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At least 127 records · Page 7Linked to original sources
PubMed1986

Evidence of an immunopathogenic basis for central nervous system disease in primary Sjögren's syndrome.

The pathogenesis of central nervous system complications in primary Sjögren's syndrome (CNS-SS) is unknown. In order to determine whether patients with active CNS-SS have cerebrospinal fluid (CSF) abnormalities indicative of CNS inflammation, CSF analyses from 30 patients with active CNS-SS (SSA) were contrasted with those from 20 SS patients without CNS involvement (SSI) and 20 patients with systemic lupus erythematosus and active CNS disease (SLEA). Elevations of total protein concentration, IgG concentration, IgG to total protein ratio, and IgG index were observed in patients with SSA, but not in those with SSI. Agarose gel electrophoresis results were abnormal, with 1 or more bands, in 25 of 29 SSA patients (86%), but in only 3 of 18 SSI patients (17%). Similar, but less striking, CSF abnormalities were seen in a minority of SLEA patients. Fifteen SSA patients (50%) had transient, mild-to-moderate CSF pleocytosis, while only 1 SSI patient and 2 SLEA patients had similar findings. Cytologic findings were abnormal in 18 SSA patients (60%); these included atypical mononuclear cells, lymphoblastoid cells, and plasma cells. The presence of immunocompetent cells and evidence for the intrathecal synthesis of IgG within the CSF of SSA, but not SSI, patients provide diagnostic parameters which are indicative of active disease and which can be monitored serially during therapy.

Central Nervous System Diseases↗
PubMed1975

Central nervous system disease in systemic lupus erythematosus. Therapy and prognosis.

The effect of corticosteroid therapy in 28 patients with 52 episodes of neuropyciatric disease in systemic lupus erythematosus (SLE) was elevated. Categories of organic central nervous system disease were seizures (eight patients), organic brain syndromes (nine patients), aseptic meningitis (four patients) and a variety of focal neurologic findings (seven patinets). Fourteen pateints had 15 episodes of functional psychosis without other evidence of neurologic disease. Although there was a general correlation between clinical and serologic evidnce of active SLE and the development of organic neurolgic disease, there was no evidence that therapy with very large doses of corticosteroids was beneficial. Of the deaths in this series, two were due to probable active SLE involving the central nervous system wheras five were attributable to complications of therapy. The long-term morbidity, likewise, was high in the patients who recieved large doses of corticosteroids. In all, 12 patients had major complications of corticosteroid therapy. Functional psychosis was usually preciptated by corticsoteroid therapy and respond to a reduction in steroid dosage and administration of psychotropic drugs.

Adolescent↗
PubMed1998

[Cerebrospinal fluid proteins in the diagnosis of disorders of the blood-cerebrospinal fluid barrier in central nervous system diseases].

BACKGROUND: Many neurological diseases are connected with the dysfunction of blood-CSF barrier. The quantitative determination of CSF proteins has already been used in the diagnosis of barrier impairments and inflammatory diseases of the central nervous system. PATIENTS: Serum and CSF, totaling 264 samples, were obtained from 15 controls and 117 patients with various diseases of the nervous system. Laurell's electroimmunoassay was used for estimation of albumin and IgG levels in serum and CSF. CSF-protein profile was evaluated according to Reiber's graph for the evaluation of the CSF-protein profile. RESULTS: The graph for the protein profile can be divided into 5 functionally different parts (1--normal range, 2, 3, 4--different types of barrier dysfunctions and 5--local humoral response in CNS without any barrier impairment). There was a good correlation of CSF-protein profiles and neurological diseases in our group of patients. CONCLUSIONS: According to our results, Reiber's graph was helpful for the diagnosis of blood-CSF-barrier dysfunctions. The graph has the following advantages: a) possibility of simultaneous assessment of the functional state of blood-CSF-barrier and the inflammatory response of the CNS, b)sensitivity for the determination of pathological local IgG-production in CNS and c) minimal number of protein assays necessary.

Blood-Brain Barrier↗
PubMed1997

Capillary electrophoretic analyses of beta-trace protein and other low molecular weight proteins in cerebrospinal fluid from patients with central nervous system diseases.

Ordinary capillary-zone electrophoresis (CZE), as well as CZE in a sodium dodecylsulfate-containing polymer solution (SDS-CZE) and capillary isoelectrofocusing (CIEF), was applied to the analysis of low molecular weight proteins in cerebrospinal fluid (CSF) from patients with various neuropsychiatric disorders. Under the CZE conditions employed, a peaks of beta-trace protein (beta TP), which is the most abundant low MW protein in CSF, was clearly detected on the electropherograms of all the samples examined, and the CSF beta TP level could be tentatively determined using allylamine added at a constant concentration as the internal standard. The results revealed that beta TP in CSF was non-specifically increased in organic disease in the central nervous system (CNS), especially in ones giving severe physical damage to the brain tissues. On the other hand, SDS-CZE allowed us to determine simultaneously the CSF minor low MW proteins other than beta TP, such as beta 2-microglobulin, gamma-trace protein, myelin basic protein, etc., while the CIEF electropherograms suggested that beta TP were separated into several fractions with the different PI values. These capillary electrophoresis systems seem to be powerful as aids in the biochemical examinations of beta TP and other low molecular weight proteins in CSF from patients with CNS diseases.

