[Portuguese-type familial amyloidotic polyneuropathy: presentation of a case].
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Biomedical subjects
Publications and source records attributed to F Bermejo.
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The immediate clinical course of 42 patients with cerebral embolism secondary to rheumatic heart disease (RHD) was analyzed retrospectively. All the cases included cranial computed tomographic (CT) findings. Twenty-five patients received early anticoagulant therapy (AT) and 17 did not. Recurrent embolic events occurred in only one case. Seven instances of hemorrhagic infarction (HI) were found. In five cases, the development of HI correlated with a recurrent stroke, which occurred in each case within 48 hours after the initial cerebral embolism. Three of the patients with HI died (all of them were receiving AT). We believe that HI is a frequent cause of recurrent stroke after a cerebral embolic event, that it generally occurs in the first 48 hours, and that its outcome is possibly worsened by AT. Anticoagulant therapy should be delayed for three days after a cerebral embolic event secondary to RHD.
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The association of truncal ataxia with a number of different factors has been studied in a group of 95 epileptic outpatients on chronic anticonvulsant treatment. The 28 patients showing truncal ataxia had been epileptic for a longer period of time, received a significantly larger number of drugs, and had higher serum levels of phenobarbital than the non-ataxic group. Serum folate levels were significantly lower in the ataxic group. A role is postulated for anticonvulsant-induced folate deficiency in the appearance of truncal ataxia presenting after prolonged anti-convulsant therapy, either by increasing the serum levels of the anticonvulsants or through other, unknown mechanisms. The presence of tonic-clonic seizures, presumably associated with brain anoxia, was not associated with the appearance of truncal ataxia.
A series of 100 epileptic patients in whom the incidence of toxic effects due to antiepileptic drugs was retrospectively studied form the basis of this report. The appearance of toxic effects depended mainly on the number of drugs used, the length of therapy and the evolution of the epileptic crisis; they were more important in focal epilepsies, which were those with more resistance to therapeutic control and requiring increasing number and doses of antiepileptic drugs. Some side effects were observed in 60% of the patients involving generally the nervous system, skin, connective tissue, skeletal system, and hematopoietic organs. The drugs had to be reduced in 19% of these patients because of excessive sedation, mild central nervous system intoxication and various psychological effects, while treatment had to be changed in 11% due to acute intoxication with skin involvement, hematologic alterations and excessive sedation.
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An approach to the controversy of the physiopathology and classification of ischemic stroke is attempted in this study. The computed tomographies (CT) of 88 patients with transient ischemic attacks (TIA), 46 with reversible ischemic neurologic deficits (RIND) and 70 with ischemic strokes with minimum residuum (SMR) are analysed. The incidence of focal ischemic lesions on CT is 25% in TIA and RIND and 35% in SMR, when the study was performed after the first 24 hours. The incidence of cerebral infarction was much lower when the CT was performed within the first 24 hours after the clinical event. No significant differences in size or location of the infarction were found between the different groups. Deep infarctions were smaller than superficial ones. TIA duration correlated neither with the incidence of CT abnormalities nor with the size of the lesions. No correlation was found between doppler or oculoplethysmography abnormalities, clinical groups and CT findings. In reference to the structural lesions that underlie the clinical syndromes, TIA, RIND and SMR should not be considered as different groups.
In a case-control study of 73 cases of cerebral hematoma diagnosed by CT scan, significant risk factors were history of hypertension, chronic alcoholism, evidence of hepatic disease, EKG abnormalities and high hematocrit values. Initial blood pressure was significantly higher in cases, but blood pressure on the third day after admission was not different from controls. Hypertension and alcoholism did not show a clear correlation, but data from other studies explain the role of alcoholism in vascular disease through a relation with high blood pressure. Risk factors were similar in lobar and basal ganglia hematomas.
Hematocrits of 131 cerebral infarction cases were correlated with the outcome at 2 weeks. Bivariate analysis showed that cases with more intense admission deficit had lower admission hematocrit and that cases with poorer outcome had lower Day 2 and 4 hematocrits. However, multivariate analysis of several prognostic factors (including hematocrit, glycemia, blood pressure, age, and sex) showed that hematocrit was not independently related to outcome. Higher hematocrit thus is not indicative of less favorable short-term outcome.
INTRODUCTION: Several studies suggested a role of 'oxidative stress' (increased production of prooxidants, antioxidants deficiencies or both) in the pathogenesis of Parkinson's disease. In this study we have measured the serum levels of a number of prooxidant and antioxidant substances to evaluate their possible relation with the risk for Parkinson's disease. PATIENTS AND METHODS: We assessed the serum levels of iron, ferritin, ansferrin, ceruloplasmine, vitamin A, alpha-carotene, beta-carotene, and alpha-tocopherol, in 28 patients with Parkinson's disease and 85 matched controls. All of them were recruited from a population study. RESULTS: None of the values studied differed significantly between the two study groups, and none of them were correlated with age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale or the Hoehn and Yahr staging in the Parkinson's disease group. CONCLUSIONS: These results confirm the previous findings of classic case-control studies, suggesting the absence of relationship of the studied values with the risk for Parkinson's disease.
