The purpose of this paper is to propose a preliminary scheme which standardizes the terminology and the manner of classifying comatose states due to organic cerebral lesions. This attempt is based on recognition of the need to use a common language in order to facilitate the transmission of information in this field.

Acute Disease↗

PubMedDate not supplied

[The genetics of Alzheimer's disease].

This paper examines recent epidemiological and molecular genetic studies on the genetic basis of Alzheimer's disease (AD). Recent epidemiological studies have shown the existence of a genetic etiology in some cases of Alzheimer's disease. Several pedigrees with an increased incidence of AD (familial Alzheimer's disease--FAD) have been described in the literature. Some of these contain sufficient numbers of affected individuals in multiple generations to provide a rigorous argument for an autosomal dominant inheritance of the AD phenotype. FAD pedigrees show several evidences of as phenotypic heterogeneity of the disease. Molecular genetic studies have shown a linkage between several polymorphic DNA markers specific for the pericentromeric region of chromosome 21 and early-onset FAD. In late-onset FAD pedigrees preliminary reports showed evidence for a linkage with chromosome 19 markers. Molecular genetic studies have clearly demonstrated the genetic heterogeneity of familial Alzheimer's disease. The analysis of new, multigenerational pedigrees with FAD and the study of patients with Down's syndrome and Alzheimer's disease should provide useful informations for the characterization of the gene(s) responsible for familial Alzheimer's disease.

Alzheimer Disease↗

PubMedDate not supplied

Multiple sclerosis. I. The immune pathogenetic hypothesis.

Animal models indicate that chronic relapsing demyelinating diseases of the central nervous system (CNS) can be induced both by certain viruses and by sensitization to myelinic antigens. Epidemiological data (studies on emigrants and on so-called "Multiple Sclerosis (MS) epidemics") suggest that an environmental transmissible agent, acting on a genetic substrate, could play a role in the pathogenesis of the disease. The transmissible agent could be a virus. Data to this effect are insufficiently indicative, but the hypothesis has been recently put forward that it could be antigenically related to the lymphotropic viruses (HTLV). The transmissible agent could act either by desegregating myelinic antigens or by inducing an alteration of the immune system with a reduction of T lymphocyte suppressor activity. There appears to be rapid and intense activated T lymphocyte "traffic" across the blood-brain barrier in patients affected with MS. Cells specifically sensitized to the unknown antigen find within the CNS other cells able to perpetuate presentation of the antigen (HLA-DR+ astrocytes and endothelial cells, not present in normal brain) and then activate the macrophages which in turn begin immuno-mediated phagocytosis of the healthy myelin. Aspecific immune cells are also recruited into CNS where seem to abnormally proliferate (possibly owing to reduced suppressor activity) producing antibodies against various viral or cerebral antigens which are not clearly related to the pathogenesis of the disease (production of intra-CNS "nonsense" antibodies and synthesis of the oligoclonal immunoglobulin bands seen at the cerebrospinal fluid electrophoresis.)

Antibodies, Monoclonal↗

PubMedDate not supplied

Multiple sclerosis. II. A critical assessment of immunotherapy.

The profound changes undergone by the immune system in Multiple Sclerosis (MS) suggest that any therapeutic protocol should take immunosuppressive therapy into consideration. The results of the numerous clinical trials should be assessed extremely cautiously in the light of the variable and unpredictable course of MS. Immunosuppressive therapies may act specifically by inhibiting a certain stage in the immune response, or, by contrast, by inducing an overall inhibition of the immune system. Low dosage, aspecific immunosuppressive therapeutic protocols with corticosteroids or azathioprine are used routinely, although there is no sure evidence of their effects. There are, however, unquestionable data on the numerous (and serious) side effects. High dosage, aspecific immunosuppression appears to be better tolerated (probably due to the brevity of the therapies) and to have certain immunodepressant effect within the CNS. ACTH and methylprednisolone are recommended for short-term relapse therapy. Research work on high dosage cyclophosphamide and total lymphoid irradiation is still too limited. Specific immunosuppressive treatment will no doubt be part of future autoimmune disease therapy, but for the time being is no more than theoretically stimulating experimentation (antiidiotypic monoclonal antibodies, specific T cell suppressor factor, T cell "vaccination"). Important multicentric studies on Cyclosporin-A and Copolymer 1 are almost complete once again without reassuring data and with documentation on the numerous side effects as regard to Cyclosporin-A. Clinical trials with Beta-interferon are still in progress and, so far at least, this drug appears to be characterized by the absence of important side effects.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

[Effects of argon laser on the skin].

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Argon↗