RESUMEN
Neurogenic neuroprotection is a promising approach for treating patients with ischemic brain lesions. In rats, stimulation of the deep brain nuclei has been shown to reduce the volume of focal infarction. In this context, protection of neural tissue can be a rapid intervention that has a relatively long-lasting effect, making fastigial nucleus stimulation (FNS) a potentially valuable method for clinical application. Although the mechanisms of neuroprotection induced by FNS remain partially unclear, important data have been presented in the last two decades. A 1-h electrical FNS reduced, by 59%, infarctions triggered by permanent occlusion of the middle cerebral artery in Fisher rats. The acute effect of electrical FNS is likely mediated by a prolonged opening of potassium channels, and the sustained effect appears to be linked to inhibition of the apoptotic cascade. A better understanding of the neuronal circuitry underlying neurogenic neuroprotection may contribute to improving neurological outcomes in ischemic brain insults.
Asunto(s)
Infarto Encefálico/prevención & control , Núcleos Cerebelosos/fisiología , Estimulación Encefálica Profunda/métodos , Animales , Infarto Encefálico/etiología , Núcleos Cerebelosos/anatomía & histología , Núcleos Cerebelosos/metabolismo , Circulación Cerebrovascular/fisiología , Modelos Animales de Enfermedad , Encefalitis/etiología , Encefalitis/prevención & control , Humanos , Infarto de la Arteria Cerebral Media/complicaciones , Vías Nerviosas/fisiología , Lóbulo Parietal/fisiologíaRESUMEN
To analyse the effect of ageing on the projection of the anterior interposed nucleus to the red nucleus, we injected the retrograde tracer fluorogold in the red nucleus of 3-, 6- and 12-month-old mice. The number of labelled neurones in the anterior interposed nucleus fell by 9% between 3 and 6 months and by another 9% between 6 and 12 months (all P < 0.001). This suggests that loss of neurones from the cerebellar nuclei starts well before old age.
Asunto(s)
Vías Aferentes/anatomía & histología , Envejecimiento/fisiología , Mapeo Encefálico , Núcleos Cerebelosos/citología , Neuronas/fisiología , Núcleo Rojo/citología , Animales , Núcleos Cerebelosos/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Degeneración Nerviosa/metabolismo , Neuronas/patología , Núcleo Rojo/anatomía & histología , Núcleo Rojo/metabolismo , Coloración y EtiquetadoRESUMEN
OBJECTIVE: To explore the frequency and course of neurodegenerative central nervous system (CNS) disease in Langerhans cell histiocytosis (ND-LCH). STUDY DESIGN: We studied 83 patients with LCH in whom magnetic resonance imaging (MRI) of the brain was performed at least twice for various clinical indications. We defined radiologic ND-LCH as an MRI pattern comprising bilateral symmetric lesions in the dentate nucleus of the cerebellum or basal ganglia. RESULTS: Forty-seven of 83 patients (57%) had radiologic ND-LCH, at a median of 34 months (range 0-16 years) from the diagnosis of LCH. The MRI findings deteriorated in 31/47 (66%) patients over a median of 3 years (range 2 months to 12 years 6 months) and did not reverse in any patient. In 12 patients with radiologic ND-LCH (25%), clinical ND-LCH with overt symptoms were found 3 to 15 years (median 6 years) after initial LCH diagnosis. These symptoms included intention tremor, cerebellar ataxia, dysarthria, dysdiadochokinesis, concentration deficits, psychomotor retardation, severe headaches, and psychosis. CONCLUSION: We conclude that radiologic ND-LCH is serious, not uncommon in patients studied by MRI, irreversible, and may be followed by severe clinical ND-LCH many years after the initial diagnosis of LCH.