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Biomedical subjects

D G Cogan

Publications and source records attributed to D G Cogan.

At least 73 records · Page 4Linked to original sources
PubMed1977

Experimental myelin intrusion in the nerve head.

On the assumption that myelin intrusion into the papilla and peripapillary region might occur with traumatic lesions of the optic nerve, a study was made of the clinical and histopathologic changes that might be expected. Nine monkey eyes were subjected to hemostat compression of the nerve close to the globe and studied over variable periods up to 28 days. Myelin was demonstrable ophthalmoscopically, followed by variable and increasing amounts of hemorrhage. The myelin was demonstrable histopathologically only during the first 2 weeks after the manipulation and was then masked by the associated hemorrhage and gliosis. The optic nerve showed expected myelinolytic reactions.

Animals↗
PubMed1976

Experimental allergic encephalomyelitis. Passive transfer by the intraocular injection of sensitized cells.

Experimental allergic encephalomyelitis is a disease of cell-mediated immunity and can be transferred passively to virgin recipients by lymphoid cells from sensitized donors. The rabbit eye contains myelinated medullary rays that can be visualized ophthalmoscopically. Intraocular injection of autologous lymph node cells from myelin basic protein (BP)-immunized rabbits into the vitreous leads to readily visualized optic neuritis while injection of cells from adjuvant immunized control rabbits does not. Microscopical study confirmed the presence of myelin destruction in recipients of cells from BP-sensitized donors. This eye chamber technique provides a simple model for the study of demyelination in vivo under direct observation.

Animals↗
PubMed1976

Ophthalmoplegia and dissociated nystagmus in adetalipoproteinemia.

A characteristic pattern of acquired exotropia, progressive paresis of the medial rectus muscles, and dissociated nystagmus on lateral gaze was found in three patients with abetalipoproteinemia. Study with electronystagmography of the eye movements of one patient revealed abnormally slow voluntary saccades and slow or absent fast components of vestibular nystagmus, optokinetic nystagmus, and jerk-type, disassociated nystagmus. Defects in central nervous system centers generating saccadic eye movements are postulated.

Abetalipoproteinemia↗
PubMed1976

Rapid eye movements in myasthenia gravis. I. Clinical observations.

Rapid eye movements, having high velocity and low amplitude, are described in 11 patients with myasthenia gravis. These movements occur with various degrees of ophthalmoplegia. To distinguish them from the somewhat similar lid-twitch phenomenon, they are called quiver movements. We believed that their presence is pathognomonic of myasthenia and results from a differential involvement of the two myoneural mechanisms that are peculiar to the extraocular muscles.

Adolescent↗
PubMed1976

Rapid eye movements in myasthenia gravis. II. Electro-oculographic analysis.

Voluntary saccades were studied by electro-oculography in ten patients with myasthenia gravis (MG) and in eight patients with other types of ophthalmoplegia. Despite limited range of eye movements, maximum velocities of 20 degree and 40 degree saccades in patients with MG were not significantly different from those in normal individuals, whereas maximum velocities in patients with other types of ophthalmoplegia were significantly decreased. In some myasthenic patients, small amplitude saccades were hypermetric and had high velocities, appearing clinically as "quiver" movements characteristic of MG. In MG the preservation of saccades with high initial velocities, even in the presence of severe ophthalmoplegia, suggests that muscle fibers generating rapid movements during saccades (twitch fibers) can be relatively spared when muscle fibers responsible for maintenance of excentric gaze (tonic fibers) are severely affected.

Adolescent↗
PubMed1976

Ocular manifestations of acute pandysautonomia.

A 33-year-old white man developed premature presbyopia and anisocoria as initial manifestations of acute pandysautonomia. Nine months later signs and symptoms of generalized, severe autonomic dysfunction developed, and six years later only paralysis of pupillary reactions, presbyopia, and orthostatic hypotension were unresolved. Pharmacologic testing of the pupils demonstrated no mydriasis to cocaine 4% or hydroxyamphetamine 1% and hypersensitivity to epinephrine 0.1%, methacholine 2.5%, and pilocarpine 0.0625%, suggesting the presence of sympathetic and parasympathetic, postganglionic blockage of autonomic innervation of the iris.

Adult↗
PubMed1976

Adrenoleukodystrophy with disease of the eye and optic nerve.

Adrenoleukodystrophy is an X-chromosome-linked recessive disease characterized by primary atrophy of the adrenal glands with or without Addison's disease and low plasma cortisol levels, and a degeneration of white matter of the central nervous system with blindness. In suspected cases of adrenoleukodystrophy an impaired rise in plasma cortisol levels after adrenocorticotrophin stimulation may be diagnostic. With the electron microscope, pathognomonic intracytoplasmic lamellar inclusions have been seen in adrenal cortical cells, peripheral nerve Schwann's cells, testicular interstitial cells, and in macrophages of the brain. Adrenoleukodystrophy appears to be a genetically determined lipid storage disease with an error in membrane sterol metabolism. A 10-year-old boy with adrenoleukodystrophy had visual loss, a prominent early symptom. The ocular abnormality consisted of a disproportionate loss of nerve fibers from the macular region. No intracytoplasmic lamellar inclusions were identified in cells representing macrophages within the optic nerve. They contained myelin debris suggestive of end-stage disease.