Beta-Globulins↗
PubMed2003

Cytomegalovirus glycoprotein B genotypes and central nervous system disease in AIDS patients.

To investigate any association between cytomegalovirus glycoprotein B (CMV gB) subtypes and central nervous system (CNS) disease in AIDS patients, proportions of different gB genotypes detected in AIDS patients with CNS disease were compared with the gB genotypes detected in AIDS patients with no neurological disorder. The patients were matched by CD4+ cell counts. CMV was detected by PCR in cerebrospinal fluid (CSF) samples obtained from AIDS patients with CNS disease and from urine and saliva samples obtained from AIDS patients without CNS disease. CMV strains obtained were digested by restriction enzymes HinffI and RsaI to classify the genotypes. The CMV gB genotype was determined in 26 CSF samples. Of these, 11/26 (42.3%) typed as gB group 1, seven (26.9%) as gB2, four (15.4%) as gB3, and four (15.4%) as gB4. The CMV gB genotype frequency distribution in the 42 AIDS patients without CNS disease showed that 18/42 (42.8%) were classified as gB group 1, 10 (23.8%) as gB2, seven (16.6%) as gB3, and seven (16.6%) as gB4. In the present study, no association was found between CMV gB genotypes and CMV-related central nervous system disease.

AIDS-Related Opportunistic Infections↗
PubMed2002

Searching for clues: tracking the pathogenesis of human immunodeficiency virus central nervous system disease by use of an accelerated, consistent simian immunodeficiency virus macaque model.

An accelerated model of human immunodeficiency virus central nervous system disease was developed in which more than 90% of infected macaques develop typical simian immunodeficiency virus (SIV) encephalitis with neuronal dysfunction by postinoculation (pi) day 84. Infected macaques had replicating virus and microglial activation in the brain 10 days after inoculation; viral replication and microglial activation were suppressed at pi day 21. By pi day 56, viral recrudescence in the brain was detected in 2 of 6 infected macaques. CD4 cells were the predominant lymphocytes in the brain during acute and asymptomatic infection; cytotoxic T lymphocytes and NK cells predominated in macaques with encephalitis. Low levels of peripheral blood NK lytic activity at pi day 10, elevated cerebrospinal fluid (CSF) monocyte chemoattractant protein-1 after 28 days, and high CSF viral RNA after 42 days predicted SIV encephalitis. This model is ideal to track the viral, cellular, and immunologic changes in the brain during acute and asymptomatic infection and during viral recrudescence and SIV encephalitis.

AIDS Dementia Complex↗
PubMed1996

[We're moving closer and closer to the insane asylum...": Modern life and nervous system diseases by Johann CHristian Reil (1759-1813)].

Johann Christian Reil is usually portrayed as a pioneer in the realm of neuroanatomy and psychiatry, and as a pragmatic physician engaged in contemporary problems of social medicine and hygiene. In this article, the connection between these two fields of interest is focused: Reil's ideas on the relation between the "modern" way of life and the occurrence of diseases of the nervous system. The first part of the paper summarizes Reil's statements on the issue, as laid out e.g. in his "Ueber die Erkenntnis und Cur der Fieber" (1802), and in the "Rhapsodieen über die Anwendung der psychischen Curmethode auf Geisteszerrüttungen" (1803). The second part gives an outline of Reil's neurophysiological model of the interaction between the organ of the soul ("Seelenorgan") and the social environment. In the third part, Reil's conceptions of culture, civilisation, and history are investigated. For Reil, madness is not an alienation from reason, but from a postulated healthy state of nature which is located in the past. Modern life causes and steadily increases a contradiction between the needs of the body and those of the soul, resulting in a concomitant tension and irritability of the nerves. Modern culture is thus criticized for its potentially harmful effects on mental health. The balance between physical and mental activities, and the constitution of a decentralized state would be means to prevent the manifestation of the ensuing diseases.

Germany↗
PubMed1997

Gene transfer and delivery in central nervous system disease.

Gene transfer offers the potential to explore basic physiological processes and to intervene in human disease. The central nervous system (CNS) presents a fertile field in which to develop novel therapeutic modalities to treat intractable and pervasive malignant tumors and neurodegenerative disease. The extension of gene therapy to the CNS, however, faces the delivery obstacles of a target population that is postmitotic and isolated behind a blood-brain barrier (BBB). Approaches to this problem have included grafting of genetically modified cells to deliver novel proteins or introducing genes by viral or synthetic vectors geared toward the CNS cell population. Direct inoculation and bulk flow, as well as osmotic and pharmacological disruption, have been used to circumvent the BBB's exclusionary role. Once the gene is delivered, myriad strategies have been used to affect a therapeutic result. Genes activating prodrugs are the most common antitumor approach. Other approaches focus on activating immune responses, targeting angiogenesis, and influencing apoptosis and tumor suppression. At this time, therapy directed at neurodegenerative diseases has centered on ex vivo gene therapy for supply of trophic factors to promote neuronal survival, axonal outgrowth, and target tissue function. Despite early promise, gene therapy for CNS disorders will require advancements in methods for delivery and long-term expression before becoming feasible for human disease.

Journal Article↗