PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11321196

Episodic hyperlibidinism in multiple sclerosis.

F A Gondim·F P Thomas
View original source ↗Export metadata ↓

Abstract

BACKGROUND: Changes in sexual function are commonly associated with MS and occur in many forms. Hypersexual thoughts or behavior are rare, but can present on the background of persistent cognitive impairment or psychiatric conditions such as mania, whereas isolated hypersexuality is still rarer. CASE REPORT: We describe the clinical, neuropsychological, electrodiagnostic, neuroimaging and endocrine findings in a MS patient with episodes of greatly increased libido. Imaging and neuropsychologicol studies indicated frontal lobe dysfunction; hormone studies showed no significant changes. CONCLUSION: Episodic hypersexuality can be a recurrent transient manifestation of MS.

Explore related subjects

Autoimmune DiseasesElectroencephalographyFemaleFrontal LobeGonadal Steroid HormonesHumansLibidoMagnetic Resonance ImagingMasturbationMiddle AgedMultiple SclerosisNeuropsychological TestsSexual Dysfunctions, PsychologicalCase ReportsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

F A Gondim, F P Thomas. 2001. Episodic hyperlibidinism in multiple sclerosis.. https://doi.org/10.1177/135245850100700111

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

The impact of variation at the KIR gene cluster on human disease.

Leukocyte behavior is controlled by a balance of inhibitory and stimulatory signals generated on ligand binding to a complex set of receptors located on the cell surface. The killer cell immunoglobulin-like receptor (KIR) genes encode one such, family of receptors expressed by natural killer (NK) cells, key components of the innate immune system that participate in early responses against infected or transformed cells through production of cytokines and direct cytotoxicity. KIRs are also expressed on a subset of T cells, where they contribute to the intensity of acquired immune responses. Recognition of self HLA class I ligands by inhibitory KIR allows NK cells to identify normal cells, preventing an NK cell-mediated response against healthy autologous cells. Activation of NK cells through stimulatory receptors is directed toward cells with altered expression of class I, a situation characteristic of some virally infected cells and tumor cells. The "missing self" model for NK cell activation was proposed to explain killing of cells that express little or no class I, while cells expressing normal levels of class I are spared. Studies performed over the last several years have revealed extensive diversity at the KIR gene locus, which stems from both its polygenic (variable numbers of genes depending on KIR haplotype) and multiallelic polymorphism. Given the role of KIR in both arms of the immune response, their specificity for HLA class I allotypes, and their extensive genomic diversity, it is reasonable to imagine that KIR gene variation affects resistance and susceptibility to the pathogenesis of numerous diseases. Consequently, the evolution of KIR locus diversity within and across populations may be a function of disease morbidity and mortality. Here we review a growing body of evidence purporting the influence of KIR polymorphism in human disease.

Autoimmune Diseases↗
PubMed2006

Immunobiology of human NKG2D and its ligands.

The NKG2D-DAP10 receptor complex activates natural killer (NK) cells and costimulates effector T cell subsets upon engagement of ligands that can be conditionally expressed under physiologically harmful conditions such as microbial infections and malignancies. These characteristics have given rise to the widely embraced concept of immunorecognition of "induced or damaged self," complementing the "missing self" paradigm that is represented by MHC class I allotypes and their interactions with inhibitory receptors on NK cells. However, this notion may only be partially sustainable, as various patterns of constitutive tissue distributions have become apparent among members of one NKG2D ligand family. This review summarizes the biological properties of NKG2D and its ligands and discusses the interactions and regulation of these molecules with emphasis of their significance in microbial infections, tumor immunology, and autoimmune disease.

Autoimmune Diseases↗
PubMed2006

Musculoskeletal and autoimmune manifestations of HIV, syphilis and tuberculosis.

PURPOSE OF REVIEW: The HIV pandemic continues to increase at an alarming rate, and is the leading cause of death worldwide from a single pathogen. The number of HIV-1-infected individuals currently exceeds 40 million, the majority of whom live in the developing countries of Asia, sub-Saharan Africa and south America. In the past 5 years, there has concurrently been an increase in the reported cases of tuberculosis and primary and secondary syphilis. This review addresses the musculoskeletal and autoimmune manifestations associated with HIV, syphilis and tuberculosis infections or their treatments. RECENT FINDINGS: During HIV infection the immune system becomes dysfunctional because of the coexistence of immunodeficiency and immune hyperactivity, and a disregulated production or activity of cytokines. Some of these mechanisms explain the development of rheumatic manifestations associated with HIV infection. Highly active antiretroviral therapy changes the course of HIV infection and the spectrum of the HIV-associated rheumatic manifestations. New syndromes such as the immune reconstitution inflammatory syndrome have emerged. HIV, tuberculosis and syphilis infections offer special epidemiological, clinical, and therapeutic challenges. SUMMARY: These observations highlight the complexity and multiplicity of the interactions between the pathogen and host that could result in the development of rheumatic manifestations.

Autoimmune Diseases↗