Postural tremor after thalamic infarction.
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Biomedical subjects
Publications and source records attributed to F Vivancos.
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Brain single photon emission computed tomography (SPECT) findings are described in four adult patients with the transient syndrome of headache with neurological deficits and cerebrospinal fluid (CSF) pleocytosis. Focal deficits consisted of right-sided hemisensory changes with or without motor dysphasia or dysarthric speech (n = 4) and confusional episodes (n = 1). All patients had a CSF pleocytosis (with a mean of 309 cells/mm3 on the first spinal tap; range 75 to 590) and an elevated total protein (mean 130.5 mg/dL; range 70 to 193). The EEG showed excessive focal slowing (n = 2). A technetium Tc 99m hexamethyl propylenamine oxime (HMPAO) brain SPECT was performed during a symptom-free period, within 8 and 25 days after the onset of symptoms (n = 4). Three patients showed a decreased tracer uptake in the anterior left hemisphere, topographically consistent with the neurological deficits and EEG slowing. One patient showed no abnormalities. These findings indicate either focally impaired neuronal metabolism or hypoperfusion in regional cerebral blood flow, which could bear some relationship with the clinical features. The possibility that SPECT abnormalities may represent an epiphenomenon was also considered.
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INTRODUCTION AND OBJECTIVE: The use of cocaine has been increasingly associated with cerebrovascular disease specially in young adults. We review the cases of stroke related to cocaine abuse in this group. PATIENTS AND METHODS: We performed a retrospective study between 1989-1998. Data were obtained from the Young Adults Stroke Registry. To investigate the etiology of stroke all patients underwent cardiologic examination, coagulation and neuroimaging tests. RESULTS: We identified 13 patients under 45 years of age with stroke related to cocaine abuse (0.39% of all strokes and 7.60% of the ones in young adults). Mean age in this group was 28.30 years. Eight developed ischemic manifestations (5 infarcts, 2 TIAs and 1 encephalopathy with multiple ischemic lesions), 4 had intraparenchymal hemorrhages and 1 had a subarachnoid hemorrhage. The principal route of administration was intranasal and the time course from cocaine use to stroke ranged from several hours to several years. 61.53% had history of other drug abuse and in 84.61% other risk factors were identified. Angiographic studies demonstrated: arterial occlusions (3 cases), changes consistent with vasospasm (1), segmental narrowing (1) and arterial wall irregularities (1). No aneurysms or arterio-venous malformations were found. The frequency of cocaine-related stroke in young adults has decreased from 8.33% in 1989 to 5% in 1998. CONCLUSIONS: Cocaine is a well known cause of stroke, specially in young adults. In most cases other risk factors can be identified. Multiple overlapping mechanisms may be involved (vasospasm-thrombosis, high blood pressure, embolism.
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The most frequent neurological lesions found on Cranial Computerized Tomography (CT scan) in patients with Systemic Lupus Erythematosus (SLE) are cortical atrophy (psychosis, although in general atrophy is not associated with a particular clinical presentation), infarcts and haemorraghes (strokes). We describe a patient diagnosed of SLE who developed a psychotic clinical picture followed by generalized epileptic seizures within a context of diffuse lupus encephalopathy. On the neurological examination, she presented cortical blindness, generalized piramidalism and extrapiramidal rigidity. Various electroencephalographic recordings showed signs of diffuse cerebral involvement predominantly in posterior regions. Cerebrospinal fluid analysis showed a slight increase of IgG without oligoclonal bands and a positive anti-DNA antibody with an homogeneous pattern. Sequential CT images were carried out demonstrating hypodense areas initially in the occipital regions that extended progressively to the temporal, parietal and finally to the frontal lobes, with a moderate mass effect on the lateral ventricles and with no contrast enhancement. The images of the lesions on the CT disappeared completely with the adequate treatment as the symptomatology resolved. A MRI and cerebral angiography were performed when the patient recovered. Both MRI and angiography showed no alterations. We consider that this neuroradiological finding is exceptional, because of its total resolution. Nevertheless, more observations will be necessary to determine the exact meaning of these abnormalities.
The present investigation uses electrooculogram to evaluate multiple system atrophy (MSA) and late onset cerebellar atrophies (LOCAs), both idiopathic (ILOCA) and late onset autosomal dominant cerebellar ataxia (ADCA). Forty cases were clinically examined using scales for cerebellar, pyramidal, parkinsonian, mental status and neuroimaging quantitative evaluations. The patients were classified into three groups: olivopontocerebellar atrophy (OPCA), striatonigral degeneration (SND), Shy-Drager syndrome (SDS), and LOCA. We have used direct current electro-oculography in order to establish their validity in making the diagnosis. Cerebellar signs were significantly correlated with impaired VOR-fix gain and OKN, abnormalities of saccades, and reduced smooth pursuit gain (p < 0.05). Pons atrophy was significantly correlated with impaired VOR-fix gain (p < 0.01), abnormalities of saccades (p < 0.01), and reduced smooth pursuit gain (p < 0.05). Cerebellar hemisphere atrophy was significantly correlated only with impaired VOR-fix gain (p < 0.05), and medulla oblongata atrophy only with abnormalities of saccades (p < 0.05). Gaze-evoked nystagmus was found in 42.8% of patients with OPCA, and only in 14.2% with SND, but was not found in LOCA patients (t test, p < 0.05). In patients with OPCA, the combination of gaze-evoked nystagmus, abnormalities of sinusoidal VOR and reduced OKN gain measurements was very frequent, while infrequent in both LOCA (Fisher's exact test, p < 0.05) and SND subjects (p < 0.01). SDS also showed abnormalities of the oculomotor system.