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Cerebellum development

DahmaneN, Ruiz i Altaba A (1999) Sonic hedgehog regulates the growth and patterning of the cerebellum. Development 126 3089—3100. [Pg.166]

Pons S, Trejo JL, Marhnez-Morales JR, Marti E (2001) Vitronectin regulates sonic hedgehog activity during cerebellum development through CREB phosphorylation. Development 128 1481—1492. [Pg.169]

Ye, P., Xing, Y., Dai, Z., and D Ercole, A. J. (1996). In vivo actions of insulin-like growth factor-I (IGF-I) on cerebellum development in transgenic mice Evidence that IGF-I increases proliferation of granule cell progenitors. Brain Res. Dev. Brain Res. 95, 44-54. [Pg.188]

Schwarz, M., Alvarez-Bolado, G., Urbanek, P., Busslinger, M. and Grass, P. (1997) Conserved biological function between Pax-2 and Pax-5 in midbrain and cerebellum development evidence from targeted mutations . Proceedings of the National Academy of Sciences of the United States of America, 94, 14518-23. [Pg.31]

Johanson CE. 1980. Permeability and vascularity of the developing brain Cerebellum vs cerebral cortex. Brain Res 190 3-16. [Pg.214]

Brain metastasis is the most common neurologic complication seen in patients with cancer. Approximately 170,000 patients develop brain metastases in the United States each year.20 Many malignancies are frequently associated with brain metastases (Table 96-7). While melanoma is the tumor type most likely to metastasize to the brain, brain metastases owing to lung and breast cancers are seen more often because they are among the most common cancers. In addition, brain metastasis may be diagnosed at the same time as the primary malignancy in around 20% of cases.22 Around 80% of brain metastases occur in the cerebral hemispheres, 15% in the cerebellum, and 5% in the brain stem. [Pg.1477]

Clinical findings include mental retardation, severe metabolic acidosis, and evidence of a spastic quadripare-sis and cerebellar disease. Some patients develop normally until late childhood, when a progressive loss of intellectual function became appreciated. Patients also may manifest a mild hemolysis. Pathological changes have included atrophy of the cerebellum and lesions in the cortex and thalamus. There is no specific therapy. [Pg.681]

Dystonia due to identifiable structural or biochemical abnormalities ( secondary dystonia) often occurs weeks or months after strokes or other focal lesions, which commonly involve the basal ganglia, but may also involve the thalamus or cerebellum. Dystonia is also seen in children with cerebral palsy and in patients with abnormalities of dopaminergic transmission. For instance, dystonia may develop in the context of Parkinson s disease, either as an early parkinsonian sign, or in response to dopaminergic drugs. A particularly interesting inherited disease results in a combination of dystonia and parkinsonian features at a young age, which responds dramatically to treatment with low-dose levodopa ( dopamine-responsive dystonia ). [Pg.775]


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