Internal Medicine - Cerebrovascular Diseases
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Internal Medicine - Cerebrovascular Diseases

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Internal Medicine - Cerebrovascular Diseases Internal Medicine - Cerebrovascular Diseases Presentation Transcript

  • INTERNAL MEDICINE:Cerebrovascular DiseasesnianderthalNOTES
  • INTRODUCTION-include the following most common devastating disorders: 1. Ischemic Stroke 2. Hemorrhagic Stroke 3. Cerebrovascular anomalies -Intracranial aneurysms -Arteriovenous malformations (AVMs)-most cerebrovascular diseases manifest by the abrupt onset of a focal neurologic deficit
  • STROKE-DEFINITION: abrupt onset of a neurologic deficit that is attributable to a focal vascular cause-laboratory studies and brain imaging are used to support the diagnosis-clinical manifestations are highly variable because of the complex anatomy of the brain and its vasculature
  • STROKE-OTHER TERMS:-Cerebral ischemia – caused by reduction in blood flow that lasts longer than several seconds-Cerebral infarction – if the cessation of flow lasts for more than a few minutes, death of brain tissue results-Transient ischemic attack (TIA) – when blood flow is quickly restored, brain tissue can recover fully and the patient’s symptoms are only transient-Ischemic Penumbra: tissue surrounding the core region of infarction that is ischemic but reversibly dysfunctional; imaged by using perfusion-diffusion imaging with MRI or CT
  • STROKE-a generalized reduction in cerebral blood flow due to systemic hypotension usually produces SYNCOPE-Global hypoxia-ischemia: widespread brain injury due to infarction in the border zones between the major cerebral artery distributions if low cerebral blood flow persists for a longer duration-Hypoxic-ischemic encephalopathy: the constellation of cognitive sequelae that ensues-Focal ischemia: usually caused by thrombosis of the cerebral vessels or by an emboli from a proximal arterial source or the heart-Intracranial hemorrhage: bleeding directly into or around the brain; produces symptoms by: a.) mass effect of neural structures b.) toxic effect of blood itself c.) increasing intracranial pressure
  • APPROACH TO THE PATIENT-patients with acute stroke often do not seek medical assistance on their own because: 1. they are rarely in pain 2. they may lose appreciation that something is wrong (ANOSOGNOSIA) *sudden onset of any of the following: -unilateral loss of sensory/motor function -changes in vision, gait, speech or comprehension -sudden severe headache
  • APPROACH TO THE PATIENT-Neurologic symptoms may mimic strokeSYMPTOM THAT MIMICS STROKE GUIDES TO DIAGNOSIS-Seizure -history that indicates prior convulsive activity excludes seizure-Intracranial tumor -present with acute neurologic symptoms due to hemorrhage, seizure or hydrocephalus-Migraine -sensory disturbance is often prominent, sensory/motor deficits tend to migrate slowly across limbs over minutes rather than seconds as with stroke-Metabolic encephalopathy -produce fluctuating mental status without focal neurologic finding
  • APPROACH TO THE PATIENT-Once a clinical diagnosis of stroke is made, a brain imaging study is necessary to determine if the cause of stroke is ischemia or hemorrhage-CT IMAGING of the brain is the STANDARD MODALITY to detect the presence or absence of intracranial hemorrhage-Medical management to reduce the risk of complications becomes the next priority, then plans for secondary prevention
  • OVERVIEW OF DIFFERENCESISCHEMIC STROKE HEMORRHAGIC STROKE-85% of stroke cases -15% of stroke cases-administration of -BP lowering primarilyrecombinant tissue consideredplasminogen activator (rTPA) -usually caused by aneurysmalor endovascular mechanical subarachnoid hemorrhagethrombectomy may be (SAH) and hypertensivebeneficial in restoring cerebral intracranial hemorrhageperfusion
  • ISCHEMIC STROKEPATHOPHYSIOLOGY:MAJOR MECHANISMS THAT UNDERLIE ISCHEMIC STROKE:1. Occlusion of an intracranial vessel by an embolus that arises at a distant site – often affects large intracranial vessels2. In situ thrombosis of an intracranial vessel – typically affecting the small penetrating arteries that arise from the major intracranial arteries3. Hypoperfusion caused by flow-limiting stenosis of a major extracranial or intracranial vessel
  • ISCHEMIC STROKEPATHOPHYSIOLOGY:1st: acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies -magnitude of flow reduction is a function of collateral blood flow and is dependent on: 1. individual vascular anatomy 2. site of occlusion 3. systemic blood pressure
  • ISCHEMIC STROKEPATHOPHYSIOLOGY:2nd: decrease in cerebral blood flow to zero causes death of brain tissue within 4-10 minutes -infarction within an hour: <16-18ml/100g tissue per minute -ischemia without infarction (unless prolonged for hours or days): <20ml/100g tissue per minute
  • ISCHEMIC STROKEPATHOPHYSIOLOGY:3rd: -if with restored blood flow: patient experiences TRANSIENT ISCHEMIC ATTACK -if no change in flow: infarction of ischemic penumbra *hence, saving the ischemic penumbra is the goal of REVASCULARIZATION THERAPIES
  • ISCHEMIC STROKEPATHWAYS OF FOCAL CEREBRAL INFARCTION:1. Necrotic pathway -with rapid cellular cytoskeletal breakdown due principally to energy failure of the cell2. Apoptotic pathway -cells are programmed to die
  • ISCHEMIC STROKE1. NECROTIC PATHWAY:-Ischemia produces necrosis by starving neurons of glucose and oxygen-Mitochondria then fails to produce ATP-NO ATP means cessation of membrane ion pump function causing neuronal depolarization which leads to: a. increase in intracellular Calcium b. glutamate release from pre-synaptic terminals -produces neurotoxicity*free radicals are produced by membrane lipid degradation and mitochondrial dysfunction
  • ISCHEMIC STROKE2. APOPTOTIC PATHWAY:-Lesser degrees of ischemia within the ischemic penumbra favor apoptotic cellular death causing cells to die days to weeks later*fever and hyperglycemia worsens brain injury during ischemia, both must be suppressed as much as possible
  • ISCHEMIC STROKETREATMENT OF ACUTE ISCHEMIC STROKE:-After the clinical diagnosis of stroke is made, an orderly process of evaluation and treatment should follow-FIRST GOAL: PREVENT OR REVERSE BRAIN INJURY -attend to the patient’s airway, breathing and circulation (ABCs) -treat hypoglycemia or hyperglycemia -perform a non-contrast head CT scan *differentiates ischemic and hemorrhagic stroke since NO reliable clinical finding conclusively separate the twoHEMORRHAGIC ISCHEMIA-more depressed level of consciousness -deficit is maximal at onset, or remits-higher initial blood pressure-worsening of symptoms after onset
  • ISCHEMIC STROKECATEGORIES OF TREATMENT:-designed to reverse or lessen the amount of tissue infarction and improve clinical outcome 1. Medical Support 2. IV Thrombolysis 3. Endovascular Techniques 4. Antithrombotic Treatment 5. Neuroprotection 6. Stroke Centers and Rehabilitation
  • ISCHEMIC STROKE1. MEDICAL SUPPORT-IMMEDIATE GOAL: optimize cerebral perfusion in the surrounding ischemic penumbra-attention is also directed toward preventing the common complications of bedridden patients: -infections -deep venous thrombosis (DVT)-blood pressure is lowered in: -malignant hypertension -concomitant myocardial ischemia -BP >185/110 mmHg and thrombolytic therapy is anticipated *B1-adrenergic blocker such as ESMOLOL can be a first step to decrease cardiac work and maintain BP
