Download ocular manifestations of impending stroke

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
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An ischemic event that results in permanent dysfunction
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Exceeded only by heart disease and cancer as the leading
cause of death in the United States
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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:
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I Ischemia (80%)
II Hemorrhage (20%)
“Ischemic” cerebrovascular disease may occur in older patients, young adults and
even in children
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In the USA, historically intracranial hemorrhage (nontraumatic) has been
due to uncontrolled arterial hypertension and its eventual sequelae:
arteriolosclerosis
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Hypertensive hemorrhages typically occur in areas where
arteriolosclerosis is most severe:
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Basal ganglia (60%)
Thalamus (10%)
Pons (10%)
Cerebellum (10%)
Transient ischemic attack
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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
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The brain weighs ~ 3 pounds (1.4 kilograms)
One of the body’s biggest organs
Has ~ 100 billion nerve cells
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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.
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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:
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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:
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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
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Monitor patient closely with Primary Care
Physician
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Coumadin, Heparin, Aspirin therapy
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Treat ocular conditions accordingly
Ocular Manifestations of Impending Stroke:
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Emboli
Amaurosis Fugax (Transient Monocular Blindness)
Ocular Ischemic Syndrome (Hypoperfusion Retinopathy
Central Retinal Artery Occlusion
Branch Retinal Artery Occlusion
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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
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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:
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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)
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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 )
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European Carotid Surgery Trial