Nervous System Involvement in Infectious Mononucleosis

Silverstein, Allen; Steinberg, Gerald G.; Nathanson, M

doi:10.1001/archneur.1972.00490100083009

Cited by 162 publications

(53 citation statements)

References 24 publications

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“…Peripheral and/or central nervous system (CNS) involvement is rare in IM, occurring in <5% of the patients (Silverstein et al 1972). The most frequent neurological disturbances observed in IM are meningitis and encephalitis.…”

Section: Isolated Oculomotor Nerve Palsy Revealing Infectious Mononucmentioning

confidence: 99%

Isolated oculomotor nerve palsy revealing infectious mononucleosis

Malclès

Ronsin

Agard

et al. 2015

Acta Ophthalmologica

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Section: Isolated Oculomotor Nerve Palsy Revealing Infectious Mononucmentioning

confidence: 99%

Isolated oculomotor nerve palsy revealing infectious mononucleosis

Malclès

Ronsin

Agard

et al. 2015

Acta Ophthalmologica

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“…Most symptoms tend to disappear in 2 to 4 weeks, although complications, including neurological disorders, can occur. The incidence of neurologic complications from infectious mononucleosis in the literature range from 0.3 % to 7.3 % and include encephalitis, seizures, optic neuritis, facial palsy, and Guillain-Barré syndrome among others [31][32][33]. Although most of the neurologic complications from viral infections are acute, it is conceivable that a combination of the mutations in the susceptibility gene CACNA1H and the patient's viral infection combined triggered persistent changes in Cav3.2 channel function, thus giving rise to epilepsy and pain syndrome.…”

Section: Discussionmentioning

confidence: 99%

Two heterozygous Cav3.2 channel mutations in a pediatric chronic pain patient: recording condition-dependent biophysical effects

Souza

Gandini

Wan

et al. 2015

Pflugers Arch - Eur J Physiol

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We report expression system-dependent effects of heterozygous mutations (P769L and A1059S) in the Cav3.2 CACNA1H gene identified in a pediatric patient with chronic pain and absence seizures. The mutations were introduced individually into recombinant channels and then analyzed by means of electrophysiology. When both mutants were coexpressed in tsA-201 cells, we observed a loss of channel function, with significantly smaller current densities across a wide range of voltages (−40 to +20 mV). In addition, when both mutant channels were co-expressed, the channels opened at a more depolarizing potential with a~5-mV right shift in the half-activation potential, with no changes in half-inactivation potential and the rate of recovery from inactivation. Interestingly, when both mutants were co-expressed in the neuronalderived CAD cells in a different extracellular milieu, the effect was remarkably different. Although not statistically significant (p < 0.07), current densities appeared augmented compared to wild-type channels and the difference in the halfactivation potential was lost. This could be attributed to the replacement of extracellular sodium and potassium with tetraethylammonium chloride. Our results show that experimental conditions can be a confounding factor in the biophysical effects of T-type calcium channel mutations found in certain neurological disorders.

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“…Various neurological disorders have been described in association with infectious mononucleosis (Bernstein and Wolff, 1950;Schnell et al, 1966). The classical clinical features of the disease need not even be present (Silverstein, Steinberg and Nathanson, 1972;Grose et al, 1975).…”

Section: Discussionmentioning

confidence: 99%