  • ISCHEMIC STROKE1. MEDICAL SUPPORT-Fever should be treated with antipyretics and surface cooling-Serum glucose should be monitored and kept at less than 110mg/dl using an insulin infusion if necessary-Cerebral edema is treated in 5-10% of patients with water restriction and IV mannitol to reduce serum osmolarity  watch out for HYPOVOLEMIA as this may contribute to hypotension and worsening infarction *cerebral edema causes obtundation or brain herniation *peaks on 2nd or 3rd day but can cause mass effect for 10 days
  • ISCHEMIC STROKE1. MEDICAL SUPPORTMEDICAL SUPPORT:-Hemicraniectomy: craniotomy with temporary removal of part of the skull; markedly reduces mortality-Things that should alert physician: -Cerebellar infarction may mimic labyrinthitis because of prominent vertigo and vomiting -Head or neck pain mimics cerebellar stroke from vertebral artery dissection -increasing ICP may lead to brainstem compression and cause respiratory arrest *prophylactic suboccipital decompression of large cerebral infarcts before brainstem compression
  • ISCHEMIC STROKE2. IV THROMBOLYSISrtPA:-causes an increased incidence of symptomatic intracerebral hemorrhage-treatment of IV rtPA within 3 hours of the onset of ischemic stroke improved clinical outcome *efficacy likely extended to 4.5 hours if not 6 hours-time of stroke onset: the time the patient’s symptoms began or the time the patient was last seen as normal. Patients who awaken with a stroke have the onset defined as the time they went to bed
  • ISCHEMIC STROKE2. IV THROMBOLYSISrtPA: INDICATIONS CONTRAINDICATIONS-Clinical diagnosis of STROKE -sustained BP > 185/110 mmHg despite Rx-onset of symptoms to time of drug -Platelets LESS THAN 100,000; Hematocritadministration is LESS THAN 3 HOURS LESS THAN 25%; Glucose LESS THAN 50 or GREATER THAN 400 mg/dl-CT scan show no hemorrhage or edema of Use of Heparin within 48 HOURS andGREATER THAN 1/3 of the MCA territory prolonged PTT or elevated INR ; GI bleeding preceding 21 DAYS-Age > 18 years old -rapidly improving , minor stroke symptoms-consent by patient or surrogate -prior stroke or head injury within 3 MONTHS; recent myocardial infarction -Major surgery in preceding 14 days -Coma or stupor
  • ISCHEMIC STROKE2. IV THROMBOLYSISrtPA:-administer through IV access with TWO PERIPHERAL LINES (avoid arterial or central line placement-0.9 mg/kg IV (maximum 90 mg) IV as 10% of total dose by bolus, followed by remainder of total dose over 1 hour-frequent BP monitoring-no other antithrombotic treatment in 24 hours-for decline in neurologic status or uncontrolled BP  STOP INFUSION, give CRYOPRECIPITATE and reimage brain emergently-avoid urethral catheterization for > 2 HOURS
  • ISCHEMIC STROKE3. ENDOVASCULAR TECHNIQUES-Vessels that involve a large clot volume and often fail to open with IV rtPA alone: -middle cerebral artery (MCA) -internal carotid artery -basilar artery-Endovascular mechanical thrombectomy: -adjunctive treatment of acute stroke in patients who are ineligible for, or have contraindications to thrombolytics, or those who have failed to have vascular recanalization with IV thrombolytics
  • ISCHEMIC STROKE3. ENDOVASCULAR TECHNIQUES-MERCI: novel endovascular thrombectomy device restores patency of the occluded vessel within 8 hours of ischemic stroke symptoms; with successful recanalization at 90 days
  • ISCHEMIC STROKE4. ANTITHROMBOTIC TREATMENTPLATELET INHIBITION:-ASPIRIN: the ONLY antiplatelet agent that has been proven effective for the acute treatment of ischemic stroke-the use of aspirin within 48 hours of stroke onset reduced both stroke recurrence risk and mortality minimally-ABCIXIMAB: a glycoprotein IIb/IIIa receptor inhibitor was found to cause excess intracranial hemorrhage and should be avoided in acute stroke-CLOPIDOGREL: still being tested to prevent stroke following TIA and minor ischemic stroke
  • ISCHEMIC STROKE4. ANTITHROMBOTIC TREATMENTANTICOAGULATION:-low molecular weight Heparin: failed to show any benefit over aspirin, and increased bleeding rates
  • ISCHEMIC STROKE5. NEUROPROTECTION-the concept of providing a treatment that prolongs the brain’s tolerance to ischemia-includes: a. use of drugs that block excitatory amino acid pathways – protects neurons and glia in animals b. hypothermia – neuroprotective in patients with cardiac arrest
  • ISCHEMIC STROKE6. STROKE CENTERS AND REHABILITATION-patient care in comprehensive stroke units followed by rehabilitation services improves neurologic outcomes and reduces mortality-proper rehabilitation of the stroke patient includes early physical, occupational and speech therapy-GOAL OF REHABILITATION: return the patient home and to maximize recovery by providing a safe, progressive regimen suited to the individual patient
  • ISCHEMIC STROKE6. STROKE CENTERS AND REHABILITATION-RESTRAINT THERAPY: immobilizing the unaffected side has shown to improve hemiparesis following stroke
  • ISCHEMIC STROKEETIOLOGY:-Although the initial management of acute ischemic stroke often does not depend on the etiology, establishing a cause is essential in reducing the risk of recurrence-Focus on: a.) atrial fibrillation and b.) carotid atherosclerosis
  • ISCHEMIC STROKECLINICAL EXAMINATION: FOCUS FINDINGS -Peripheral and cervical -carotid auscultation for bruits, vascular system BP, pressure comparison between arms -Heart -dysrhythmias, murmurs -Extremities -peripheral emboli -Retina -effects of hypertension and cholesterol emboli (Hollenhorst plaques)
  • ISCHEMIC STROKE: Cardioembolic StrokeEXAM/LABORATORIES/IMAGING:-a complete neurologic examination is performed to localized the site of stroke-an imaging study of the brain is required for patients being considered for thrombolysis-an ECG may demonstrate arrhythmias or reveal MI-Other tests include: -CXR -ESR -urinalysis -serum electrolytes -CBC -Creatinine/BUN -blood sugar -PT/PTT -serum lipid profile -serologic test for syphilis
  • ISCHEMIC STROKE: Cardioembolic Stroke-responsible for 20% of all ischemic strokes-stroke caused by heart disease is PRIMARILY DUE TO EMBOLISM of thrombotic material forming on the atrial or ventricular wall of the left heart valves-TIA: if the thrombus fragment or lyse quickly-Characteristics: -sudden onset -maximum neurologic deficit at once -petechial hemorrhage can occur within the ischemic territory-Emboli from the HEART most often LODGE IN THE MCA, posterior cerebral artery or one of their branches, infrequently, the anterior cerebral artery is involved
  • ISCHEMIC STROKE: Cardioembolic Stroke-Most significant causes: 1. non-rheumatic (non-valvular) atrial fibrillation -MOST COMMON cause of cerebral embolism -stroke risk can be calculated using CHADS2 score CHADS2 score: CHADS2 RECOMMENDATION POINTS CONDITION SCORE 1 > 75 years old 0 Aspirin or no 1 Hypertension antithrombotic 1 Congestive heart failure 1 Aspirin or VKA 1 Diabetes Greater than VKA 2 Stroke or TIA (>) 1
  • ISCHEMIC STROKE: Cardioembolic Stroke-Most significant causes: 2. Myocardial Infarction -especially when transmural and involves anteroapical ventricular wall -risk is reduced by anticoagulation 3. prosthetic valves 4. rheumatic heart disease -increased incidence with prominent mitral stenosis or atrial fibrillation 5. ischemic cardiomyopathy
  • ISCHEMIC STROKE: Cardioembolic Stroke-paradoxical embolization occurs when venous thrombi migrate to arterial circulation, usually via a PATENT FORAMEN OVALE or ATRIAL SEPTAL DEFECT; detected through bubble-contrast ECG-Bacterial endocarditis can cause valvular vegatations that can give rise to septic emboli *Mycotic aneurysms caused by septic emboli give rise to SAH or intracerebral hemorrhage
