Ocular tilt reaction following lateral pontomedullary infarction.
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Biomedical subjects
Publications and source records attributed to J R Keane.
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Injury to cranial nerves is a common sequela of blunt head trauma. The olfactory, facial, and audiovestibular nerves are damaged most often, followed by the optic and ocular motor nerves. The trigeminal and lower cranial nerves are rarely involved. Chances of recovery are greatest for the facial nerve, intermediate for the ocular motor nerves, and least likely for the olfactory, optic, and audiovestibular nerves. Treatment is usually symptomatic, although steroids or surgical decompression of the optic and facial nerves can lead to dramatic results in selected patients.
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In 50 hospitalized patients with acquired immunodeficiency syndrome, signs of central eye movement limitation (28 cases) were most common. Peripheral eye movement limitations (18), abnormalities of vision (18), and abnormal spontaneous eye movements (15) occurred with about equal frequency. Meningitis (17), usually due to lymphoma (8) or Cryptococcus (8), was the usual cause of peripheral nervous system involvement, while toxoplasmosis (18) was more common than lymphoma (4) or presumed viral causes (8) in producing CNS dysfunction. The midbrain and pretectal (8) were affected about as often as the pontine tegmentum (9), but rostral brainstem lesions appeared to be the result of toxoplasmosis (4) or lymphoma (3), whereas a viral etiology was the presumed cause of most caudal stem involvement.
The pretectal syndrome occurred in 2.3% of patients personally examined over an 18-year period. The symptoms were nonspecific, but the signs (abnormal pupils in 198 patients, vertical gaze limitation in 180, disjunctive horizontal eye position in 90 and vertical in 79, lid retraction in 83, and convergence-retraction nystagmus in 71) were exquisitely localizing. The etiology, skewed by the local prevalence of cysticercosis, was hydrocephalus in 80 patients, stroke in 53, and tumor in 45. The importance of timely diagnosis was underscored by the relatively good prognosis of many patients.
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In 1887, the New York Neurological Society appointed a committee of distinguished neurologists to investigate the claim of ophthalmic surgeon George Thomas Stevens that he could cure chorea and epilepsy through correction of refractive errors and strabismus. After 2 1/2 years, the supervised therapeutic trial collapsed amid mutual recriminations. The commission issued a bland statement to the effect that the treatment was not curative and was insufficiently helpful to recommend. The idea of ocular reflex causation and surgical cure of "neuroses" persisted for several more decades in the face of increasing skepticism and resistance.
An automobile accident left a 26-year-old man in stupor with a complete right third-nerve palsy. Although fixed to light, the right pupil (only) exhibited continual concentric oscillations, initially at 1 Hz but slowing to 0.3 Hz during 2 weeks' observation. The pathophysiologic characteristics of this unique movement are uncertain but may involve central parasympathetic nervous system dysfunction.
Of 100 consecutive, adult, hospitalized inpatients with acquired unilateral oculosympathetic palsy, in 63 the central neuron was involved-usually due to strokes; in 21, tumor or trauma affected the preganglionic neuron; and in 13, postganglionic damage was sustained from a variety of causes. The preponderance of first neuron involvement by stroke is in part a reflection of patient sampling, but emphasizes the fact that central causes of Horner's syndrome are common.
Further evidence that the blink reflex to light is a brain stem reflex was provided by a patient who continued to blink to sudden illumination despite anoxic neocortical death with electrocerebral silence and absent summated cortical visual evoked responses.
A total of 94 patients had subarachnoid hemorrhage and it was strongly suspected in the remaining six patients. Acute encephalopathy associated with independent ocular hemorrhage due to hypoxia, multiple emboli, or bleeding tendencies was not a diagnostic problem during this study. Aneurysms occurred in 64 patients (combined with vascular malformations in four), isolated vascular malformations in four; "spontaneous" hematomas in 13, evidence of cryptic head trauma in six, hemorrhage from a glioblastoma in one, and no cause was identified in six patients. Retinal hemorrhages were more prominent ipsilateral to the site of intracranial bleeding. No single aneurysm location predominated and multiple aneurysms were common. The high mortality of 56% supports previous conclusions that retinal hemorrhages tend to accompany severe intracranial bleeding.
Hysterical hemianopias are uncommon and usually occur in association with other lateralized complaints. The most frequent pattern consists of decreased vision in one eye, an ipsilateral hemianopia on testing the "affected" eye, full fields in the other eye, and a complete hemianopia toward the affected side on testng with both eyes open. The incompatibility of the monocular and binocular fields quickly demonstrates the functional nature of this alleged visual loss.
Internuclear ophthalmoplegia (INO) is caused by lesions in the median longitudinal fasciculus. It is generally the result of primary intraaxial disorders, most commonly multiple sclerosis in young adults and infarction in older adults. Rarely, extraaxial disorders cause INO by compressing the brainstem. We report two patients with INO resulting from subdural hematoma with transtentorial herniation. These cases demonstrate that INO is a reliable, but not a pathognomonic, sign of a primary intraaxial disorder.
For 24 hours after an automobile accident, a 19-year-old comatose man exhibited spontaneous, intermittent, see-saw, rotatory, and downward eye movements with synchronous lid elevation. These unusual movements, which appear most closely related to nonpendular see-saw nystagmus and atypical ocular bobbing, probably resulted from the severe pontomedullary tegmental damage found at autopsy.
Painful bilateral orbicularis clonus on eccentric gaze developed in 2 patients with demyelinating disease. This unusual phenomenon was of variable intensity but persisted for years and did not respond to phenytoin or carbamazepine therapy.