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Biomedical subjects

E Tolosa

Publications and source records attributed to E Tolosa.

At least 163 records · Page 9Linked to original sources
PubMed1993

Choreas, hereditary and other ataxias, tics, myoclonus, and other movement disorders.

Developments in the field of Huntington's disease have focused on the potential benefits of predictive testing. Markers have been described for autosomal dominant cerebellar ataxia and for certain subtypes of Friedrich's ataxia. Argentophilic neuronal and glial inclusions appear to be the first specific pathologic hallmark of multiple system atrophy. "Pure" hereditary spastic paraplegia is not a multisystem disorder of the central nervous system, but a monomorphic and stereotyped disease. Advances in Tourette's syndrome are limited because the presumed gene eludes identification. A new type of myoclonus, propiospinal myoclonus, has been described. Clinical and electrophysiologic criteria for defining primary orthostatic tremor have been proposed. Understanding of the neurophysiologic substrate of essential tremor and myoclonus is improving. New neurologic disorders presenting clinically with prominent movement disorder continue to be described.

Ataxia↗
PubMed1992

Clinical and pathological study of two patients with progressive supranuclear palsy and Alzheimer's changes. Antigenic determinants that distinguish cortical and subcortical neurofibrillary tangles.

Two cases with classical clinical manifestations of progressive supranuclear palsy (PSP) showed severe progressive dementia as an additional clinical feature. Neuropathological study demonstrated typical features of PSP in the brainstem. Additionally, histological criteria of Alzheimer's disease (AD) were observed. A topographic and immunohistological study (with neurofilament subunit and Tau and Ubiquitin antibodies) of the distribution of neurofibrillary tangles (NFTs) was performed in order to compare the characteristics of NFTs from cortex and brainstem. NFTs from cortex were positive with all antibodies used and were predominantly distributed in cortical layers III and V and affected medium size neurons. Brainstem NFTs were positive only for neurofilament subunits and Tau. Cortical and brainstem NFTs showed immunohistological differences. Cortical NFTs in our two cases had a similar distribution as in control AD cases. On the basis of our observations we believe (1) that cortical tangles in our PSP cases are related to Alzheimer's disease and (2) that the cortical NFTs of PSP and AD are morphologically and immunohistologically distinct. Mechanisms concerned with the production of cortical and brainstem NFTs in PSP and AD are discussed.

Aged↗
PubMed1992

[Study of neurological and cognitive changes in patients in stage III and initial phases of stage IV of infection by human immunodeficiency virus type 1].

BACKGROUND: To evaluate the prevalence of neurological and cognitive disorders in patients with the human immunodeficiency virus type 1 (HIV-1). METHODS: A transversal prospective study was carried out in 56 patients with HIV-1 and in 18 seronegative subjects by a protocolized neurological and cognitive examination. RESULTS: Twenty-seven patients were intravenous drug users (IVDU) and 29 were male homosexuals. Nineteen were in stage III of HIV-1 infection and 37 were in the initial phases of stage IV. No significant differences were found in the cognitive performance of patients in stage III when the control group was compared with seropositive patients. Significant differences were observed in stage IV in the Rey figure complex tests the B trace test and the number key. Three stage IV patients presented dementia criteria. No significant differences were seen in test performance upon comparing the ex-iVDU seropositive subgroup with the male homosexuals nor in the stage III or stage IV groups. CONCLUSIONS: Cognitive performance of stage III patients did not significantly differ from that of the seronegative control group; a global diminution in cognitive performance was observed in the stage IV group and there were no differences in the cognitive state between the two risk groups analyzed.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Immunohistological study of grumose degeneration of the dentate nucleus in progressive supranuclear palsy.

The grumose degeneration observed in the dentate nuclei of 7 cases of progressive supranuclear palsy (PSP) was studied with a panel of antibodies which included 2 neurofilaments, Tau and ubiquitin. Dentate nucleus neurons were negative with all antibodies except ubiquitin which showed a slightly positive homogeneous pattern of staining. The amorphous material surrounding swollen or normal neurons was strongly positive for neurofilament and subunits and numerous torpedoes were observed in the granular layer of the cerebellar cortex. Our results confirm that grumose degeneration consists in degeneration of terminal axons of Purkinje cells in the dentate nucleus. The positivity of dentate nucleus neurons for ubiquitin may support the concept of synaptic dysfunction between Purkinje cells and dentate nucleus neurons.

Aged↗
PubMed1992

Ubiquitin in cerebral amyloid angiopathy.

Immunohistological findings in cerebral blood vessels of 4 cases with cerebral amyloid angiopathy (CAA) were compared with those of 4 Alzheimer's (AD) cases. A panel of antibodies against 2 neurofilament subunits (BF10 and RT97), a microtubule-associated protein (TAU) and ubiquitin were used. CAA cases showed a strong immunoreactivity for ubiquitin in blood vessel wall. Senile plaques (SPs) in CAA cases showed strong ubiquitin positivity but the central amyloid core was negative. AD brains showed immunoreactivity with all antibodies in SPs and neurofibrillary tangles (NFTs); blood vessels were consistently negative for ubiquitin. Control brains showed few SPs and NFTs; these were positive for ubiquitin, but blood vessels were negative. These results indicate that vascular amyloid deposition in CAA and AD may have different pathophysiological mechanisms.

