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OCULAR MANIFESTATIONS OF IMPENDING STROKE Carlo J. Pelino O.D., F.A.A.O. Assistant Professor Retina / Emergency Clinic The Eye Institute The Pennsylvania College of Optometry • An ischemic event that results in permanent dysfunction • Exceeded only by heart disease and cancer as the leading cause of death in the United States • Hypoxia – reduction in the normal concentration of tissue oxygen Usually occurs from decreased blood flow ( Ischemia ) Prolonged ischemia leads to tissue death ( Infarction ) Infarction of neural tissue includes all cell bodies, blood vessels and nerve Epidemiology: Cerebrovascular Accidents result from two major causes: I Ischemia (80%) II Hemorrhage (20%) “Ischemic” cerebrovascular disease may occur in older patients, young adults and even in children • In the USA, historically intracranial hemorrhage (nontraumatic) has been due to uncontrolled arterial hypertension and its eventual sequelae: arteriolosclerosis • Hypertensive hemorrhages typically occur in areas where arteriolosclerosis is most severe: • • • • Basal ganglia (60%) Thalamus (10%) Pons (10%) Cerebellum (10%) Transient ischemic attack • • • • Abrupt, focal loss of neurological function caused by an ischemic event Most often they occur for only a few minutes with no residual deficit Arbitrarily defined as 24 hours or less .… now thought to be 1- 4 hours or less The maximum duration for a TIA is somewhat controversial Anatomy • • • The brain weighs ~ 3 pounds (1.4 kilograms) One of the body’s biggest organs Has ~ 100 billion nerve cells • • • The cerebrum is the largest part of the brain ~ 85 % brain’s weight. The outer surface is the cerebral cortex consisting of gray matter. Beneath this lies the white matter. • • • More glia than nerve cells found in the brain = invol brain tumors Astroglia = transports nutrients, holds neurons in place Oligodendroglia = provides insulation (myelin) to neurons The brain receives 20% of the cardiac output Needs oxygen and glucose Brain can not store nutrients or use protein or fat for its metabolic needs More glia than nerve cells found in the brain = involved in brain tumors Astroglia = transports nutrients, holds neurons in place Oligodendroglia = provides insulation (myelin) to neurons • Almost always due to an embolism to the MCA branch point at the circle of Willis from a cardiac or carotid bifurcation thrombus. Almost never due to primary MCA thrombosis Patient History: Interrogate and Investigate !!!! The patient’s history is a very important tool in the evaluation of a complaint of headache. History is the key to diagnosis. ~ 90 % of the diagnosis comes from the history ! Stroke symptoms Stroke Etiology: • • • • • Hypertension Diabetes Hypercholesterolemia Smoking Atrial fibrillation (4-5 X increase in stroke risk) 75% of all strokes occur after the age of 65 Atherosclerosis – Most common cause of thrombosis Grading of Hypertensive Retinopathy: Causes of Thrombosis Hypercoaguable State: • • • • It is a risk factor for artery and venous occlusions Has and association with coronary artery disease Has and association with cerebral vascular accidents (CVA) Hypercoaguable state is associated with peripheral vascular disease Hypercoaguable State: Treatment • Monitor patient closely with Primary Care Physician • Coumadin, Heparin, Aspirin therapy • Treat ocular conditions accordingly Ocular Manifestations of Impending Stroke: Emboli Amaurosis Fugax (Transient Monocular Blindness) Ocular Ischemic Syndrome (Hypoperfusion Retinopathy Central Retinal Artery Occlusion Branch Retinal Artery Occlusion Anterior Ischemic Optic Neuropathy Arteritic NonArteritic Carotid artery dissection Causes of Embolism Embolus: The most common found in the retinal circulation are • Cholesterol (Hollenhorst) • Fibrin-Platelet • Calcific • Beaver Dam Study – Found that the overall prevalence of retinal emboli in a population of 4926 patients was 1.3 % and increased to 3.1 % in patients 75 years or older !!! Amaurosis Fugax: • Abrupt loss of vision (Transient Monocular Blindness) secondary to ischemia or vascular insufficiency • Amaurosis Fugax is not equivalent to a TIA • If a patient does present with a new onset of amaurosis fugax, they should be treated as if they have had a TIA. The patient should see their Primary Care Physician (PCP) stat for a Cerebrovascular Accident (CVA) work up. Ocular Ischemic Syndrome: • Ocular and Periorbital pain (40%) • Prolonged recovery of vision following exposure bright light • Transient Monocular Blindness • Transient Ischemic Attack (TIA) • Giant Cell Arteritis Transient Monocular Blindness – may occur initially May be a predisposing factor for stroke • Thrombosis and occlusion Non Arteritic Anterior Ischemic Optic Neuropathy Treatment of Stroke: Diagnosis of Stroke: Two major prospective studies: • North American Symptomatic Carotid Endarterectomy Trial ( NASCET ) • European Carotid Surgery Trial