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Neuro: Strokes


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formation of a blood clot within a blood vessel
object migreate from one part of the body and causes a blockage of a blood vessel in another part of the body
Facts/Stats about strokes
-3rd leading cause of death in U.S.
-1 occurs every 53 seconds in U.S.
-1 death from stroke occurs every 3.3 min
-28% who suffer stroke are <65 yo
-1/3 of people with stroke die
-15-30% of stroke survivers are permanently disabled
Transient Ischemic Attack (TIA)
-stroke signs and sx which completely resolve within 24 hours with no residual effect
-necrosis of tissue due to upstream obstruction of its arterial blood supply
-it is the culmination of ischemia
-restriction in blood supply, generally due to factors in the blood vessels that result in damage or dysfunction of tissue
-no visible abnormalities on CT or MRI
Reversible Ischemic Neurologic Deficit (RIND)
-Similar to TIA but signs and syx last >24 hours, thenr resolve no residual effect
-outdated term (now condidered a small stoke)
-no visible abnormalities on CT or MRI
Stroke (Cerebrovascular Accident, CVA)
-sudden and rapid onset of a neurologic deficit that fits a vascular territory and is due to an underlying cerebrovascular disease
2 types of stroke
1. strokes due to infarction

2. strokes due to hemorrhage
Strokes to do infarction (ischemia)
-account for 80+% of strokes seen today
-many have TIAs before stroke or at time of stroke
Athero-Thrombotic Ischemic Stroke
-caused by blood clot in an artery leading to the brain
-larger sized strokes
-usually from thrombus (clot) in an atherosclerotic plaque
-2/3 are extracranial stenosis with an ulcerative plaque in the carotid artery
-1/3 are extracranial stenosis with an ulcerative plaque in the basilar artery
-average age 70 yo
Embolic Ischemic Stroke
-smaller size strokes caused by an embolus that moves to progressively smaller arterial branches until it gets stuck
Emboli may come from...
-arthersclerotic plaque
-heart valve vegetation
-mural thrombus
-atrial myxoma
Lacunar Ischemic Stroke
-due to occulsive disease of small penetrating arterioles
-usually seen in diabetic or hypertensive pts, but may be in previously healthy persons
-produce small (< 5mm diameter)lesions
Lacunar Ischemic Stroke is most commonly seen where?
-Most commonly seen in deep white matter of the brain in areas such as the basal ganglia, pons, cerecellum, internal capsule, etc
Lacunar Ischemic Stroke Prognosis
-Prognosis is good
-Most have partial or complete recovery in 4-6 weeks
-but cummultive lacunar infarcts eventually result in dementia if brain tissue is detroyed
-damage is not as big, but long term is harder to fix since it is due to a small vessel disease
Vasculitic Infarct Stroke
-Arteritis-type illness
-inflammation of blood vessels
-may involve intracerebral arteries
-causing arterial spasms and edema that leads to brain ischemia
Hematological-Related Infarct Stroke
-sickle cell anemia, polycythemic and hyperviscosity syndromes may lead to occlusion of intercerebral arteries
Subclavian Steal Syndrome
-retrograde (reversed) arterial flow in the vertebral artery
-compensatory action due to compromised vascular territory beyond the subclavian stenosis/occluded
-extremeties "steal" blood away from other side of the body through the vertebal artery
Strokes associated with Hypercoagulable States
-persons with hypercoagulable states form clots easier and clot can eventually cut off blood supply
-also pts with C/S deficiency, hyperfibrinogenemia
Strokes due to hypoglycemia
-blood sugar drops and brain is particularly sensitive to needing glucose, so brain cells are the first to die d/t lack of glucose
-tends to be large strokes with residual problems such as dementia
Strokes due to Anoxia
-brain is first to die from lack of oxygen
-e.g. drowning
Strokes due to prolonged hypotension
-BP drops so dec oxygen and glucose to brain
-watershed attack
Watershed areas
-areas between vessels that get a little blood from the right and a little blood from the left. If BP decreases of there is an occulsion somewhere, then blood flow to these peripheral areas is lessened
Strokes due to hemmorrhage
-<20% of strokes seen today
-hemorrhagic strokes are NOT associated with TIAs
-area of bleeding is not letting new blood get pastbc it is all bleeding out, so body beyond the hemorrhage is not getting adequate oxygen and glucose
Catergorizing of Cerebral Hemorrhages
-intracerebral hemorrhage (primary and secondary)
-subarachnoid hemorrhage
Primary Intracerebral hemorrhage
-d/t weak artery that spontaneously bleeds
-most common in hypertensive and diabetic pts
Primary Intracerebral Hemorrhage ususally occurs in..
deep brain:
-basal gaglia
