neurology: stroke
DESCRIPTION
Neurology: STROKE. superKAT :). Stroke. Condition characterized by rapidly developing signs and symptoms of a focal brain legion with symptoms lasting for more than 24 hours or leading to death no apparent reason - PowerPoint PPT PresentationTRANSCRIPT
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Neurology: STROKE
superKAT :)
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Stroke
• Condition characterized by rapidly developing signs and symptoms of a focal brain legion with symptoms lasting for more than 24 hours or leading to death no apparent reason
• Sudden neurologic syndrome, cerebrovascular disease – pathologic process of blood vessels– Occlusion of lumen by embolus/thrombus– Dissection – Permeability of blood vessel wall
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Primary disorder
• Atherosclerosis• Hypertensive
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Epidemiology
• 2nd most common cause of death around the world, next to heart disease
• Out of 2 million, 2% will have a stroke• If you will have stroke, 30% will die, 30%
permanently disabled, 30% recover• 10,000/1 mil (Philippines) = 1%• Cerebrovascular disease (stroke) = highest
percentage of disability computed in life years
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Morbidity and mortality
• 700,000 strokes per year in US• 22% men and 25% of women, higher among
65 years old• 1st leading cause of long-term disability• 2.7 million related stroke death in Asia,
leading cause of death in China– Intracranial atherosclerosis, common in Asians
31%
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Risk factors (non-modifiable)
• Age: Elderly• Gender : Males more susceptible• Genetic predisposition• Race/ethnicity: Non white groups have greater
disk• Prior stroke or MI: Higher risk• Existing heart disease: increase risk for stroke
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Modifiable• Lifestyle
– Smoking– Low physical exercise– Obesity– Alcohol consumption– Dietary restrictions
• Pharmacotherapy– Hypertension– Arterial disease– Heart disease– Thrombotic phenomenon or embolic – Diabetes mellitus
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Diagnosis
• Clinical• Based on history• Characteristic signs
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Subtypes
• Ischemic– Thrombotic– Embolic– Hyperfusion
• Hemorrhagic – Intracranial haemorrhage – Subarachnoid hemorrhagic
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Mechanism
• Borderzone – 5%• Lacunar – 20%• Cryptogenic/rare cases – 20%• Artery to artery – 20%• Aortic arch -20%
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Stroke sub classifications according to clinical presentation
• TACI – total anterior circulation infarct– Higher dysfunction– Homonymous hemianopsia– Motor/sensory deficit • 2/3 face arm/arm/leg
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PACI – partial anterior circulation (1/3 to ¼ of the brain)
• 2 of 3 of TACI• Higher dysfunction alone• Limited motor/sensory deficit
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LACI - lacunar anterior circulation infarct
• Pure motor stroke (2/3 parts)• Pure sensory• Sensorimotor• Ataxic hemiparesis– New dysphagis– New visuosptial problem– Proprioceptie sensory loss only– Vertebrobasilar features
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POCI – posterior
• Crossed motor sensory deficit• Bilateral motor or sensory deficit• Conjugate eye movements problems• Cerebellar dysfunction• Isolated homonymous hemianopsia
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The brain
15% of cardiac output20% of all O225% of all glucose 2-3% body weight
*50ml/100gms/min*500mlof O2/min*75-100ml of glucose/min
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• Oligemia – diminished blood flow(increased O2 extraction
• Mild ischemia – increase in glycolysis, below 20cc – threshold for electrical failure
• 10-20 cc per 100 grams per brain tissue per min = PENUMBRA – moderate ischemia
• Severe ischemia – anoxic depolarization
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If perfusion of the cerebrum is suspended or critically reduced there are limited capacities for compensation and minimal energy reserves
*auto regulation
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Vascular anatomy
• Anterior circulation – from carotid system (80% supply of brain)
• Posterior circulation – from vertebral system (20% supply of brain)
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Atherosclerosis and Thrombus foundation
• Main pathology that can bring about stroke • Site of endothelial injury• Thrombus formation = ischemia• Formation of a plaque (atherosclerotic)• Atherosclerotic develops in time
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Thrombus formation and embolism
• Leads to infract in brain• Thrombus = impedes laminar flow of blood,
time characteristic• Embolism = small piece of clot, thrown off that
can block, smaller than thrombus
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Extant and size of ischemia
• Rate of occlusion – paulit-ulit ba?• Adequacy of collateral circulation • Resistance of brain structures to ischemia –
dependent on function of cerebral autoregulation (ability of the blood vessel to respond, elasticity of blood vessels)
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Sites of atherosclerosis
• Common area where it forms the junction • Junction between MCA and ACA• Mas malakas ang laminar flow sa junctions =
increased pressure
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Types of stroke
• Ischemic stroke (infarct)• Hemorrhagic stroke = intracerebral
haemorrhages, compression, herniation and shifting of structure
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Ischemic stroke
• 85% of stroke• Thrombotic or embolic• One month mortality: 15%
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Middle cerebral artery
• Most common intracranially involved in ischemic stroke
• Supply almost all parts of the convex surface of brain
• Supply deep tissue: basal ganglia, putamen, parts of globus pallidus...
