Impairment of intellectual functions after surgery and posterior fossa irradiation in children with ependymoma is related to age and neurologic complications. (33/77)

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Cerebellar mutism following posterior fossa tumor resection in children. (34/77)

AIM: Cerebellar mutism is a documented complication of posterior fossa surgery in pediatric ages. Risk factors such as the type of tumor, size, and location of tumor, hyrdrocephalus, postoperative cerebellar swelling for cerebellar mutism were investigated in this study. MATERIAL AND METHODS: A consecutive series of 32 children with a cerebellar tumor were operated on at the Haseki Educational and Research Hospital, Department of Neurosurgery, between 1990 and 2005. Their speech and neuroradiological studies were systematically analysed both preoperatively and postoperatively RESULTS: Cerebellar mutism developed in ten children (32%) in the early postoperative period. The type of tumor, midline localization, and vermian incision were significant single independent risk factors. In addition, an interdependency of possible risk factors (tumor > 5 cm, medulloblastoma) was found. The latency for the development of mutism ranged from 0 to 90 days (mean 15.6 d). The speech returned to normal in eight patients. All cases were accompanied by cerebellar ataxia. CONCLUSION: Mutism after posterior fossa tumor resection is also associated with ataxia. Cerebellar mutism usually has a self-limiting course and a favorable prognosis.  (+info)

Brain structural abnormalities in survivors of pediatric posterior fossa brain tumors: a voxel-based morphometry study using free-form deformation. (35/77)

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Survivors of pediatric posterior fossa tumors: cognitive outcome, intervention, and risk-based care. (36/77)

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Intensive multimodality treatment for children with newly diagnosed CNS atypical teratoid rhabdoid tumor. (37/77)

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Injuries to inferior vermis and dentate nuclei predict poor neurological and neuropsychological outcome in children with malignant posterior fossa tumors. (38/77)

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Candidate genes on chromosome 9q33-34 involved in the progression of childhood ependymomas. (39/77)

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Evolution of neurological impairment in pediatric infratentorial ependymoma patients. (40/77)

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