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PubMedDate not supplied

[Usefulness of volumetric studies in the evaluation of respiratory efficiency in nervous system diseases].

In nervous system diseases impairing the efficiency of respiratory muscles the authors determined vital capacity, minute ventilation and respiratory capacity. On the basis of volumetric investigations the authors tried to find an optimal schedule for administration of drugs in myasthenia and determine the usefulness of volumetric and gasometric measurements for the evaluation of respiratory efficiency in neurological diseases.

Body Weight↗
PubMed1989

Familial aggregation of multiple myeloma and central nervous system diseases.

Degenerative central nervous system diseases such as Alzheimer's disease and lymphoreticular malignancies such as multiple myeloma occur with increased frequency with advancing age. Relatives of early-onset Alzheimer's disease patients may have an increased risk of lymphoreticular malignancies. This led us to evaluate the family history of central nervous system diseases in a case-control study of multiple myeloma. Thirteen of 439 multiple myeloma cases had one or more first-degree relatives with degenerative or demyelinating central nervous system disease. In comparison, there were nine "positive" family histories in 1,317 matched hospital controls (relative risk = 4.4, 95% confidence interval = 1.9-10.3). Relative risks for the component categories of Parkinson's disease, multiple sclerosis, and miscellaneous degenerative central nervous system diseases were 3.0, 4.0 and 11.9, respectively. Our findings suggest that the degenerative and demyelinating central nervous system diseases and the lymphoreticular malignancies may comprise an etiologically related group of "protean diseases." These diseases may have a shared genetic susceptibility, possibly an immunologic abnormality. The varied disease manifestation in family members suggests a second necessary etiologic step of a variable and possibly environmental nature.

Aged↗
PubMed1994

The radiographic diagnosis and treatment of paraneoplastic central nervous system disease.

Paraneoplastic nervous system syndromes are being identified with increasing frequency because of greater physician awareness and the availability of serodiagnostic tests for some syndromes. Frequently, paraneoplastic syndromes develop in the setting of an indolent, limited stage, or otherwise occult malignancy. As a result, the paraneoplastic disorder often becomes the most disabling part of a patient's disease. Effective treatment appears to require early identification. For these reasons, the ability to diagnose a paraneoplastic syndrome, follow its course, and treat it successfully are important. The authors describe four patients with neurologic paraneoplastic syndromes and identical magnetic resonance imaging abnormalities. Three patients responded to immunosuppressive or immunomodulatory therapy, and in one, corresponding radiographic improvement was documented. Strategies for early diagnosis and options for treatment of paraneoplastic nervous system disorders are discussed.

Aged↗
PubMed1997

Animal models for nervous system disease in systemic lupus erythematosus.

Animal models have much to teach us about nervous system dysfunction in SLE. It should be stressed that the murine strains described in this review have variable expression in the onset and severity of clinical and serological features, perhaps making them more like a heterogeneous human population with SLE. With this in mind, studies involving animal models like those involving human subjects should use a sample size that ensures adequate power. It is not surprising that studies that use sample sizes as low as four to five animals per group would find discrepant results, especially in outcomes that are measured prior to the terminal phases of the disease. Similar to human SLE patients, murine models have systemic autoimmune as well as neurological manifestations. Studies with murine models must continue to consider some type of SLE disease activity measures in order to control for the effects of systemic disease on nervous system dysfunction. Because of the short time window between the earliest evidence of neurologic dysfunction and severe autoimmune disease manifestations, especially in MRL/lpr mice, the disease acceleration model may allow a more careful dissection of how immunological events are related to nervous system dysfunction. Alternatively, the study of MRL/lpr mice ultraearly (e.g., 3 weeks of age) could also provide invaluable information about the first events leading to nervous system dysfunction in SLE. Both approaches promise to identify predictors of specific nervous system manifestations that may suggest novel and more specific therapeutic interventions.

Animals↗
PubMed1994

Amyloid and peripheral nervous system disease.

The peripheral nervous system can be involved in the following amyloid deposition diseases. (1) Amyloid deposition composed of beta 2-microglobulin in patients on long term hemodialysis causing a carpal tunnel syndrome; (2) deposition of light chain immunoglobulin derived amyloid leading to polyneuropathy, carpal tunnel syndrome and autonomic nervous system involvement in patients with primary amyloidosis, or amyloidosis secondary to or associated with multiple myeloma, Waldenström's macroglobulinemia, non-Hodgkin's lymphoma, and solid neoplasms like hypernephroma; and (3) several types of heredofamilial amyloid polyneuropathies, which are mainly caused by a point-mutation in the transthyretin gene on chromosome 18. The clinical and biochemical features of these three groups will be discussed, with special attention for recently developed therapy. In clinical practice, amyloid polyneuropathy should be considered in case of familial occurrence of a polyneuropathy and when a patient presents with a polyneuropathy and a monoclonal gammopathy.

