PubMed Health⌕ Search

Biomedical subjects

J N Alpert

Publications and source records attributed to J N Alpert.

16 recordsLinked to original sources
PubMed1994

Acute hemorrhagic leukoencephalitis: a cause of acute brainstem dysfunction.

A 37-year-old female physician was admitted to the hospital with severe headache, facial and hand paresthesias, dysarthria, and ataxia. Neurologic examination disclosed signs of brain stem dysfunction. There was rapid neurologic deterioration, and she died in 28 hours. Postmortem studies showed the characteristic features of acute hemorrhagic leukoencephalitis.

Acute Disease↗
PubMed1989

Polyradiculoneuropathy in transfusion-associated AIDS and dorsal root pathology.

A 68-year-old woman developed a clinical picture of a painful subacute polyradiculoneuropathy. Her condition improved dramatically after treatment with plasmapheresis. A few months later she was found to have serologic evidence for the human immunodeficiency virus. This infection was traced to a contaminated transfusion received three years earlier. Postmortem studies disclosed pathology affecting mainly dorsal roots.

Acquired Immunodeficiency Syndrome↗
PubMed1978

Downbeat nystagmus due to anticonvulsant toxicity.

Isolated downbeat nystagmus was observed in 2 patients on multiple anticonvulsant regimens. The nystagmus disappeared when phenytoin dosage was reduced. Electrooculographic analysis revealed impaired downward tracking, supporting the concept of "pursuit" nystagmus.

Adult↗
PubMed1977

Glossopharyngeal neuralgia, asystole, and seizures.

Glossopharyngeal neuralgia, asystole, and seizures occurred in a patient with an internal carotid occlusion and external carotid stenosis. Swallowing was the triggering mechanism for these events. Mechanical stimulation of the pharynx failed to reproduce the symptoms. An ischemic injury to the glossopharyngeal nerve in the region of the jugular foramen that resulted in an artificial synapse is the proposed etiology.

Aged↗
PubMed1976

Lightning eye movements.

Physiologic studies were performed on a patient who demonstrated lightning eye movements, palatal myoclonus and myoclonic jerks of the left platysma and sternocleidomastoid muscles. The myoclonus and lightning eye movements were separate phenomena with no defined relationship to each other. Analysis of this ocular dyskinesia identified strictly horizontal saccadic oscillations, 2 to 5 Hz in frequency, with amplitudes varying greatly but often reaching 25 degrees. A brief stationary period between each saccadic oscillation was frequently observed. They were particularly induced by vertical or horizontal ocular pursuit as well as sustained upward or downward ocular deviation. Caloric nystagmus abolished the oscillations but they persisted, irregularly, during optokinetic nystagmus. Thus a faulty visual fixation mechanism is postulated to precipitate lightning eye movements. Constrast studies revealed a mass lesion arising from the right dorsolateral portion of the medulla. These results indicate that lightning eye movements occur with caudal as well as rostral brain-stem lesions. From the clinical findings cerebellar pathway involvement is likely.

Adult↗
PubMed1975

"Saccadic nystagmus" in cerebellar cortical atrophy.

An ocular dyskinesia designated "saccadic nystagmus" was observed in a patient with cerebellar cortical atrophy. Saccadic nystagmus is a sustained ocular dyskinesia present during visual fixation and abolished by eye closure. It is difficult to distinguish visually from either pendular or jerk nystagmus without eye movement recordings. The oscillations are horizontal and rapid and may be influenced by direction of gaze. Caloric nystagmus (eye closed) and optokinetic nystagmus were normal in our patient. Visual fixation abolished caloric nystagmus, which was replaced by saccadic nystagmus.

Caloric Tests↗
PubMedDate not supplied

Reversible angiography.

A 26 year old woman presented with a subacute onset of headache, hypertension, and neurologic impairment. Angiography revealed severe extracranial carotid and vertebral artery disease. Long segmental stenoses, lumen irregularities, and aneurysmal dilatations were noted. She improved with medical management and was followed for one year. Because recurrent neurologic symptoms developed, angiography was repeated and disclosed normal vasculature. "Spontaneous dissections" with recovery are the most probable explanation for this phenomenon.

Adult↗