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Biomedical subjects

A R Seay

Publications and source records attributed to A R Seay.

At least 19 recordsLinked to original sources
PubMed1998

Management of status epilepticus in children.

Treatment of SE is based on the age of the patient and the possible underlying etiology. Initial treatment should include a benzodiazepine (lorazepam 0.1 mg/kg or diazepam 0.5 mg/kg). Specimens for laboratory tests should be drawn early in the event of a prolonged seizure and geared toward the clinical presentation and age of the patient. If a seizure lasts longer than 10 minutes, phenobarbital 20 mg/kg dose should be administered with strict adherence to the proper rate of administration. Further seizure activity during drug administration can be treated with additional doses of lorazepam or diazepam. If a seizure lasts longer than 10 minutes, a second long-acting anticonvulsant should be administered, followed by induction of general anesthesia.

Anticonvulsants↗
PubMed1989

Pattern and concentration of IgG in cerebrospinal fluid in neurosarcoidosis.

Reports have suggested that the pattern of CSF IgG differentiates neurosarcoidosis from multiple sclerosis. We examined CSF and serum of 7 patients with neurosarcoidosis to determine concentrations of IgG and albumin and the presence of oligoclonal bands. Our results showed that neurosarcoidosis may have associated abnormalities of IgG synthesis and oligoclonal bands present in CSF, but without a consistent pattern.

Adolescent↗
PubMed1987

Interferon treatment of experimental Ross River virus polymyositis.

Ross River virus (RRV), an alpha togavirus, causes an inflammatory myopathy in mice, which probably results from direct lytic effects of virus or viral products on myofibers. Administration of recombinant hybrid human leukocyte interferon-alpha A/D (rIFN-alpha A/D) ameliorates clinical illness and reduces mortality from 86 to 42%. Peak concentrations of virus are reduced by 1,000-fold in serum and by 30-fold in muscle, but anti-RRV antibody production is not altered. Treatment with rIFN-alpha A/D dramatically reduces inflammation and necrosis in muscle. Beneficial effects of rIFN-alpha A/D on experimental, RRV-induced polymyositis result in part from inhibition of viral replication and spread, though immunomodulation might also play an important role.

Animals↗
PubMed1984

Spinal cord dysfunction complicating bacterial meningitis.

Cervical transverse myelopathy developed in an 8-month-old girl during the early stages of Klebsiella pneumoniae meningitis. Spinal cord dysfunction is an uncommon complication of bacterial meningitis and has not been previously described in patients younger than 1 year old. A literature review of patients 2 years old or older with similar complications showed that young children have cervical cord lesions, whereas the majority of adolescents and adults have thoracic or lumbar lesions. In four of five previously reported cases of patients between 2 and 3 years old, a cardiorespiratory arrest probably played a critical role in the pathogenesis of cord dysfunction. The patient described herein, however, did not experience any cardiorespiratory insufficiency, and cord dysfunction was probably the direct result of local vascular changes and cord ischemia. On follow-up assessment, all patients had persistent neurologic deficits, regardless of age.

Female↗
PubMed1984

Clinical features of carbamyl phosphate synthetase-I deficiency in an adult.

Carbamyl phosphate synthetase-I (CPS-I) catalyzes the first reaction required for the conversion of ammonia to urea through the urea cycle. Severe CPS-I deficiency causes marked hyperammonemia with encephalopathy in infancy and usually results in death within the first few months of life. We describe a 33-year-old woman whose CPS-I activity is less than 5% of normal. She has had mild, intermittent symptoms throughout life but has never experienced severe encephalopathy. Although mildly retarded, she has no major neurological deficits. Therapy with a low-protein diet, lactulose, and sodium benzoate has prevented recurrence of hyperammonemia and symptoms. Cranial computed tomographic scans demonstrate prominent lucency of cerebral white matter, and cerebral evoked potential recordings indicate slowed central conduction. These findings suggest that the metabolic disturbances in this patient may have adversely affected central myelin formation or maintenance. This woman represents, to our knowledge, the oldest reported patient with CPS-I deficiency, and the case illustrates the need to consider urea cycle disorders in the differential diagnosis of intermittent neurological symptoms regardless of the patient's age.

Adult↗
PubMed1983

Ross River virus--induced demyelination: II. Ultrastructural studies.

Focal central nervous system demyelination is a prominent feature of Ross River virus encephalitis in mice. The present ultrastructural study shows that oligodendrocytes are a primary site of viral replication. The earliest myelin disruption occurs in association with an inflammatory infiltrate composed primarily of polymorphonuclear leukocytes, which are later replaced by macrophages. Viral particles are found in oligodendrocytes, selected neuronal populations, macrophages, and polymorphonuclear leukocytes through the end of the first week of infection as macrophages remove myelin from normal-appearing axons. Between the second and third weeks of infection, axons within foci of demyelination partially remyelinate with central myelin. Schwann cells are not found within regions of central remyelination. Cyclophosphamide treatment does not prevent or delay demyelination or remyelination. Results of this and previous studies strongly suggest that Ross River virus--induced demyelination is not immune mediated but rather the direct result of viral infection of oligodendrocytes.

