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Biomedical subjects

S Lessell

Publications and source records attributed to S Lessell.

At least 55 records · Page 3Linked to original sources
PubMed1994

Choroidal infarction after optic nerve sheath fenestration.

PURPOSE: To describe a visual complication of optic nerve sheath fenestration. METHODS: Case review of two patients who underwent seemingly uncomplicated optic nerve sheath fenestration. FINDINGS: Both patients had a surgical complication that resulted in significant depression of their temporal visual field and development of a wedge-shaped region of subretinal pigmentation in the nasal fundus. CONCLUSIONS: Both patients had choroidal infarctions as a complication of optic nerve sheath fenestration. Choroidal infarction should be considered in cases of unexpected loss of visual field after this type of surgery, although the funduscopic signs that assist in making the diagnosis may not be evident for several weeks after surgery.

Adult↗
PubMed1994

Optic canal decompression in indirect optic nerve trauma.

BACKGROUND: The proper management of neurogenic visual loss after blunt head trauma is controversial. Non-treatment, corticosteroids, and surgical decompression of the optic canal are all currently considered to be reasonable alternatives. The goal of this study was to identify factors affecting improvement in patients treated with canal decompression. METHODS: A retrospective analysis of 31 cases in which transethmoidal decompression of the optic canal had been performed for neurogenic visual loss after closed head trauma was conducted. Each patient was alert and free of injury to the globe when evaluated before surgery. Surgery was performed within 6 days of injury, and all were given perioperative steroids. RESULTS: Visual acuity improved in 22 (71%) patients, with 6 (19%) regaining visual acuity of 20/40 or better. The mean improvement from preoperative visual deficit was 42.0% +/- 6.6%, with a median improvement of 45.2%. Both univariate and multivariate analysis suggested that vision improved more in patients who were younger than 40 years of age than in patients who were 40 years of age or older. Interval between injury and surgery, preoperative visual acuity, and the presence of optic canal fracture did not affect outcome. CONCLUSION: Any future randomized trials of therapy should stratify patients based on age. Enrollment of patients with no light perception or who experienced delay between injury and treatment may be reasonably considered.

Adolescent↗
PubMed1994

Neuro-ophthalmology of multiple sclerosis.

Neuro-ophthalmic manifestations are important in multiple sclerosis. Optic neuritis is a frequent harbinger of the disease, and is characterized by subacute painful visual loss, with disproportionate loss of color and contrast sensitivity, central or cecocentral scotoma, and an afferent pupillary defect. Visual recovery is the rule, but tests have been developed to detect most cases of recovered optic neuritis. Intraocular inflammation has come to be recognized as a frequent accompaniment of multiple sclerosis. Because of the predilection of multiple sclerosis for the infratentorial white matter, defects in eye movement control are common, particularly internuclear ophthalmoplegias and nystagmus.

Humans↗
PubMed1993

Tobacco amblyopia.

Tobacco amblyopia, once an important cause of bilateral optic neuropathy, has become so rare in the United States that some investigators doubt its existence. However, we treated two men who appeared to have this disorder. These two patients demonstrate that tobacco amblyopia can develop without malnutrition, alcoholism, or disordered vitamin B12 metabolism. Both patients recovered, one with cessation of smoking and the other with intramuscular administration of hydroxocobalamin despite continued smoking.

Adult↗
PubMed1993

Atypical Leber's hereditary optic neuropathy with molecular confirmation.

OBJECTIVE: Leber's hereditary optic neuropathy (LHON) is typically a familial disease of primarily young, male adults. Analysis of mitochondrial DNA has identified point mutations associated with LHON and allowed us to identify cases of LHON not consistent with traditional descriptions of the disease. DATA SOURCES: The collective experience of three tertiary referral centers contributed to this report. STUDY SELECTION: Patients with bilateral optic neuropathies who were positive for the 11778 LHON mutation were included in this study if they were female and there was no family history of visual loss. DATA EXTRACTION: Six case histories are presented. DATA SYNTHESIS: The diagnosis of LHON remained unknown in six female patients with bilateral optic neuropathies until molecular analysis revealed the 11778 mitochondrial DNA mutation. None of the patients had a family history of visual loss, and five were initially diagnosed as having factitious visual loss. Other individual features atypical for LHON included lack of the characteristic LHON funduscopic appearance, bitemporal hemianopia, optic disc cupping, and premonitory episodes of transient visual loss. In one patient the correct diagnosis was delayed 17 years. CONCLUSIONS: The diagnosis of LHON should be considered in all cases of unexplained optic neuropathy, including those with negative family history, late or early age at onset, female gender, or normal funduscopic appearance.

Adult↗
PubMed1993

Remitting sixth nerve palsy in skull base tumors.

