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Biomedical subjects

M J Sá

Publications and source records attributed to M J Sá.

10 recordsLinked to original sources

Tau protein seems not to be a useful routine clinical marker of axonal damage in multiple sclerosis.

BACKGROUND: The descriptions of early axonal damage in patients with multiple sclerosis (MS) prompted the search of body fluid markers. However, the studies addressing this issue in MS present conflicting results. AIM: To assess the levels of tau protein in patients with definite MS. PATIENTS AND METHODS: Cerebrospinal fluid (CSF) samples from 50 patients with definite diagnosis of MS (33 F, 17 M; mean age: 33.6 years) and from 19 age-matched individuals without organic neurological diseases (11 F, 8 M), entered this study. With regard to the clinical course, the MS patients were classified as follows: 32 relapsing-remitting (RR); two secondary progressive (SP), and four primary progressive (PP). Twelve patients had clinical isolated syndromes (CIS). The mean duration was 36.1 months (range: 15 days to 20 years). Tau protein was measured in the CSF by double antibody sandwich ELISA. RESULTS: The median tau and the cut-off values of the controls were 104.9 and 175.3 pg/mL, respectively. We found that most MS patients presented normal values. In addition, the clinical features - course, duration, Expanded Disability Status Scale (EDSS) value, Poser index of progression, Multiple Sclerosis Severity Score - did not significantly influence the tau levels in the MS group. CONCLUSION: Our study showed similar CSF tau concentrations in MS patients with different clinical characteristics. This suggests that tau protein does not seem to be a useful routine clinical marker of axonal damage.

Adolescent↗

Dendritic changes in the hippocampal formation of AIDS patients: a quantitative Golgi study.

We have previously shown that in the hippocampal formation of patients with acquired immunodeficiency syndrome (AIDS) there is neuronal atrophy, without cell loss. Because reductions in neuronal size are suggestive of associated neuritic alterations, we decided to study the dendritic trees of the main neuronal populations in the hippocampal formation. Material was obtained in five male AIDS patients and five male controls. After Golgi impregnation, the dendritic arborizations of dentate granule and hilar basket cells, and of CA3 and CA1 pyramidal cells, were hand traced, and their segments classified, counted and measured. We found an impoverishment of the dendritic trees in all neuronal populations in the AIDS group, which was more striking in the hilus and CA3 field. Specifically, hilar neurons had fewer dendritic segments, and reduced branching density and dendritic extent; in CA3 pyramids there was a decrease in the number of terminal segments in the basal trees, and a reduction in the total number of segments, number of medium order terminals, dendritic branching density and dendritic extent in the apical trees. In CA1 pyramids, the terminals were shorter in the apical trees and the dendritic spine density decreased in the basal trees, whereas in granule cells only the dendritic spine density was reduced in AIDS patients. Subtle signs suggestive of dendritic reorganization were observed. These results point to a regional vulnerability of the hippocampal formation to HIV infection, and might contribute to explaining the occurrence of dementia, as a consequence of overall reduction in the hippocampal neuronal receptive surface.

Acquired Immunodeficiency Syndrome↗

A whole genome screen for association with multiple sclerosis in Portuguese patients.

Multiple sclerosis (MS) is common in Europe affecting up to 1:500 people. In an effort to identify genes influencing susceptibility to the disease, we have performed a population-based whole genome screen for association. In this study, 6000 microsatellite markers were typed in separately pooled DNA samples from MS patients (n=188) and matched controls (n=188). Interpretable data was obtained from 4661 of these markers. Refining analysis of the most promising markers identified 10 showing potential evidence for association.

Adolescent↗

AIDS does not alter the total number of neurons in the hippocampal formation but induces cell atrophy: a stereological study.

Although cognitive dysfunction is a common finding in patients with acquired immunodeficiency syndrome (AIDS) its pathogenesis remains controversial. Given the involvement of the hippocampal formation in the processing of cognitive information and the scarcity of quantitative studies in this brain region, we have examined, using stereological methods, the hippocampal formations of AIDS patients. The study was performed in ten AIDS patients and ten age-matched controls. All cases were male. The Principle of Cavalieri was applied to estimate the volume of the layers of the dentate gyrus and of the CA3 and CA1 hippocampal fields. The fractionator and the nucleator were used as estimators of the total number, and mean somatic and nuclear volumes of the neurons in the cell-containing layers of all hippocampal subdivisions. No cell death was detected in AIDS patients but the global volume of their hippocampal formations was significantly decreased due to the reduced volume of its layers, mainly the cell-containing layers. Furthermore, the somatic and nuclear volumes of the neurons in the hippocampal formation were significantly decreased in AIDS patients. No correlation was found between the estimates obtained and the presence or absence of neurological involvement. Our results show that neurons in the hippocampal formation of AIDS patients display marked morphological changes, despite the maintenance of their total number. These alterations are likely to lead to dysfunction of the hippocampal circuitries and, thus, might contribute to explaining the dementia features which occur in this condition.

AIDS Dementia Complex↗

Morphometric study of the frontal cortex in subacute sclerosing panencephalitis.

In biopsic material collected from the frontal cortex of 6 patients with subacute sclerosing panencephalitis (SSPE) and 5 patients with posterior fossa tumors, we estimated the neuronal and synaptic numerical densities as well as the mean volume of the neurons from layers II and III. The thickness of these layers was also determined. The evaluation of the layer's thickness suggested that there was no difference in the shrinkage in SSPE as compared to controls. No differences were found between the neuronal numerical densities and the neuronal soma sizes from SSPE and controls. Conversely the synaptic numerical density was reduced in SSPE. Given the maintenance of the neuronal numerical density in the frontal cortex of patients with SSPE, the presence of a decreased density of synapses must be regarded as a consequence of the dendritic and axonal degeneration that we previously described in this condition. It must then be borne in mind that SSPE's functional and behavioral changes might spring from alterations of the frontal cortex neuronal circuitry.