  • ISCHEMIC STROKE: Artery-Artery Embolic Stroke-thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing an artery-to- artery embolic stroke-Unlike the myocardial vessels, artery-to-artery embolism, RATHER THAN local thrombosis, is the DOMINANT VASCULAR MECHANISM causing brain ischemia.-embolic sources are diseased vessels in the: -aortic arch -common carotid arteries -internal carotid arteries -basilar arteries -vertebral arteries -carotid bifurcation – MOST COMMON SOURCE
  • ISCHEMIC STROKE: Artery-Artery Embolic Stroke-Carotid Atherosclerosis: -atheroscerois within the carotid artery occurs most frequently with the common carotid bifurcation and proximal internal carotid artery -Risk factors: -male -smoking -older age -hypertension -diabetes -hypercholesterolemia -produces 10% of ischemic stroke
  • ISCHEMIC STROKE: Artery-Artery Embolic Stroke-Carotid Atherosclerosis: -Classification is based on: 1. whether stenosis is symptomatic or asymptomatic -symptomatic – patient has experienced a stroke within the vascular distribution of the artery - associated with greater risk of subsequent stroke 2. degree of stenosis
  • ISCHEMIC STROKE: Artery-to-Artery Embolic Stroke-Other causes of Artery-to-Artery embolic stroke: 1. Intracranial atherosclerosis -produces stroke through an embolic mechanism or by in situ thrombosis -common in Asian and African-Americans
  • ISCHEMIC STROKE: Artery-to-Artery Embolic Stroke-Other causes of Artery-to-Artery embolic stroke: 2. Dissection -common source in the young: internal carotid, vertebral arteries or vessels beyond the circle of Willis -characteristic: painful, precedes stroke by hours or days -causes: -connective tissue disorders (such as Ehlers- Danlos type IV, Marfan’s disease, cystic medial necrosis and fibromuscular dysplasia), trauma (usually on carotid and vertebral arteries) -most dissections heal spontaneously, and stroke or TIA beyond 2 weeks are uncommon -treatment: anticoagulants  antiplatelets EXTRACRANIAL dissection INTRACRANIAL dissection -do not cause hemorrhage because of -may produce SAH because vessels are tough adventitia of vessels thin and may form pseudoaneurysms
  • ISCHEMIC STROKE: Small-Vessel Stroke-lacunar infarction: infarction following atherothrombotic or lipohyalinotic occlusion a small artery (30-300 micrometer) in the brain -account for 20% of all strokesPATHOPHYSIOLOGY:-arteries that give rise to 30-300 micrometer branches that penetrate the cerebrum or brainstem: -MCA -circle of Willis -anterior and posterior communicating -basilar vertebral
  • ISCHEMIC STROKE: Small-Vessel StrokePATHOPHYSIOLOGY:-small branches can occlude either by: 1. atherothrombotic disease at its origin -thrombosis cause small infarcts called lacunes -infarct size: 3mm to 2cm 2. development of lipohyalinotic thickening-Principal risk factors: -age -hypertension
  • ISCHEMIC STROKE: Small-Vessel StrokeCLINICAL MANIFESTATIONS:-Lacunar Syndromes: 1. Pure motor hemiparesis -infarct location: posterior limb of the internal capsule or basis pontis -involves mostly the arms, face, legs 2. Pure sensory stroke -infarct location: ventral thalamus 3. Ataxic hemiparesis -infarct location: ventral pons or internal capsule 4. Dysarthria and clumsy hand -infarct location: ventral pons or genu of internal capsule
  • ISCHEMIC STROKE: Small-Vessel StrokeCLINICAL MANIFESTATIONS:-transient symptoms may occur several times a day and last only a few minutes-a large-vessel source may manifest initially as a lacunar syndromeSECONDARY PREVENTION:-risk factor modification especially BP reduction
  • STROKE: LESS COMMON CAUSES1. Hypercoagulable disorders2. Venous sinus thrombosis3. Sickle cell anemia4. Fibromuscular dysplasia5. Temporal giant cell arteritis6. Necrotizing (granulomatous) arteritis7. Primary Central Nervous System Vasculitis8. Drugs: amphetamines, cocaine9. Moyamoya Disease10. Reversible posterior leukoencephalopathy11. Leukoaraiosis / periventricular white matter disease12. CADASIL (cerebral autosomal dominant arteriopathy withsubcortical infarcts and leukoencephalopathy)
  • LESS COMMON CAUSES OF STROKE: Hypercoagulable disorders-primarily cause INCREASED RISK of VENOUS THROMBOSIS and therefore may cause VENOUS SINUS THROMBOSIS-Protein S deficiency & Homocysteinemia: may cause arterial thromboses-SLE with Libmann-Sacks endocarditis: can cause embolic stroke-requires long term anticoagulation to prevent further stroke
  • LESS COMMON CAUSES OF STROKE: Venous sinus thrombosis-affected location: lateral or sagittal sinus or small cortical vessels-occurs as a complication of: -oral contraceptive use -pregnancy and the post-partum period -inflammatory bowel disease -intracranial infections (meningitis) -dehydration -thrombophilia
  • LESS COMMON CAUSES OF STROKE: Venous sinus thrombosis-manifestations: -headache -focal neurologic symptoms -paraparesis and seizures -CT is normal unless presence of hemorrhage -signs of increased ICP/coma in greater degrees-Venous thrombosis is readily visualized by MR or CT venography-treatment: IV heparin regardless of intracranial hemorrhage -Vitamin K antagonists – if without hypercoagulability *anticoagulation is continued indefinitely if thrombophilia is diagnosed
  • LESS COMMON CAUSES OF STROKE: Sickle cell anemia (SS Disease)-common cause of stroke in children-predicted by high velocity of blood flow within MCAs using transcranial Doppler ultrasonography-Treatment: aggressive exchange transfusion
  • LESS COMMON CAUSES OF STROKE: Fibromuscular dysplasia-affects the cervical arteries *carotid/vertebral arteries show multiple rings of segmental narrowing alternating with dilatation-OCCLUSION is usually INCOMPLETE-more common in women-often asymptomatic but may be associated with audible bruit, TIA or stroke-may involve renal arteries and cause hypertension-Treatment: anticoagulation or antiplatelet
  • LESS COMMON CAUSES OF STROKE: Temporal giant cell arteritis-common in elderly with the temporal arteries undergoing subacute granulomatous inflammation with giant cells-blindness: due to occlusion of posterior ciliary arteries; prevented with GLUCOCORTiCOIDS-rarely causes stroke because the internal carotid artery is not inflamed-Takayasu’s arteritis: idiopathic giant cell arteritis involving great vessels arising from the aortic arch; may cause carotid or vertebral thrombosis
  • LESS COMMON CAUSES OF STROKE: Necrotizing (granulomatous) arteritis-occurs alone or in association with generalized polyarteritis nodosa or granulomatosis with polyangiitis (Wgener’s)-involves the distal small branches (<2mm diameter) of the main intracranial arteries-produces small ischemic effects on the brain, optic nerve and spinal cord-CSF: pleocytosis, increased protein level
  • LESS COMMON CAUSES OF STROKE:Primary Central Nervous System Vasculitis-rare-affects small or medium-sized vessels-without apparent systemic vasculitis-can follow the post-partum period and are self- limited-differential diagnosis includes inflammatory and non-inflammatory causes
  • LESS COMMON CAUSES OF STROKE: Drugs – amphetamines, cocaine-cause stroke by acute hypertension or drug induced vasculopathy-Phenylpropanolamine, cocaine, methamphetamine: linked with intracranial hemorrhage
  • LESS COMMON CAUSES OF STROKE: Moyamoya Disease-occlusive disease involving large intracranial arteries especially: -distal internal carotid -stem of MCA and ACA-lenticulostriate arteries develop rich collateral circulation around the occlusive lesion, which gives the “puff of smoke” impression-common in Asian chilren or young adults but appears the same in adults with atherosclerosis associated with diabetes-Treatment: anticoagulation is risky -surgical bypass of extracranial carotid arteries to the dura or MCAs may prevent stroke and hemorrhage
