CIPark脑瘫早期的神经成像诊断.ppt

MRI Evaluation Highly sensitive to detect gross structural abnormalities in CP 1. Is PVL etiologic factor in the pathogenesis of spastic type of CP ? Not always because 25% of CP shows normal MRI findings 2. Is the Damage of the corticospinal tract caused by PVL ? 2. Is the damage of the corticospinal tract is caused by PVL ? No relationship with the damage of corticospinal track and PVL 3. Is the spasticity and motor dysfunction of CP caused by damaged corticospinal tract ? 3. Is the spasticity and motor dysfunction of CP caused by damaged corticospinal tract ? Alteration of GABAA receptor binding might play an important role in the pathogenesis of motor dysfunction and spasticity in patients with spastic CP. Evaluation Tools 1. Conventional Brain MRI 2. Diffusion Tensor Imaging with Tractography 3. 18F-fluoroflumazenil PET Methods 1st AOCPRM Normal Group SD Group CP spastic diplegia with PVL 1st AOCPRM SD Normal Rt Lt CP spastic diplegia with PVL P 0.0005 1st AOCPRM CST Optic radiation Corpus callosum CSTs CP spastic diplegia without PVL P 0.0005 1st AOCPRM Decreased F-18-FFMZ Binding Sites in Spastic Diplegia Decreased 18F-FFMZ Binding Sites in Spastic Diplegia 1st AOCPRM Conclusions 1. PVL may not be the etiologic factor in the pathogenesis of spastic type of CP . 2.There is no relationship with the damage of corticospinal track and PVL 3.Alteration of GABAA receptor binding might play an important role in the pathogenesis of motor dysfunction and spasticity in patients with spastic CP. 1st AOCPRM * * * * * * * * * Activation of GABA A receptors generate an efflux of chloride and an exitation of immature neurons, and an influx of chloride and an inhibition of adult neurons. * * * The corticospinal tracts in patient without PVL were grossly normal in terms of connectivity and white matter volume, however, the FA value was significantly decreased. * * The Early Diagnosis of