Bns Dubisky Lecture #5

Front 1

What is the leading cause of neurological disability?

Back 1

-stroke

Front 2

Are strokes more common in men or women?

Back 2

-men!

Front 3

What are some odd modifiable risk factors?

Back 3

-CAD, drugs (esp.cocaine use), alcohol, atrial fibrillation, hypercholesterolemia/dyslipidemia

Front 4

Define a transient ischemic attack? Anterior circulation TIA (the ispsilateral and contralateral signs)? Poster TIA?

Back 4

-a TEMPORARY focal neurlogical deficit that lasts less than 24 hours (most only a few minutes)
-ipsilateral symptoms:amaurosis fugax (painless vision loss). Contralateral: sensory or motor dysfunction.
-aphasia (language difficulty)
-Posterior: bilateral or shifting sensory or motors symptoms, vision field loss, often see diplopia, vertigo, dysphagia, dysarthria

Front 5

How would a pt. present with an thrombotic stroke?

Back 5

-a thrombotic stroke occurs from a blood clot (aka thrombus) in an intracranial vessel affected by atherosclerosis
-think platelets!!
-often preceded by TIAs, can progress over hours to days, often in a stepwise fashion
-the prenumbra can be reversed, there is cell death but it is not the site of destruction (so you still have blood flow. Also see neuronal paralysis and perfusion abnormality)
-at ground zero you have irreversible ischemia, cytotoxic edema and diffusion abnormality

Front 6

How would a pt. present with an embolic stroke?

Back 6

-occlusion of a cerebral vessel by material from a distant site
-heart: atrial fibrillation, patent foramen ovale, prosthetic valves, endocarditis, atrial myxoma (benign tumor found in heart), aortic arch plaques
-sudden onset with max symptoms at onset. Also fewer TIAs beforehand

Front 7

How would a pt. present with a lacunar stroke? What is special about thisstroke? What are some distinct clinical syndromes it can cause?

Back 7

-ischemic stroke resulting from disease of small vessels or penetrating arteries (so happens deep in the brainstem). Happens bc of long standing hypertension causing hypertrophy which causes then deposition of fibriod
-can be asymptomatic
-pure motor stroke, pure sensory stroke, clumsy hand dysarthria syndrome, various brainstem syndromes

Front 8

How would a pt. present with diffuse hypoperfusion

Back 8

-it is usually as a result of cardiac pump failure or systemic HYPOtension
-it occurs right at the interface of two vessel territories

Front 9

What are some uncommon causes of stroke?

Back 9

-vasculitis, arterial disseciton (tear in the vessel) (carotid and vertebral)

Front 10

What are the pre-hospital assessment screening tool?

Back 10

-FAST: face (ask person to smile), arms (ask to raise both arms, see if one drifts downward) , speech (ask pt. to repeat asimple sentence, look for slurred speech or confusion), time (call 911 is pt. shows any of these symptoms)

Front 11

What would you include in your evaluation of a pt. suspected of having a stroke?

Back 11

-MRI, CT, angiography (carotid ultrasound and digital subtraciton), history, physical exam, lab studies, echocardiography, national institute for neurological disorders and stroke scale (NINDS), cardiac monitoring, lumbar puncture

Front 12

How would you treat a stroke?

Back 12

-ABC's (make sure stable), determine if pt. is a candidate for thrombolytic therapy for ACUTE ISCHEMIC STROKE

Front 13

Describe the purpose of TPA? What is the criteria to be a candidate for this treatment?

Back 13

-purpose is to improve functional outcome at three months.
-you need to explain the risks and benefits to pt. and family and get WRITTEN CONSENT (bc there is a small risk of intracranial hemorrhage)
-must be at least 18, onset of stroke symptoms began 3.5 to 4 hours ago, non contrasted CT brain is negative for evidence of acute intracranial hemorrhage and does not show evidence of acute ischemic changes

Front 14

What is the exclusion criteria for for thrombolytic therapy?

Back 14

-platelet count less than 100,000
-seizure at onset of stroke
-head trauma within 3 months
-systolic and diastolic cannot be maintained below 185/110
-evidence of active internal bleeding
-pt. is currently on anticoagulation therapy (warfarin or heparin)
-no surgery in past 14 days
-history suggestive of subarachnoid hemmorhage
-NINDS >22
-recent arterial puncture at non compressible site
-if symptoms are improving

Front 15

How do you administer the TPA?

Back 15

.9 mg/kgwith max of 90mg (the first 10% is administered as a bolus over 60 seconds, the remainder is administered over 1 hour)

Front 16

What happens after TPA is adminitered?

Back 16

-pt. is admitted to ICU for at least 24 hours
-no heparin, warfarin or ASA for 24 hours
-pt. is monitores closely for evidence of decline

Front 17

What are other treatments besides TPA? What is the best treatment?

Back 17

-physical, occupational, and speech therapies
-address modifiable risk factors (bp, sugars, lipids, smoking cessation, alcohol and drug use, vascular surgical evaluation
-antiplatelet therapy
-anticoagulation therapy
-serial neurological checks
-DVT prophylaxis
-best treatment is preventing strokes!!!