Eye movement disorders

Professor Dr. Ayman Youssef Ezeddin Eassa

Diplopia

 Concomitant strabismus (ophthalmological) deviation is constant. Non concomitant strabismus (neurological) varies with gaze deviation (paralyticrestrictive)

 Heterophoria: tendency for ocular misalignment Heterotropia: manifest under stress;

Fatigue Bright sun Alcohol Anticonvulsants Sedatives

Double vision
Onset is always abrupt. Cover one eye relieves the problem. May be intermittent. Solved by or compensated by head position as:
Congenital superior oblique palsy Ocular myasthenia Thyroid ophthalmopathy

Double vision

Present as:

Overlapping images (ghosting) Frank diplopia Blurred vision

Physiologic diplopia

Double vision
Image may be
Tilted oblique muscle Vertical lateral muscles Horizontal depressor & elevator muscles

 Monocular diplopia: (double vision persists when closing one eye.)

Refractory error Psychogenic Retinal Cerebral cortex Pinhole test solves the problem of diagnosis. **

Clinical assessment
Cover one eye Daily variation (morning and evening). Affected by fatigue Images separated
Vertically Horizontally Or oblique

Distance between images constant despite the gaze direction or vary. Worse for near or distance. Do eye lids drop Influenced by head posture. The progression course

Clinical assessment (cont.)

Associated symptoms
Headache Dizziness Vertigo Weakness (general)

Medications received Family history Eye surgery

Clinical assessment (cont.)

Lateral rectus
Worse at distance & looking to the side of weak muscle.

Superior oblique
Worse on downward to side opposite weak muscle Difficult reading, watching TV in bed, going downstairs

Medial rectus
Worse for near than far & to contralateral side more

Clinical assessment (cont.)

General inspection
Ptosis (MG) Ptosis + dilated pupil occulomotor nerve palsy Lid lag thyroid Lid retraction
3rd nerve Dorsal midbrain lesion Hypokalemic periodic paralysis Chronic steroid use Orbital lesion Inflammatory (periorbital swelling, conjunctival injection) Psseudotumor Lymphoma Dural sinus

Proptosis

Clinical assessment (cont.)

Head posture to compensate Sensory visual function
Acuity Color vision Confrontation Field of vision

Stability of fixation
Stability of gaze holding mechanism

Clinical assessment (cont.)

Versions (pursuit, saccades & ocular muscle over reaction) Convergence
( )

Ductions

Ocular alignment & muscle balance

Should neutralize the head tilt

Clinical assessment (cont.)

Pupils Lids Dolls eyes Bells phenomenon Bruit Edrophonium test Forced ductions

Causes
Encephalopathy HIV Basilar meningitis or neoplastic infiltrates Botulism Brain stem lesions (stroke, encephalitis) Carotid cavernous fistula Cavernous sinus thrombosis Fisher syndrome Intoxications MS myasthenia

Causes (cont.)
Leighs disease (subacute necrotizing encephalopathy) Orbital pseudotumor Paraneoplastic encephalopathy Associated with polyradiculopathy Psychogenic Tolosa-Hunt syndrome Trauma Wernickes encephalopathy Myopathies: mitochondrial, fiber type disproportion Vitamin E deficiency Supra-para nuclear gaze palsy

Abnormalities of optic nerve and retina

Swollen optic disc

True Pseudo
Clear peripapillary nerve fibers No spontaneous venous pulsations (SVP) Presence of hemorrhages Hereditary optic disc drusen white people more (more axonal degeneration) Retinitis pigmentosa

Unilateral optic nerve (disc) edema

Optic neuritis (papillitis if swollen disc occur) Anterior ischemic optic neuropathy Orbital comprssion lesions Central retinal vein occlusion Leukemia infiltrates Neuropathy delayed radiation effect Lebers hereditary optic neuropathy

Differentiation of early papilledema and pseudo one

Papilledema Pseudopapilledema

Disc color Margins

Disc elevation & vessels Nerve fiber layer

hemorrhages

Hyperemic Indistinct at superior & inferior poles, later entire Minimal SVP (-) Dull May obscur blood vessels Splinter

Pink yellowish Irregular blurred

Center of disc most elevated SVP No edema

Retinal, subretinal

Papilledema
= optic disc swelling secondary to ICP. Acutely central visual acuity is generally normal. Enlargement of the physiological blind spot, concentric constriction and inferior visual fields loss. 4 stages for papilledema:
Early Acute Chronic atrophic

Papilledema (cont.)
Malignant hypertension. Diabetic papillopathy. Anemia. Hyperviscosity syndromes. Pickwickian syndrome. Hypotension. Severe blood loss. COPD ? Giant cell temporal arteritis. Methanol poisoning.

Optic neuropathy with normally appearing optic disc = retrobulbar optic neuritis

Unilateral Optic neuritis Compressive lesion (visual loss)examination: ? Normal (=field defects in fellow eye compressive) Giant celll arteritis Other vasculitides Post stroke, severe blood loss

Bilateral Nutritional Tobacco-alcohol Vitamin B12 deficiencies Folate deficiency Toxic heavy metal Drug related
Chloramphenicol Isoniazide Chloroprpamide

Bilateral compressive Bilateral retrobulbar