-pons "pontine hemorrhage"
Primary Intracerebral Hemorrage in the Cerebellum
-neurosurgical emergency
-presents as dizzy spells, coordination problem, nystagmus, ataxia
-if not surgucally treated, edema and hemorrhage may obstruct the outflow of CSF, leading to increased ICP and tonsillar or uncal herniation
Secondary Intracerebeal Hemorrhage
-d/t identifiable causes such as anticoagulation, aneurysm, AVM, hemophila, tumor etc
-suspect hemorrhage is noted in an unusual location
-muscular wall is weak, gets stretch out and balloons out, can break and lead to hemorrhage
aneursym Tx
-can be surgically clipped or excised
-arteriovenous malformations
-most lesions are congenital
-bleeding or sx commonly onset bwn 10-30 y/o
-no heretary component
-may remain clinical silent for life
-can be surgically resected
Subarachnoid Hemorrhage
-hemorrhage into the ventricles and subarachnoid spaces where CSF circulates
Subarachnoid Hemmorrhage is often due to..
-ruptured berry aneurysm in the area of the Circle of Willis
Berry Aneurysm
-small outpouching that looks like a berry; dilations of an intracranial artery
-most occur at anterior part of circle of willis especially at arterial bifurcations
-most remain assymptomatic throughout life
-often multiple
-associated with polycystic kidney disease and coarctation of the aorta
Subarachnoid Hemmorrhage signs and sx
-sudden onset of a very severe HA
-signs of meningeal irriation (meningismus)
-"the worst HA I ever had" along with a stiff neck
-must R/O meningitis
Obstrcutive Hydrocephalus
-complication from subarachnoid hemorrhage
-d/t CSF ouflow obstruction from the blood
-usually occurs ~2+ weeks after subarachnoid hemorrhage
Subarachnoid prognosis
-may progress to coma and death
-extremely poor prognosis when hemorrhage into cerebral ventricles
Work up: to determine the site and extent of brain injury
1. CT scan
2. MRI scan
Stroke: CT Scan
-best for acute hemorrhage stroke
-appears white on CT-brain window
-misses acute infarct (appears dark on CT-brain window)
Stroke: MRI Scan
-best for acute infarct (appears dark on T1, white on T2)
-may miss acute hemorrhage (appears white on T1, whiter on T2)
Work up: Routine Studies for Stroke Patient
-CBC (R/O infection, check RBC counts)
-chemistry panel
-lipid panel (check cholesteral, see if they are set-up for stroke)
-sed rate (R/O vasculitis, other autoimmune dz)
-CXR (chest xray for heart size)
-PT/PTT (check clotting time)
Work up: Determine the source of embolism
1. ECG
2. Duplex (Ultrasound) Scan of Carotid Arteries
3. Echocardiogram (transesophageal echo is the most sensitive)
4. MR Angiography (MRA) or CT-Angiography (CTA)
5. Cerebral Arteriogram
-look for atrial fibrilation (causes stasis of blood in atria with clot formation)
Duplex Ultrasound Scan of Carotid Arteries
-look for thrombus and plaque
-look for mural (wall) thrombus in heart, valve vegetation, atrial myxoma
MR-Angiography (MRA) or CT-Angiography (CTA)
-be sure to order both an intra-cerebral and extra-cerebral scan
-no contrast dye required for MR-Angiography
Cerebral Arteriogram
-used to confirm MRA & Duplex findings
-gold standard for imaging the cerebral cirulation, but carries risks
-contrast dye is injeced into cranial arteries via a catheter introduced in the groin
-surgeons ususally require before doing surgery
Selective arteriogram
-only certain intrcranial arteries are injected with contrast
Complete arteriogram
-both vertebrals and both carotids are injected with contrast
If vasculitis is suspected...
-erythrocyte sedimentation rate (ESR, Sed, Rate)
-anti-nuclear antibody (ANA)
-Lupus Analyzer Profile
-Cerebral agiogram demonstrates arteries that look like "linked sausages"
If hypercoagulability is suspected...
-Lupus anticoagulant
-cardiolipin antibody
-leyden factor V (in young female athletes)
Treatment of Acute Stoke of the Infart Type
1. Intravenous thombolytic Therapy
2. Anticoagulant Therapy for Ischemic Stroke
3. manage increased intracranial pressure, if indicated
4. Supportive Care
5. Post Stroke rehab
6. Surgical Treatment
Intravenous Thrombolytic Therapy for Ischemic strokes
-"clot busters"
-thomboltyics dissolve existing clots
-tPA is only thrombolytic currently approved for use in infarct stroke
-not particularly effective for stroke
-significant side effects
Admin of Thrombolytics
-admin within 3 hours of stroke onset (after that, clot is mature and cells beyond clot that have not been getting any blood are dead by now)
-admin via catheter directly into area of clot
Risks of Thombolytics
-10% risk of intracranial hemorrhage (and half of these are lethal)
(bc it decreases clotting ability so increases bleeding - pts essentially get 2 strokes: 1st is the ischemic stroke they presented with and 2nd is a hemorrhagic stroke from the new bleed d/t drugs)

