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Outline
Clinical Presentation
Anterior Circulation Posterior Circulation
Stroke Mechanism
Heart Vessel Blood
Treatment T t t
Acute Management Long Term Prevention
Ischemic Stroke
Acute onset of neurologic deficits caused by impaired blood flow to the central y nervous system. 3rd leading cause of death leading cause of adult disability
30% impaired ADLs 20% impaired ambulation 16% require institutional care
Stroke
persisting neurologic deficit after 24hrs f f infarct on CT or MRI
TIA
most TIAs last 5-20 minutes 5 if >1hr usually small infarction on MRI
TIA Syndromes
Amaurosis fugax
sudden onset painless vision l dd t i l i i loss, curtain over one eye, b i f 1-5 i t i brief 1-5min ophthalmic artery emboli
Subclavian steal
gives B/S ischemia, worse with arm exercise
Crescendo TIAs
cerebral ischemia increasing in frequency, severity and duration Capsular warning syndrome: repeated weakness face arm leg face, arm,
DDx TIA
Migraine, Seizure, Syncope Tumor, Subdural, SAH Hypoglycemia Labyrinthine dz TIA rarely march across body
suggests Sz, migraine Sz involuntary movements more Sz fortification/scintillating light more migraine
Approach to TIA
Rule out other causes of transient events Imaging of Carotid arteries
Carotid U/S, MRA neck, CT angio neck Urgent for high risk patients Carotid endarterectomy early for stenosis >70%
Start ASA Control Vascular risk factors Follow up stroke prevention clinic if not admitted
Stroke Syndromes
Anterior Circulation
MCA ACA
MCA Strokes
most common ischemic stroke arm + face > leg weakness and sensory loss can see aphasia neglect homonymous aphasia, neglect, hemianopia
MCA Strokes
Proximal MCA
contralateral hemiplegia, conjugate eye deviation, hemisanesthesia, homonymous hemianopsia, aphasia or neglect
Upper MCA
f face + arm affected more than leg, Brocas aphasia ff t d th l B h i
Lower MCA
leg> face + arm, Wernicke aphasia or behavioural disturbance (non dominant hemisphere), homonymous hemianopia hemisphere)
Angular gyrus
Gerstmanns syndrome: fi G t d finger agnosia, acalculia, R-L di i t ti i l li R- disorientation, agraphia
Right parietal
anosognosia, neglect apraxia impaired prosody confusion/delirium anosognosia neglect, apraxia, prosody,
ACA Strokes
less common 3% weakness LE >UE abulia, akinetic mutism, emotional di b li ki i i i l disturbance b transcortical motor aphasia head deviation toward lesion Paratonia Ant choroidal a. syndrome ant limb int capsule
hemiparesis, hemisensory loss, hemianopia
Lacunar Strokes
Infarct from small penetrating arteries p g 20 syndromes, 5 most common y ,
1. Pure motor weakness face, arm and leg 2. Pure sensory paresthesias & numbness, face, arm and leg 3. Sensory-Motor weakness and sensory loss Sensoryp 4. Ataxia hemiparesis -weakness LE, incoordination ipsilateral arm and leg 5. Dysarthria-Clumsy hand syndrome Dysarthria-dysarthria dysphagia dec fine motor hand dysarthria, dysphagia,
Cerebellar Strokes
Present with vertigo, nystagmus, gait ataxia, truncal g , y g ,g , ataxia, dysmetria, dysarthria Often associated with Brainstem Strokes
See cranial nerve involvement and Horners syndrome
If infarct large can cause decreased LOC, hydrocephalus, herniation and death need close observation should consult neurosurgery
Brainstem Strokes
Suspect based on involvement of cranial nerves, cerebellum, altered LOC, crossed motor and crossed , , sensory findings Midbrain
CN III ipsilateral paresis, dil t d pupil i il t l i dilated il
Pons
-CN V facial numbness weakness jaw movements numbness, -CN VI lateral rectus palsy -CN VII facial weakness
Medulla
CN VIII vertigo, hearing loss -CN IX, X dysphagia -CN XII tongue weakness
Brainstem Syndromes
Locked in Syndrome y
bilateral ventral pons lesion quadriplegia, aphonia, impairment horizontal eye movements can move eyes vertically, can blink normal wake/sleep cyles
Sensory Changes
paresthesias, altered position, pain, temperature sensation
Language
anomic or transcortical sensory aphasia alexia without agraphia difficulty naming colors, objects, photographs, but can name letters, letters, numbers can get amnesia agitated delirium amnesia,
ParietalParietal-Occipital Syndromes
Antons syndrome Anton s cortical blindness with denial of blindness Balints syndrome optic ataxia psychic paralysis of fixation (cant ataxia, (can t look to peripheral field), disturbance of visual atte t o , s u tago os a attention, simultagonosia
Thalamic Strokes
aphasia, akinetic mutism DejerineDejerine-Roussy syndrome (thalamic pain pain, sensory loss) visual field defects (quadrantanopia, secto a op a) sectoranopia)
Watershed Infarcts
Hypoperfusion of CNS
post CABG, cardiac arrest, respiratory hypoxia, bilateral carotid stenosis
PICA-AICA-SCA PICA-AICA-
Exam Tips
Cortical infarcts are suspect based on the presence of
visual field impairment language impairment neglect or anosognosia graphethesia or stereoagnosia