  • LESS COMMON CAUSES OF STROKE:Reversible posterior leukoencephalopathy-can occur in head injury, seizure, migraine, sympathomimetic drug use, eclampsia and postpartum period-may involve widespread cerebral segmental vasoconstriction and edema-manifestation: headache, fluctuating neurologic symptoms especially visual-ischemia reverses completely
  • LESS COMMON CAUSES OF STROKE:Leukoaraiosis / periventricular white matter disease-result of multiple small-vessel infarcts within the subcortical white matter-CT/MRI: areas of white matter injury surrounding the ventricles within the corona radiata; lacunar infarction are also seen-caused by chronic hypertension leading to lipohyalanosis of small penetrating arteries within the white matter-may lead to SUBCORTICAL DEMENTIA SYNDROME – which may be prevented/delayed with antihypertensive medications
  • LESS COMMON CAUSES OF STROKE:CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)-an inherited disorder that presents as: -small-vessel stroke -progressive dementia -extensive white matter changes seen in MRI-manifestation: migraine with aura, transient motor or sensory deficits-onset is usually on the 4th or 5th decade of life-caused by mutation in Notch-3
  • LESS COMMON CAUSES OF STROKE: Other monogenic ischemic stroke syndrome- CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy)- Hereditary endotheliopathy, retinopathy, nephropathy, and stroke (HERNS)- Fabry’s disease
  • TRANSIENT ISCHEMIC ATTACK-episodes of stroke symptoms that last only briefly-standard definition of duration is <24 hours, but most TIAs last <1 hour-has similar causes as ischemic stroke; may herald stroke-may arise from an emboli to the brain or an in situ thrombosis-newer definitions of TIA categorize those with new infarct as having ischemic stroke rather than TIA regardless of symptom duration
  • TRANSIENT ISCHEMIC ATTACK-Amaurosis fugax: transient monocular blindness, occurs from emboli to the central retinal artery of one eye -indicates carotid stenosis or local opthalmic artery disease-risk of stroke after TIA is 10-15% in the first 3 months with most events occuring in the first 2 days-risk is estimated using ABCD2 method-improvement characteristic of TIA is contraindication to thrombolysis CLINICAL FACTOR SCORE A: AGE: greater than/equal to 60 years 1 B: BLOOD PRESSURE: SBP >140 mmhg or DBP >90 mmHg 1 C: CLINICAL SYMPTOMS -Unilateral weakness 2 -Speech disturbance without weakness 1 D1: DURATION - greater than 60 minutes 2 -10 to 59 minutes 1 D2: DIABETES (oral medications or insulin) 1
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAGENERAL PRINCIPLES:-identification and control of modifiable risk factors is the best strategy to reduce the burden of stroke
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAATHEROSCLEROSIS RISK FACTORS:1. Older age2. Family history of thrombotic stroke3. Hypertension -most significant risk factor -Rx: use of thiazide diuretics, ACE-inhibitors4. Tobacco smoking – discouraged5. Abnormal blood cholesterol (high LDL, low HDL) -Rx: statin drugs6. Prior stroke or TIA – greater risk7. Cardiac conditions – atrial fibrillation, MI8. Oral contraceptives and hormone replacement therapy9. Hypercoagulable states10. Diabetes -Rx: pioglitazone – agonist of peroxisome proliferator-activated receptor gamma
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAANTIPLATELET AGENTS:-inhibits the formation of intraarterial platelet aggregates-most commonly used: 1. Aspirin – acetylates platelate cyclooxygenase, which irreversibly inhibits the formation in platelets of thromboxane A2, a platelet aggregating and vasoconstricting prostaglandin -paradoxically inhibits formation of prostacyclin, an antiaggregating and vasodilating prostaglandin -50-325 mg/day of aspirin for stroke prevention 2. Clopidogrel – block ADP receptor on platelets and thus prevent the cascade resulting in activation of glycoprotein IIB/IIIa that leads to fibrinogen binding to the platelet and consequent platelet activation -rarely causes TTP, but does not cause neutropenia
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAANTIPLATELET AGENTS: 3. Dipyridamole (extended-release) – an antiplatelet agent that inhibits the uptake of adenosine by a variety of cells, including those of the vascular endothelium  accumulated adenosine is an inhibitor of aggregation -potentiates effects of prostacyclin and nitrous oxide 4. Ticlopidine – rarely used, alternative to Clopidogrel -same action as Clopidogrel -more effective than aspirin but causes more side effects such as diarrhea, neutropenia, thrombotic thrombocytopenic purpura (TTP)
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAANTICOAGULATION THERAPY AND EMBOLIC STROKE:-anticoagulation is safe for patients with chronic nonrheumatic atrial fibrillation and prevent cerebral embolism-the decision to use anticoagulation for primary prevention is based primarily on risk factors *history of TIA or stroke favors anticoagulation-anticoagulation also reduces the risk of embolism in acute MI-3-month course of anticoagulation when there is: -Q wave infarction -substantial left ventricular dysfunction -congestive heart failure -mural thrombosis -atrial fibrillation (VKA if atrial fibrillation persists)
  • TREATMENT: Primary and Secondary Prevention of Stroke and TIAANTICOAGULATION THERAPY AND NONCARDIOGENIC STROKE:-warfarin has no benefit over aspirin-no support for long-term use of VKAs for preventing atherothrombotic stroke for either intracranial or extracranial cerebrovascular disease
  • TREATMENT: Carotid Atherosclerosis-can be removed surgically (endarterectomy) or mitigated with endovascular stenting with or without balloon angioplasty-Surgical: - Endarterectomy is most beneficial when performed within 2 weeks of symtpom onset, benefit is more pronounced in patients >75 years old, and benefit men more than women-Endovascular Therapy: -endovascular stenting with balloon angioplasty used to open stenotic carotid arteries
  • STROKE SYNDROMESDIVISION OF STROKE SYNDROMES: 1. LARGE-vessel stroke within the ANTERIOR circulation 2. LARGE-vessel stroke within the POSTERIOR circulation 3. SMALL-vessel of either vascular bed
  • STROKE SYNDROMESCEREBRAL HEMISPHERE, LATERAL ASPECT: STRUCTURES INVOLVED SIGNS AND SYMPTOMS-Somatic motor area for -paralysis of the contralateral face, arm and legface and arm -sensory impairment over the same are (pinprick, cotton-Fibers descending from the touch, vibration, position, 2-point discrimination,leg area to enter the corona stereognosis, tactile localization, barognosis,radiata and corresponding cutaneographia)somatic sensory sytem-Motor speech area of the -Motor aphasiaDOMINANT hemisphere-Central, suprasylvian -Central aphasia -word deafness -sensoryspeech area agraphia-Parietooccipital cortex of -anomia -jargon speechthe dominant hemisphere GERSTMANN SYNDROME: -acalculia -alexia -finger agnosia -right-left confusion-Central speech area -Conduction aphasia
  • STROKE SYNDROMESCEREBRAL HEMISPHERE, LATERAL ASPECT: STRUCTURES INVOLVED SIGNS AND SYMPTOMS-non-dominant parietal lobe -Apractagnosia of the dominant hemisphere(corresponds to speech area -inaccurate localization on the half fieldin dominant hemisphere) -distortion of visual coordinates -agnosia for the left half of external space -visual illusions -upside-down reading -anosognosia -unilateral neglect -hemiasomatognosia -dressing apraxia -constructional apraxia -inability to judge distance-Optic radiation deep to -homonymous hemianopiasecond temporal -homonymous inferior quadrantonopiaconvolution-Frontal contraversive eye -paralysis of the conjugate gaze to the opposite sidefield-Projecting fibers
