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We report 2 patients who had eyelid retraction and eyelid lag with minimal impairment of vertical gaze. In both patients, magnetic resonance imaging demonstrated a circumscribed unilateral lesion immediately rostral and dorsal to the red nucleus involving the lateral periaqueductal gray area. Our clinical and radiological findings support the existence of a premotor eyelid control center in the region of the nucleus of the posterior commissure.

We report thirty-three patients with alternating skew deviation on lateral gaze. The right eye was hypertropic in right gaze, and the left eye was hypertropic in left gaze. Most patients had associated downbeat nystagmus and ataxia and were diagnosed as having lesions of the cerebellar pathways or the cervicomedullary junction. This contrasts with a previous report in which alternating skew was seen mainly in lesions of the midbrain pretectum.

Three patients who had slowly alternating skew deviation are described; each had elements of the Sylvian aqueduct syndrome. This combination of signs supports a pretectal location for lesions associated with alternating skew movements. Postmortem examination of a patient who died of chronic herpes simplex encephalitis showed extensive demyelination and periaqueductal spongiform degeneration; there was preservation of the oculomotor and trochlear nuclei, the medial longitudinal fasciculus, vestibular nuclei, and the interstitial nucleus of Cajal bilaterally. The slowly alternating dysconjugate vertical movements bear a resemblance to both see-saw nystagmus and the ocular tilt response.

We used [18F]fluoro-2-deoxyglucose positron emission tomography (PET) to study serial changes in the local cerebral metabolic rate of glucose in 5 patients with ischemic lesions of the posterior afferent visual system causing homonymous visual field defects. All 5 patients had striking impairment of glucose metabolism in the striate cortex shortly after ictus. In 2 patients, visual field defects abated, and repeat PET scans showed reduced size of the metabolic lesion and improvement of striate metabolism. Three patients did not recover vision, and repeat PET scans did not show improvement. Patients who recovered vision had ischemic lesions outside the occipital lobe, while those who did not experience improvement had primary damage to the occipital lobe itself.

Twenty-four patients with myasthenia gravis were treated with azathioprine. Eighteen of the patients tolerated the drug. Six discontinued azathioprine therapy because of toxicity. Of the 18 patients, 15 (83%) improved while receiving azathioprine; in 8 (44%) improvement was felt to result solely from azathioprine. Initial response was seen after 4 to 10 months of treatment, with a mean of 6.4 months. Patients continued to improve for up to 24 months, with the mean time of peak improvement being 14 months. Relapse occurred within one year in all 6 patients in whom azathioprine administration was discontinued. Azathioprine is a reasonable alternative to corticosteroids in selected myasthenic patients requiring immunosuppression.