Carotid endarterectomy and its alternatives in managing amaurosis fugax.
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Blindness↗
Biomedical subjects
J D Trobe
Publications and source records attributed to J D Trobe.
Visual loss in tuberous sclerosis.
Of 11 patients with tuberous sclerosis complex (TSC) treated from 1980 to 1990 for obstructive hydrocephalus secondary to subependymal giant-cell astrocytoma, four had adequate documentation to determine visual outcome. Despite surgical relief of elevated intracranial pressure in all cases, two patients sustained further visual loss. In one patient, visual loss was arrested, and in one patient, it was prevented. Although hydrocephalus is uncommon in TSC, its effects on the optic nerves are serious and eventually irreversible. Because TSC patients may not be able to express early symptoms of increased intracranial pressure, periodic ophthalmologic examination and brain imaging may be advisable when a subependymal lesion has been identified.
Adolescent↗
Idiopathic photoreceptor dysfunction causes unexplained visual acuity loss in later adulthood.
Progressive visual loss, caused by initially unrecognized retinal photoreceptor dysfunction predominantly affecting cones, developed in six patients in late adulthood. Because of minimal ophthalmoscopic retinal abnormalities, the patients initially had been suspected of having optic neuropathy or psychogenic visual loss. The correct diagnosis was ultimately established by finding electroretinographic abnormalities and color discrimination losses out of proportion to visual acuity loss. In no case was a causative agent or a family history of photoreceptor disease identified. In many other respects, however, features of the patients' illness resemble those described previously under the headings of cone dysfunction syndrome, cone dystrophy, cone degeneration, and cone-rod dystrophy.
Aged↗
MR imaging of the brain in five members of a family with Pelizaeus-Merzbacher disease.
MR imaging was performed in five members of a family afflicted with Pelizaeus-Merzbacher disease. The individuals imaged included a male proband, his mother, and three maternal uncles. Clinically affected members showed generalized white matter signal aberration consistent with dys- and demyelination, basal ganglia, and thalamic signal aberration suggestive of pathologic iron storage and diffuse brain atrophy. These findings are similar to those seen in other leukodystrophies. The proband's mother was normal by neurologic examination but showed a suspicious but not definitely abnormal similar pattern of basal ganglionic and white matter signal aberration. In our limited patient sample, MR appears to be able to: (1) demonstrate a pattern of imaging abnormalities characteristic of Pelizaeus-Merzbacher disease (we do not know if this pattern is specific); (2) potentially detect the obligate carrier state; and (3) detect the facultative carrier state.
Adult↗
Angle-closure glaucoma as initial presentation of myelodysplastic syndrome.
A 57-year-old man presented with proptosis of the right eye and findings consistent with bilateral angle-closure glaucoma. Subsequent evaluation revealed severe bilateral uveal effusions and associated nonrhegmatogenous retinal detachments, which were felt to be related to orbital pseudotumour and associated scleritis. Hematologic studies were consistent with a diagnosis of myelodysplastic syndrome. Although myelodysplastic syndrome has been reported in one patient with orbital inflammation and myositis, to our knowledge ciliochoroidal effusion and secondary angle closure have not previously been reported in myelodysplastic syndrome.
Exophthalmos↗
Visual outcome in cystic craniopharyngiomas treated with intracavitary phosphorus-32.
Seven patients with cystic craniopharyngiomas were treated with stereotactic instillation of radioactive phosphorus-32 (32P). Five patients had been previously treated with various combinations of surgery and external beam irradiation, whereas two had the 32P instillation at a primary therapy. Visual acuity improved in 13 eyes and remained stable in 1. Visual fields normalized in three patients, improved in two, and remained stable in two. Two patients received single treatments with 32P, whereas five required multiple instillations for recurrent cyst expansion.
Adolescent↗
Bilateral optic nerve compression as a mechanism for the Foster Kennedy syndrome.
