Diplopia/Nystagmus

Diplopia/Nystagmus: Excerpt from Field Guide to Bedside Diagnosis

Differential Overview

Diplopia

❑ Alcohol

❑ Diabetes

❑ Brainstem ischemia/lesion

❑ Grave disease

❑ Multiple sclerosis

❑ Ophthalmoplegic migraine

❑ Myasthenia gravis

❑ Wernicke encephalopathy

❑ Zygoma fracture

❑ Basilar meningitis

❑ Posterior communicating artery aneurysm

❑ Cavernous sinus thrombosis

❑ Syphilis

❑ Guillain-Barré variant

❑ Botulism

Nystagmus

❑ Labyrinthitis

❑ Multiple sclerosis

❑ Oculogyric crisis

❑ Cerebellar lesion

❑ Brainstem lesion

❑ Frontal lesion

❑ Occipital lesion

❑ Dorsal midbrain lesion

❑ Heavy metal intoxication

❑ Congenital

Diagnostic Approach

The direction of gaze with the most prominent diplopia reflects the action of the paretic muscle. Binocular diplopia is due to ocular misalignment, and the patient will usually close one eye to compensate. Acute monocular diplopia can occur with corneal aberrations, cataract, or foveal traction.

CN III paresis: The lateral rectus and superior oblique are unopposed, turning the eye outward and downward. An acute lesion may be peripheral (diabetic or ischemic) or central (posterior communicating artery aneurysm or
cavernous sinus lesion). Both have ptosis, absent eye elevation, and adduction, but a peripheral lesion has normal pupil size and movement (“pupillary sparing”). A central lesion produces a pupil that is dilated and unresponsive to light or accomodation. Causes include tumor, aneurysm, or severe trauma. Unilateral third nerve palsy with contralateral superior rectus palsy and bilateral partial ptosis, and bilateral third nerve palsy always represents a central lesion. Unilateral external ophthalmoplegia with normal contralateral superior rectus function, unilateral internal ophthalmoplegia, and unilateral ptosis represents a peripheral lesion.

CN IV paresis: Superior oblique weakness produces vertical diplopia. The patient tilts his or her head to the opposite side to lessen the displacement. Typical causes are a relatively minor head blow, and idiopathic.

CN VI paresis: Lateral rectus palsy produces weakness in abduction and horizontal diplopia that is better in near than in distant vision. When CN V is also affected (reduced facial sensation around the upper face and cornea), a cavernous sinus lesion should be suspected. Papilledema should also be looked for, as it indicates a mass lesion displacing the brainstem.

If the patient has an isolated lesion of one of the cranial nerves, pain will be localized to just above the eyebrow on the weak side. Intraorbital pathology is indicated by pain in the eye itself or on eye movement. The worst headache of the patient’s life raises concern for intracranial aneurysm.

True nystagmus is characterized by rapid regular oscillations around a fixed point not just with lateral gaze but also when the eyes are looking forward. A few beats of nystagmus at extremes of gaze are not pathologic. Nystagmus of ocular causes has a pendular motion whereas disease in the central nervous system produces fast and slow components. Irregular bursts of rapid eye movements (saccadic intrusions) almost always indicate a cerebellar lesion.

Internuclear ophthalmoplegia occurs when the oculomotor and abducens nerves (CN III and VI) are disconnected at the medial longitudinal fasciculus. When conjugate gaze is attempted, one eye will not adduct medially and the abducting eye (lateral gaze) will show nystagmus. This finding is seen in persons with multiple sclerosis and pontine vascular lesions.

Clinical Findings

Alcohol  Diplopia occurs with acute intoxication.

Diabetes  The third nerve is typically affected with sparing of pupillary fibers.

