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Apraxia of eyelid opening (AEO) is a syndrome characterized by the patient's difficulty in initiating eyelid elevation spontaneously. Most of the reported cases were associated with extrapyramidal diseases. We report a case of AEO presented after traumatic brain injury, not with extrapyramidal diseases, and improved by dopaminergic treatment. A 49-year-old man underwent a traffic accident and was transferred to the emergency room in an unconscious state. Brain computed tomography (CT) revealed a subdural and epidural hemorrhage at right temporal and bilateral frontal lobes, and he received burr-hole trephination. After receiving comprehensive treatment including occupational therapy, cognition and mobility gradually improved, but he could not open his eyes voluntarily. With dopaminergic treatment (levodopa/benserazide 200/50 mg), he started to open his eyes spontaneously, especially when eating and undergoing physical training. This case showed that AEO may occur after brain injury and that dopaminergic treatment is beneficial also in AEO patients without extrapyramidal diseases.
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To investigate the effect of combined therapy of exercise and nootropic agent on cognitive function in a focal cerebral infarction rat model.
Forty 10-week old male Sprague-Dawley rats were subjected to photothrombotic cerebral infarction of the left parietal lobe. All rats were randomly divided into 4 groups: group A was photothrombotic cerebral infarction rats without any treatment (n=10); group B was photothrombotic cerebral infarction rats with swimming exercise (n=10); group C was photothrombotic cerebral infarction rats with oral administration of acetyl-L-carnitine (n=10); group D was photothrombotic cerebral infarction rats with swimming exercise and oral administration of acetyl-L-carnitine (n=10). Cognitive function was evaluated using the Morris water maze test on the 1st day, and the 1st, 2nd, and 4th week after the induction of cerebral infarction. The activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in the hippocampus were measured. The neuronal cells of the hippocampus were histopathologically evaluated.
The escape latency was shorter in groups B, C, and D than in group A. However, the differences were not statistically significant at the 1st, 2nd and 4th week. The activity of SOD was the highest in group D. The level of MDA was the lowest in group D. We observed more normal neuronal cells in groups B, C, and D.
The combined therapy of exercise and nootropic agent was helpful in ameliorating oxidative stress in the focal cerebral infarction rat model. However, the effect did not translate into improvement of cognitive function.
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