Adolescent↗

Cerebrospinal fluid cytomorphologic findings in 41 intracranial tumors: a retrospective review.

The main objective of this retrospective review of clinical and cerebrospinal fluid (CSF) data from 41 patients with intracranial tumors diagnosed between 1975 and 1989, is to report the role that the finding of neoplastic cells in CSF plays, specially when cerebral CT-scanning and MRI were not currently done. Another objective is to study the CSF proteic abnormalities in cerebral tumors. CSF cell count, cytomorphologic pictures obtained after sedimentation and protein findings are described. Tumor cells were seen in 12 cases (29%): medulloblastomas--6, meningeal carcinomatosis--3, multiforme glioblastoma--1, ependymoma--1, cerebral metastasis--1; in two cases it was an unexpected finding. We noticed that tumoral localization next to the ventricles favoured cell exfoliation. Although pleocytosis was rare and uncorrelated with the presence of neoplastic cells, pathological cytomorphologic pictures appeared in most of the cases including all "positive" ones. Our results stress that the appearance of neoplastic cells in CSF remains helpful specially when it is an unexpected finding.

Adolescent↗

Cytoproteic CSF findings in 33 MS patients: usefulness for diagnosis.

Although multiple sclerosis (MS) is mainly defined on clinical grounds, CSF parameters still remain important diagnostic and scoring tools. To demonstrate the usefulness of some easy laboratory techniques, a CSF cytomorphological and agarose gel electrophoresis (AGE) evaluation was undertaken in 33 MS patients: 79% presented a lymphoid cell profile and in 73% the gamma globulin fraction was abnormal. In the great majority of cases (97%) either or both cytological and electrophoretical abnormalities were found.

Adolescent↗

Clinical and CSF cyto-proteic findings in 23 patients with CSF eosinophilia.

Clinical diagnosis and cerebrospinal fluid (CSF) protein pattern were studied in 23 patients who had eosinophilic granulocytes in the CSF. Clinical data revealed that an inflammatory disorder of the central nervous system (CNS) was evident in 20 cases. A lymphoid reaction and elevated CSF total protein were found in most of the cases, but the most important finding was an increase of CSF gamma-globulin in 12 patients, of whom 10 had oligoclonal patterns. Our results may give support to a relationship between intrathecal eosinophilic reaction and inflammatory diseases of the CNS with subacute or chronic course accompanied by intrathecal synthesis of immunoglobulins.

Cerebrospinal Fluid Proteins↗

Tetanus antibody production in serum and cerebrospinal fluid in the rabbit and correlated histopathological features of the central nervous system.

The histopathological features in the central nervous system (CNS) developing during the active phase of tetanus antibody formation in the cerebrospinal fluid (CSF) as induced in 15 rabbits were studied. The measurement of antibody titres in serum and CSF by electroimmunodiffusion and histological examination were done sequentially at the 1st, 3rd, 5th, 7th and 9th days after cisternal secondary inoculation with fluid tetanus toxoid. Tetanus antibodies appeared in serum after the 1st and in CSF after the 5th day. Decreasing values of CSF total protein were found. The meaning of an elevated Q ratio as observed in this situation of strong antibody formation in the CSF was enhanced. The histopathological features in the central nervous system consisted of perivascular inflammatory infiltration, at first polymorphic and then composed almost exclusively of mononuclear cells with a predominantly leptomeningeal and subpial localization, which might represent the origin of CSF tetanus antibodies. The localization was related to the contact zone between the antigen- and antibody-containing compartments, respectively the subarachnoid space and vascularized structures of the brain and spinal cord. Four control rabbits presented neither tetanus antibodies in the CSF nor perivascular inflammatory infiltration in the CNS. Similarity between the present experimental results and the immunopathological features of the primary demyelinating diseases provides some useful information about the immunological inflammatory events in these diseases.

Animals↗

[Young-onset multiple sclerosis].

INTRODUCTION: Young onset multiple sclerosis is an infrequent situation which may present with atypical symptoms and uncertain outcome. OBJECTIVE: Our aim was to assess the clinical presentation and course in young onset multiple sclerosis, and analyze eventual data which might be helpful in establishing its prognosis. PATIENTS AND METHODS: We have retrospectively reviewed the clinical protocols of 17 patients with young onset multiple sclerosis, defined as presentation of symptoms before 21 years. Diagnosis was made according to Poser's criteria including clinical features, magnetic resonance imaging, cerebrospinal fluid findings, and evoked potentials. RESULTS: The mean age at onset was 16.9 +/- 4.4 and median time to diagnosis was four weeks. The clinical course was relapsing-remitting in 76.5% and secondary progressive in 23.5%. The mean annual exacerbation rate was 1.5 +/- 0.9 and median time to second exacerbation was 12 months. The actual Expanded Disability Status Scale score is 2.6 +/- 2 after a mean disease duration of 11.4 +/- 8.0 years. The correlation between the Expanded Disability Status Scale score and the mean disease duration was the only statistically significant result. CONCLUSIONS: These results are similar to other studies, namely, age at onset did not correlate with final neurological disability. However, we must emphasize that any primary progressive form was found in our study. We conclude that in young onset multiple sclerosis, progression is not dependent on the age of onset and does not necessarily lead to an unfavorable outcome.

Adolescent↗