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Biomedical subjects

S Lessell

Publications and source records attributed to S Lessell.

At least 145 records · Page 8Linked to original sources
PubMed1977

Acquired cerebral dyschromatopsia.

Color blindness developed in five patients apparently because of lesions in the posterior portions of both cerebral hemispheres. Three of them also had symptoms of prosopagnosia. The lesions were neoplastic in two and vascular in three of the patients. It would appear that bilateral, inferior, occipital lobe lesions may be responsible both for acquired cerebral dyschromatopsia and prosopagnosia. Evidence from experimental investigations in primates suggests that the areas of the cerebral hemispheres analogous to those involved in these patients, may be specialized for the processing of colored stimuli.

Adult↗
PubMed1977

Retinopathy in systemic lupus erythematosus.

A 32-year-old black woman with systemic lupus erythematosus went rapidly blind due to severe bilateral retinal vasculitis. The mechanism appeared to be total arrest of the retinal circulation by thrombosis of most of the retinal vasculature including major arterioles.

Adult↗
PubMed1976

Electron microscopic study of extraocular muscles in myotonic dystrophy.

The extraocular muscles of two middle-aged men with ophthalmoplegia secondary to myotonic dystrophy were studied by electron microscopy. The main change was disorganization in the arrangement of myofibrils rather than degeneration of the cells. Diseased muscle cells contained randomly distributed, short and irregular myofibrils and individual myofilaments. The cytologic appearance of these muscle cells was similar to that of developing muscle cells. The pathogenesis of the myopathy in myotonic dystrophy may be related to myofibrillogenesis and its maintenance.

Humans↗
PubMed1976

Optic neuritis in the Landry-Guillain-Barré-Strohl syndrome.

A patient with typical Landry-Guillain-Barré-Strohl syndrome (LG-BS) developed bilateral optic neuritis. Laboratory studies showed hypersensitivity to both central and peripheral nervous tissue myelin. The occurrence of optic neuritis is presumably due to autohypersensitivity to central nervous tissue myelin. The initial lesions of the LG-BS syndrome in the peripheral nerves might have liberated sequestered antigens that cross-reacted with central nervous system myelin.

Adolescent↗
PubMed1976

Histopathology of experimental ethambutol intoxication.

Ethambutol was administered to albino rats in their drinking water in doses of 105 to 2,500 mg. per kilogram per day for 18 to 102 days. Sixteen per cent developed bilateral lesions consisting of focal axonal swelling without demyelination, in their optic chiasms and the intracranial portions of their optic nerves.

Animals↗
PubMed1975

Unilateral exophthalmos. Occurrence after treatment for perichiasmatic neoplasms.

Unilateral exophthalmos developed shortly after treatment in three patients with chromophobe adenoma of the pituitary gland and craniopharyngioma. In two patients, the exophthalmos followed surgery, while in the third it did not appear until after radiation treatment. The pathogenesis of the exophthalmos in these cases in obscure. However, the other findings and subsequent course indicate that the exophthalmos is not due to recurrence of the neoplasm nor to a complication of therapy.

Adenoma, Chromophobe↗
PubMed1975

Limited form of Wegener granulomatosis. Eye involvement as a major sign.

Bilateral uveitis was the initial manifestation of a limited form of Wegener granulomatosis in a 47-year-old man. Diagnosis was established by biopsy of a pulmonary nodule. Subsequently, evidence of lesions developed in the patient's central and peripheral nervous systems, but renal lesions were absent. Pulmonary lesions regressed on therapy with azathioprine and prednisone. Blindness ultimately resulted from retinal phlebitis, vitreous hemorrhages, and neovascular glaucoma.

Azathioprine↗
PubMed1975

Prolonged vertical nystagmus after pentobarbital sodium administration.

Of 17 healthy adults without nystagmus who ingested 100 mg of pentobarbital sodium, six had up-beating, gaze-evoked vertical nystagmus 12 hours later. Three of them had nystgmus 36 hours later, but none of them had it 60 hours later. Therefore, one should be reluctant to ascribe this type of nystagmus to a disease of the central nervous system in patients who received a barbiturate within several days of examination.

Adult↗
PubMed1975

Supranuclear paralysis of monocular elevation.

A man with bronchogenic carcinoma lost the ability to elevate his left eye voluntarily. His eyes were level in the primary position and the Bell phenomenon was normal, indicating that the ophthalmoplegia was caused by a supranuclear lesion. Other clinical and radiologic evedence indicated that there was a lesion in the rostral midbrain. A metastatic tumor, found in the right pretectum at autopsy, probably produced the ophthalmoplegia by interrupting axons destined for the superior rectus portion of the homolateral oculomotor nucleus and the interior oblique portion of the contralateral oculomotor nucleus.

Brain Neoplasms↗
PubMed1975

Cerebral disorders of vision in systemic lupus erythematosus.

Sensory neuroophthalmic abnormalities due to cerebral lupus erythematosus, with involvement of visual pathways posterior to the optic chiasm, occurred in 12 patients with systemic lupus erhthematosus. Five underwent detailed evaluation because of an hallucination, 4 for visual loss, and 3 for both. Hallucinations were either unformed (for example, bright lights, straight lines) or highly formed (for example, faces), in which case they were invariably recognized by the patient as inappropriate. In no instance did they occur in association with delirium, confusion, or use of hallucinogenic drugs. Patients with loss of vision had scotomas, homonymous field defects, and cortical blindness. These features indicate disease in the posterior cerebral artery circulation, a localization often supported by ancillary neurologic findings, for example, vocal cord paralysis, diminished gag reflex. Thus, various visual dysfunctions may occur in systemic lupus erythematosus due to cerebral vasculitis. At times they may be the most prominent and disabling feature of the disorder.

Adrenal Cortex Hormones↗