INTRODUCTION: The dementias are one of the commonest conditions seen in Neurology Clinics. Potentially reversible causes are described amongst the various aetiologies although there are doubts as to whether the use of indiscriminate testing to detect them is worthwhile. OBJECTIVE: In a group of demented persons to determine how many had a potentially reversible condition and how many improved, in a prospective, descriptive study in a Neurology Outpatient Clinic. PATIENTS AND METHODS: Using the Mini-Mental State Examination of Folstein and the DSM-III-R criteria for dementia, 121 demented patients were selected. An ordinary biochemical study was made (vitamin B12, thyroid hormones), serology (lues) and neuroimaging (cerebral CT), and when a potentially reversible condition was found, each case was treated. The patients treated were followed-up periodically for an average of 9.6 months (range 2 to 24 months). RESULTS: A potentially reversible condition was seen in 19.8% of the patients. On prospective evaluation only 3.3% had reversible symptoms and in no case were these completely reversed. Improvement was seen in conditions of depressive pseudo-dementia. CONCLUSIONS: Since some causes of dementia are reversible, the neurologist is obliged to investigate and seek these possible aetiologies. This study should be individualized according to clinical criteria to improve profitability of the complementary tests. Our results suggest that there are doubts as to the usefulness of indiscriminate investigation of possible reversible causes of the cases of dementia referred to Outpatient neurologists.
OBJECTIVES: The published data on neurological resources and the demand for neurological care in Spain were reviewed. Also, this demand was analysed in a specific health district (area 11, Hospital Universitario 12 de Octubre, Madrid). DEVELOPMENT: About 2.5 neurologists per 100,000 inhabitants in Spain was estimated to practice in the National Health Service in 1998. The published demand for first outpatient neurological consultations per 1,000 inhabitants/year in the National Health Service in Spain have a range of 8-35 consultations. The same demand in the health district analyzed was 14.5 consultations per 1,000 inhabitants/year in 1996. CONCLUSIONS: The demand for neurological care is high in Spain and will increase in the future mainly due to the population aging; the resources of neurologists and neurological beds would be adequate to this increasing neurological demands.
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OBJECTIVE: To study histologic gastric mucosa lesions in patients with gastric ulcer disease and to assess their evolution in the year after Helicobacter pylori eradication. METHODS: Seventy-three patients with gastric ulcer were prospectively studied. On endoscopy, biopsy specimens were taken from the antrum and gastric body for hematoxylin and eosin staining and urease testing. Serology and 13C-urea breath test were carried out. Fifty-six patients treated for H. pylori infection were monitored with histologic study at months 1, 6 and 12 after therapy to eradicate H. pylori infection. RESULTS: In patients with gastric ulcer, the prevalence of H. pylori was 86.3% (95% CI: 76-92%). Similar percentages in patients with chronic gastritis (CG) and in those with active chronic gastritis (ACG) were noted in the antrum and gastric body. However, severe active chronic gastritis was more prevalent in the antrum (p < 0.01). In patients with H. pylori infection who were not treated with non-steroidal anti-inflammatory drugs (NSAIDs), the percentages of both CG and ACG were higher than those observed in patients with both risk factors (p < 0.01) and in those treated with NSAIDs and with no infection (p < 0.0001). The prevalence of glandular atrophy (17.8%; 11-28%) and of intestinal metaplasia (68.5%; 57-78%) was higher in the antrum than in the gastric body (4.1%; 1-11% and 16.4%; 10-26%, respectively) (p < 0.01). In the antrum of patients with successful treatment, the percentages of CG:ACG before treatment and 1, 6, and 12 months after treatment completion were: 100%:97%, 74%:14%, 44%:11% and 11%:2%, respectively. In the gastric body these rates were: 88%:86%, 51%:14%, 23%:4% and 4%:0%. Improvement of CG was observed at month 1 after treatment completion, which was then confirmed at months 6 and 12 (p < 0.01) whereas improvement of ACG was most often achieved at month 1 after treatment completion (p > 0.001). No changes in atrophy and intestinal metaplasia were observed after H. pylori eradication. CONCLUSIONS: Histologic gastritis associated with gastric ulcer disease involves both the antrum and gastric body, although prevalence of severe ACG, atrophy and intestinal metaplasia were higher in the antrum. Histologic gastritis were closely related to H. pylori infection but is unrelated to NSAIDs. H. pylori eradication results in progressive CG improvement over the first year, as well as in early ACG improvement (as soon as 1 month after treatment completion); however, atrophy and intestinal metaplasia remain unchanged.