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Biomedical subjects

L Rabinowich

Publications and source records attributed to L Rabinowich.

5 recordsLinked to original sources

Inflammatory myelinoclastic diffuse sclerosis.

We report on a 12-year-old girl with a severe subacute to chronic bifrontal leukoencephalopathy. By clinical, biochemical, radiological, and neuropathological criteria, a diagnosis of inflammatory myelinoclastic diffuse sclerosis was reached. This is the third fully documented case.

Child↗

The clinical neuro-ophthalmologic spectrum of temporal arteritis.

The range of neuro-ophthalmologic signs in temporal arteritis is broad and includes diverse presentations of ischemic optic neuropathy, retinal infarction, transient ischemic phenomena, ophthalmoparesis, pupillary autonomic and anterior ocular segment dysfunction, cortical blindness and associated post-chiasmal field defects, and complex visual hallucinations. Neurovascular compromise can follow arteritic lesions at multiple neuroanatomic sites, and reflects different pathogenetic mechanisms and displays distinctive clinical features. A variety of temporal clinical profiles and differential responses to corticosteroids occur. This article reviews the broad range of neuroanatomic pathways affected by diverse and potentially interactive etiologic factors in this systemic arteritis.

Autonomic Nervous System Diseases↗

Parasympathetic pupillary involvement in biopsy-proven temporal arteritis.

The neuro-ophthalmologic spectrum of temporal arteritis (TA) is broad and includes such diverse presentations as ischemic optic neuropathy, retinal infarction, anterior ocular segment dysfunction, ophthalmoparesis, and cortical blindness. A common clinical dictum suggests that third nerve palsies are associated with pupillary sparing in this systemic arteritis. We present a biopsy-proven case of TA with parasympathetic pupillary involvement and ophthalmoparesis. Relative light-near dissociation and differential clinical response to adrenocorticosteroids occurred. Previous pathologic studies have suggested that clinically apparent parasympathetic pupillary dysfunction could follow arteritic lesions at several neuroanatomic sites and may, therefore, reflect different pathogenetic mechanisms and display distinctive clinical features. Our case effectively broadens the clinicopathologic locus of neuro-ophthalmologic expression in TA.

Aged↗