

Avoid sedating meds

Fall risk

Aspiration risk


Inpatient workup for stroke

Echo (w/bubble)
Vessel imaging (carotid doppler/TCD)
Speech and swallow eval
Hypercoag workup (PFO, SLE, anticardiolipin)
PT/OT/Rehab eval
TEE (L atrial dilatation, it sees the aortic arch better)
Fasting lipids, A1C, hypercoag


Anterior circulation syndromes

From carotids

Can include deficits related to damage to cortex of frontal, parietal, or temporal lobes, basal ganglia, internal capsule

Aphasia and heminopsia can only be cortical

Agraphesthesia, extinction to dual simultaneous stimulation and neglect are all cortical as well

Lesion with dense hemiparesis is likely internal capsule from lacunae


Posterior circulation syndromes


usually diplopia (cranial nerve nucleii), vertigo (vestibular nucleii), ataxia (cerebellum or its connections), n/v, crossed deficits (hemisensory loss on ipsilateral face and contralateral body), dysarthria/dysphagia (nucleus ambiguus)

Wallenberg syndrome AKA Dorsolateral medullary syndrome: dysarthria, n/v, vertigo, crossed sensory defecit, horners

Weber syndrome: ipsilateral oculomotor paresis with contralateral hemiparesis

Medial medullary syndrome: contralateral hemiparesis and ipsilateral tongue paresis

Ataxia-hemiparesis syndrome: from pontine lacunae

Dysarthria-clumsy hand syndrome: also in pons


Hyperacute onset with full deficit present from the beginning

Embolic etiology likely, esp is patient has AFib


Stuttering onset

Usually thrombotic


Stuttering onset with sudden deterioration

may suggest hemorrhagic conversion


Carotid bruit on exam on the suspected side of lesion

Suspicious for large vessel atherosclerotic disease


Irregular pulse

May suggest underlying AFib and cardioembolic stroke


Methods for evaluating the carotid arteries

MRA, CTA, duplex US and catheter based carotid angiogram

Most common is Doppler US

MRA can be done with or without contrast

CTA MUST have contrast. CTA without contrast may demonstrate calcification in the wall of the carotid artery but will not evaluate the patency or degree of stenosis


Amaurosis fugax

Transient monocular blindness

Most commonly caused by atheroembolus to ophthalmic artery from internal carotid.

If a patient with retinal or cerebral ischemia in the anterior circulation has ipsilateral carotid stenosis that is high grade, then carotid revasculatization is indicated.

CEA is better than stenting.

Confirm high grade stenosis by concordance on 2 different noninvasive tests (doppler, CTA, MRA) OR with catheter angio


Risk of stroke in untreated vs treated Carotid artery stenosis

In patients with high grade stenosis who are symptomatic in the distribution of the stenotic ICA, the 2yr stroke risk is 24% with medical treatment and 9% with addition of CEA


Wallenburg syndrome

Caused by infarct in distribution of PICA. Lesion in dorsolateral medulla. Look out for chiropractic treatment. PICA is first branch of vertebral artery. Patients can dissect the vert during chiropractic treatment. In young patients, cerebral infarction is usually caused by unusual things like this, paradoxical emboli or hypercoagulable states.

1) Vertigo - vestibular nuclei
2) Dysarthria and paralyzed L palate - L nucleus ambiggus
3) L ptosis, miosis (horner) - L descending sympathetics
4) L facial numbness - L spinal trigeminal tract
5) R body numbess to pinprick - L spinothalamic tract
6) L sided dysmetria - L inf cereballar peduncle


Is Horners easier to diagnose in dark or light rooms?


In the light, both pupils are small (the good pupil is constricted due to parasympathetics)

In the dark, the affected pupil would be unable to dilate due to sympathetic damage. The good pupil dilates so the anisocoria is more pronounced.


Some key signs of transtentorial uncal herniation

Blown pupil and lethargy


Hemorrhage vs infarct

If there is acute onset of FND with associated depression of consciousness that is more typical for acute ICH

Likely due to HTN. HTN is an even bigger risk factor than smoking.


Damage to putamen

Hemorrhage to R putamen could compress the R internal capsule leading to L hemiplegia and compressing the R thalamus causing L hemisensory loss


Pathology of HTN ICHs

same as for lacunar strokes

Both occur in deep penetrating branches of ACA, MCA and PCA

Lipohyalinosis - can develop very small aneurysms which rupture causing ICH (this is Charcot-Bouchard aneurysm)