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At least 19 recordsLinked to original sources
PubMed1978

Autoimmune and virus-induced demyelinating diseases. A review.

Patterns of demyelination are described in several autoimmune and virus-induced demyelinating diseases of the peripheral and central nervous system. Myelin can be destroyed by injuries that affect either the myelin-supporting cells and/or the myelin lamellae. After destruction of the supporting cells, the related disintegrating sheaths are stripped off axons by invading phagocytes. Virus-induced cytolysis can occur with or without participation of immune responses, as demonstrated in subacute sclerosing panencephalitis and progressive mutlifocal leukoencephalopathy, respectively. Autoimmune demyelination is characterized by disintegration of myelin sheaths in periventular, mononuclear cell infiltrates. Myelin lamellae rather than the myelin-supporting cells are the target of the allergic reaction. The lamellae are lysed in focal areas when in contact with presumably sensitized mononuclear cells. The damaged sheaths are then removed in a nonspecific manner by invading macrophages that strip the myelin remnant off the axons. This sequence of changes is best revealed in experimental and human autoimmune demyelination of peripheral nerves, ie, allergic neuritis and idiopathic polyneutris (the Guillain-Barré syndrome). Autoimmune demyelination triggered by virus infection is described in Marek's disease and postinfectious Theiler's virus myelitis. Changes in canine distemper are discussed with reference to both autoimmune and virus-induced demyelination. The observations are compared with lesions in multiple sclerosis, the most common human demyelinating disease of unknown etiology.

Adolescent↗
PubMed1978

Virus infection in demyelinating diseases.

Several animal and human demyelinating diseases of the central nervous system (CNS) are associated with RNA or DNA viruses. These viruses infect CNS cells lytically or persistently. They mainly belong to the group of envelope viruses which derive their envelope partly from the host cell membrane. The process of virus release may result in the appearance of new antigens of virus-infected cells or the incorporation of cell membrane material into the viral envelope. These changes may lead to an immune response which selectively injures the CNS. These alterations of host cell membranes and host cell functions, together with the immune mechanism, are central to many of the hypotheses regarding virus-induced demyelination. The role of virus infection in progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis, visna and mouse hepatitis virus infections, is discussed in relation to the demyelinating process of these diseases.

Animals↗
PubMed1977

Tissue culture studies of demyelinating disease: a critical review.

Tissue culture studies of human and experimental demyelinating diseases have demonstrated that sera from patients with multiple sclerosis reversibly demyelinate central nervous system cultures. Similar changes are evoked by sera from animals with experimental allergic encephalomyelitis induced by inoculation with whole central nervous system tissue but not by encephalitogenic myelin basic protein. Sera and buffy coat or lymph node cells from humans with idiopathic polyneuritis and animals with experimental allergic neuritis demyelinate cultures of peripheral nervous system tissue. While these studies have contributed to speculations about pathogenetic mechanisms of demyelinating diseases, including the role of both circulating antibodies and delayed hypersensitivity factors, a number of important questions remain unanswered. Among these are the identity of the antigens that evoke antimyelin antibodies and the precise relationship of serum or cellular antimyelin factors to the pathogenesis or clinical course of the demyelinating diseases. Further studies with this technique may provide more complete information about the role of immunological events in induction of disease.

Animals↗
PubMed1977

[Abnormal scintigrams in demyelinating diseases of the brain (author's transl)].

In 6 patients with acute or exacerbating demyelinating disease and in 2 cases suffering from adrenoleucodystrophy (Schilder's disease) brain scintigraphy revealed areas with increased isotope uptake. The pathological foci were verified by autopsy in 4 cases and by inspection in 1. These foci are difficult to distinguish from other localized brain diseases causing increased isotope uptake; in addition to the clinical course and to spinal fluid abnormalities reversibility of the scintigraphic lesions indicate demyelinating diseases. The typical pattern of symmetrical lesions within the white matter and the progression of abnormalities from the occipital to the frontal lobe speak in favor of Schilder's disease.

Adult↗
PubMed1977

In vitro cell-mediated immunity of cerebrospinal-fluid lymphocytes to myelin basic protein in primary demyelinating diseases.

In an attempt to characterize the immunologic reactivity of cerebrospinal-fluid lymphocytes in demyelinating diseases, we compared the myelin-basic-protein-induced in vitro responses of these cells to peripheral blood lymphocytes from the same subjects with a variety of neurologic diseases. Peripheral blood lymphocytes from patients with acute disseminated encephalomyelitis and progressive multiple sclerosis had increased reactivity as compared to those of normal volunteers (P less than 0.01 and P less than 0.05, respectively). Cerebrospinal-fluid lymphocytes from patients with acute disseminated encephalomyelitis and acute and progressive (but not stable) multiple sclerosis were more reactive than cells from subjects with other neurologic diseases (P less than 0.005, P less than 0.02 and P less than 0.05, respectively). Cerebrospinal-fluid lymphocytes manifested a greater reactivity than peripheral blood lymphocytes in acute and progressive multiple sclerosis but not in acute disseminated encephalomyelitis. These findings demonstrate that lymphocytic cells reactive to myelin basic protein are present in the spinal fluid during active demyelinating disease; and that these cells may be more reactive than peripheral blood lymphocytes.

Acute Disease↗
PubMed1979

Measurement of visual resolution at high luminance levels in patients with possible demyelinating disease.