-no benefit is noted if given 24 hrs after onset
Anticoagulant Therapy for ischemic Strokes
-IV heparin or PO warfarin (Coumadin)
-cannot be used until hemorragic stroke is R/O by CT
-may help to limit or halt spread of a thrombotic stroke, but are of NO help for completed strokes (except if there is ongoing source of emboli), ie they prevent clot from getting worse but don't really dissolve the clot
Risks of Anticoagulant therapy
-sometimes an infart stroke is converted into a hemorrhagic stroke d/t use of these agents
Onset of Anticoagularnt therapy
-IV herparin: immediately
-Coumadin: couple of days to work; involves subatances in the clotting cascade so it doesn't work until stores of these chemicals are used up by the body
Carotid Artery Surgical Tx
->65% stenosis or <2mm residual vessel lumen indicated surgery ("critical" stenosis)
-Ulcerated or hemorrhagic plaque with <65% stenosis indicates surgery
when vessel is blocked >65%
Not amenable to surgical treatment:
-vertebral arteries and basilar artery are not accessable, except by means of special instrumentation
-lacunar (small vessel disease) infarcts deep in brain
-embolic type strokes
Surgical Prophylaxis
-carotid endarterectomy (removing occlusive artherosclerotic plaque)
Surgical prophlaxis vs medical propphylaxis
-recent studies show surigcal is superior to medical
- but surgical is higher cost
Stoke Prophylaxis
-anti-platelet agents
-cholesteral-lowering agents
Antiplatelet agents
-Dipyridamole (persantine)
-Ticlopidine (Ticlid)
-Clopidogrel (Plavix)
Acetosalycilic Acid (ASA)
-cyclooxygenase inhibitor that inhibits platelet aggregation by preventing formation of thomboxane A2
ASA uses
-low dose ASA works well for CV disease prevention
-does NOT work as well for stroke prevention
-shown to prevent strokes in males
Unbuffered vs Buffered
Unbuffered: Bayer

Buffered: Ascriptin, Bufferin
Dipyridamole (Persantine)
-cyclooxygenase inhibits that inhibits platelet aggregation by inhibiting the uptake of adensoine and as a weak phosphodiesterase inhibitor
-extended release capsule that is a combination of Dipyridamole and Aspirin
-twice as effective as ASA alone
-BUT more expensive!
Ticlopidine (Ticlid)
-30% more effective than ASA
-but more expensive
-can cause neutropenia and thrombocytopenia so must monitor WBC count
-use for pts who can't tolerate other meds
-250 mg PO bid c food
Clopidogrel (Plavix)
-50% better than ASA without SE of ASA
-safer than Ticlopidine & same cost
-use for pts who are allergic to, or can't tolerate ASA
-75 mg qd
Other Pharm agents for Stroke
-ACE inhibitors
-angiotensin II antagonists

both lower BP
-heparin sodium
-warfarin sodium (coumadin)
Heparin Sodium
-IV form only, initiated in hospital
-monitored by Activated partial thromboplastin test (aPTT) which measures certain part of coagulation cascade
If aPTT is high..
give less heparin sodium
Warfarin Sodium (Coumadin)
-takes several days to work
-monitored by pro time (PT) or International Normalization Ratio (INR)
-wait 24 hrs before starting heparin
Recommendation for INR control
INR at 2.5X control
Normal protocol for anti-coag drugs
start IV heparin and warfarin at the same time, then discontinue heparin after the warfarin reached therapeutic levels
Warfarin is absolutely indicated for:
-pts with cardiac source of embolization (atrial fib, mural thrombus)