Adenosine Triphosphate↗
PubMed1992

Expression of intercellular adhesion molecule-1 in thyroid follicular cells in autoimmune, non-autoimmune and neoplastic diseases of the thyroid gland: discordance with HLA.

The presence of intercellular adhesion molecule-1 (ICAM-1) on epithelial cells facilitates their recognition by specific T lymphocytes. To assess the possible role of ICAM-1 in the recognition of thyroid follicular cells by T cells in thyroid autoimmune disease, we investigated the expression of ICAM-1 in thyrocytes from thyroid glands affected by Graves' disease, in glands with non-autoimmune pathology and normal glands using immunofluorescence staining on cryostat sections and on dispersed cell preparations. Sequential tissue sections from glands affected by Graves' disease (n = 15), multinodular goitre (MNG, n = 26), benign nodules (n = 11), primary carcinomas (n = 12) and control thyroid glands (n = 5) were stained for ICAM-1, HLA class I, HLA class II, CD3 and thyroid peroxidase (TPO). Weak and patchy ICAM-1 expression was found in the thyrocytes of 4/15 (27%) Graves' disease and of 1/26 (4%) multinodular goitre glands. In contrast, ICAM-1 expression was detected in the thyrocytes of 5/11 (45%) benign nodules and of 8/12 (67%) thyroid carcinomas in which it was sometimes strong. Thyrocytes in the five control glands were negative. These results correlated well with flow cytometry data from 23 of these glands which showed that ICAM-1 expression in thyrocytes from Graves' patients was, when present, 'dull', while in some malignant thyrocytes it was 'bright'. In preparations of thyrocytes from Graves' disease glands we found a striking discordance between the high levels of expression of HLA class I and HLA class II and the low expression of ICAM-1. This is surprising since in vitro the expression of these three molecules is equally induced by IFN-gamma and TNF-alpha. These results suggest that additional factors are involved in the induction of the inappropriate HLA class II expression observed in the thyrocytes of glands affected by Graves' disease.

Antigens, CD↗
PubMed1992

Induction of intercellular adhesion molecule-1 but not of lymphocyte function-associated antigen-3 in thyroid follicular cells.

We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3) by thyrocytes and their regulation by cytokines. Immunofluorescence studies on cryostat sections and on freshly dispersed cell preparations showed that ICAM-1 and LFA-3 are barely detectable in non-autoimmune thyrocytes. However, thyrocytes acquired ICAM-1 expression in culture. IFN-gamma, IL-1 beta and TNF-alpha produced a clear enhancement of ICAM-1 expression. When tested in combination, IL-1 beta and TNF-alpha were additive to the IFN-gamma effect. LFA-3 expression was not modulated by these cytokines. In the HT93 thyroid cell line generated by transfection with SV40, ICAM-1 and LFA-3 were both constitutively expressed at high levels. Cytokines modulated ICAM-1 expression similarly, but to a greater extent than in normal thyrocytes. LFA-3 remained unmodified. These results support the notion that normal thyrocytes are immunologically silent cells. The capability of cytokines to induce ICAM-1 together with HLA class I and class II-expression on thyrocytes suggests that under their influence, these cells may express all the surface molecules required for antigen presentation and/or for being recognized as target cells in the context of thyroid autoimmune disease.

Antibodies, Monoclonal↗
PubMed1992

Plasmapheresis and antineoplastic treatment in CNS paraneoplastic syndromes with antineuronal autoantibodies.

We retrospectively evaluated the effect of plasmapheresis (PE) in seven patients with paraneoplastic encephalomyelitis (PEM), small-cell lung carcinoma, and anti-Hu antibodies, and four patients with paraneoplastic cerebellar degeneration (PCD), ovarian or breast cancer, and anti-Yo antibodies. In addition to PE, patients received prednisone (nine), cyclophosphamide (eight), or treatment of the tumor (five). All but one patient were severely disabled by the time PE began. The clinical outcome was compared with that of five patients (PEM, four; PCD, one) who only had treatment of the tumor. Only one of these five patients had a severe neurologic deficit at the onset of the antineoplastic treatment. No patient improved. Two patients treated with PE and antineoplastic therapy and three who only received treatment of the tumor remained stable for at least 6 months. Four of the five patients with a stable course started the treatment when the neurologic deficit was not severe. We conclude that the efficacy of PE with other immunosuppressive therapies in the stabilization of the neurologic deficit is uncertain.

Aged↗
PubMed1992

Neuronal changes in the nigrostriatal pathway of 1-methyl-4-phenylpyridine-treated mice.

