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Conjugate Gaze Palsies

By Michael Rubin, MDCM, Professor of Clinical Neurology;Attending Neurologist and Director, Neuromuscular Service and EMG Laboratory, Weill Cornell Medical College;New York Presbyterian Hospital-Cornell Medical Center

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A conjugate gaze palsy is inability to move both eyes in a single horizontal (most commonly) or vertical direction.

Gaze palsies most commonly affect horizontal gaze; some affect upward gaze, and fewer affect downward gaze.

Horizontal gaze palsies

Conjugate horizontal gaze is controlled by neural input from the cerebral hemispheres, cerebellum, vestibular nuclei, and neck. Neural input from these sites converges at the horizontal gaze center (paramedian pontine reticular formation) and is integrated into a final command to the adjacent 6th cranial nerve nucleus, which controls the lateral rectus on the same side, and, via the medial longitudinal fasciculus (MLF), to the contralateral 3rd cranial nerve nucleus and the medial rectus it controls. Inhibitory signals to opposing eye muscles occur simultaneously.

The most common and devastating impairment of horizontal gaze results from pontine lesions that affect the horizontal gaze center and the 6th cranial nerve nucleus. Strokes are a common cause, resulting in loss of horizontal gaze ipsilateral to the lesion. In palsies due to stroke, the eyes may not move in response to any stimulus (eg, voluntary or vestibular). Milder palsies may cause only nystagmus or inability to maintain fixation.

Another common cause is a lesion in the contralateral cerebral hemisphere rostral to the frontal gyrus. These lesions are typically caused by a stroke. The resulting palsy usually abates with time. Horizontal conjugate gaze mediated by brain stem reflexes (eg, in response to cold-water caloric stimulation) is preserved.

Vertical gaze palsies

Upward and downward gaze depends on input from fiber pathways that ascend from the vestibular system through the MLF on both sides to the 3rd and 4th cranial nerve nuclei, the interstitial nucleus of Cajal, and the rostral interstitial nucleus of the MLF. A separate system descends, presumably from the cerebral hemispheres, through the midbrain pretectum to the 3rd and 4th cranial nerve nuclei. The rostral interstitial nucleus of the MLF integrates the neural input into a final command for vertical gaze.

Vertical gaze becomes more limited with aging.

Vertical gaze palsies commonly result from midbrain lesions, usually infarcts and tumors. In upward vertical gaze palsies, the pupils may be dilated, and vertical nystagmus occurs during upward gaze.

Parinaud syndrome (dorsal midbrain syndrome), a conjugate upward vertical gaze palsy, may result from a pineal tumor or, less commonly, a tumor or infarct of the midbrain pretectum. This syndrome is characterized by impaired upward gaze, lid retraction (Collier sign), downward gaze preference (setting-sun sign), convergence-retraction nystagmus, and dilated pupils (about 6 mm) that respond poorly to light but better to accommodation (light-near dissociation).

Downward gaze palsies

Impaired downward gaze with preservation of upward gaze usually indicates progressive supranuclear palsy; other causes are rare.