Tai Kwok-Keung, Truong Daniel D
The Parkinson's and Movement Disorder Research Laboratory, Long Beach Memorial Medical Center, 2625 Pasadena Ave., Long Beach, CA 90806, USA.
Neurosci Lett. 2007 Sep 20;425(1):34-8. doi: 10.1016/j.neulet.2007.08.007. Epub 2007 Aug 10.
Although the mechanism underlying the anti-epileptic effects of a ketogenic diet (KD) is not known, KD is reported to be an effective treatment for intractable epilepsy, in particular among children. Here, we evaluated whether a KD can reduce posthypoxic seizure and myoclonic jerks in a rat model of cardiac arrest-induced cerebral hypoxia. In this study, rats were divided into two groups: one group received a normal diet while the other group was fed a KD for 25 days before being subjected to cardiac arrest-induced cerebral hypoxia. We found that rats fed a normal diet developed seizures and severe myoclonic jerks in response to auditory stimuli after the hypoxic insults, whereas the rats on the KD did not develop seizure and showed much less severe myoclonic jerks in response to auditory stimuli. The results suggested that the KD has beneficial effects against posthypoxic seizure and myoclonus.
尽管生酮饮食（KD）抗癫痫作用的潜在机制尚不清楚，但据报道KD是治疗难治性癫痫的有效方法，尤其是在儿童中。在此，我们评估了KD是否能减少心脏骤停诱导的脑缺氧大鼠模型中的缺氧后癫痫发作和肌阵挛。在本研究中，大鼠被分为两组：一组给予正常饮食，另一组在经历心脏骤停诱导的脑缺氧前25天给予KD。我们发现，给予正常饮食的大鼠在缺氧损伤后对听觉刺激会出现癫痫发作和严重的肌阵挛，而接受KD的大鼠没有出现癫痫发作，并且对听觉刺激的肌阵挛严重程度要低得多。结果表明，KD对缺氧后癫痫发作和肌阵挛具有有益作用。
