Download Neuro-Ophthalmic Manifestations of Stroke

Neuro-Ophthalmic Manifestations of Stroke
Kelly A. Malloy, OD, FAAO, Diplomate, Neuro-Ophthalmic Disease
Course Description: This course uses a case-based approach to focus on the prevention, diagnosis, and
treatment of stroke. Presented cases revolve around presenting features of stroke and causes of stroke in
younger versus older patients. Emphasis is placed on detailed history and exam techniques, as well as
proper work-up and referral.
Course Learning Objectives:
1. To be able to recognize visual field and ocular motility manifestations of stroke.
2. To be able to recognize visual, ocular, and systemic manifestations which suggest risk for stroke.
3. To be able to take the clinical ocular presentation and transform it into an anatomic localization of stroke.
4. To understand the importance of measuring blood pressure and pulse in patients suspected of stroke.
5. To understand the proper work-up related to stroke, both in acute and non-acute presentations.
6. To understand the necessary referrals and follow-up needed in dealing with stroke patients.
Course Outline:
I.
Neuro-Ophthalmic Manifestations Of Stroke
a. Types of Stroke
i. Ischemic
1. Embolic
2. Thrombotic
ii. Hemorrhagic
1. Intracerebral hemorrhage
2. Subarachnoid hemorrhage
b. Stroke Associations/ Risk Factors
i. Stroke in Older Patients
1.
2.
3.
4.
5.
6.
7.
8.
9.
Giant Cell Artertis
Hypertension
Diabetes
Hypercholesterolemia
Smoking
Sleep Apnea
Atrial Fibrillation
Carotid Stenosis
Ocular Ischemic Syndrome
a. Statistics Regarding Ocular Ischemic Syndrome:
i. A 40% Mortality Rate Reported In Patients With OIS
ii. The Most Common Symptom Is Slowly Progressive Vision
Loss, But 10% Report Sudden Vision Loss
iii. 40% Present With Pain
iv. 67-87% Present With Iris Neovascularization
v. 10-20% Are Asymptomatic At Time Of Diagnosis
vi. 86% Of Patients Are Smokers
vii. Risk Factors Include Diabetes, Ischemic Heart Disease, CerebroVascular Disease, Trauma, And Vasculitis (Need To R/O GCA)
b. Ocular / Visual Manifestations Of OIS
i. Transient Vision Loss (Amarosis Fugax)
ii. Red Eye (Episcleral Injection)
iii. Eye Pain
iv. Mid-Peripheral Retinal Hemorrhages
v. Uveitis
vi. Iris Neovascularization
vii. Neovascular Glaucoma
viii. Emboli (Hollenhorst Plaques)
ix. Optic Disc Edema (Ischemic Optic Neuropathy)
x. Retinal Artery Occlusion (CRAO / BRAO)
xi. Ophthalmic Artery Occlusion
xii. Retinal Or Disc Neovascularization
xiii. Venous Stasis Retinopathy
xiv. Homonymous Hemianopia
xv. Ocular Motility Problems (Cranial Nerve Palsy/Brainstem
Motility Disorder)
xvi. Supranuclear Gaze Abnormalities
ii. Stroke in Younger Patients
1. Hypercoaguable States
2. Sickle Cell Disease
a. Sickle gene present in 8% of black Americans
b. > 2 million Americans have sickle cell trait
c. > 30,000 have sickle cell disease, or sickle cell anemia (Hb SS)
d. Incidence of stroke in Hb SS = 10%
e. Incidence of stroke in Hb Sc = 2-5%
f. Vasculopathy and stasis in small arteries
g. Progressive segmental narrowing of arteries
h. Strokes are mostly thrombotic, but can be hemorrhagic
i. Incidence of stroke is highest at age 2-10, but can occur at any age
j. All children with sickle cell disease should be screened with
transcranial Doppler
i. Consider chronic transfusion therapy if at risk
k. Patients with a high number of sickle cell crises may be at higher
risk for stroke
3. Patent Foramen Ovale
a. Normally the foramen ovale closes at birth when increased blood pressure
on the left side of the heart forces the opening to close.
b. If the atrial septum does not close properly, it is called a patent foramen
ovale.
c. This type of defect generally works like a flap valve, only opening during
d.
e.
f.
g.
certain conditions when there is more pressure inside the chest. This
increased pressure occurs when people strain while having a bowel
movement, cough, or sneeze.
If the pressure is great enough, blood may travel from the right atrium to
the left atrium. If there is a clot or particles in the blood traveling in the right
side of the heart, it can cross the PFO, enter the left atrium, and travel out
of the heart and to the brain causing a stroke
25% of general population – usually asymptomatic
Diagnosis – Bubble Echocardiogram
Treatment – Medical, Surgical Closure
4. Carotid Artery Dissection
a. Pain On Side Of Face, Head, Or Neck
b.
c.
d.
e.
f.
g.