Coumadin rx reduced A-fib associated stroke risk from 4.5%/year to 1.4%/year
Warfarin is relatively indicated for:
-pts c positive hypercoagulability tests
-if TIAs continue on platelet inhibitor therapy
Deciding between Anti-platelet and anti-coagulant therapy
-For TIAs, start with anti-platelet agent
-If TIAs persist while on antiplatelet agent, use anticoagulant
-for cardiac thromboemboli, use anticoagulant
-for abnormal protein C, protein S, etc, use anticoagulant
Cholesteral-lowering agents
-shown to cause regression of atherosclerotic plaques
-if >70 yo, it is too late to expect them to work
How to Manage pts who can't/won't have surgery
-if ASA doesn't control sx, try clopidogrel or ticlopidine
-if that doesn't work, try ASA + clopidogrel
-if that doesn't control sx, try warfarin alone
-if that doesn't control sx, try warfarin + ASA (RISKY!! can cause death from bleeding ulcers)
2 pairs of blood vessesl that supply the brain
-internal carotid arteries
-vertebral arteries (join to form basilar artery)
Clinical feature with occlusion of Anterior cerebral artery
-Contralateral leg weakness
Clinical feature with occlusion of middle cerebral artery
-contralateral face and arm > leg weakness
-sensory loss
-visual field deficit
Clinical feature with occlusion of posterior cerebral artery
-contralateral visual field deficit
Clinical feature with occlusion of basilar artery
-oculomotor deficits and/or ataxia with opposite side motor and sensory deficits
Clinical feature with occlusion of vertebral artery
-lower CN deficits and/or ataxia with opposite side sensory deficits
Clinical feature with occlusion of penetrators
-contralateral motor or sensory deficit without cortical signs
Cortical signs include:
-other cognitive abnormalities
-unsteady and clumsy motion of the limbs and trunk d/t failure of the gross coordination of muscle movements
-loss or impairment of the ability to produce and/or comprehend language
-loss of the ability to execute or carry out learned movements depsite having the desire, and physical ability to perform the movements
AVM pathophysiology
-shunt bwn arterial and venous system typically as a tangle of abnormal vessels
-vessels that tangle are typically very thin compared to intercranial vessels
AVM most frequent location
posterior half of the hemispheres
AVM presentation
-intercranial hemorrhage
-bruits over eye or mastoid processes may be heard in pts with intercerebral AVMs
-MRI better than CT
-except CT may show calcifications or bleeds if any are present
AVM tx
-surgical treatment if symptomatic (clip off AVM)
-stereotactic radiation treatment
AVM prognosis
-15% moratility rate if lesions bleeds
-small lesions bleed more often
Cavernous Angioma
-similar to AVM but usually not connecting high pressure arteries to low pressure veins (ususally connecting high pressure to high pressure or low pressure to low pressure)
-may or may not be hereditary
-low bleed risk
-seizure risk depending on location
Cavernous Angioma pathophysiology
-capillary grouping that forms deep within the white matter and brainstem with no intervening neural structures
-typically <1 cm in diameter and often associated with a venous anomaly
-may form large pool of blood (like one vessel that grows really large)
cavernous angioma tx
Chiari Malformation/Syrinx: Etiology
-cerebellar tonsils protrude though foramen magnum and into cervical spinal canal
Chiari Malformation/Syrinx: Pathophysiology
-d/t blockage created by the tonsils, CSF flow is interupted or occluded resulting in the formation of syringomyelia (or syrinx cavities)
Chiari Malformation/Syrinx: presentation
-present like central cord syndrome (from high cervical pressure)
-cough HA, neck/arm/facial pain
Chiari Malformation/Syrinx Dx
MRI (white line in middle of spinal cord from fluid/CSF being pushed further and further down into spinal cord)
Chiari Malformation/Syrinx Tx
-conservative tx is usually unsuccessful
-surgical decompression of the posterior fossa is typically necessary
-shunt if recurrent syrinx (through neck, through chest cavity, into abdominal cavity)

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