Amyloid Neuropathies↗
PubMed1999

Primary Sjögren's syndrome with severe central nervous system disease.

OBJECTIVE: Central nervous system (CNS) involvement in primary Sjögren's syndrome (pSS) is controversial with regard to frequency, significance, and etiology. METHODS: We describe a young woman with pSS and severe CNS disease and review the literature on the pathophysiology, clinical significance, symptoms, diagnostic examinations, and treatment of CNS disease with concomitant pSS (CNS-SS). RESULTS: Our patient with pSS had a 5-month history of benign lymphadenopathy and myositis, after which she developed severe CNS disease, vasculitic lesions on her hands, and a neurogenic bladder attributable to spinal cord involvement. The diagnosis was based on the clinical picture and the results of a brain magnetic resonance imaging (MRI) scan, electroencephalography (EEG), and cerebrospinal fluid (CSF) analysis. The disease did not respond to corticosteroids, but the administration of cyclophosphamide resulted in recovery. In the literature, the incidence of CNS-SS varies widely, from rare to incidence rates of 20% to 25%. The clinical picture is diverse, ranging from mild cognitive symptoms to fatal cerebrovascular accidents. The pathophysiology of CNS-SS is unclear, specific diagnostic methods are not available, and diagnosis is based on the clinical picture and a combination of examinations. MRI is the most sensitive test and cerebral angiography the most specific. CSF reflects involvement of the leptomeninges, and EEG is nonspecific. There are no controlled studies of the treatment of CNS-SS. Regimens for vasculitis are commonly used. CONCLUSIONS: CNS-SS is uncommonly recognized and difficult to diagnose. Increasingly accurate and available diagnostic examinations will yield more information about the association of CNS disease with pSS.

Adult↗
PubMed1998

Microglia in cell culture and in transplantation therapy for central nervous system disease.

The central nervous system (CNS) is host to a significant population of macrophage-like cells known as microglia. In addition to these cells which reside within the parenchyma, a diverse array of macrophages are present in meningeal, perivascular, and other peripheral locations. The role that microglia and other CNS macrophages play in disease and injury is under intensive investigation, and functions in development and in the normal adult are just beginning to be explored. At present the biology of these cells represents one of the most fertile areas of CNS research. This article describes methodology for the isolation and maintenance of microglia in cell cultures prepared from murine and feline animals. Various approaches to identify microglia are provided, using antibody, lectin, or scavenger receptor ligand. Assays to confirm macrophage-like functional activity, including phagocytosis, lysosomal enzyme activity, and motility, are described. Findings regarding the origin and development of microglia and results of transplantation studies are reviewed. Based on these data, a strategy is presented that proposes to use the microglial cell lineage to effectively deliver therapeutic compounds to the CNS from the peripheral circulation.

Animals↗
PubMed1991

HIV-1, macrophages, glial cells, and cytokines in AIDS nervous system disease.

Hallmarks of central nervous system (CNS) disease in AIDS patients are headaches, fever, subtle cognitive changes, abnormal reflexes, and ataxia. Dementia and severe sensory and motor dysfunction characterize more severe disease. Autoimmune-like peripheral neuropathies, cerebrovascular disease, and brain tumors are also observed. Histological changes include inflammation, astrocytosis, microglial nodule formation, and diffuse de- or dysmyelination. Focal demyelination can also be seen. It is clear that AIDS-associated neurological diseases are correlated with greater levels of HIV-1 antigen or genome in tissues. In AIDS dementia, macrophages and microglial cells of the CNS are the predominant cell types infected and producing HIV-1. However, manifestations of the disease make it unlikely that direct infection by HIV-1 is responsible. It seems more likely that the effects are mediated through secretion of viral proteins or viral induction of cytokines that bind to glial cells and neurons. HIV-1 induction of such cytokines as interleukin 1 (IL 1) and tumor necrosis factor-alpha (TNF alpha) may lead to an autocrine feedback loop involving further productive virus replication and induction of other cytokines such as interleukin 6 (IL 6) and granulocyte-macrophage colony-stimulating factor (GMCSF). Interleukin 1 and TNF alpha in combination with IL 6 and GMCSF could account for many clinical and histopathological findings in AIDS nervous system diseases. As HIV-1 infected patients produce elevated levels of IL 1, TNF alpha, and IL 6, it will be important to make a formal connection between the presence of these factors in the CNS, which are all products of activated macrophages, astroglia, and microglia, their in vivo induction directly by virus or indirectly by virus-induced intermediates, and the clinical and pathological conditions seen in the nervous system in this disease.

AIDS Dementia Complex↗
PubMed2002

Nervous system Lyme disease.

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.

Europe↗