These findings suggest that RFE may be more effective than conventional rehabilitation in lessening impairment and improving upper-limb motor function during the subacute phase of stroke.

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Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor involved in the survival and proliferation of neurons. However, there have been few reports examining the relationship between GDNF and functional recovery after cerebral infarction. The authors investigated the change in the expression of GDNF proteins during functional recovery in rats following photochemically induced cerebral infarctions. Functional recovery for the first 14 days after the infarction was evaluated using a beam-walking test. The number of GDNF-like immunoreactive cells around the infarction were counted at various times (24 h, 72 h, 7 days, and 14 days) post-infarction. Immunohistochemical analysis of brain sections showed that the expression of GDNF-like immunoreactive cells was significantly increased in the temporal cortex until 7 days on the side ipsilateral to the infarction, and had decreased by 14 days. Likewise, the functional recovery of paralysis was substantial until 7 days post-infarction, after which the improvement was mild. Therefore, the expression of GDNF protein might have some relationship with the functional recovery of paralysis. There are great hopes that GDNF could be used as a therapeutic agent for cerebral infarction.

Genetic polymorphisms in the cytochrome P450 family are widely known to contribute to inter-individual differences in drug pharmacokinetics. In this study we report a case of a patient with cytochrome P450 2C19 polymorphism. A 57-year-old woman presented with right cerebral hemorrhage and left hemiplegia. She was administrated phenytoin 200 mg day and phenobarbital 60 mg day to prevent convulsions. After a change in phenytoin dosage 97 grains to 10 grains , she developed ataxia and experienced a disturbance in her activities of daily living. She was admitted to our hospital. Her serum concentration of phenytoin was found to be at a toxic level 45.9 mg ml and serum phenobarbital was relatively high 19.1 mg ml. She showed an extremely low clearance of phenytoin, so we checked the genotype of her P450 2C9 and P450 2C19 cytochromes, which are metabolic enzymes of phenytoin. For cytochrome P450 2C9, the patient was a homozygous extensive metabolizer wild type, 1 1 , but for cytochrome P450 2C19, she was a poor metabolizer 3 3. Her phenytoin dosage was reduced, and her ataxia, activities of daily living, left hemiplegia, and cerebral blood flow in Xe-CT improved.

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