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PubMed1999

[Molecular analysis of hereditary nervous system diseases].

The molecular genetic basis of a large group of monogenic hereditary neurological diseases is analyzed. Emphasis is laid on different types of mutations causing Huntington's chorea, autosomal dominant ataxias, Friedreich's disease, dopa-responsive and nondopa-responsive forms of torsion dystonia: the frequencies of these mutations and their molecular characteristics have been first investigated in the Russian population. Relationships between particular genotypes and various clinical variants of these disorders are analyzed. Genetic loci for two novel hereditary diseases of the nervous system, such as X-linked congenital cerebellar hypoplasia and an atypical form of autosomal recessive muscular dystrophy are characterized. Nosological entities of these clinical forms are substantiated in accordance with molecular genetic findings. DNA diagnostic techniques have been developed, which allows medical genetic counselling and prevention of relapses to be made in genetically burden families.

DNA↗
PubMed1990

Amyloid in central nervous system disease.

A review is presented of diseases of the central nervous system associated with amyloid deposition. The name amyloid is given to substances with particular physical characteristics which are independent of the chemical constitution of the proteins in the substance. Ideally, a classification of amyloid diseases should be based on the chemical composition of the amyloid deposits; this has only been partially realized. The best documented group of diseases with amyloid deposition in the central nervous system is the group of 'cerebral beta amyloid diseases', characterized by the deposition of beta-protein. This group includes: Alzheimer's disease, sporadic cerebral amyloid angiopathy, Down's syndrome, Parkinson-dementia of Guam, hereditary cerebral hemorrhage with amyloidosis-Dutch type and age-related asymptomatic amyloid angiopathy.

Amyloid↗
PubMed1991

Gastroesophageal reflux: a significant association with central nervous system disease in children.

An association between gastroesophageal reflux (GER) and central nervous system (CNS) disease has been suggested, but not defined clearly in children. We report on 613 children (ages 1 week to 16 years; mean, 16 months) studied at three institutions who were referred to the pediatric surgical service for documentation of GER by an abnormal pH score derived from 18- to 24-hour esophageal pH monitoring. Follow-up (range, 1 to 115 months; mean, 25 months) was obtained in 368 patients. One hundred thirty-two children had CNS disease documented prior to the evaluation for GER. In children older than 1 year, there was an increased incidence of GER (31/45, 69%) in those children with CNS disease compared with those without CNS disease (38/81, 47%; P = .014). On follow-up, only 4.6% (14/282) of children who were not diagnosed initially with CNS disease were found later to have overt CNS disease. There was no significant difference in the prevalence of newly diagnosed CNS disease in children with and without GER in long-term follow-up. In conclusion, in the population of children referred to the pediatric surgeon for evaluation of GER, children older than 1 year with CNS disease are at high risk to have associated GER documented by extended esophageal pH monitoring. Despite this association, those children with GER and no obvious CNS disease do not appear to be at increased risk to develop CNS disease.

Adolescent↗
PubMed2006

Platelet decline: an early predictive hematologic marker of simian immunodeficiency virus central nervous system disease.

As the prevalence of human immunodeficiency virus (HIV)-induced central nervous system (CNS) disease has increased with antiretroviral treatment, there is a critical need for identifying biomarkers that predict HIV CNS disease. To identify novel hematologic markers that precede and predict CNS disease, the authors examined longitudinal hematology data from 47 simian immunodeficiency virus (SIV)-infected macaques. This study demonstrated that the magnitude of decline in circulating platelet counts beginning at day 28 post infection, during asymptomatic SIV infection, predicted the eventual development of SIV encephalitis. Univariate analysis performed on platelet values obtained day 56 post inoculation demonstrated that SIV-infected macaques with the greatest decline in platelet numbers were 18 times more likely to develop SIV CNS disease than SIV-infected animals with minimal to no decline in circulating platelet counts. Decline in platelet number was a more robust marker than decline in hemoglobin levels, a previously identified marker of HIV CNS disease. The identification of an association between decline in platelets and the development of encephalitis demonstrates that monitoring platelet decline in HIV-infected individuals may serve as a predictive marker for clinical progression to HIV-induced CNS disease. Identifying those HIV-infected individuals at risk for CNS disease during asymptomatic stages of infection would promote early interventive, neuroprotective therapy to prevent neuronal damage and loss.