An 11-year-old boy with a juvenile nasopharyngeal angiofibroma developed optic disc pallor in one eye and optic disc edema in the other eye (Foster Kennedy Syndrome [FKS]). The mechanism was believed to be bilateral, asymmetric optic nerve compression. Review of the 36 previously reported cases of FKS revealed that 12 cases (33%) were probably also caused by bilateral optic nerve compression. Only eight (22%) of the cases satisfied Foster Kennedy's original hypothesis for the pathogenesis of his syndrome, namely, direct compression of one optic nerve causing atrophy and increased intracranial pressure causing contralateral papilledema. In 15 (41%) reported cases of FKS, descriptions were inadequate to determine a mechanism, while two (5%) were probably caused by long-standing increased intracranial pressure without direct optic nerve compression. The authors believe that as sophisticated imaging permits earlier diagnosis and more precise localization, most future cases of FKS caused by mass lesions will be found to result from bilateral direct optic nerve compression.
Child↗
Optic tract injury after anterior temporal lobectomy.
Three patients had complete homonymous hemianopia with clinical and neuroimaging characteristics of ipsilateral optic tract infarction after anterior temporal lobectomy for seizure control. This injury presumably resulted from irritative vasospasm of the anterior choroidal artery. The features of this pure optic tract syndrome should be distinguished from the more common compressive optic tract syndrome which generally also impairs ipsilateral optic nerve function.
Adult↗
Don't let high-tech tests beget low-quality care.
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Health Services↗
Third nerve palsy and the pupil. Footnotes to the rule.
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Humans↗
Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension. A clinicopathologic case study.
A 59-year-old woman with anemia became totally blind after repeated gastrointestinal bleeding and acute hypotension. Neuropathologic examination was normal apart from bilateral infarctions centered on the orbital portion of the optic nerves. This is the only "pure" histopathologic study of visual loss after hemorrhage and hypotension in the recent literature, the single previous case being complicated by arteriosclerosis and vasculitis. The authors suggest that visual loss after hypotension is of three types. Profound hypotension in patients with neither anemia nor arteriosclerosis generally causes water-shed infarctions in the parietal and occipital lobes. Brief hypotension combined with arteriosclerosis favors juxtalaminar optic nerve infarction indistinguishable from spontaneous anterior ischemic optic neuropathy. In anemic patients without arteriosclerotic risk factors, hypotension is likely to cause infarction in the orbital optic nerve, where pial end vessels are subject to compression from hypoxic edema.
Blindness↗
Carotid endarterectomy. Who needs it?
Although carotid endarterectomy is one of the most frequently performed operations in this country, recent evidence casts doubt on its advisability, particularly for patients with ocular manifestations of cerebral ischemia. The following evidence is that: the risk of future stroke in untreated patients with amaurosis fugax, retinal plaques, and infarcts is less than 3% per year, far lower than that expected for cerebral (hemispheric) transient ischemic attacks (TIAs); the perioperative risk of stroke and death after endarterectomy may be much higher than previously suspected; and aspirin is a comparatively risk-free and moderately effective alternative to endarterectomy. Because of the questions raised about the risk-to-benefit ratio of endarterectomy, patients with ocular manifestations of cerebral ischemia should be considered for this operation only as part of a proposed randomized collaborative study.
Carotid Arteries↗
Isolated third nerve palsies.
In the diagnostic assessment of patients with N III palsies, the examiner should first endeavor to determine if the palsy is isolated, that is, unassociated with other contributory neurologic findings. If any other abnormalities are present, they should be used to localize the lesion and to help direct ensuing neuroradiologic studies. If the palsy is isolated, the presence of pupil sparing, together with advanced age or a vasculopathic background probably indicates that an extra-axial infarction of the nerve has taken place. The patient may safely be observed periodically without radiographic studies. In younger patients or those without significant vasculopathy, the status of the pupil should not be a major determinant of management. Moreover, the clinician must be aware that pupil sparing is expected when the vulnerable superior division of N III is selectively involved in cavernous sinus compressive lesions. "Pseudo pupil-sparing" in aberrant N III regeneration and in coexisting parasympathetic and sympathetic pupillomotor paresis is a pitfall to be avoided. When one of the muscles subserved by N III appears to be misfunctioning, the diagnosis is rarely that of a partial N III palsy. Instead, the causative lesion is more likely to be in the muscles themselves, the neuromuscular junction, or in the gaze pathways converging on the N III subnuclei.
