Singla Monika, Singh Parampreet, Kaushal Sandeep, Bansal Rajinder, Singh Gagandeep
Neurology Unit, Dayanand Medical College, Ludhiana, India.
Epileptic Disord. 2007 Sep;9(3):292-9. doi: 10.1684/epd.2007.0122. Epub 2007 Sep 20.
To discuss the possible mechanisms underlying a dual pathology combining neurocysticercosis and hippocampal atrophy, illustrated by the observation of four patients with epilepsy.
The first patient presented at the age of four years with a first episode of status epilepticus, presumably due to an inflamed, calcified, parenchymal cysticercus granuloma. Thereafter, he had occasional seizures. Routine MRI undertaken several years later revealed unilateral hippocampal atrophy and sclerosis. Two other patients with initial imaging evidence of active neurocysticercosis located close to the hippocampus, and occasional seizures, developed ipsilateral hippocampal sclerosis. The seizure disorder of our fourth patient, with medically intractable epilepsy, was initially attributed to a calcified cysticercus granuloma. Clinical description, video-EEG telemetry and imaging work-up suggested a diagnosis of mesial temporal lobe epilepsy due to hippocampal sclerosis.
Definitive conclusions as to the underlying mechanisms cannot be derived from the present, retrospective series of only four patients. However, the following suggestions can be made: 1) seizures due to neurocysticercosis may constitute the initial precipitating illness for the development of hippocampal sclerosis, 2) the hippocampus may be involved in host brain inflammation and gliosis in response to a nearby, degenerating cysticercus, 3) the seizure focus formed by the degenerating cysticercus, engenders epileptogenic changes in the hippocampus through kindling, and 4) the two conditions may coexist purely by chance. Systematic and prospective, serial MRI evaluations of hippocampal structures in patients with neurocysticercosis should contribute to further clarify the underlying mechanisms.
通过对4例癫痫患者的观察,探讨神经囊尾蚴病与海马萎缩合并存在的双重病理可能的潜在机制。
首例患者4岁时首次出现癫痫持续状态,推测是由于实质内囊尾蚴肉芽肿发炎、钙化所致。此后,他偶尔发作癫痫。几年后进行的常规MRI显示单侧海马萎缩和硬化。另外两名患者最初的影像学证据显示在海马附近有活动性神经囊尾蚴病,且偶尔发作癫痫,随后出现同侧海马硬化。我们的第四例患者患有药物难治性癫痫,其癫痫发作最初归因于钙化的囊尾蚴肉芽肿。临床描述、视频脑电图遥测和影像学检查提示诊断为海马硬化所致的内侧颞叶癫痫。
仅基于目前这例仅4名患者的回顾性系列研究,无法得出关于潜在机制的确切结论。然而,可以提出以下建议:1)神经囊尾蚴病引起的癫痫发作可能是海马硬化发展的初始促发疾病;2)海马可能参与宿主对附近正在退变的囊尾蚴的脑部炎症和胶质增生反应;3)退变的囊尾蚴形成的癫痫病灶通过点燃作用在海马中引发致痫性变化;4)这两种情况可能纯属偶然共存。对神经囊尾蚴病患者的海马结构进行系统的、前瞻性的系列MRI评估,应有助于进一步阐明潜在机制。