• Usually hypodense lesion – left MCA stroke• Contralateral paresis – pyramidal decussation,
unilateral lesion
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Left hemisphere = dominant
• Right motor deficits– Face– Upper and lower extremitiesRight sensory loss
All modalitiesDecreased stereognosisAgraphesthesia
Language deficitsRight homonymous hemianopsiaAgraphia, acalculia, apraxia of left limbs
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Right hemisphere
• Left hemiparesis• Left weakness of upper and lower extremities• Left hemineglect• Asomatognosia• Flat affect• Loss of prosody of speech
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Anterior cerebral artery
• Supply medial and basal aspects of cerebral hemisphere
• Extends to anterior two thirds• Caudate nucleus, parts if internal capsule,
putamen and hypothalamus
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ACA stroke
• Weakness of leg• +/- proximal muscle weakness in upper ex• Affect frontal lobe: impaired judgement and
insight, change in affect• Presence of primitive grasp and suck reflex
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Vertebrobasilar system
• Supplies:– Brainstem– Cerebellum– Thalamus– Visual occipital cortex
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Vertebrobasilar
• Level of consciousness– Ranges from alert to coma– No cognitive impairments– Confusion or agitation uncommon
• Motor impairments– Contralateral paresis of upper and lower ex– Quadriparesis – buong basilar artery involved– Crossed paresis– Dysarthria, hoarseness, dysphagia, ipisilateral ataxia, gait
or truncal instability (cerebellar vermis involvement)
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• Sensory impairments• Abnormalities of extraocular movement• Vertigo, nasuea, vomitting• Horner’s syndrome
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Hemorrhagic stroke
• 15% of all total strokes• Intracerebaral > subarachnoid haemorrhage• Occur during stress or exertion• Focal deficits rapidly evolve• Confusion, coma, immediate death
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Intracerebral• Classic: sudden onset• Vomiting, elevated BP• Focal neurologic deficits that progress over minutes• Larger the deficits, the poorer the prognosis will be• Hypertensive damage to small penetrating vessels and has the
same vascular distribution as lipophyalinosis• Charcot and Bouchard – mcircoaneurysm which ruptured,
causing ICH• Other causes: trauma, ruptured aneurysm, AV malformation,
anticoagulant intake, thrombolytic agents, cerebrovascular amyloidosis, bleeding disorders (leukemia)
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ICH
• Most common site: putamen and adjacebt structures
• Rupture of small penetrating branches of thalamus, pons, cerbellum
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Subarachnoid hemorrhage
• Rupture of an aneurysm (usually located in the circle of Willis)
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Subarachnoid hemorrhage• Headache– Severe– Sudden or cataclysmic onset– Described as worst headache of life
• Transient loss of consciousness, seizure, syncope, prolonged unresponsiveness, confusion, agitation
• Nausea and vomitting• Photophobia and phonophobia• Hypertension and abnormal vital signs• Nuchal rigidity• Retinal haemorrhage
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• May be secondary to ruptured aneurysm or arteriovenous malformation
• 3 major risks affect subsequent events– Rebleeding– Vasoconstriction (delayed ischemic deficit)– Hydrocephalus (blood impedes normal flow)
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Management goals
• Goals immediate diagnosis and evaluation:– Determine symptoms due to stroke– Advisability for acute treatment with thrombolytic
therapy
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Management goals
• History of physical examination– Note vital signs– Cardiac examination– Check for Carotid bruit
• Validated scoring systems e.g. NIHSS to determine stroke severity
• Immediate diagnostic studies– Cranial CT scan– ECG– Bloof glucose level– Serum electrolyte– Renal function test– CBC including platelet count