OBJECTIVE: Spontaneous recovery of a sixth nerve palsy is thought to rule out a neoplastic origin. We reviewed cases of sixth nerve palsy that improved without treatment but that ultimately proved to be caused by a tumor at the base of the skull. DESIGN: Case series. SETTING: Hospital-based, neuro-ophthalmology referral practice. PATIENTS: Seven patients with an age range from 7 to 61 years had sixth nerve palsy secondary to a slow-growing neoplasm at the skull base. MAIN OUTCOME MEASURES: Return of lateral rectus function and resolution of diplopia without intervention. RESULTS: Seven patients with sixth nerve palsy caused by skull base tumors experienced spontaneous improvement of their deficit. Recovery time ranged from 1 week to 18 months. No patient was diabetic or had evidence of vascular disease. In one patient, the palsy improved once prior to becoming a fixed deficit, and spontaneous improvement occurred on two to five occasions in the other patients. CONCLUSION: Spontaneous recovery of a sixth nerve palsy can occur in the presence of an extramedullary compression by a tumor at the base of the brain. Possible mechanisms for recovery include remyelination, axonal regeneration, relief of transient compression (eg, resorption of hemorrhage), restoration of impaired blood flow, slippage of a nerve previously stretched over the tumor, or immune responses to the tumor.

Abducens Nerve↗
PubMed1993

Neuro-ophthalmologic findings in chordoma and chondrosarcoma of the skull base.

Review of the clinical features of 48 patients with chordoma and 49 patients with low-grade chondrosarcoma of the skull base disclosed overlapping clinical profiles but distinctive features. Both tumors occurred at all ages but chondrosarcoma tended to occur in the third and fourth decades. Twenty-five (52%) of the patients with chordoma and 24 (49%) of the patients with chondrosarcoma had ocular symptoms (diplopia or visual impairment) as the initial manifestation of the disease. Of the 59 patients (both groups) with diplopia, the diplopia was initially intermittent in 25 (42%). Headache and diplopia from an insidious abducens nerve palsy was most common in both groups. Abducens nerve palsy occurred in 22 (46%) of the patients with chordoma and 23 (47%) of the patients with chondrosarcoma. Normal examination results were more common in patients with chordoma, whereas visual loss, facial numbness, and multiple cranial neuropathies were more common in patients with chondrosarcoma. The similarities in the clinical features of these tumors reflect their common origin at the central skull base and the vulnerability of the abducens nerves at that site. The differences reflect the tendency of chordomas to originate from the clivus and chondrosarcomas to originate from the temporal bone.

Adolescent↗
PubMed1993

Idiopathic hypertrophic cranial pachymeningitis.

We evaluated 3 patients with biopsy-proven hypertrophic cranial pachymeningitis apparently unrelated to any systemic disease. Each patient had chronic headache, cranial neuropathy, an elevated ESR, and a mild CSF pleocytosis. Neuro-ophthalmic findings included bilateral sixth nerve palsies in two patients and the third had bilateral optic neuropathies. MR imaging revealed thickened dura that enhanced with Gd-DTPA administration. Histologic examination showed thickened, fibrotic dura with a sterile, chronic, nongranulomatous inflammation. The response to treatment was variable with corticosteroids, immunosuppressive drugs, or radiation. The distinctive MR appearance should help physicians recognize this rarely reported disease.

Abducens Nerve↗
PubMed1992

Spontaneous visual improvement in chiasmal gliomas.

Three untreated patients with presumed chiasmal gliomas had spontaneous visual improvement, although serial magnetic resonance imaging in two of the patients showed the lesions to be unchanged. Two patients had evidence of neurofibromatosis. Three other patients with similar disease courses have been documented in the medical literature. These cases demonstrate that conservative management of optic chiasmal gliomas may sometimes be associated with favorable outcomes.

Adolescent↗
PubMed1992

Retinocalcarine function in Alzheimer's disease. A clinical and electrophysiological study.

Impaired visual function in Alzheimer's disease (AD) could result from either precortical or cortical lesions, or both. In a parallel psychophysical study of visual function in AD, we found that contrast sensitivity function, color vision, stereoacuity, and backward masking were impaired relative to the performance of age-matched control subjects, whereas performance on a critical flicker fusion test was normal. The intent of the present study was to determine whether abnormalities of the retinocalcarine pathway contribute to visual dysfunction. We performed neuro-ophthalmological examinations on 38 patients with AD; from this group, 25 received additional psychophysical testing and 13 underwent electrophysiological testing. Clinical neuro-ophthalmological examinations, full-field electroretinograms, focal electroretinograms, and pattern visual evoked potentials were normal in all patients tested. There was no evidence of retinocalcarine abnormality specific to AD. We conclude that the visual impairment experienced by some patients with AD primarily results from involvement of the visual association cortices rather than from precortical damage, at least before the end stage of the disease.

Aged↗