Brainstem ischemia/lesion  Vertebrobasilar transient ischemia is associated with vertigo, numbness of the ipsilateral face and contralateral limbs, dysarthria, and dysphagia in addition to the diplopia. A third nerve lesion with contralateral tremor results from a lesion of the red nucleus. A third nerve lesion with contralateral spastic hemiparesis is caused by a ventral lesion involving the corticospinal tract (Weber syndrome). A brainstem lesion characteristically produces vertical nystagmus, which is more marked when the patient gazes toward the side of the lesion. An abducens nucleus lesion produces an ipsilateral gaze palsy with ipsilateral absent “doll’s eyes” and calorics.

Grave disease  Exophthalmos and lid lag are present as are general symptoms of hypermetabolism. Primary position strabismus and incomplete eye movements may be present. Diplopia is due to muscle tightness, so the involved muscle works opposite the position of worst images.

Multiple sclerosis  Important clues are optic neuritis, internuclear ophthalmoplegia, and a prior history of sensory neurological lesions. The Charcot triad of nystagmus, intention tremor, and scanning speech is a classic
presentation.

Ophthalmoplegic migraine  Unilateral headache, nausea, and visual phenomena such as scintillating scotoma are clues to a migraine.

Myasthenia gravis  Diplopia fluctuates. An isolated fourth or sixth nerve palsy is associated with unilateral or bilateral ptosis. The pupillary reaction is normal.

Wernicke encephalopathy  Paresis of the abducens nerve, horizontal diplopia, and nystagmus occur in a malnourished alcoholic patient.

Zygoma fracture  Following facial trauma, the inferior oblique muscle may become trapped leading to paresis of upward gaze. Ataxia, confusion, and polyneuropathy are additional findings.

Basilar meningitis  Unilateral or bilateral sixth nerve palsy is an early sign. Cancer, tuberculosis, sarcoidosis, or cryptococcosis may cause this syndrome.

Posterior communicating artery aneurysm  Most patients have intense headache, stupor or coma, and complete (central) third nerve paralysis.

Cavernous sinus thrombosis  Retro-orbital headache is followed by polyneuropathic ophthalmoplegia (III, IV, V, VI), proptosis, and chemosis.

Syphilis  An Argyll-Robertson pupil accommodates but does not react. A self-limited genital chancre is usually recalled.

Guillain-Barré variant  Bilateral polyneuropathic ophthalmoplegia is associated with areflexia and ataxia.

Botulism  Diplopia is a common presenting symptom. Concomitant features include bilateral ptosis, mydriasis, dysphagia, dysphonia, vomiting, limb cramping, and generalized muscle weakness. Consumption of possibly contaminated canned food within 6 to 36 hours is a key clue.

Labyrinthitis  Nystagmus responds to positional changes of the head (Dix-Hallpike maneuver) with a latency of response of 3 to 10 seconds and is fatigable. Rotatory nystagmus is typical.

Oculogyric crisis  Tonic upgaze is seen in Parkinson disease, and tonic downgaze, in phenothiazine reaction.

Cerebellar lesion  An irritative lesion produces coarse movement toward the side of the lesion, and fine movement away from it. There is no latency with head movement and little vertigo.

Frontal lesion  There is tonic deviation ipsilateral to the lesion and saccadic palsy contralateral to the lesion. Calorics are normal.

Occipital lesion  There is ipsilateral pursuit palsy with normal calorics.

Dorsal midbrain lesion  It presents with paralysis of upgaze, large Argyll-Robertson pupils, no vertical pursuit, and lid retraction. Causes include thalamic hemorrhage, metabolic encephalopathy, pineal tumor, and syphilis.

Heavy metal intoxication  Nystagmus occurs in intoxication, particularly with manganese or lead.

Congenital  Nystagmus is present from childhood, and the macula is hypopigmented.

Book Source Details

• Book Title: Field Guide to Bedside Diagnosis
• Author(s): David S. Smith
• Year of Publication: 2007
• Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.

More About Diplopia

• Back to disease: Diplopia: Introduction
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Field Guide to Bedside Diagnosis Authors: David S. Smith Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-78178-165-5

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