Tebartz Van Elst L, Baeumer D, Lemieux L, Woermann F G, Koepp M, Krishnamoorthy S, Thompson P J, Ebert D, Trimble M R
Raymond Way Research Group, Epilepsy Research Group, Institute of Neurology, University College London, UK.
Brain. 2002 Jan;125(Pt 1):140-9. doi: 10.1093/brain/awf008.
Psychosis of epilepsy (POE) has been recognized as a severe complication of chronic intractable epilepsy for more than a century. Most of the clinical symptoms of POE are reminiscent of schizophrenia. Nevertheless, there is general agreement that the phenomenology of POE differs from classical schizophrenia. The temporal lobe hypothesis of schizophrenia put forward in the 1960s notes that episodes with paranoid psychoses are more prevalent in temporal lobe epilepsy (TLE). However, the aetiology and pathogenesis of POE are poorly understood. One of the strongest biological findings in schizophrenia is volume loss of temporal lobe structures and the hippocampus in particular. In order to test the hypothesis that atrophy of the hippocampus and the amygdala is found in patients with TLE and POE, we performed a retrospective study of all patients with TLE who were admitted to the assessment unit of the Chalfont Centre for Epilepsy from 1995 until 1999. Twenty-six (2.6%) of these 1008 patients fulfilled inclusion criteria and were compared with 24 patients with TLE without psychopathology and 20 healthy volunteers. All patients underwent extensive MRI investigations, including volumetric data sets and quantitative T(2 )relaxometry. We found that patients with TLE and POE differed from patients with TLE alone and healthy volunteers in that the total brain volumes were significantly smaller. While there were no differences in hippocampal volumes between the three study groups, there was a significant 16-18% enlargement of the amygdala on both sides in patients with POE. Our findings support the notion that POE is a distinct nosologic entity differing from schizophrenia not only in clinical details but also in neurobiological aspects. The finding of amygdala enlargement agrees with the observation of an association between dysphoric disorders of epilepsy and POE described nearly 100 years ago.
癫痫性精神病（POE）在一个多世纪以来一直被认为是慢性难治性癫痫的一种严重并发症。POE的大多数临床症状让人联想到精神分裂症。然而，人们普遍认为POE的现象学与经典精神分裂症不同。20世纪60年代提出的精神分裂症颞叶假说指出，偏执性精神病发作在颞叶癫痫（TLE）中更为普遍。然而，POE的病因和发病机制仍知之甚少。精神分裂症最有力的生物学发现之一是颞叶结构尤其是海马体体积缩小。为了验证在TLE和POE患者中发现海马体和杏仁核萎缩这一假说，我们对1995年至1999年入住查尔方特癫痫中心评估单元的所有TLE患者进行了一项回顾性研究。这1008名患者中有26名（2.6%）符合纳入标准，并与24名无精神病理学的TLE患者和20名健康志愿者进行了比较。所有患者均接受了广泛的MRI检查，包括容积数据集和定量T2弛豫测量。我们发现，TLE和POE患者与单纯TLE患者及健康志愿者的不同之处在于，前者的全脑体积明显较小。虽然三个研究组之间海马体体积没有差异，但POE患者双侧杏仁核显著增大了16% - 18%。我们的研究结果支持这样一种观点，即POE是一种独特的疾病实体，不仅在临床细节上，而且在神经生物学方面都与精神分裂症不同。杏仁核增大的发现与近100年前所描述的癫痫烦躁症与POE之间的关联观察结果相符。