Oculosympathetic Paresis Without Anhydrosis
Delayed Retinal Or Cerebral Ischemia (50-95% Of Patients)
Annual Incidence 2.5 – 3/100,000
2% Of All Ischemic Strokes
Affects All Age Groups Including Kids
10-25% Of All Ischemic Strokes In Young And Middle Aged
Patients!
h. Carotid Artery Dissection Causes
i. Spontaneous
ii. Traumatic (Neck Extension)
iii. Fibromuscular Dysplasia
iv. Marfan’s Syndrome
v. Carotid Artery Dissection Manifestations
1. Horner’s Syndrome (painful)
- MRI / MRA/ CTA/ Angiogram
2. Carotid Artery Dissection Treatment
- Prevent Thromboembolic Complications
With Anticoagulation
i. IV Heparin; Oral Warfarin
ii. @3 Mos: MRA To Evaluate Intra
Luminal Irregularties
iii. @3 Mos: High Rate Of
Recanalization
iv. Heal Spontaneously
c. Neuro-Ophthalmic Features of Stroke
i. Homonymous Hemianopia
1. More Congruous = More Posterior
2. Less Congruous = More Anterior
3. Calcarine Artery
4. Most Occluded PCA Branch (Isolated Homonymous Hemianopia)
5. Occluding Mechanisms:
a. Vertebral-Basilar Emboli
b. Emboli From Distant Site
c. PCA Stenosis
6. Homonymous Hemianopia Prognosis
a. Some Improvement Possible With Resolution Of Acute Edema
b. Improvement usually occurs in first year
c. Over Age 40 – Think Infarct
d. Under Age 40 – Think Non-Infarctive Cause
7. If has respect for BOTH horizontal and vertical meridian, think occipital lobe
infarct
8. Bilateral occipital lobe infarcts can look like bilateral altitudinal VF defects
9. Visual fields give evidence of the size, shape and location of the infarct in the
occipital lobe
ii. Ocular Motility Issues
1. Internuclear Ophthalmoplegia (INO)
a. Adduction deficit
b. Abducting Nystagmus in fellow eye
c. Can be unilateral (INO) or bilateral (BINO)
d. Medial Longitudinal Fasciculus (MLF) in brainstem
e. If convergence affected, think Midbrain
f. If convergence spared, think Pons or Medulla
2. Skew Deviation
a. Vertical Misalignment
3.
4.
5.
6.
iii.
Visual Field Neglect
1.
2.
3.
4.
iv.
b. Higher Eye Is Intorted, Lower Eye Is Extorted
c. May Have Head Tilt
d. May Have Tilt Of Subjective Visual Vertical
i. Double Maddox Rod test to check for torsion
e. Localization:Vestibular Nerve/Nuclei, Medulla, Pons, Midbrain
Gaze Palsy
a. Lesion of CN VI nucleus or PPRF (brainstem)
i. Eyes Do Not Look To The Ipsilateral Side
ii. Eyes May Point Away From The Lesion
- Contralateral Hemiparesis – Corticospinals
iii. Eyes Point To The Paralyzed Side
b. Supranuclear Origin
i. Gaze Palsy / Gaze Preference (Supranuclear Cause)
1. Cerebral Infarct – Supranuclear
2. Contralateral Eye Movements Affected – Eyes
Point Toward Side Of Lesion
3. Often Associated With Hemiparesis
4. Eyes Pointing Away From Paralyzed Side
One-and –a – Half Syndrome
a. Gaze Palsy in one direction of gaze
b. INO in opposite direction of gaze
Vertical Eye Movement Restrictions
a. Thalamic infarcts
Nystagmus
a. Brainstem infarcts
Anterior Circulation Problem
Neglect Of The Left Visual Field
May Have A Superior Left Homonymous
Often Accompanied By Left Hemisparesis & Hemisensory Loss
a. Large Inferior Division MCA Territory Infarct Of Right Temporal
Lobe
Disorders Of Visual Association Cortex / Higher Visual Function
Ventromesial Pathway “What It Is”
a. Association Cortices Beneath Calcarine Fissure & Adjacent
Temporal Regions
b. Visual Object Recognition, Reading, Color Vision
2. Dorsolateral Pathway “Where It Is”
a. Association Cortices Above Calcarine Fissures And In Adjacent
Parietal, Temporo-Parieto-Occipital Regions
3. Visual Agnosia
a. Unable To Recognize Objects That Are Seen
b. Aperceptive Agnosia – Image Of The Object Is In Some Way
Distorted And Cannot Be Recognized
c. Associative Agnosia – Image Is Clear, But Connections To
Association Visual Cortex Are Impaired Not Allowing Recognition
i. Prosopagnosia
1. Cannot Recognize Familiar & Own Face
2. Bilateral Occipital Temporal Lesions
3. Damage To Inferior Longitudinal Fasciculus Near
Its Occipital Temporal Origin
4. Disconnection Of Occipitotemporal Cortex
Specialized For Facial Recognition
1.
