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Biomedical subjects

S B Elias

Publications and source records attributed to S B Elias.

14 recordsLinked to original sources
PubMed1990

Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: a prospective magnetic resonance imaging study.

The rate at which profound hyponatremia should be corrected is the focus of a recent clinical debate. We prospectively studied neurological outcomes with serial magnetic resonance imaging in 13 hyponatremic subjects with serum sodium concentrations of less than 115 mmol/L (mean initial serum sodium concentration, 103.7; range, 93-113 mmol/L). All subjects were corrected to mildly hyponatremic levels at 24 hours and ultimately underwent an increase in serum sodium concentration of 25 mmol/L without development of hypernatremia. Magnetic resonance imaging revealed the development of pontine lesions in 3 patients. The correction rate of hyponatremia over the first 24 hours was significantly faster in patients with pontine lesions (mean +/- SD, 1.25 +/- 0.4 mmol/(L . hr) versus 0.74 +/- 0.3 mmol/(L . hr); p less than 0.05). Initial sodium concentration was also significantly lower in the pontine lesion group (97.3 +/- 6.7 vs 105.6 +/- 5.2 mmol/L, p less than 0.05). We conclude that the correction rate of hyponatremia plays a significant role in the pathogenesis of pontine lesions in individuals with profound hyponatremia who undergo large increases in sodium concentration as a result of severe initial hyponatremia.

Adult↗
PubMed1989

Myasthenia gravis.

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Combined Modality Therapy↗
PubMed1988

Central pontine myelinolysis after rapid correction of hyponatremia: a magnetic resonance imaging study.

We describe a patient with severe hyponatremia (serum sodium 94 mmol/L) who developed encephalopathy and decorticate posturing after a 29 mmol/L rise in serum sodium concentration during the first 24 hours of correction. High-resolution computed tomography of the pons was normal during the first, second, and twelfth weeks of the illness. Subsequent magnetic resonance imaging revealed a pontine lesion consistent with central pontine myelinolysis.

Adult↗
PubMed1987

Recurrent stroke associated with thymoma and anticardiolipin antibodies.

A 44-year-old woman developed recurrent thrombotic cerebral cortical infarctions. IgG and IgM anticardiolipin antibodies were found, as was a thymoma. To our knowledge, these antiphospholipid antibodies, which may inhibit prostacyclin formation and alter platelet function, have not been previously associated with this thymic neoplasm, an association we believe is not coincidental.

Adult↗
PubMed1987

Oligodendrocyte development and the natural history of multiple sclerosis. A new hypothesis for the pathogenesis of the disease.

The cause of multiple sclerosis (MS) is not known. This article presents a review of recent studies concerned with the development of oligodendrocytes and suggests that the primary lesion in MS could be related to damage to oligodendroglial progenitor cells. Loss of the capacity to generate oligodendrocytes could alter the course of normal development such that insufficient cells are produced to support growth and replace cells lost through attrition, and as a result, regions of demyelination appear. The site and extent of the primary loss of oligodendroglial precursors would then predetermine the time of onset, site, and severity of the neurologic manifestations of MS. It is suggested that MS is a single, continuous process and that clinical, pathologic, and immunologic findings may be understood as the consequences of the acquired inability to generate sufficient oligodendrocytes to maintain myelin.

Cell Differentiation↗
PubMed1979

Neonatal myasthenia gravis in the infant of a myasthenic mother in remission.

A 26-year-old woman was in spontaneous clinical remission from myasthenia gravis (MG) for six months, yet gave birth to a full-term infant with typical neonatal MG. It is believed that transplacental transfer of anti-acetylcholine (ACh) receptor antibodies is responsible for neonatal MG; therefore, neonatal MG represents an in vivo assay of the pathogenic potential of anti-ACh receptor antibodies in 2 human individuals. Anti-ACh receptor antibodies were present in both mother and infant (titers 12.3 X 10(-9) and 4.4 X 10(-9) moles per liter, respectively) at the time of birth, and both mother's and infant's sera accelerated the degradation of ACh receptors in myotube cultures. This case suggests that "host factors" unique to the individual appear to modify or even determine whether the presence of anti-ACh receptor antibodies will result in clinical myasthenia.

Adult↗
PubMed1979

The role of acetylcholine receptor antibodies in myasthenia gravis.

Myasthenia gravis is an autoimmune disease of man characterized by remitting and relapsing muscle fatigability. Although the etiology and pathogenesis are incompletely understood, the presence of circulating antibodies directed against the nicotinic acetylcholine (ACh) receptor in 80--90% of patients with myasthenia gravis and the identification of immune complexes at their neuromuscular junction have helped explain the altered neuromuscular transmission. The ACh receptor antibodies do not block access of ACh to the receptor, but do decrease the number of receptors by accelerating their degradation both in rat myotube cultures and in vivo models. In vitro these antibodies play a major role in myasthenia gravis. However, correlations of antibody titers with the clinical state following thymectomy or in neonatal myasthenia suggest that host factors may be equally important in determining whether the ACh receptor antibodies will result in clinical myasthenia.

Acetylcholine↗
PubMed1978

Acetylcholine receptor in myasthenia gravis: increased affinity for alpha-bungarotoxin.

Studies of the binding of 125 I-labeled alpha-bungarotoxin to myasthenic motor end-plates have been interpreted as showing a decrease in the number of acetylcholine (ACh) receptors at these end-plates. Equilibrium binding studies of 125 I-tagged alpha-bungarotoxin rather than to a decreased number of receoptors. Our results show increased rather than decreased affinity of myasthenic receptors for alpha-bungarotoxin and also suggest that the number of ACh receptors is indeed reduced. The presence of a change in binding affinity, in addition to the reduced number of ACh receptors, suggests the presence of membrane changes that may contribute to the pathogenesis of myasthenia gravis.

Acetylcholine↗