Animals↗
PubMed1982

Ross River virus-induced demyelination: I. Pathogenesis and histopathology.

Ross River virus (strain T48) infection in mice causes an encephalomyelitis characterized by focal, primary demyelination in the cerebellum, brain stem, and spinal cord. Maximal serum and brain content of virus occurs on days 2 and 4, respectively. Virus is not detectable in serum after day 3 or in brain after day 9. Histopathological lesions are present by day 2 and consist of perivascular macrophage and polymorphonuclear leukocyte infiltration, focal necrosis in the internal granule cell layer, and myelin disruption. Mononuclear cell infiltrates are present by day 5. Foci of demyelination in the presence of preserved axons become more widespread by day 8, and early partial remyelination occurs by day 13. Immunosuppression reduces the mononuclear cell infiltration but does not alter the demyelination . Although the mechanism of Ross River virus-induced demyelination is not known, these findings suggest that it is not immune mediated.

Animals↗
PubMed1981

Experimental viral polymyositis: age dependency and immune responses to Ross River virus infection in mice.

Ross River virus (RRV) causes an age-dependent myositis in mice. Infected 4-week-old mice develop no clinical signs, but 1-week-old mice develop weakness and myositis. Humoral and cell-mediated immune responses to RRV in the two age groups are comparable, and immunosuppression does not alter age-dependent resistance to clinical disease. Immunosuppression of 1-week-old mice protracts clinical signs and reduces muscle inflammation but does not alter muscle necrosis or regeneration. These studies suggest that immune responses do not determine age dependency of RRV myositis and that muscle necrosis results from direct viral lysis of muscle fibers.

Age Factors↗
PubMed1979

Abnormal leukocyte electrophoretic mobility in myotonic dystrophy.

Electrophoretic mobility of polymorphonuclear leukocytes (PMNs) was studied in 10 patients with myotonic dystrophy. The mobility of patients' PMNs differed significantly from that of controls. Following incubation with bacterial chemotactic factor the PMNs from patients showed significantly less change in net surface charge compared to that in controls. Our data support a leukocyte membrane defect in myotonic dystrophy.

Adolescent↗
PubMed1979

CT scans in Menkes disease.

The clinical courses and serial computerized tomography (CT) scans of four patients with Menkes disease are described. Although the initial clinical presentations were similar, head growth and serial CT scans showed striking individual differences. The CT scans varied from showing no abnormalities early in the disease to showing diffuse cortical atrophy, subdural accumulation of fluid, or multifocal areas of ischemic infarction. The pathologic findings in one patient showed only cerebral and cerebellar atrophy, whereas the findings in another patient showed areas of ischemic infarction, probably secondary to abnormal vessels. Menkes disease should be suspected in male infants with psychomotor deterioration and seizures, or when trauma is suspected from subdural hematoma and multiple fractures.

Brain↗
PubMed1978

Defective neutrophil function in myotonic dystrophy.

Polymorphonuclear leukocytes (PMNs), obtained from 10 patients with myotonic dystrophy and 39 age-matched controls, were tested for chemotactic activity, chemiluminescence (CL), and phagocytosis. PMNs from 8 of the 10 patients had depressed chemotactic indexes (30 +/- 23) as compared to controls (61 +/- 18) (P less than 0.0003), and 6 of the 10 patients' PMNs produced lower peaks in CL (less than 90%) than those of controls. Phagocytosis and bactericidal activity were evaluated in 7 patients and were normal. Control PMNs incubated in patient serum produced normal chemotactic activity and CL. These results indicate defects in 2 PMN membrane-associated activities in myotonic dystrophy and suggest that the PMN is affected by the generalized membrane abnormality underlying myotonic dystrophy.

Adolescent↗
PubMed1978

Serum creatine phosphokinase and pyruvate kinase in neuromuscular disorders and Duchenne dystrophy carriers.

Serum levels of creatine phosphokinase (CPK) and pyruvic kinase (PK) were determined in 42 controls, 57 patients with various neuromuscular disorders, and 23 female relatives of Duchenne dystrophy patients. CPK and PK enzyme activities were increased in comparable numbers of muscle disease patients and female carriers; there was no advantage in the combined use of the two tests. We did not confirm earlier reports suggesting that determination of PK is more valuable than CPK in carrier detection.

Adolescent↗