4. Alexia Without Agraphia
a. Cannot Read But Can Write; “Word Blind”
b. Can Read Numbers
c. Can Spell Words Upon Request
d. Difficulty Naming Colors May Have Right Homonymous,
Prospagnosia, Or Visual Object Agnosia
e. Infarct Of Left Visual Association Cortex And Splenium Of Corpus
Callosum; Occlusion Of PCA
5. Alexia With Agraphia
a. Cannot Read, Write Or Spell
b. Cannot Recognize A Word That Is Spelled
c. Cannot Interpret Word Pictures
d. Cannot Evoke The Images Of Words To Write Them Down
e. Ok With Spoken Language
f. Infarct In The Angular Gyrus Of Dominant Hemisphere
6. Central Achromotopsia
a. Acquired Disorder Of Color Perception Involving All Or Part Of The
Visual Field
b. Visual Association Cortices In The Middle Third Of The Fusiform
And Lingual Gyrus
c. Area V1 With Underlying Radiations Are Spared
7. Balint’s Syndrome
a. Optic Ataxia- Defective Hand Control
b. Ocular Apraxia- Defective Gaze Control
c. Simultanagnosia- Unable To Synthesize All The Features In An
Array
d. Bilateral Posterior Parietal Occipital Infarction
8. Akinetopsia
a. Motion Blindness
b. Area V5 Of Association Visual Cortex
c. Posterior Bank Of Superior Temporal Sulcus
d. A “Motion Funnel” – All Information Related To Motion Is Relayed
Through V5
e. Retina Must Be Normal
II.
Other Neurologic Manifestations Of Stroke
1.
2.
3.
4.
5.
6.
Carotid Bruit
Hemiplegia
Hemianesthesia
Aphasia
Headache
Speech Disturbances
b. Quality of Life Issues Related to Stroke
i. Loss of independence
ii. Inability to drive / loss of driver license
iii. Inability to communicate
c. Stroke Work-up
i. In-office testing
1. Blood Pressure
a. Should be done in BOTH arms
2. Pulse
a. Rate
b. Rhythm
c. Need to consider Atrial Fibrillation
3. Neurologic assessment
a. Cranial nerve testing
b. Motor
i. weakness
c. Sensory
d. Coordination
i. ataxia
e. Rhomberg test
ii. Additional Work-up
1. Neuro-Imaging
a. MRI / MRA / CT/ CTA of head / neck
b. Does location of stroke correlate with clinical presentation
c. Could the presentation indicate a new stroke?
2. Carotid Doppler
3. Cardiology Consult
a. Echocardiogram
b. EKG
c. Bubble Echocardiogram
4. Neurology Consult
5. Consult with vascular surgeon (if carotid stenosis present)
a. NASCET (N Eng J Med. 1991; 325: 445-453.)
b. North American Symptomatic Carotid Endarterectomy Trial
i. Symptomatic With Stenosis > 70%
1. Carotid Endarterectomy Is Recommended
ii. Symptomatic With Stenosis 50-70%
1. Carotid Endarterectomy Is Indicated
iii. 2.1% Perioperative Risk Of Stroke And Death
iv. Surgical Tx Of Asymptomatic Carotid Stenosis Is
Controversial
c. Other Surgical Treatment Options
i. Pericutaneous Transluminal Angioplasty
ii. Internal Carotid Artery Stent
6. Lab testing
a. CBC, platelets, ESR, C-reactive protein (r/o GCA)
b. Hypercoagulable states
i. Homocysteine levels
1. Amino acid in blood
2. Increased with vit B 12 deficiency, folate deficiency,
genetic causes or renal disease
3. Related to greater risk of
- Cardiovascular disease
- Stroke
- Peripheral vascular disease
- Heart attack
- Alzheimer’s disease
- Deep Venous Thrombosis
ii. Sickle Cell Screen
iii. other hypercoagulable states (especially in young pts with no
other risk factors)
c. Lipid Panel
d. ANA, etc
d. Treatment
i. Controlling risk factors
ii. t-PA
iii. Blood thinners
iv. Therapy
v. Managing symptoms