  • STROKE SYNDROMESCEREBRAL HEMISPHERE, MEDIAL ASPECT: STRUCTURES INVOLVED SIGNS AND SYMPTOMS-Motor leg area -Paralysis of the opposite foot and leg-Arm area of cortex -A lesser degree of paresis of opposite arm-fibers descending to coronaradiata-Sensory area for foot and -Cortical sensory loss over toes, foot, and legleg-Sensorimotor area in -Urinary incontinenceparacentral lobule-Medial surface of the -Contralateral grasp reflexposterior frontal lobe; likely -sucking reflexsupplemental motor area - gegenhalten (paratonic rigidity)
  • STROKE SYNDROMESCEREBRAL HEMISPHERE, MEDIAL ASPECT: STRUCTURES INVOLVED SIGNS AND SYMPTOMS-Uncertain localization— -Abulia (akinetic mutism)probably cingulate gyrus -reflex distraction to sights and soundsand medial inferior portion -intermittent interruptionof frontal, parietal, and -slowness -lack of spontaneitytemporal lobes -delay -whispering-Frontal cortex near leg -Impairment of gait and stance (gait apraxia)motor area-Corpus callosum -Dyspraxia of left limbs -tactile aphasia in left limbs
  • STROKE SYNDROMESLEVEL OF MEDULLA:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -vertebral artery - -same -Ipsilateral twelfth -Paralysis with atrophy ofmedullary branch of nerve one-half half the tonguesyndrome vertebral or lower basilar artery -opposite -Contralateral -Paralysis of arm and leg, pyramidal tract sparing face and medial -impaired tactile and lemniscus proprioceptive sense over one-half the body-Lateral -vertebral artery -same -Descending tract -Pain, numbness, impairedmedullary -posterior inferior -nucleus fifth sensation over one-half thesyndrome cerebellar artery nerve face -superior, middle, or inferior lateral medullary arteries
  • STROKE SYNDROMESLEVEL OF MEDULLA:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -vertebral artery -same -Uncertain— -Ataxia of limbs, falling tomedullary -posterior inferior restiform body, side of lesionsyndrome cerebellar artery cerebellar -superior, middle, hemisphere, or inferior lateral cerebellar fibers, medullary arteries spinocerebellar tract -same -Vestibular nucleus -Nystagmus -diplopia -oscillopsia -vertigo -nausea -vomiting -same -Nucleus and -Loss of taste tractus solitarius
  • STROKE SYNDROMESLEVEL OF MEDULLA:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -vertebral artery -same -Descending Horners syndrome:medullary -posterior inferior sympathetic tract -Miosissyndrome cerebellar artery -Ptosis -superior, middle, -Decreased sweating or inferior lateral medullary arteries -same -Issuing fibers -Dysphagia ninth and tenth -hoarseness nerves -paralysis of palate -paralysis of vocal cord -diminished gag reflex -same -Cuneate -Numbness of ipsilateral -gracile nuclei arm, trunk, or leg
  • STROKE SYNDROMESLEVEL OF MEDULLA:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -vertebral artery -same -Genuflected -Weakness of lower facemedullary -posterior inferior upper motorsyndrome cerebellar artery neuron fibers to -superior, middle, ipsilateral facial or inferior lateral nucleus medullary arteries -opposite -Spinothalamic -Impaired pain and thermal tract sense over half the body, sometimes face-Total -vertebral artery -Combination of medial andunilateral lateral syndromesmedullarysyndrome
  • STROKE SYNDROMESLEVEL OF MEDULLA:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -vertebral artery -Combination of lateralpontomedul medullary and laterallary inferior pontine syndromesyndrome-Basilar -basilar artery -Bilateral long tract -Bilateral long tract signsartery -arteries arising in -cerebellar and (sensory and motor;syndrome the posterior peripheral cranial cerebellar and peripheral cerebral artery nerves cranial nerve abnormalities) distribution -Corticobulbar and -Paralysis or weakness of all corticospinal tracts extremities, plus all bulbar bilaterally musculature
  • STROKE SYNDROMESLEVEL OF THE INFERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -same -Center for -Paralysis of conjugate gazeinferior branch of basilar conjugate lateral to side of lesionpontine artery gaze (preservation ofsyndrome convergence) -Vestibular nucleus -Nystagmus -Likely middle -Ataxia of limbs and gait cerebellar peduncle -Abducens nerve -Diplopia on lateral gaze -opposite -Corticobulbar and -Paralysis of face, arm, and corticospinal tract leg in lower pons
  • STROKE SYNDROMESLEVEL OF THE INFERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -opposite -Medial lemniscus -Impaired tactile andinferior branch of basilar proprioceptive sense overpontine artery one-half of the bodysyndrome-Lateral -anterior inferior -same -Vestibular nerve -Horizontal and verticalinferior cerebellar artery or nucleus nystagmuspontine -vertigosyndrome -nausea -vomiting -oscillopsia -Seventh nerve -Facial paralysis -Center for -Paralysis of conjugate gaze conjugate lateral to side of lesion gaze
  • STROKE SYNDROMESLEVEL OF THE INFERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -anterior inferior -same -Auditory nerve or -Deafnessinferior cerebellar artery cochlear nucleus -tinnituspontinesyndrome -Middle cerebellar -Ataxia peduncle and cerebellar hemisphere -Descending tract -Impaired sensation over and nucleus fifth face nerve -opposite -Spinothalamic -Impaired pain and thermal tract sense over one-half the body (may include face)
  • STROKE SYNDROMESLEVEL OF THE MIDPONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -same -Pontine nuclei -Ataxia of limbs and gaitmidpontine branch of (more prominent in bilateralsyndrome midbasilar artery involvement) -opposite -Corticobulbar and -Paralysis of face, arm, and corticospinal tract leg -Medial lemniscus -Variable impaired touch and proprioception when lesion extends posteriorly-Lateral -short -same -Middle cerebellar -Ataxia of limbsmidpontine circumferential pedunclesyndrome artery Motor fibers or -Paralysis of muscles of nucleus of fifth mastication nerve
  • STROKE SYNDROMESLEVEL OF THE MIDPONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -short -same -Sensory fibers or -Impaired sensation overmidpontine circumferential nucleus of fifth side of facesyndrome artery nerve -opposite -Spinothalamic -Impaired pain and thermal tract sense on limbs and trunk
  • STROKE SYNDROMESLEVEL OF THE SUPERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -same -Superior and/or -Cerebellar ataxiasuperior branches of upper middle cerebellar (probably)pontine basilar artery pedunclesyndrome -Medial -Internuclear longitudinal ophthalmoplegia fasciculus -Localization -Myoclonic syndrome, uncertain—central palate, pharynx, vocal tegmental bundle, cords, respiratory dentate projection, apparatus, face, oculomotor inferior olivary apparatus, etc nucleus
  • STROKE SYNDROMESLEVEL OF THE SUPERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -opposite -Corticobulbar and -Paralysis of face, arm, andsuperior branches of upper corticospinal tract legpontine basilar arterysyndrome -Medial lemniscus -Rarely touch, vibration, and position are affected-Lateral -superior -same -Middle and -Ataxia of limbs and gait,superior cerebellar artery superior cerebellar falling to side of lesionpontine peduncles,syndrome superior surface of cerebellum, dentate nucleus -Vestibular nucleus -Dizziness -nausea, vomiting -horizontal nystagmus
  • STROKE SYNDROMESLEVEL OF THE SUPERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -superior -same -Pontine -Paresis of conjugate gazesuperior cerebellar artery contralateral gaze (ipsilateral)pontinesyndrome -Uncertain -Skew deviation -Descending Horners syndrome: sympathetic fibers -Miosis -Ptosis -Decreased sweating over face -Dentate nucleus -Tremor -superior cerebellar peduncle
