Neurologia-Neurocirugia Psiquiatria最新文献

Central nervous system (CNS) lesions were studied from weanling hamsters inoculated with the HBS strain of subacute sclerosing panencephalitis (SSPE) virus. The animals showed clincial signs of acute encephalitis between 8 and 18 days post-inoculation (PI), but all survivors were clinically recovered by day 21 PI. Nevertheless, 13 of 14 hamster brains examined by light and electron microscopy between days 21 and 59 PI had chronic lesions which contained morphologic evidence of persistent viral infection. The lesions developed preferentially in the subependymal areas of the lateral and fourth ventricles and involved degeneration of ependyma with subsequent damage to adjacent parenchyma. All CNS cell types were involved in degeneration. Viral inclusions occurred in both CNS parenchymal cells and in inflammatory cells. Giant cells were particularly common. No budding virus was seen in chronically infected animals, a finding in accord with previous studies. Demyelination was a common constituent of most lesions. It occurred in the presence of inflammatory cells and macrophages, and in later lesions, some remyelination was seen. It is suggested that the damage to myelin is a secondary phenomenon and is not a cellular immune reaction. The possible reasons underlying the latent nature of the virus and the similarities between this condition, canine distemper encephalomyelitis and human SSPE are discussed. It is concluded that the experimental chronic disease is a valid model for the study of human SSPE and may have usefulness in the understanding of other chronic CNS conditions of man, e.g. multiple sclerosis. Additional Key Words: Latent infection; Paramyxovirus; Slow Viruses; Demyelination; Inmmunologic defects; Multiple Sclerosis.

In an attempt to describe epidemiologic features to generate etiological hypotheses and to study natural history, 121 cases of childhood CNS neoplasms under 15 years of age, occurring during 1950-66 in Manitoba, were analyzed. The incidence of CNS neoplasms in childhood (2.4/100 000 per annum) ranks second only to leukemia in Manitoba. For both sexes somewhat elevated incidences were noted for both extreme age groups; i.e. 0-4 and 10-14. Such peaks were more prominent for gliomas, which may indicate differential factors operation in the genesis of gliomas between early and late childhood. The former may be related to genetic and/or perinatal environmental factors and the latter, to environmental factors, in early childhood. Excess occurrences of gliomas among Irish, Scottish and Icelandic offsprings were observed, which possibly indicates the importance of either genetic or environmental factors peculiar to these ethnic groups. There was no evidence of time clustering (i.e. season and year) by estimated conception or by birth. Further investigation into the relative role of genetic and environmental factor in the genesis of childhood gliomas are in order.

A hamster-adapted SSPE agent was shown to cause a productive infection in weanling hamster brain, which changed to a cell-associated or defective infection coincident with the appearance of measles antibodies in serum. Antibodies to measles hemagglutinin, hemolysin and neucleocapsid antigens developed in serum, which also contained neutralizing activity for regular measles virus. The agent recovered from the brains prior to the appearance of serum antibodies was infectious in cell-free media, capable of rapidly destroying Vero-cell cultures and able to progressively destroy primary hamster brain cultures. In contrast the agent recovered from the brain after serum antibodies were present, was infectious only within cells destroyed Vero-cells ineffectively and spread slowly through primary brain tissue cultures releasing minute amounts of extracellular virus intermittently. Nevertheless, infected giant cells in the primary brain cultures contained both the HA & HL measles antigens in their cytoplasmic membranes. This in vivo conversion of a productive to a cell-associated cerebral infection appeared to be caused by the host antibody response and may mirror the initial events of human SSPE and possibly other slow or latent measles infections of the CNS.