Animals↗
PubMed2002

Molecular studies of cerebrospinal fluid in human immunodeficiency virus type 1-associated opportunistic central nervous system diseases--an update.

Although the incidence of opportunistic central nervous system (CNS) diseases has markedly declined in developed countries following the advent of highly active antiretroviral therapies (HAARTs), they still represent a major diagnostic and therapeutic challenge over the world. The application of nucleic acid amplification techniques to the study of cerebrospinal fluid (CSF) has contributed substantially to their diagnosis. The detection of specific microbial genomes in the CSF is now the preferred test for some CNS opportunistic diseases, such as progressive multifocal leukoencephalopathy or cytomegalovirus encephalitis. More recent developments of these techniques are the quantitative amplification techniques and postamplification studies. Quantification of nucleic acids in CSF is an important aid both at the time of diagnosis, for the interpretation of positive findings, and during patient follow-up. Postamplification analyses can provide important information with regard to clinical patient management, e.g., detection of genotypic resistance to antimicrobial drugs, and in the attempt to elucidate disease epidemiology and pathogenesis.

AIDS Dementia Complex↗
PubMed1995

Association of antiphospholipid antibodies with central nervous system disease in systemic lupus erythematosus.

OBJECTIVE: To determine the prevalence and characteristics of central nervous system disease in systemic lupus erythematosus (CNS/SLE) with particular reference to disease activity and to the presence of antiphospholipid (aPL) antibodies. PATIENTS AND METHODS: From 340 unselected SLE patients attending our lupus clinic, we found 96 (28%) to have definite CNS manifestations not attributed to any cause other than SLE. Patients with mild migraine or cognitive disorders were excluded. The control group consisted of 100 SLE patients without CNS or thromboembolic manifestations. RESULTS: Fifty-six of our CNS patients had transient ischemic attacks or strokes, 24 had epilepsy, and 12 had psychiatric disorders; the other 4 did not fulfill SLE criteria. In all, 55% of patients (53) were found to be positive for aPL antibodies, whereas only 20% of the SLE control group were positive (P < 0.001). Based on a physicians' global clinical assessment tool together with laboratory analysis, only 42 (44%) patients were found to be active at the onset of CNS manifestations, and the other 54 (56%) were nonactive. A finding of aPL antibodies was associated strongly with the inactive CNS/SLE group (P = 0.001). Of the 53 patients who underwent magnetic resonance imaging (MRI) study, 33 showed small high-density lesions suggestive of vasculopathy. Twenty-six (79%) of them were positive for aPL antibodies; whereas of the 20 patients with normal MRIs, only 8 (40%) were positive for aPL antibodies (P < 0.01). CONCLUSION: We confirm that CNS disease in SLE is significantly associated with the presence of aPL antibodies. The CNS manifestations can occur in about half of SLE patients without any other evidence of lupus activity. Abnormal MRIs highly correlate with positive aPL antibodies.

Antibodies, Antiphospholipid↗
PubMed1982

[Basic principles of health resort treatment of children with sequelae in nervous system diseases].

As a result of many-year studies of the effectiveness of using health resort factors for treating children with various nervous system diseases basic principles of that treatment have been determined. A particular importance is attached to combined application of different health resort factors with consideration for the specificity of their therapeutic action and the peculiarities of the disease. The scope of the therapeutic measures should be dynamic in character and dose, so as to preserve the effect of each principal therapeutic factor on the patient's body. Attention is paid to the necessity of careful selection of patients for the health resort treatment, as well as to he therapeutic strategy in subsequent periods. Data on the effectiveness of treating various groups of patients at health resorts are presented.

Aftercare↗