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PubMed · 12804165

Nervous system Lyme disease.

Abstract

Nervous system involvement in Lyme borreliosis is a much-feared, often-misunderstood disorder. Both the peripheral and central nervous systems may be involved, typically in a multifocal, patchy fashion, perhaps suggesting a vasocentric mechanism. Clinical manifestations vary widely, depending on the site and severity of involvement. Although neurologic manifestations observed in Europe differ somewhat from those reported in the United States, there are also striking similarities, permitting some generalization of information obtained in each population. In general, diagnosis of neurologic disease requires objective evidence of nervous system damage, and must be differentiated from both psychiatric disorders and metabolic encephalopathies, both of which typically occur in the absence of significant neurologic damage or infection. Laboratory confirmation of nervous system involvement by Borrelia burgdorferi has limitations. However, neurophysiologic testing of the peripheral nervous system, imaging of the neuraxis, and examination of the cerebrospinal fluid can all be informative. In contrast, to date functional brain imaging has been of limited specificity. Treatment with one of several straightforward antimicrobial regimens, typically 2-4 weeks in duration, generally results in microbiologic cure. Although some symptoms may persist after this, the data do not suggest that these are responsive to further antimicrobial therapy.

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BibTeXRIS

John J Halperin. 2002. Nervous system Lyme disease.. https://doi.org/10.1089/153036602321653824

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Recurrence risk to offspring in extended multiplex schizophrenia pedigrees from a Pacific Island isolate.

Genetic transmission plays a major role in the pathogenesis of schizophrenia. Family, twin, and adoption studies have consistently shown that risks in relatives are many times greater than the general population risk of approximately 1%. McGue, Gottesman, and Rao (1983; Am J Hum Genet 35:1161-1178) calculated risk estimates of 12.8% for offspring and 3.5% for nieces/nephews of schizophrenia patients based on a large data set of Western European families. The present study evaluated corresponding risk levels in Palau, an isolated population in Micronesia where the prevalence of narrowly (broadly) defined schizophrenia is 1.99% (2.67%) and cases cluster in extended pedigrees, 20 of which contain 80% of affected individuals. We hypothesized that offspring in these extended families would have a higher risk for schizophrenia than offspring in smaller schizophrenia pedigrees from more genetically heterogeneous populations. RDC diagnostic data based on complete ascertainment of cases and their families covering the past two generations were used to quantify empirical recurrence risks in the offspring and nieces/nephews of Palauan schizophrenia patients. Risks to 1st- and 2nd-degree offspring were approximately double the rates found in the smaller Western European families: 23.4% in the offspring of an affected parent, 6.4% in offspring with one affected aunt/uncle, and 15.0% in offspring with two or more affected aunts/uncles. Recurrence rates in offspring of an affected parent were 1.6 times higher in males (27.9%) than in females (17.7%). The high risk levels we found in Palauan offspring reflect the elevated population prevalence, strong familial aggregation, and multi-lineal transmission pattern of schizophrenia in Palau.

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