Theiler's encephalomyelitis virus (TMEV) in mice represents one of the few existing animal models of virus-induced demyelination and may provide further information about the human disease, Multiple Sclerosis. An inbred strain of mice (SJL/j) employed in the present ultrastructural study, develops a life-long neurologic illness characterized by profound spasticity after intracerebral inoculation of TMEV. Anesthetized animals were sacrificed sequentially by total body perfusion with gluteraldehyde from 7 days to 9 months after infection. An intense mononuclear inflammatory infiltrate appeared in the leptomeninges and white matter of spinal cord by 15 days and persisted for as long as one year. These infiltrates contained numerous plasma cells, and perivascular demyelination could be found in almost every 1 micron section. Vesiculation and stripping of myelin by mononuclear cell processes were seen as mechanisms of myelin break-down. However, virions were not found in cells in grey or white matter and the integrity of oligodendrocytes was maintained. At one year, active demyelination was still seen in areas containing naked and remyelinated axons. The relevance of these ultrastructural findings to postulated mechanisms of virus-induced demyelination will be discussed.

This paper justifies the consideration of epilepsy as a social problem and an important public health problem in Latinamerica. It comments on the lack of proper statistical studies and the particular composition of the Latinamerican population where epilepsy has no clear differences according to age, in reference to mortality. It considers the labor structure of the population with low income and exposed to morbility and malnutrition for different causes, making notice that the social problems of epilepsy are by and large going along with the economic deficits and the unequal social system. The article mentions the problem of neonatal anoxia and other perinatal hazards so much influenced by poor hygiene and ignorance, going along with other poorly understood or non existing hygienic prevention problems. Among other points it touches on human and material resources in relation to epilepsy.

Histoplasma meningitis (HM) has been reported to occur primarily in association with disseminated histoplasmosis (DH). We report a case of histoplasma meningitis occurring in a patient with common variable hypogammaglobulinemia (CVH) in which no manifestations of DH were observed. L. L., a 66-year-old Caucasian male, clerical worker, developed occasional episodes of dizziness and tinnitus in mid-1971. During 1972, increasing frequency of these episodes and gradually progressive confusion were noted. In January 1973, vomiting, forther confusion, obnubilation, and a left central facial paresis developed and he was hospitalized. Physical examination revealed no pulmonary abnormalities, lymphadenopathy or hepatosplenomegaly. Over the ensuing 6-week evaluation, there was occasional fever to 38.5 degrees C. Chest roentgenogram was normal. Cerebral angiography suggested a mass in the left cerebellar hemisphere. EEG was diffusely slow. Multiple CSF examinations revealed: Glucose 7-18 mg/with a normal blood glucose, protein 109-256 mg/and cells 66-140 (95 + % mononuclear). Histoplasma capsulatum was cultured from CSF but not from sputum, urine, blood or bone marrow. Skin tests for PPD, histoplasmosis, coccidiodomycosis, blastomycosis, mumps, dinitrochlorobenzene and streptokinase-streptodornase were negative then and 6 months later. Histoplasma serum antibody was absent. Immunoglobulin analysis revealed IgG 430 mg %, IgA 46 mg %, and IgM 35 mg %, which with the history and skin test results suggested CVH. Treatment with 2.51 gm of amphotericin B given intravenously over a 3-month period resulted in complete reversal of all neurologic signs and clearing of the confusion. The remission has been maintained for two years. This case represents a primary infection of the CNS by histoplasma. The relationship between the HM and the CVH will be discussed.

This article points out that it is possible to carry out institutional psychotherapy, if one knows a theory and a technique which will foster the psychotherapeutic process through an approach following the psychoanalytic model, but with a limited number of sessions. A therapeutic alliance with limited goals is established; it permits to work with the demands of the patient, promoting and maintaining a positive transference which will eliminate the sense of rejection in the process of termination. The author insists on team work, necessary to review the material obtained in each session and on formulation of a psychodynamic diagnosis.

A neurophysiological hypothesis for hypnosis is suggested. Frequently, a hypnotic state is considered close to sleep. Experiments show that it closer to wakefulness, that attention is present and, at times, increased. Physiological changes under hypnosis, changes in suggestibility, conditionability, memory, visceral and endocrine changes, are outlined. Four large neuronal groups with diverse functions are described: wakefulness system, sleep system, that of conscious experience and the executive system; these last two, localized in the midbrain, pons and medulla, are considered the structural basis for the hypnotic state which arises from their increased or decreased functions. In the hypnotic state, through functional variations in these groups, modifications are seen in the spinal chord, in afferent fibers such as the optic ribbon and in complicated cortical functions such as memory.