Transcript Slide 1
CEREBROVASCULAR DISEASE CEREBROVASCULAR DISEASE “STROKE” • Macrovascular disease • Microvascular disease • Emboli • Venous thrombosis Blood supply to the brain - or better, the supratentorial level, posterior fossa level and (upper) spinal level. Describe the “two” vascular arterial supplies to the intracranial compartment, and their distribution to the portions of the neuraxis Closer view of the vertebral-basilar and carotid arterial systems. Know their distribution, branches, “territories” and syndromes associated with the named vessels. Mid sagittal view of the supratentorial level and posterior fossa level with their respective blood supplies. The vertebral-basilar vessels supply a portion of the supratentorial level. Angiography to demonstrate the middle cerebral artery. The utility of a number of imaging techniques allows for the demonstration of vascular integrity and disease in vivo. The blood vessels of the “base” of the brain and their distribution. Vessels of the supratentorial level, medial left hemisphere. Which is carotid, and which is vertebral-basilar? Vessels of the supratentorial level, medial left hemisphere. Which is carotid, and which is vertebral-basilar? Sometimes there appears to be less significance given to the veins, but their location and distribution give rise to some interesting findings, especially in hypercoagulable states, and trauma. Blood drains from the veins into the sinuses, the dural sinuses. Define and differentiate hypoxia, ischemia and infarction Discuss the etiology and pathogenesis of ischemic encephalopathy Define and differentiate hypoxia, ischemia and infarction STRAIGHT FROM ROBBINS Discuss the etiology and pathogenesis of ischemic encephalopathy Ischemic (hypoxic) Encephalopathy Vulnerability to ischemia Neurons First to die Glial cells Tissue necrosis Prolonged ischemia Mechanism of neuron cell death Excitotoxin release Persistent opening of NMDA receptor channels Influx of Ca++ NO toxicity Why is this important? NO synthase inhibitors protect against effects of ischemia in some model systems!!!! Treatment for ischemia? Define and differentiate hypoxia, ischemia and infarction Discuss the etiology and pathogenesis of ischemic encephalopathy STRAIGHT FROM ROBBINS Ischemic encephalopathy Episodes of hypotension Transient (if mild) Severe global ischemia Survivor = persistent vegetative state Isoelectric (flat) EEG Respirator brain Morphology Brain swollen Flat surface Poor gray-white distinction Acute neuronal changes (12 - 24 hours) Glial cell death Vulnerability factor Necrosis, macrophages, vascular proliferation, gliosis What is a watershed infarct, and how does it relate to the discussion of ischemic encephalopathy? Vessels of the supratentorial level, medial left hemisphere. Which is carotid, and which is vertebral-basilar? Differentiate between ischemic and hemorrhagic (white vs. red) infarcts, and define the most likely causes of each A B A B Infarct, acute. Acute infarcts may be red or white, hemorrhagic or ischemic, leaks or plugs. In A, the lesion is an acute hemorrhage. In B, on the right, the lesion is ischemic, with secondary congestion of the tissue, but no large hemorrhage. “A” could be caused by a ruptured aneurysm (hypertensive, for example) whereas (B) would be caused by a thrombus. Note that in B, the damage is confined to the territory of the middle cerebral artery, What is the lesion on the left side of picture B? Differentiate between thrombotic and embolic infarction, and given a gross or microscopic picture, be able to recognize the difference between the two CEREBROVASCULAR DISEASE “STROKE” • Macrovascular disease • Microvascular disease • Emboli • Venous thrombosis STROKE: EPIDEMOLOGIC FACTORS • 0.5 million / year • 3 X 106 ‘survivors’ • 150,000 deaths / year • Incidence 100 / 100,000 ages 45-54 1800 / 100,000 ages 85+ • Risk factors • Infarction 10 X > Hemorrhage STR0KE: RISK FACTORS MAJOR FACTORS • Age • Family history • Diabetes Mellitus • Cigarette smoking • Hypertension • Lipid Metabolism • Truncal obesity OTHER FACTORS • Oral contraceptives • Hematologic Sickle cell Polycythemia • Coagulation disorders • Cardiac disease • Vascular disease ATHEROSCLEROSIS & STROKE • Documented risk factors • TIA -- common presentation • TIA -- high risk • Embolization • Occlusive thrombosis Extracranial -- common Intracranial -- less often Vascular, acute thrombosis. The hemostat is positioned to show the internal carotid artery on the right (yellow arrow) in which there is a fresh thrombus. The patient had severe atherosclerosis; note the left internal carotid and the patchy yellow-white plaques in