Brain Diseases↗
Isolated pupil-sparing third nerve palsy.
The challenge in managing patients with pupil-sparing third nerve palsies is met most efficiently by dividing such patients into three groups according to the relative deficits in pupillomotor and extraocular muscle function: (1) patients with a normal pupillary sphincter and completely palsied extraocular muscles. Such patients should not have cerebral angiography if they are aged 50 or more; (2) patients with a normal pupillary sphincter and incompletely palsied extraocular muscles. Such patients should have angiography, particularly if the inferior oculomotor division is spared; (3) patients with a subnormal pupillary sphincter and completely palsied extraocular muscles ("relative pupil-sparing"). Such patients should have angiography unless they have clear-cut vasculopathic findings.
Aged↗
Upgaze paralysis caused by lesion of the periaqueductal gray matter.
A 61-year-old man with upgaze paralysis was found on postmortem examination to have had a single lesion of the brain stem confined to the periaqueductal gray matter between the levels of the superior and inferior colliculi. Most previous neuropathologic cases reported in human beings have consisted of much larger lesions with common involvement of the posterior commissure and pretectum. We suggest that the lesion in this case caused upgaze paralysis either by interrupting descending fibers from the interstitial nucleus of Cajal or by destroying neurons located within the periaqueductal gray matter.
Brain Diseases↗
Septic cavernous sinus thrombosis associated with gingivitis and parapharyngeal abscess.
A 29-year-old previously healthy man died of spread of infection from gingivitis to both parapharyngeal (pharyngomaxillary) spaces and to the cavernous sinus. The diagnosis was delayed because gingival and parapharyngeal sources of cavernous sinus thrombosis were not initially considered, and the ophthalmic congestion was believed at first to represent orbital cellulitis rather than cavernous sinus thrombosis.
Abscess↗
Cyclodeviation in acquired vertical strabismus.
The prevalence and pattern of cyclodeviation can differentiate among superior oblique palsy, dysthyroid ophthalmopathy, myasthenia gravis, and skew deviation. Excyclodeviation was detected in 30 of 33 patients with superior oblique palsy, eight of 15 patients with dysthyroid ophthalmopathy, three of six patients with nondysthyroid restrictive ophthalmopathy, and one of 13 patients with myasthenia. No cyclodeviation was found in cases of skew. Incyclodeviation was found in two patients with dysthyroid ophthalmopathy, two with nondysthyroid restrictive ophthalmopathy, and three with myasthenia. The amount of cyclodeviation did not vary between head-tilt positions, but did vary between primary and eccentric gaze positions, usually in the same direction as the amount of hyperdeviation. The patient's awareness of the presence of cyclodeviation varied with the degree of cyclodeviation, being 100% (4/4) for 15 degrees, 86% (12/14) for 10 degrees, and only 55% (11/21) for 5 degrees.
Eye Movements↗
Microcomputer-based testing of proficiency with the visual field examination.
A system for computer-assisted instruction in performing ophthalmic visual field examinations is presented. The system is implemented on a microcomputer making use of specially developed algorithms to summarize the information contained in a visual field in a very compact, efficient manner and to determine cursor position relative to stored visual field landmarks. The computer program presents a challenging testing situation by using visual fields, based on those of actual patients, of differing degrees of complexity. It is particularly well suited for trainees as well as for the physicians and ophthalmic technicians who frequently perform this examination.
Computer-Assisted Instruction↗