Thirty young-adult mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) 30 mg/kg/day for 2 days and sacrificed 24 hours later in order to determine striatal catecholamines and to study morphological changes in the nigrostriatal pathway. Immunohistological techniques were also used with polyclonal antibodies for glial fibrillary acidic protein (GFAP) and tyrosine hydroxylase (TH), and monoclonal antibodies for two subunits of neurofilaments. Silver impregnation demonstrated conspicuous neuronal changes affecting cellular processes from substantia nigra in all treated mice. Terminal and axonal degeneration were also observed in striata. These changes were associated with a moderate to marked gliosis. The TH immunoreactivity was normal in cell bodies of substantia nigra but was decreased in striata from MPTP-treated mice. These data indicate that in mice the deterioration of dendritic and axonal neuropil may constitute a significant causal factor of MPTP neurotoxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

[Tropical spastic paraparesis and HTLV-I. The first case in Spain].

The first patient with myelopathy associated with T-cell leukemia/lymphoma virus infection (HTLV-I) in Spain is reported. Although this condition is endemic in several areas from the Caribbean Sea, South America, Africa and Japan, some cases have been reported in European countries, generally in immigrant patients, residents in endemic zones or patients having received transfusions. In the present case the infection was probably acquired in a tropical zone through blood transfusion. The patient was a 60-year-old female who had been living in Peru during the last 25 years. In that country aortocoronary bypass was carried out for ischemic heart disease. During operation she received blood transfusion. One and a half year later she developed progressive spastic parapesia with impaired sphincter control. Other causes were ruled out, and the diagnosis was confirmed by HTLV-I antibody determination with ELISA and Western blot.

Female↗
PubMed1991

Plasma and saliva levels of PGI2 and TXA2 in the headache-free period of classical migraine patients. The effects of nicardipine.

The levels of Prostacyclin (PGI2) and Thromboxane A2 (TXA2) were assayed simultaneously (RIA) in the plasma and saliva of 9 patients suffering from classical migraine attacks. The assays were done during an attack-free period. In relation to the control group we observed a significant decrease in the plasma levels of PGI2 together with a sharp increase in TXA2 in saliva. When the patients were treated with nicardipine, a calcium antagonist, the TXA2 increase in saliva did not occur. These results suggest both a systemic and local effect in the classical migraine attacks. We explain and discuss our results by referring to the PGI2: TXA2 equilibrium system. Nicardipine action might be related to its ability to reduce the calcium entry into the cell induced by thromboxane.

Adolescent↗
PubMed1990

[Postherpetic vasculopathy. A study of 3 cases in immunosuppressed patients].

We report three cases of postherpetic vasculopathy in immunologically compromised patients. Two had ophthalmic herpes zoster, contralateral to the physical signs, and the third case developed after disseminated herpes zoster. The initial CT images consisted of small ischemic infarcts in capsular regions and basal ganglia. The arteriography showed images consistent with vasculitis or thrombosis of great vessels of the Willis' polygon, which were ipsilateral to the herpetic lesion in two cases. In one patient the neurological defect remained stable, while the other two developed new ischemic episodes, all in the same cerebral hemisphere. It can be assumed from the delayed development of neurologic disease after cutaneous lesions that some cases go unnoticed if the zoster infection is not specifically looked for in retrospect.

Adult↗
PubMed1990

Subacute cerebellar syndrome as the first manifestation of AIDS dementia complex.

A patient presented with a subacute cerebellar syndrome in absence of cognitive impairment or other symptoms. He became demented several months after the onset of the disease. Necropsy demonstrated the typical features of the AIDS dementia complex and severe loss of Purkinje cells of the cerebellum. Patients with subacute cerebellar dysfunction should be evaluated for the presence of human immunodeficiency virus infection.

AIDS Dementia Complex↗
PubMed1990

Cerebrospinal fluid neuropeptide Y in Alzheimer's disease.

The cerebrospinal fluid neuropeptide Y level was measured by radioimmunoassay in 20 patients with probable Alzheimer's disease and in 19 controls. The mean level was lower in patients (69.5 +/- 36.7 pg/ml) than in controls (103 +/- 21.8 pg/ml; p less than 0.001). Patients with a disease duration of greater than 2 years had cerebrospinal fluid neuropeptide Y levels lower than those with shorter disease duration (p less than 0.02). These results suggest that neuropeptide Y containing cells may be involved in Alzheimer's disease. No correlation was found between neuropeptide Y levels and degree of cognitive impairment or age at disease onset.

Aged↗
PubMed1989

[AIDS dementia complex as the 1st manifestation of the acquired immunodeficiency syndrome].

In a prospective follow-up period from September 1987 to August 1988, the AIDS dementia complex (ADC) was the presenting clinical feature in six of 102 patients in whom AIDS was diagnosed in the Hospital Clínic i Provincial from Barcelona. The clinical picture was characterized by subcortical type deterioration and motor disturbances. Cerebrospinal fluid investigation and imaging techniques excluded other types of neurological involvement, and the diagnosis was confirmed at autopsy in two patients. The present study suggested that: 1) the ADC may be the presenting feature of AIDS in patients with unknown seropositive status; 2) in our area, ADC represents one of the most common causes of dementia in young patients, and 3) although a specific marker permitting a definitive clinical diagnosis is not available, at the time of diagnosis all patients had a severe degree of cellular immunosuppression induced by type 1 human immunodeficiency virus.

AIDS Dementia Complex↗