Stroke (Week 4--Ali) Flashcards
Definition of stroke
Permanent injury to brain or spinal cord of vascular origin (either reduced blood flow or bleedint into or around the brain or spinal cord)
1) Cerebral infarction
2) Intracerebral hemorrhage
3) Subarachnoid hemorrhage
Transient ischemic attack
Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction
Note: this tissue-based definition recently replaced prior, time-based (24 hour) definition
After TIA, 10x risk of ischemic stroke (risk highest in first 48 hours following TIA; 35% stroke risk within 3-5 years after TIA)
Facts about stroke
Leading cause of adult disability in US
3rd leading cause of death in US
>5 million stroke survivors and 90% have deficit
Pathogenesis of cerebrovascular disease
Ischemic stroke (83%): atherothrombotic (30%), cardioembolic (30%), lacunar (25%), other (10%), cryptogenic (5%)
Hemorrhagic stroke (17%): intracerebral hemorrhage (70%), SAH (30%)
Stroke risk factors
Nonmodifiable: age, gender, race, heredity
Medical conditions: HTN, cardiac disease, a-fib, hyperlipidemia, DM, carotid stenosis, prior TIA or stroke
Behaviors: cigarette smoking, heavy alcohol use, physical inactivity
Pathogenesis of brain infarction
1) Sudden interruption of cerebral blood supply
2) Alteration of brain metabolism (after 30 sec)
3) Cessation of neuronal function (after 1 min)
4) Formation of infarct (5 min - 10 hours)
5) Tissue necrosis and softening (days)
6) Replacement by fluid and gliosis (weeks - months)
Ischemic penumbra
Area outside core infarct
Zone of salvageable tissue surrounding core infarct
Anterior cerebral artery (ACA) syndrome
Contralateral leg weakness
Contralateral leg sensory loss
Bladder incontinence
Middle cerebral artery (MCA) syndromes
Superior division: contralateral face and arm > leg weakness; contralateral face and arm > leg sensory loss; broca/nonfluent aphasia (left hemisphere); contralateral neglect (right hemisphere)
Inferior division: contralateral hemianopia, superior quadrantanopic; Wernicke/fluent aphasia (left hemisphere); contralateral neglect (right hemisphere)
Posterior cerebral artery (PCA) syndrome
Contralateral hemanopia, quadrantanopia
Alexia (can’t read) without agraphia (left hemisphere)
Visual agnosias with bilateral PCA infarcts (visual object agnosia, prosopagnosia, simultagnosia, cortical blindness)
Vertebrobasilar syndromes
Ataxia, vertigo, diplopia, dysarthria, dysphagia, bilateral weakness, bilateral sensory loss, crossed cranial and body signs
Lacunar syndromes
Pure motor hemiparesis: isolated face, arm, leg weakness
Pure sensory stroke: isolated face, arm, leg sensory loss
Ataxic hemiparesis: homolateral ataxia and hemiparesis
Dysarthria clumsy hand syndrome
Large artery atherothromboembolic stroke
Risk factors: age, HTN, DM, tobacco, hyperlipidemia, hx CAD, PAD
Clinical features: progressive deficits (frequently stepwise) in 50%, onset while asleep in 30-40%, preceeding TIAs in 40%
Cardioembolic stroke
Risk factors: a-fib, sick sinus syndrome, rheumatic valvular disease, prosthetic cardiac valve, dilated cardiomyopathy
Clinical features: maximal deficits at onset in 80-90%, usually not onset while asleep, usually no preceding TIAs
Sources of cardiogenic embolism
45% nonvalvular a-fib
15% acute MI
10% ventricular aneurysm
10% rheumatic heart disease
10% prosthetic cardiac valves
10% other
Small vessel (lacunar) stroke
Risk factors: arteriosclerosis and atherosclerosis, age, HTN
Clinical features: progressive deficits in 45%, onset while asleep in 40-50%, preceding TIAs fairly common 20%
Small vessel symdromes cortical signs rare
Diagnosis: clinical, CT/MRI confirmation
Mortality low, 1%
Rate of recurrence 12% annual
Intracerebral hemorrhage
Smoothly progressive deficits over 10-20 minutes
Onset while asleep uncommon 15%
Focal symptoms
Symptoms of raised intracranial pressure (headache, nausea/vomiting, decreased level of consciousness)
Subarachnoid hemorrhage
Thunderclap headache
Usually no onset while asleep
Symptoms of raised intracranial pressure (headache, nausea/vomiting, decreased level of consciousness)
Focal symptoms uncommon
Diagnosis: CT, LP mandatory with clinical suspicion and normal CT (elevated CSF pressure and protein, large # RBCs, SAH has xanthochromic centrifuged supernatant and trauma doesn’t), angiography gold standard (if neg repeat in 2 weeks)
Clinical grading of aneurysmal SAH
Grade I: normal LOC, no clinical features, yes surgical candidate
Grade II: normal LOC, HA/stiff neck, yes surgical candidate
Grade III: confused/drowsy, focal neuro deficits, yes surgical candidate
Grade IV: stupor, focal neuro deficits, not surgical candidate
Grade V: coma, decerebrate posturing, not surgical candidate
Outcome after SAH
32% mortality from aneurysmal SAH (most in first few days)
Neurologic condition at arrival at hospital is most important determinant of outcome
Permanent disability (cognitive usually) in 50% of survivors
Better prognosis with ruptured AVMs compared to aneurysmal rupture (recovery in almost 90%)