the basilar and posterior cerebral arteries (blue arrows). COAGULATION DEFECTS & BRAIN INFARCTS • Protein C deficiency • Factor V Leiden mutation (Arg506Gln) • Protein S deficiency • Antithrombin III abnormalities • Carbohydrate-deficient glycoprotein synthase type I MICROANGIOPATHY • Angitis and vasculitis • Primary angitis of CNS • Vasculitides Polyarteritis nodosa Allergic angitis and granulomatosis Wegener’s granulomatosis Lymphomatoid granulomatosis • Microvasculopathy associated with dementia Binswanger’s Autosomal dominant arteriopathy BINSWANGER’S SUBCORTICAL ARTERIOSCLEROTIC LEUKOENCEPHALOPATHY • Slowly progressive, but “stairstep” • 6th to 7th decade • Memory, mood, cognition • Pseudobulbar: gait and sphincter control EMBOLIC DISEASES Embolic stroke results when solid material: forms in the arterial circulation is introduced into arterial circulation shifts from venous to arterial circulation Resultant infarct is: abrupt hemorrhagic (reperfusion Differential diagnosis is: ischemic infarct cerebral hemorrhage SOURCES OF BRAIN & SPINAL CORD EMBOLI • Atheroma • • • • • Cardiogenic Fat Neoplasms and parasites Iatrogenic Miscellaneous SOURCES OF BRAIN & SPINAL CORD EMBOLI • Atheroma Complicated atherosclerosis • Cardiogenic Left atrium (noncontractile) Mural thrombi Endocarditis Valve lesions CNS INFARCTION • Acute 5-8 hours undetectable 12-36 hours blurring gray/white interface, dusky, softening territorial • Subacute 2-4 days softening, blurring, dusky, EDEMA • Chronic Stage I: liquefactive necrosis to cavitation Stage II: (months) cavitary ACA MCA A B Infarcts, recent (A) and old (B). A. The infarct is in the distribution of the middle cerebral artery on the right. It began as an ischemic infarct, there is no large mass of hemorrhage. What is present now is the soft, necrotic resorbing tissue (inflammatory process at work). B. An example of ischemia of the internal carotid distribution on the right. The territories of both the anterior and middle cerebral arteries is involved. Again, it was an ischemic, there is no large mass of blood as in a ruptured aneurysm. Vessel territories are demonstrated on the left of B. CNS INFARCTION • Acute (hours) eosinophilia with pyknosis vacuolation of neurophil • Subacute (days) PMN infiltration necrotic microvessels foamy macrophages • Chronic (weeks to months) foamy macrophages, hemosiderin reactive astrocytes CORTICAL DYSFUNCTION: TERRITORIAL MCA hemipariesis aphasia hemisensory deficit ACA hemipariesis transcortical aphasia abulia PCA thalamic syndrome hemianopia alexia A B Infarct, remote. In the healing process of the brain, cavitation is the end result. There are several examples of old infarcts, none of which was initially fatal. They are all in the distribution of the ____________ artery? C Infarcts, microscopic. What vessel? What section of the brainstem? What is the syndrome? INTRACRANIAL HEMORRHAGE • Extradural • Subdural • Subarachnoid • Parenchymal Cerebral Cerebellar Brain stem Define the etiology and pathogenesis of hypertensive vascular disease including hemorrhage and lacunar infarcts HYPERTENSIVE PARENCHYMAL HEMORRHAGES Pathogenesis rupture of weakened arterioles replacement of muscle by fibrous tissue fragmentation of elastic tissue focal microaneurysms Associated systemic hypertension PARENCHYMAL HEMORRHAGES • Hypertension • • • • • • • • Trauma Cerebral amyloid angiopathy Saccular aneurysms Vascular malformations Bleeding diathesis (anticoagulants) Vasculitis Neoplasms Infections HYPERTENSIVE HEMORRHAGES Symptoms and Signs • Putamen • Cerebellum hemiparesis hemisensory loss visual field defects • Thalamus hemiparesis hemisensory loss gaze abnormalities vomiting & headache ataxia cranial nerve abnormalities • Large pontine coma quadriparesis or quadraplegia small reactive pupils • Small pontine gaze paresis ataxia sensorimotor deficit HYPERTENSIVE HEMORRHAGES • Gross findings acute hematoma intraventricular extension swelling, herniation resorb, cavitation does not respect vascular territory secondary Wallerian degeneration HYPERTENSIVE HEMORRHAGES Microscopic features fresh blood inflammatory cells, macrophages hemosiderin, hematoidin Small vessels “onion-skinning” lipohyalinosis microaneurysms fibrinoid necrosis HYPERTENSIVE HEMORRHAGES ARTERIOSCLEROTIC CHANGE Thickening of the media Adventitial fibrosis Fragmentation / reduplication of elastica Intimal thickening Accumulation of macrophages Charcot - Bouchard microaneurysm MICROVASCULAR DEMENTIA Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts & Leukoencephalopathy (CADASIL) Binswanger’S Subcortical Arteriosclerotic Leukoencephalopathy Cerebral Amyloid Angiopathy