  • STROKE SYNDROMESLEVEL OF THE SUPERIOR PONS:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -superior -opposite -Spinothalamic -Impaired pain and thermalsuperior cerebellar artery tract sense on face, limbs, andpontine trunksyndrome -Medial lemniscus -Impaired touch, vibration, (lateral portion) and position sense, more in leg than arm (there is a tendency to incongruity of pain and touch deficits)
  • STROKE SYNDROMESLEVEL OF THE MIDBRAIN:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Medial -paramedian -same -Third nerve fibers -Eye "down and out"midbrain branches of upper secondary to unopposedsyndrome basilar arteries action of fourth and sixth -proximal cranial nerves posterior cerebral -with dilated and arteries unresponsive pupil -opposite -Corticobulbar and -Paralysis of face, arm, and corticospinal tract leg descending in crus cerebri
  • STROKE SYNDROMESLEVEL OF THE MIDBRAIN:SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS OCCLUDED LESION STRUCTURES INVOLVED-Lateral -small penetrating -same -Third nerve fibers -Eye "down and out"midbrain arteries arising -third nerve secondary to unopposedsyndrome from posterior nucleus action of fourth and sixth cerebral artery cranial nerves -with dilated and unresponsive pupil -opposite -Red nucleus -Hemiataxia, hyperkinesias, -dentatorubro- tremor thalamic pathway
  • STROKE WITHIN THE ANTERIOR CIRCULATION-The internal carotid artery and its branches comprise the ANTERIOR CIRCULATION of the BRAIN-causes of occlusion: -intrinsic disease of the vessel -emboli from proximal source-occlusion of each major intracranial vessel has distinct clinical manifestations
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY:-occlusion of the proximal MCA or one of its major branches is MOST OFTEN due to an embolus RATHER THAN intracranial atherothrombosis-collateral formation via leptomeningeal vessels prevents MCA stenosis from becoming symptomatic-cortical branches of the MCA supply the lateral surface of the hemisphere except for: 1. the frontal pole and a strip along the superomedial border of the frontal and parietal lobes supplied by the ACA 2. the lower temporal and occipital pole convolutions supplied by the PCA
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY:-proximal MCA (M1 segment) gives rise to lenticulostriate arteries (penetrating branches) that supply the following: -putamen -outer globus pallidus -posterior limb of the internal capsule -adjacent corona radiata -most of the caudate nucleus-MCA divides into superior and inferior divisions (M2 branches) in the sylvian fissure: -inferior – supply inferior parietal & temporal complex -superior – supply frontal & superior parietal complex
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY:-occlusion of the entire MCA at its origin, with limited distal collaterals lead to the following clinical findings: -contralateral hemiplegia -hemianesthesia -homonymous hemianopia -1-2 day gaze preference to the ipsilateral side -dysarthria (due to facial weakness) DOMINANT HEMISPHERE NONDOMINANT HEMISPHERE INVOLVEMENT INVOLVEMENT -Global aphasia -anosognosia -constructional apraxia -neglect
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY: COMPLETE SYNDROME PARTIAL SYNDROME -most often occlusion of MCA stem -presence of cortical collateral blood flow -emboli that causes incomplete occlusion -occlusion of distal MCA branches or fragment and move distally
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY: LOCATION OF OCCLUSION SYMPTOMS-single branch -hand or hand and arm weakness (brachial syndrome) -facial weakness with Broca’s aphasia with or without arm weakness (opercular syndrome)-proximal superior division and -sensory disturbanceinfarcted frontal and parietal -motor weaknesscortices -Broca’s aphasia-inferior division supplying -Wernicke’s aphasia without weaknessposterior part (temporal cortex) of -Jargon speech and inability to comprehend writtenthe dominant hemisphere and spoken language -contralateral homonymous superior quadrantanopiainferior division of the -hemineglectnondominant hemisphere -spatial agnosia without weakness
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the MIDDLE CEREBRAL ARTERY: LOCATION OF OCCLUSION SYMPTOMS-lenticulostriate vessel (stroke -pure motor stroke or sensory-motor strokewithin the internal capsule) contralateral to the lesion-ischemia in the genu of the -1st: facial weakness arm weakness  leg weaknessinternal capsule (moving -contralateral hand: ataxia, dysarthriaposteriorly)-lacunar infarction in globus -few clinical symptomspallidus and putamen -parkinsonism -hemiballismus
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the ANTERIOR CEREBRAL ARTERY:-ACA is divided into 2 segments: 1. precommunal (A1) circle of Willis or stem – -connects the internal carotid to the anterior communicating artery -gives rise to deep penetrating branches that supply the: -anterior limb of the internal capsule -amygdala -anterior perforate substance -anterior hypothalamus -inferior part of the head of the caudate nucleus 2. postcommunal (A2) – -distal to the anterior communicating artery
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the ANTERIOR CEREBRAL ARTERY:-occlusion of the ACA is usually well tolerated due to collateral flow through the anterior communicating and through the MCA and PCA LOCATION OF OCCLUSION SYMPTOMS-single A2 segment -contralateral symptoms-A2 segments from a single -may affect both hemispheres and thus result to:anterior cerebral stem -profound abulia –delay verbal and motor response(contralateral A1 segment atresia) -bilateral pyramidal signs with paraparesis and quadriparesis -urinary incontinence
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the ANTERIOR CHOROIDAL ARTERY:-anterior choroidal artery arises from the internal carotid artery and supplies the posterior limb of the internal capsule and the white matter posterolateral to it, through which GENICOLOCALCARINE fibers pass-collateral: penetrating vessels of the proximal MCA, posterior communicating artery, posterior choroidal arteries *presence of collateral cause minimal deficits-anterior choroidal strokes are often caused by IN SITU thrombosis, and iatrogenic occlusion during surgical clipping of aneurysms arising from the internal carotid artery
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the ANTERIOR CHOROIDAL ARTERY: LOCATION OF OCCLUSION SYMPTOMS-anterior choroidal artery -COMPLETE syndrome consists: -contralateral hemiplegia -hemianesthesia (hypesthesia) -homonymous hemianopia
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the INTERNAL CAROTID ARTERY:-clinical picture depends on cause of ischemia: -thrombus -embolism -low flow-the cortex supplied by the MCA territory is affected MOST OFTEN-may go unnoticed with a COMPETENT circle of Willis-in stenotic lesions, a high-pitched carotid bruit fading into DIASTOLE is heard  becomes fainter and disappears when occlusion is imminent
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the INTERNAL CAROTID ARTERY: LOCATION OF OCCLUSION SYMPTOMS-propagation into the MCA -symptoms of proximal MCA -may have massive infarction of deep white matter and cortical surface-origins of ACA and MCA at the top -abuliaof carotid artery -stupor with hemiplegia -hemianesthesia -aphasia -anosognosia-fetal posterior cerebral artery -symptoms referable to its peripheral territory(PCA arises from the internalcarotid artery)-opthalmic artery -recurrent transient monocular blindness (amaurosis fugax)
  • STROKE WITHIN THE ANTERIOR CIRCULATIONOCCLUSION of the COMMON CAROTID ARTERY:-Signs and symptoms the same with internal carotid occlusion-Jaw claudication: low flow in external carotid branches-Bilateral common carotid artery occlusion: Takayasu’s arteritis
