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Nystagmus refers to the involuntary oscillations of one or, more commonly, both eyeballs. These oscillations are usually rhythmic and may be horizontal, vertical, rotary, or mixed. They may be transient or sustained and may occur spontaneously or on deviation or fixation of the eyes. Minor degrees of nystagmus at the extremes of gaze are normal. Nystagmus when the eyes are stationary and looking straight ahead is always abnormal. Although nystagmus is fairly easy to identify, the patient may be unaware of it unless it affects his vision.
Nystagmus may be classified as pendular or jerk. Pendular nystagmus consists of horizontal (pendular) or vertical (seesaw) oscillations that are equal in rate in both directions and resemble the movements of a clock’s pendulum. Jerk nystagmus (convergence-retraction, downbeat, and vestibular), which is more common than pendular nystagmus, has a fast component and then a slow — perhaps unequal — corrective component in the opposite direction. (See Classifying nystagmus.)
Nystagmus is considered a supranuclear ocular palsy — that is, it results from pathology in the visual perceptual area, vestibular system, cerebellum, or brain stem rather than in the extraocular muscles or cranial nerves III, IV, and VI. Its causes are varied and include brain stem or cerebellar lesions, multiple sclerosis, encephalitis, labyrinthine disease, and drug toxicity. Occasionally, nystagmus is entirely normal; it’s also considered a normal response in the unconscious patient during the doll’s eye test (oculocephalic stimulation) or the cold caloric water test (oculovestibular stimulation).
Begin by asking the patient how long he’s had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and an altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
An insidious onset of jerk nystagmus may occur with tumors of the brain stem and cerebellum. Associated characteristics include deafness, dysphagia, nausea and vomiting, vertigo, and ataxia. Brain stem compression by the tumor may cause signs of increased ICP, such as an altered LOC, bradycardia, a widening pulse pressure, and an elevated systolic blood pressure.
With encephalitis, jerk nystagmus is typically accompanied by an altered LOC ranging from lethargy to coma. Usually, it’s preceded by sudden onset of a fever, a headache, and vomiting. Among other features are nuchal rigidity, seizures, aphasia, ataxia, photophobia, and cranial nerve palsies, such as dysphagia and ptosis.
Brain stem injury may cause jerk nystagmus, which is usually horizontal. The patient may also display pupillary changes, an altered respiratory pattern, coma, and decerebrate posture.
Acute labyrinthitis is an inner ear inflammation that causes a sudden onset of jerk nystagmus, accompanied by dizziness, vertigo, tinnitus, nausea, and vomiting. The fast component of the nystagmus is toward the unaffected ear. Gradual sensorineural hearing loss may also occur.
Ménière’s disease is an inner ear disorder that’s characterized by acute attacks of jerk nystagmus, severe nausea and vomiting, dizziness, vertigo, progressive hearing loss, tinnitus, and diaphoresis. Typically, the direction of jerk nystagmus varies from one attack to the next. Attacks may last from 10 minutes to several hours.
A stroke involving the posterior inferior cerebellar artery may cause sudden horizontal or vertical jerk nystagmus that may be gaze dependent. Other findings include dysphagia, dysarthria, loss of pain and temperature sensation on the ipsilateral face and contralateral trunk and limbs, ipsilateral Horner’s syndrome (unilateral ptosis, pupillary constriction, and facial anhidrosis), and cerebellar signs, such as ataxia and vertigo. Signs of increased ICP (such as an altered LOC, bradycardia, a widening pulse pressure, and an elevated systolic pressure) may also occur.
Jerk nystagmus may result from barbiturate, phenytoin, or carbamazepine toxicity or from alcohol intoxication.
Prepare the patient for diagnostic tests, such as electronystagmography and a cerebral computed tomography scan.
In children, pendular nystagmus may be idiopathic or it may result from early impaired vision associated with such disorders as optic atrophy, albinism, congenital cataracts, or severe astigmatism.
Read excerpts from these other book chapters related to Nystagmus:
Copyright Details: Handbook of Signs & Symptoms (Third Edition), Copyright © 2008 Williams & Wilkins.
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More About This Book:
Title: Handbook of Signs & Symptoms (Third Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 1-58255-402-1 
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