Tone decreased on side of weakness early on, later on increased Reflexes h R fl hypereflexic on side of weakness, with up-going t fl i id f k ith up- i toe look for a Horners syndrome: ptosis, miosis listen for heart murmur take pulse for atrial fibrillation
Mechanism Stroke
Vessel
Carotid U/S, MRA, CTA, Angio
Heart
EKG, Holter, EKG Holter Echo
Blood
INR, PTT, Platelets
Vessel
Atherosclerotic
Large vessel Lacunar
Vessel: Atherosclerosis
Common in patients with vascular risk factors
Age, HTN, DM, S k H A HTN DM Smoker, Hyperlipidemia, CAD St k ABI <0.9 li id i CAD, Stroke, 09
ArteryArtery-artery embolism
-fatty streak fibrous plaque thrombosis plaque hmg / necrosis /calcification
-stenosis 50-69% may benefit from CEA if have vascular risk factors 50- % y
-male, smoker, diabetes, HTN, CAD, hemispheric stroke, ulcerative stenosis, contralateral carotid occlusion
Vessel: Lacunar
microvascular disease caused by long standing HTN, DM, smoking involves putamen, pons, thalamus, post limb internal capsule caudate nucleus capsule, associated with cognitive impairment g p CT leukoariosis
Rx: Heparin / Warfarin 3-6mts 3 avoid anticoagulation in intracranial dissections risk SAH
Homocystinuria
inc homocysteine causes endothelial damage
Cardioembolic Stroke
1515-20% of ischemic strokes suspect if infarct is l i f i large, multiple, bil l i l bilateral wedge shaped i f l d h d infarcts with hmg component Risk of Emboli High risk:
Muscle: AMI, Cardiomyopathy Valve: rheumatic mitral stenosis, mechanical valves, infective endocarditis Other: cardiac tumors (atrial myxoma, rhabdomyoma), A-fib Oth di t ( ti l h bd ) A-
Mod risk:
Muscle: remote MI, LV aneurysm, hypertrophic cardiomyopathy Valve: MVP, mitral or aortic valve calcification, valvular strands, Other: PFO, ASA, A-flutter, Chiari network A-
Low risk:
Congenital heart disease, Anemia
Cardioembolic Stroke
Atrial Fibrillation
5-6 fold higher stroke risk Risk of stroke based on CHAD2
CHF, HTN, Age >65, Diabetes 2 , previous stroke/TIA Presence of each factor increases risk of stroke in A-fib Ahigh risk group 5-7% strokes per year 5-
Cardioembolic Stroke
Patent Foramen Ovale
present in 25% of patients right to left shunt risk emboli high if larger or present with atrial septal aneurysm Invx: Bubble study or TEE Rx -no difference b/w ASA vs warfarin -transcather or surgical closure
Cardioembolic Stroke
AMIAMI -stroke occurs in 1% of AMI
85% of strokes occur in 1st wk, all by 3 months high risk: anterior wall MI, decreased ejection fraction
Cardiomyopathy C di th
dilated or congestive 2 HTN, inflammatory, infection, metabolic CHF uncommon to have embolism
Valvular
Mitral Stenosis -emboli in 9-14% 9SEM: inc t k i k Age>50 SEM i stroke risk if A 50 Infective Endocarditis vegetations by TTE Non-bacterial thrombotic endocarditis -emboli in 50% Non-
Blood Hypercoagulable
Primary y
Arterial:
Antiphospholipid Ab Syndrome Hyperhomocystenemia
Venous:
Activated Prot C resistance Factor V Leiden, Prothrombin G20210A mutation Leiden, Prothrombin Antithrombin III Deficiency Protein Protein C or S deficiency Abnormal Fibrinogen or Plasminogen
Blood Hypercoagulable
Secondary y
Malignancy Hormonal
P Pregnancy BCP -avoid in females with HTN, age>35, smokers Ovarian Hyperstimulation Syndrome
Stroke Treatment
Acute Stroke Management
Reperfusion, Neuroprotection Supportive care: BP, Glucose, Feeding
2. Neuroprotection
no approved neuroprotective agent, 120 trials prevent hyperglycemia, hypoxia, hypoperfusion, hyperthermia
Exclusion criteria:
rapidly improving deficits, Sz at onset of event prior ICH Hx suggests of SAH, stroke past 3mts ICH, suggests SAH, GI or GU hmg in past 3wks, recent MI, major surgery 14d MI, arterial puncture noncompressible site past 7d Labs: glucose <2.7mM or >22.2mM, platelet <100 000, >22.2mM, 000, INR >1.7, PT >15 SBP >186 or DBP >110, Hg<100?
Reperfusion IV TPA
Risk of intracerebral hmg 6.4% g % Absolute benefit 11-13% 1130% chance mild neurologic deficit at 3 mts g mts Good response
treatment in 90min, normal CT, mild-mod stroke severity, mildno DM, normal glucose, normal BP glucose,
Poor response
large area hypo-attenuation with mass effect, advanced age, hypoDM, DM inc BP before/during/after treatment severe deficits treatment, deficits, protocol violations
CVS
MI in 3% BP: dont decrease by >10%
Resp
aspiration occurs in 25%, swallowing assement 25%, PE / DVT Heparin sc or pneumatic compression
GI
hyperglycemia worsens stroke
Diabetes
no evidence that tighter glycemic control reduces stroke risk, but thi is recommende b t this i recommende d
Lipid
high LDL, low HDL associated with inc stroke risk statins reduce strokes 20-28% 20-
Smoking
inc RR stroke 2-3fold 2-
Antiplatelets
Primary Prevention -no role in low risk, middle y , age population Secondary prevention -start all patients with stroke or TIA on ASA -if have stroke on ASA, reasonable to change t A h to Aggrenox or Cl id Clopidogrel l -no benefit to ASA + Clopidogrel in longterm prevention, increase hemorrhage risk (MATCH) prevention ASA -irreversible inhibition of cyclo-oxygenase cyclo-reduced risk stroke, MI, vascular death by 25%