  • STROKE WITHIN THE POSTERIOR CIRCULATION-the POSTERIOR CIRCULATION is composed of: -paired vertebral arteries  join to form  -basilar artery  divides  -paired posterior cerebral arteries *these arteries give rise to circumferential and deep penetrating branches that supply the: -cerebellum -brainstem -diencephalon -hippocampus -medial temporal and occipital lobes *occlusion of each vessel produces its own distinctive symptom
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:-origin of the PCA: 75% - from bifurcation of the basilar artery 20% - one from the ipsilateral internal carotid artery via the posterior communicating artery 5% - both from the respective ipsilateral internal carotid arteries
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:-PCA syndromes: -usually result from atheroma formation or emboli that lodge at the top of the basilar artery -may also be due to vertebral artery dissection or fibromuscular dysplasia-2 clinical syndromes are COMMONLY observed with PCA occlusion: 1. P1 syndrome -midbrain, subthalamic, thalamic signs -due to disease of the proximal P1 segment or its penetrating branches 2. P2 syndrome -cortical temporal and occipital lobe signs -due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:P1 SYNDROMES LOCATION OF OCCLUSION SYMPTOMS -Ipsilateral subthalamus and medial thalamus -CLAUDE’S SYNDROME: third nerve palsy with -Ipsilateral cerebral peduncle and midbrain contralateral ataxia -WEBER’S SYNDROME: third nerve palsy with contralateral hemiplegia -red nucleus -ataxia -dentatorubrothalamic tract -cerebral peduncle -hemiplegia -subthalamic nucleus -hemiballismus -artery of Percheron -paresis of upward gaze -drowsiness -abulia -extensive infarction in the midbrain and -coma -bilateral pyramidal signs subthalamus with bilateral PCA occlusion -unreactive pupils -decerebrate rigidity
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:P1 SYNDROMES LOCATION OF OCCLUSION SYMPTOMS -penetrating branches o f thalamic and -less extensive thalamic and thalamocapsular thalamogeniculate arteries lacunar syndromesThalamic Dejerine-Roussy syndrome:-consists of: -contralateral hemisensory loss  -agonizing, searing, burning pain in the affected area-persistent and responds poorly to analgesics-anticonvulsants (carbamazepine or gabapentin) or tricyclic antidepressants show benefits
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:P2 SYNDROMES LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -distal PCA (infarction of medial temporal and -contralateral homonymous hemianopia WITH occipital lobes) macula sparing *occasionally, only the upper quadrant of visual field is involved -calcarine cortex -patient is aware of visual defects dominant hemisphere: -acute disturbance in memory but clears -medial temporal lobe -hippocampus dominant hemisphere: -alexia WITHOUT agraphia -splenium of the corpus callosum *amnestic aphasia may occur even without callosal involvement -PCA -peduncular hallucinosis: visual hallucinations of brightly colored scenes and objects
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the POSTERIOR CEREBRAL ARTERY:P2 SYNDROMES LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -bilateral infarction in the distal PCA -cortical blindness (blindness with preserved PLR) -ANTON’S SYNDROME: unaware/deny blindness -infarction secondary to low flow in the -BALINT’S SYNDROME: disorder of orderly visual “watershed” between distal PCA and MCA scanning of the environment territories -palinopsia: persistence of visual image for *as occurs after cardiac arrest several minutes -asimultanagnosia: inability to synthesize whole image -top of the basilar artery -central or peripheral territory symptoms -HALLMARK: sudden onset of bilateral signs – -ptosis -pupillary asymmetry -somnolence -lack of reaction to light
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:-The vertebral artery arises from the INNOMINATE artery on the RIGHT and the SUBCLAVIAN artery on the LEFT SEGMENT COURSE V1 -from origin to entrance of 5th/6th transverse vertebral foramen V2 -traverses the vertebral foramina from C6 to C2 V3 -passes through the vertebral foramen and circles around the arch of the atlas to pierce the dura at the foramen magnum V4 -courses upward to join the other vertebral artery to form the basilar artery -ONLY V4 gives rise to branches that SUPPLY THE BRAINSTEM and CEREBELLUM
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:-Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery -V1 may produce posterior circulation emboli but collateral flow from contralateral vertebral artery, ascending cervical, thyrocervical or occipital arteries prevent low flow TIAs or stroke -but when one vertebral artery is atretic, collateral flow may be insufficient -low flow TIAs consist of: -syncope -vertigo -alternating hemiplegia
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:-Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery -V4 can promote thrombus formation as: -embolism -basilar artery thrombosis – with propagation-if the SUBCLAVIAN ARTERY is occluded proximal to the origin of the vertebral artery there is reversal in the direction of blood flow in the ipsilateral vertebral artery *exercise of the ipsilateral arm may increase demand on vertebral flow, producing posterior circulation TIAs / “SUBCLAVIAN STEAL”
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES: -V2 and V3 are subject to: -dissection -fibromuscular dysplasia -encroachment by osteophytic spurs within the vertebral foramina
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:-The posterior inferior cerebellar artery (PICA): -PROXIMAL segment supplies the LATERAL MEDULLA -DISTAL branches supply the INFERIOR surface of the cerebellum-stenosis proximal to the origin of the PICA can threaten both the lateral medulla and the inferior surface of the cerebellum
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES: LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -V4 segment (ischemia of lateral medulla) -vertigo -numbness of ipsilateral face; contralateral limbs -diplopia -hoarseness -dysarthria -dysphagia -ipsilateral Horner’s syndrome (lateral medullary / Wallenberg’s syndrome) -medullary penetrating branches -partial syndromes -PICA -infarction of the pyramid -rarely, medial medullary syndrome -contralateral hemiparesis of the arm and leg, sparing the face
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES: LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -medial lemniscus -contralateral loss of joint position sense -emerging hypoglossal nerves -ipsilateral tongue weakness -cerebellar infarction with edema -sudden respiratory arrest (due to raised ICP in the posterior fossa) -before arrest ensues, the following are absent or present briefly: -drowsiness -Babinski signs -dysarthria -bifacial weakness-Gait unsteadiness, headache, dizziness, nausea and vomiting may be the only early symptoms and signs and should arouse suspicion of impending complication, which may require neurosurgical decompression, often with an excellent outcome
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the BASILAR ARTERY:-the basilar artery supply the base of the pons and the superior cerebellum; they fall into 3 GROUPS: 1. Paramedian -7-10 in number -supply a wedge of pons on either side of the midline 2. Short circumferential -5-7 in number -supply the lateral 2/3 of the pons and middle and superior cerebellar peduncles 3. Bilateral long circumferential -2 in number -course around the pons to supply superior and anterior inferior cerebellum
