RESUMO
OBJECTIVE: In patients with large middle cerebral artery (MCA) infarction space occupying brain edema may lead to a malignant course with up to 80% mortality under conservative treatment. As interventional treatment strategies must be started before the deterioration occurs predictors of a malignant course are necessary. PATIENTS AND METHODS: This study reports on the results of early electroencephalography (EEG) within 24h after onset of stroke in 25 patients suffering a large MCA infarct (12 patients with a malignant and 13 with a non-malignant course). EEG analysis was performed according well-established indicators for focal as well as global changes. RESULTS: Our findings indicate that the absence of delta activity and the presence of theta and fast beta frequencies within the focus predict a benign course (p < 0.05), whereas diffuse generalized slowing and slow delta activity in the ischemic hemisphere may point to a malignant course. CONCLUSION: This study shows that in patients suffering from large MCA infarction early EEG delivers useful information to select those patients who develop malignant edema.
Assuntos
Edema Encefálico/etiologia , Edema Encefálico/mortalidade , Eletroencefalografia , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/fisiopatologia , Idoso , Feminino , Seguimentos , Humanos , Infarto da Artéria Cerebral Média/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Fatores de Tempo , Tomografia Computadorizada por Raios X , Índices de Gravidade do TraumaRESUMO
The pathophysiology of sleep-related motor diseases and sleep dysfunction in movement disorders is widely unknown as yet. Functional brain imaging, in particular radioisotope and magnetic resonance techniques, are powerful tools to investigate possible pathomechanisms of combined sleep and motor dysregulation. In patients with Restless legs syndrome (RLS), only a subtle striatal dopamine deficit was found in PET and SPECT despite a good treatment effect of dopaminergic drugs. Functional MRI suggested a central generator of periodic limb movements during sleep (PLMs) in RLS. In contrast, a marked striatal dopamine depletion was demonstrated in patients with REM sleep behaviour disorder (RBD) as the base for the clinical and nosological overlap of RBD with parkinsonian disorders. PET and SPECT also suggested that sleep abnormalities in Parkinson's disease (PD), such as REM sleep diminution or increased PLMs, are indirect manifestations of the primary striatal dopamine deficiency.
Assuntos
Encéfalo , Imageamento por Ressonância Magnética , Transtornos dos Movimentos/fisiopatologia , Transtornos do Sono-Vigília/fisiopatologia , Encéfalo/irrigação sanguínea , Encéfalo/patologia , Encéfalo/fisiopatologia , Humanos , Transtornos dos Movimentos/patologia , Transtornos do Sono-Vigília/patologiaRESUMO
Sleep disturbances are common in patients with Parkinson's disease (PD). Previous studies have shown alterations of polysomnographic sleep parameters in PD, such as overall diminution of slow-wave and REM sleep duration, absence of muscle atonia during REM and increased occurrence of periodic leg movements during sleep. The pathogenesis of sleep dysregulation in PD is unknown. The aim of this study was to determine relations of abnormal polysomnographic sleep parameters and the dopaminergic function of the striatum and the upper brainstem measured with the use of positron emission and magnetic resonance tomography in 10 early-stage PD patients with a history of sleep disturbances. Our data demonstrated a significant inverse correlation of absolute and percentage REM sleep duration with the mesopontine [18F]6-fluorodopa (FDOPA) uptake in PD patients. Therefore, the results point to a REM inhibiting effect of increased monaminergic transmission within the upper brainstem in early-stage PD. This finding emphasises the pathophysiological significance of a disturbed neurotransmitter equilibrium in the rostral brainstem for REM sleep alterations in PD.
Assuntos
Tronco Encefálico/fisiologia , Di-Hidroxifenilalanina/análogos & derivados , Di-Hidroxifenilalanina/farmacocinética , Doença de Parkinson/complicações , Transtornos do Sono-Vigília/etiologia , Sono REM , Tomografia Computadorizada de Emissão , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neurotransmissores , Polissonografia , Transtornos do Sono-Vigília/fisiopatologiaRESUMO
After stroke, the interhemispheric reorganization of the neural network implicated in language is hypothesized to be a function not only at the site of the lesion but also of dynamic right hemispheric and subcortical neural systems. These neural systems may have different functional shares in the utilization of particular language tasks. Important insights in language rehabilitation have been gained by quantitative topographical electroencephalography. It has been demonstrated that abnormalities within and outside speech relevant areas are related to restitution of poststroke aphasia. In the ischemic regions they indicate local disturbances, outside they reflect failures in neuronal networks involved in the generation and propagation of the alpha-rhythm. Treatment by a neuromodulatory agent has shown a significant shift of alpha-rhythm from frontal to occipital regions which may be due to a restitution of corticothalamic circuits in parallel to an improvement of neuropsychological scores in different language domains.
RESUMO
Individual benzodiazepine receptor (BZR) binding of peri-lesional cortex was investigated in symptomatic epilepsies. Eleven patients aged 19-44 years were studied whose diagnosis was established by medical history, clinical, electroencephalographic, and magnetic resonance imaging (MRI) findings. Three-dimensional [11C]-flumazenil (FMZ) positron emission tomography and MRI scans were obtained and coregistered. Lesions (five low-grade brain tumours, one AV malformation, one cavernoma, one cystic lesion of unknown aetiology, one traumatic brain injury, one post-operative and one post-haemorrhagic defect) were outlined on individual MRI scans. Adjacent to those lesions, and in homologous contralateral structures, FMZ binding was analysed in four pairs of cortical 9 x 9-mm regions of interest (ROIs) placed on transaxial and coronal slices, respectively, as well as in the lesion volume and its mirror region. Percentage asymmetry ratios were calculated and those at or outside the 90-110% range were operationally defined significant. Peri-lesional FMZ binding asymmetries ranged from 70 to 125%, lesional asymmetries from 38 to 82%. Only one patient showed no significant change, whilst nine exhibited significant reductions of FMZ binding in at least one ROI (3 x 1, 4 x 2, 1 x 3, 1 x 4), and significant increases were observed in two ROIs of another patient. Therefore, peri-lesional disturbances of BZR binding are common but variable in location. Because a close correlation between regional decreases in FMZ binding and spiking activity was recently demonstrated in neocortical epilepsies, abnormal peri-lesional FMZ binding may bear some relation to the mechanisms of epileptogenesis in symptomatic epilepsies.