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General supportive care
• ABC – airway, breathing, circulation• Control of fever• Cardiac rhythm• Hypoglycemia/hyperglycemia
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General supportive care
• Hypertension– No clinically proven benefit for lowwering BP
among patients with acute ischemic stroke– Antihypertensive agents should be withheld
unless• DBP>120 or SBP>220• Hypertensive encephalopathy• Aortic dissection• Acute renal failure• Acute pulmonary edema• Acute myocardial infarction
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Neuroimaging
• Non-contrast enhanced CT scan of the brain– Early signs of infarction• Hyperdense MCA sign• Loss of gray-white differentiation in the cortical ribbon
(particularly the lateral margins of the insula) or the lentiform nuclues • Sulcal effacement
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Neuroimaging
• Multimodal MRI– DWI (diffusion weighted image)• Perfusion-diffusion mismatch (PWI: Perfusion weighted
image)– Potential difficulty in reliably identifying acute
intracranial hemorrhage - GRE
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Interventions
• Primary prevention• Acute phase • Secondary prevention
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Treatment options – Acute phase
• Stroke units• Thrombolysis• Neuroprotection• Aspirin and heparin• Surgery and intra-cerebral hemorrhage• Early secondary prevention
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• Risk factor • Neuroprotectants• Thrombolytics• Stroke unit Stroke Event • Hematoma evacuation 3 hours • Revascularization Hospital • Recanalization
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Treatment options – Secondary prevention
• Antiplatelet (thrombotic) and anticoagulant (embolic) therapy
• Antihypertensive treatment post stroke• Statin therapy• Carotid artery disease
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Intervention Outcome OR (95% C.I) NNTNumber needed to
treat
Stroke unit
Death
Death or institutionalization
0.81 (0.68-0.96)
0.75 (0.65-0.87)
21
14
Death or dependency 0.71 (0.60 -0.84) 15
ASA
Thrombolysis
Death or dependency
Early death (2w)
Early ICH (2w)
Death
0.95 (0.91-0.99)
1.99 (1.56-2.55)
3.6 (2.7-4.8)
1.36 (1.1-1.6)
83
-
-
-Death dependency 0.75 (0.6-0.9) 15
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Storokeunit team
1. Medical doctor2. Pyshiotherapist3. Nurses4. OT5. Social worker6. Speech pathologist7. Home care case manager8. Nutritionist
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Thrombolysis
• IV Intrevnous rtPA– The only FDA approved therapy for treatment of
patients with acute ischemic stroke• IA rtPA– Experimental
• Established as a treatment in acute ischemic stroke patients within 3 hours of stroke onset
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Secondary stroke prevention
• Aspirin recommended 50 – 325 mg/day • Clopidogrel - Plavix• Ticlid – best selling• Aggrenox
NNT
33
121
40
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Neuroprotection
• No present clinical trials that demonstrated benefit for neuroprotective agents
• Citicoline• Cerebrolycine?• Magnesium sulfate
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• Clipping – gold standard for cerebral aneurysm, craniotomy • Coiling – less invasive, angiogram procedure (endovascular
treatment)– Now preferred treatment for aneurysm– 7.4% absolute risk reduction in combined death and instability
compared to clipping– Durability of coil still unknown due to lack of long term followup– Treatment choice for basillar artery aneurysm– Commonly used to treat post SAH vasospasm
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Hypertensive hemorrhage• Recombinant activated facotr VIIa (rFVIIa)• Hemostatic agent approved for hemophilia (Novo Seven)• 3 hour time window• Decreased enlargement of the hemotoma• Improve survival and favorable clinical outcomes
• Potential thrombotic complications (arterial thrombolytic events) – 7%
• FDA approval pending due to this safety issue