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the BASILAR ARTERY:-atheromatous lesions occur anywhere the basilar trunk but are MOST FREQUENT in the PROXIMAL BASILAR and DISTAL VERTEBRAL segments-clinical picture depends on the availability of retrograde collateral flow from the posterior communicating arteries-emboli from the heart or proximal vertebral or basilar segments are MORE COMMONLY responsible for “top of the basilar” syndromes-COMPLETE BASILAR OCCLUSION: constellation of bilateral long tract signs (sensory and motor) with signs of cranial nerve and cerebellar dysfunction
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the BASILAR ARTERY:- “LOCKED-IN” state of preserved consciousness with quadriplegia and cranial nerve signs suggest COMPLETE PONTINE and LOWER MIDBRAIN infarction-TIAs in the proximal basilar distribution may produce vertigo, other symptoms include diplopia, dysarthria, facial or circumoral numbness and hemisensory symptoms-symptoms of BASILAR BRANCH affect ONE side of the brainste; symptoms of BASILAR ARTERY affect BOTH sides-TIAs are short lived (5-30 minutes) but repititive -Rx: heparin to prevent clot propagation
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the BASILAR ARTERY: LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -basilar artery with infarction -bilateral brainstem signs: -gaze paresis/internuclear opthalmoplegia -ipsilateral hemiparesis -unequivocal signs of bilateral pontine disease -branch of basilar artery -unilateral symptoms: -signs involving motor, sensory and cranial nerves -superior cerebellar artery -severe ipsilateral cerebellar ataxia -nausea and vomiting -dysarthria -contralateral loss of pain and temperature sensation over the extremities, body and face Rarely: -partial deafness -Horner’s syndrome -ataxic tremor of ipsilateral upper limb -palatal myoclonus
  • STROKE WITHIN THE POSTERIOR CIRCULATIONOCCLUSION of the BASILAR ARTERY: LOCATION OF OCCLUSION/INFARCTION SYMPTOMS -anterior inferior cerebellar artery ipsilateral : -deafness, facial weakness, vertigo, nausea and vomiting, nystagmus, tinnitus, cerebellar ataxia, Horner’s syndrome, paresis of conjugate lateral gaze contralateral: -loss of pain and temperature sensation *an occlusion close to the origin may cause CORTICOSPINAL TRACT SIGNS -one of the short circumferential branches of the -affects the lateral 2/3 of the pons and middle or basilar artery superior cerebellar peduncle -one of the paramedian branches -affects a wedge-shaped area on either side of the medial pons
  • IMAGING STUDIES: CT SCANS-identify or exclude hemorrhage as the cause of stroke and they identify extraparenchymal hemorrhages, neoplasms, abscesses, and other conditions masking as stroke-CT OBTAINED in the FIRST SEVERAL HOURS after an infarction generally SHOW NO ABNORMALITY-Infarct may not be seen reliably for 24-48 hours-CT may fail to show small ischemic stroke in the posterior fossa because of bone artifact, also on the cortical surface
  • IMAGING STUDIES: CT SCANS-contrast enhanced CT allow visualization of venous structures-CT angiography readily: - identifies carotid disease and intracranial vascular occlusions -area of brain infarct, ischemic penumbra after IV bolus of contrast -sensitive in detecting SAH-NON-CONTRAST HEAD CT IS THE IMAGING MODALITY OF CHOICE IN PATIENTS WITH ACUTE STROKE
  • IMAGING STUDIES: MRI-reliably documents the extent and location of infarction in ALL AREAS of the brain, including the posterior fossa and cortical surface-LESS SENSITIVE than CT in DETECTING ACUTE BLOOD-diffusion-weighted imaging and fluid-attenuated inversion recovery (FLAIR) is MORE SENSITIVE for EARLY BRAIN INFARCTION than MR sequences or CT-MR perfusion studies use IV GADOLINIUM contrast-MR angiography is highly sensitive for stenosis of extracranial internal carotid arteries and large intracranial vessels-MRI with fat saturation visualize extra or intracranial arterial dissection
  • IMAGING STUDIES: MRI-compared to CT, MRI is: -less sensitive for acute blood products -more expensive -time consuming -less readily available -limited with Claustrophobia-MRI is more useful outside the acute period by: -more clearly defining the extent of tissue injury -discriminating new from old regions of brain infarction
  • IMAGING STUDIES: CEREBRAL ANGIOGRAPHY-conventional X-RAY cerebral angiography is the GOLD STANDARD for: -identifying and quantifying atherosclerotic stenoses of the cerebral arteries -characterizing other pathologies-coupled with endovascular techniques for cerebral revascularization-risks of cerebral angiography: -arterial damage -groin hemorrhage -embolic stroke -renal failure from contrast nephropathy *reserved when less invasive means are inadequate
  • IMAGING STUDIES: ULTRASOUND TECHNIQUES-Transcranial Doppler (TCD) -can detect stenontic lesions in large intracranial arteries because such lesions increase systolic flow velocity -can assist thrombolysis and improve large artery recanalization following rTPA administration
  • IMAGING STUDIES: PERFUSION TECHNIQUES-both xenon techniques (xenon-CT) and PET can quantify cerebral blood flow-generally used for research BUT can be useful for determining the significance of arterial stenosis and planning for revascularization surgery-CT perfusion increases the sensitivity of detecting ischemia and can measure ischemic penumbra
  • INTRACRANIAL HEMORRHAGEINTRODUCTION:-Hemorrhages are classified by their location and underlying vascular pathology.-Types: -Subdural and epidural hemorrhage – usually caused by trauma -Subarachnoid hemorrhages – produced by trauma and rupture of intracranial aneurysms -Intraparenchymal and Intraventricular hemorrhages
  • INTRACRANIAL HEMORRHAGEDIAGNOSIS:-Intracranial hemorrhage is often discovered on non-contrast CT imaging of the brain during the acute evaluation of stroke *CT imaging is preferred method for acute stroke evaluation over MRI since it is more sensitive on acute blood
  • INTRACRANIAL HEMORRHAGEEMERGENCY MANAGEMENT:-Airway – reduction in the level of consciousness is common and progressive-Initial BP is maintained until CT scan results are reviewed *BP can be safely lowered using nicardipine , labetalol or esmolol (non-vasodilating IV drugs)-Mean arterial pressure is maintained <130mmHg, unless an increase in ICP is suspected-Stuporous or comatose patients generally are treated presumptively for elevated ICP with: -tracheal intubation -mannitol administration -hyperventilation -elevation of the head of bed
  • INTRAPARENCHYMAL HEMORRHAGE-MOST COMMON TYPE OF INTRACRANIAL HEMORRHAGE-particularly high in Asians and Blacks-Major causes: 1. hypertension 2. trauma 3. cerebral amyloid angiopathy-Risk factors: -advanced age -heavy alcohol consumption -cocaine and methamphetamine use (most important cause in the young)
  • HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGEPATHOPHYSIOLOGY:-usually results from spontaneous rupture of a small penetrating artery deep in the brain-can also be due to hemorrhagic disorders, neoplasms, vascular malformations *suspected in non-hypertensives and in uncommon sites-Most Common Sites: -basal ganglia especially the putamen -thalamus -cerebellum -pons
  • HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGEPATHOPHYSIOLOGY:-hemorrhage may lead herniation and death-most develop over 30-90 minutes compared hemorrhage caused by anticoagulant therapy that evolve for 24-48 hours
  • HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGEPATHOPHYSIOLOGY:-hemorrhage may lead herniation and death-most develop over 30-90 minutes compared hemorrhage caused by anticoagulant therapy that evolve for 24-48 hours