特发性全面性强直阵挛发作癫痫磁共振波谱改变的临床意义

Clinical significance of magnetic resonance spectroscopy of idiopathic generalized tonic clonic seizure epilepsy

目的用氢质子磁共振波谱检测丘脑、基底节区、岛叶中的代谢产物,探讨其在特发性全面性强直阵挛发作癫痫发病中的作用及意义。方法对20例特发性全面性强直阵挛发作癫痫患者进行发作间期的磁共振波谱采集,对N-乙酰天门冬氨酸、胆碱、肌酸进行半定量分析,完成检查后将以代谢物NAA/(Cho+Cr)含量为灰阶的伪彩图与横断位T1图像进行融合,直观分析双侧丘脑、基底节、岛叶代谢物的分布情况。结果GTCS组双侧丘脑NAA/Cr明显减少,NAA/(Cr+Cho)比值明显低于正常对照组,差异有统计学意义(P<0.05),而双侧基底节、岛叶的代谢物两组相比,差异无统计学意义(P>0.05)。将NAA/(Cr+Cho)含量比值伪彩图与常规MRI图像进行融合,可直观发现双侧丘脑区NAA/(Cr+Cho)比值与正常对照组存在明显差异。结论特发性GTCS患者丘脑神经元丧失及胶质细胞增生可能是其共同的病理特征;发作间期丘脑可能为其癫痫形成相关脑区,或是长期癫痫发作的脑损伤区。

Objective To detect the metabolite of thalamus, basal ganglia,insular lobe of patients with idiopathic generalized tonic clonic seizure（GTCS） and to discuss the role and significance of the change in the onset of GTCS. Methods There were twenty patients of idiopathic GTCS, two-sldes metabolites of thalamus basal ganglia, insular lobe were collected by magnetic resonance spectroscopy（MRS）, and N-aceytl aspartate（ NAA）, creatine（Cr）, chollne（Cho） were conducted with half-quantltative analysis. Amalgamated the colour-coded imaging which relative signal intensity of metabolites and TIRT1 imaging,to measure NAA/（Cho＋ Cr） singal intensity in thamalus basal ganglia,insular lobe areas. The distribution of metabolites in thalamus was analyzed straightly. Results The both NAA/Cr levels of thalamus in the GTCS group were significantly lower. The ratio of NAA/（Cr＋Cho） was either lower than that of the normal control group（P〈0.05）, but there was no difference between the two groups in basal ganglia and insular lobe . Through the amalgamation of the colour-coded imaging and the routine MRI imaging,the difference of the signal intensity of the ratio of NAA/（Cho＋Cr） in thalamus between two groups could be straightly detected. Conclusion The common pathology of idiopathic GTCS is the loss of neuron and hyperplasia of colloid cell. The abnormality NAA/（Cho＋Cr） of thalamus in idiopathic GTCS may indicate a correlated encephalic region of the form of epilepsy or injured cerebral zone caused by long time epi- leptic seizures.