Adrenal Gland Diseases↗
PubMed1976

Plasma cell infiltration of the conjunctiva associated with pancytopenia, dermatitis, and polyclonal gammopathy.

A 73-year-old man developed conjunctivitis, epiphora, pancytopenia, dermatitis, and a polyclonal gammopathy. Diffuse infiltration and thickening of the conjunctiva and lacrimal canaliculi by plasma cells was present. Histopathologic examination suggested a reactive, chronic inflammatory response rather than neoplasia. The patient's ocular manifestations appeared to be related to his pancytopenia, dermatitis, and polyclonal gammopathy.

Aged↗
PubMed1976

Optic atrophy following prophylactic chemotherapy and cranial radiation for acute lymphocytic leukemia.

Two patients with acute lymphocytic leukemia developed progressive optic nerve and chiasmal lesions eight to nine months after the initiation of identical chemotherapy protocols that included intrathecal medication and prophylactic radiation of only 2,400 rads to the central nervous system. Both patients eventually lost all vision despite additional radiotherapy, and there was no evidence of leukemia involving the central nervous system after acute lymphocytic leukemia was diagnosed. Optic nerve biopsy in one case showed changes consistent with radiation necrosis.

Adult↗
PubMed1976

Optic neuropathy presumably caused by vincristine therapy.

A 36-year-old man with Hodgkin's disease developed symmetric optic neuropathy after treatment with nitrogen mustard, vincristine, procarbazine, and prednisone. Histopathologic sections of the eyes showed loss of ganglion cells in the macular region and atrophy of the corresponding fibers in the optic nerve. Vincristine is presumed to have been the cause of the optic neuropathy because of its recognized neurotoxicity and its temporal relation to the onset of the visual complaint.

Adult↗
PubMed1976

Ocular motor abnormalities in hereditary cerebellar ataxia.

Twelve members of a family with hereditary cerebellar ataxia of late onset were examined and, in 5, quantitative recording of eye movements were obtained. The initial and most severe symptom in all patients was ataxia of gait, followed by dysarthria and later by dysmetria of the limbs. Clinical examination did not reveal involvement of structures other than the cerebellum. Ocular motor examination showed: (1) inability to hold eccentric gaze resulting in gaze-paretic nystagmus; (2) downward beating nystagmus, accentuated on lateral gaze; (3) defective smooth pursuit, with relative preservation of optokinetic nystagmus induced by full-field stimulation; (4) rebound nystagmus; (5) enhanced gain (eye velocity/head velocity) of the vestibulo-ocular reflex during rotation in darkness; (6) decreased ability to suppress the vestibulo-ocular reflex during fixation of an object rotating with the patient; (7) saccadic dysmetria, especially downward overshoot; and (8) square wave-jerks. Although each of these signs can probably occur with lesions elsewhere in the brain, in combination they are highly suggestive of cerebellar involvement. With the reservation that we do not yet have pathological confirmation of the location of our patients' lesions, our results support the suggestion that the cerebellum specifically: (1) helps maintain eccentric gaze; (2) produces smooth pursuit eye movements; and (3) modulates the amplitude of saccadic eye movements. Many of the characteristics of the altered vestibulo-ocular responses and rebound nystagmus could be explained by the underlying anomaly in the smooth pursuit system.

Adult↗
PubMed1976

Fibrin clots in the choriocapillaris and serous detachment of the retina.

Clot formation occurs preferentially in the choriocapillaris. With intraocular inflammation this clotting begins along the inner surface of the choriocapillaris suggesting that dilatation of the vessels and opening of the endothelial fenestra have initiated the process. With the systemic coagulopathy of thrombotic thrombocytopenia (TTP) and disseminated intravascular coagulopathy (DIC) clotting occurs preferentially in the submacular choriocapillaris, sometimes associated with choroidal hemorrhage and detachment of the retina. These complications are illustrated in the present paper by a patient with TTP showing relatively chronic coagulopathy and by three patients with DIC showing variations of acute coagulopathy.

Adult↗
PubMed1976

Sliding of the epithelium in experimental corneal wounds.

The corneal epithelial cell has a unique sliding capability. The epithelial cell spreads and migrates in an amebic fashion without mitotic activity when the continuity of the epithelium is broken. This movement is demonstrated both in vivo and in vitro. Prompt sliding for sealing the wound defect is apparently the first step of the wound healing of the superficial cornea. Cut edges of collagen fibers show no sign of activity towards healing the wound. The energy source of the sliding is provided mainly from stored glycogen in the epithelial cells. Sliding is inhibited by removal of glycogen from the cell or by adding glycolytic enzyme inhibitors.

Animals↗
PubMed1975

Ocular involvement in disseminated intravascular coagulopathy.

Seven cases illustrate the ocular pathology of disseminated intravascular coagulopathy in its several stages, and correlate these changes with the clinical manifestations. The prime abnormalities consisted of detachments of the retina, vacuolar disruption of the pigment epithelium, choroidal hemorrhage, and, most importantly, thrombotic occlusion of the choriocapillaris and of the juxtaposed vessels in the submacular and peripapillary regions. The changes were characteristically symmetrical in the two eyes.

Adult↗