An interferometric acuity device (Takata) has been used to study visual resolution in individuals with possible demyelinating disease. The instrument employed provides a large field with a continuous range of grid or fringe frequencies and a relatively intense (10(5) mean photopic trolands) stimulus. After a brief period of time with eyes closed, resolution thresholds of patient are repeatedly determined during a five minute period. In all individuals suspected of having a demyelinating disease tested to date, a fall off in resolution capability has been found in time when using this intense stimulus display. This occurs whether eye signs have been present, are present or have not yet been observed. Normal observers do not exhibit comparable decrements. The fall off in resolution capability may or may not occur at lower stimulus levels, and is often not revealed when testing routine Snellen acuity. Outer and inner retinal pathology (division based on vascular support) do not cause a comparable fall off in resolution in time. The interferometric acuity test is a non-invasive, easily applied test.

Adult↗
PubMed1978

Severe demyelinating diseases in childhood: a clinicopathological study.

Case reports of six children seen by the author were selected to emphasize that severe demyelinating diseases occur in childhood, even if rarely. Cases include measles encephalitis, acute and chronic, subacute sclerosing panencephalitis, neuromyelitis optica, and multiple sclerosis, confirmed by pathologic findings, and, finally, a case of multiple sclerosis in a living child. Emphasis is directed to the clinical and pathological findings of demyelinating diseases associated with viral encephalitis caused by rubeola and vaccinia viruses. Photomicrographs illustrate the principal pathologic findings.

Adolescent↗
PubMed1978

The immune response in human demyelinating diseases.

Lymphocytes present in the brain, meninges and cerebrospinal fluid (CSF) in multiple sclerosis (MS) are capable of synthesizing IgG. The CSF in MS contains more T-lymphocytes and fewer B-lymphocytes compared to blood. The reactivity of CSF lymphocytes in MS to T-cell mitogens and probably also to a combined B-and T-cell mitogen is absent or heavily reduced. This unresponsiveness of CSF lymphocytes may be a consequence of their previous activation. The blood lymphocytes in MS are not altered regarding distribution of B-and T-cells, nor regarding responsiveness to mitogens, when compared with healthy controls. An asynchronous synthesis of heavy and light immunoglobulin chains occurs within the CNS in many MS patients, giving rise to oligoclonal band patterns on electrophoresis and abnormal kappa/lambda light chain ratios of CSF. The synthesized immunoglobulins are most probably antibodies which may play a role in the pathogenesis and course of human demyelinating diseases. The brain must be regarded, from an immunological point of view, as a privileged site with its own immune system and its characteristic immune reactions, and future research concerning demyelinating diseases should, if possible, include investigations of these reactions.

Antibodies, Viral↗
PubMed1977

Cortical and cervical somatosensory evoked responses in demyelinating diseases.

In six patients suffering from a multifocal neurological disease of the demyelinating type, a somatosensory evoked response was analyzed in the cortical and cervical are after stimulating the right index finger and the right nervus suralis. The results of the investigation with this method indicate that localization of the central nervous system pathology seems to lie within the realms of possibility, in which case this method will be a useful addition to the tools used to evaluate quantitatively the results of different treatments in this type of disease.

Adult↗
PubMed1977

Computerized tomography in demyelinating disease of the young.

We have used computerized tomography (CT) to look for evidence of cerebral demyelination in children with progressive neurologic disorders. Fourteen patients with a clinical diagnosis of a demyelinating disorder were examined by CT, and five had CT findings suggesting cerebral demyelination. In two patients with a so-called myelinoclastic demyelinating disease, CT showed asymmetric, circumscribed areas of diminished radiodensity, and in three patients with a leukodystrophy, scans showed diffuse symmetric areas of low density in the centrum ovale. Autopsy examination in one patient confirmed the diagnosis of sudanophilic leukodystrophy and substantiated the abnormalities suspected from CT.

Adolescent↗
PubMed1975

Experimental autoimmune demyelinating diseases: experimental allergic encephalomyelitis and experimental allergic neuritis.

Experimental allergic encephalomyelitis (EAE) and experimental allergic neuritis (EAN) are reproducible models of auto-allergic demyelinating diseases of central and peripheral neurons tissue respectively. EAE bears a close resemblance to naturally-occuring post-infectious encephalomyelitis and EAN to Laundry-Guillain-Barré polyneuritis, in humans. In the experimental models the antigen responsible for disease induction is a different myelin basic protein in each disease. Although a variety of humoral antibodies to various neural fractions are found in both disorders, it has been shown that disease results from cell-mediated immune reactions to specific myelin antigens.

Autoantibodies↗
PubMed1977

Radioimmunoassay of herpes-simplex and measles virus antibodies in serum and cerebrospinal fluid of patients without infectious or demyelinating diseases of the central nervous system.

A solid-phase radioimmunoassay was used to detect IgG antibodies against herpes-simplex virus antigens (capsid, envelope and excreted) and against measles virus antigen in serum and cerebrospinal fluid (CSF) specimens of 61 patients with no evidence of infectious or demyelinating disease of the central nervous system. Quantitative determinations of IgG and albumin in serum and CSF were also performed. Of the 61 serum and 61 CSF samples tested, 57 and 56 respectively contained antibodies against subunit antigens of herpes simplex virus. Antibody against measles virus was found in 59 serum and 47 CSF specimens. A positive correlation (P less than 0-001) was found between each of the four serum to CSF antibody ratios and the serum to CSF total IgG ratios. This indicated that the distribution of antiviral IgG antibodies in serum and CSF normally follows the distribution of total IgG. The ratios between viral antibody in serum and CSF were also correlated with albumin ratios (P less than 0-05). An inverse relation (P less than 0-001) was found between the age of the patients and their serum to CSF albumin ratios, but not their IgG ratios, suggesting that the albumin ratio is a useful indicator of a blood brain barrier lesion and that the IgG ratio should be used in evaluating disturbed antibody ratios.

Adult↗