卡马西平治疗三叉神经痛致头晕的发病机制探讨

目的:探讨卡马西平治疗三叉神经痛致头晕的可能发病机制。方法:回顾性研究我院确诊为原发性三叉神经痛的129例患者,21例患者未服用卡马西平治疗,74例患者服用卡马西平每日剂量<600 mg,34例患者服用卡马西平每日剂量≥600 mg。通过磁共振成像和磁共振断层血管造影检查脑供血不足的情况及三叉神经根出口区周围的血管结构,探讨不同卡马西平使用剂量、不同脑供血不足状态、不同三叉神经血管结构与卡马西平致头晕的关系。结果:未服用卡马西平的患者未出现头晕,服用卡马西平每日剂量<600 mg与每日剂量≥600 mg的患者头晕的发生率比较,差异无统计学意义(P>0.05)。无脑供血不足的患者头晕的发生率较脑供血不足和脑梗死的患者显著降低,差异均有统计学意义(P<0.05),而脑梗死的患者头晕的发生率与脑供血不足的患者比较,差异无统计学意义(P>0.05)。血管未接近神经、血管接近神经未压迫、血管压迫神经的患者头晕的发生率比较,差异均无统计学意义(P>0.05)。结论:脑供血不足是卡马西平治疗三叉神经痛致头晕的可能发病机制之一,而药物剂量、神经血管结构与卡马西平治疗三叉神经痛致头晕并无显著相关性。

Pathogenesis of Carbamazepine in the Treatment of Trigeminal Neuralgia-associated Dizziness

OBJECTIVE：To investigate possible pathogenesis of carbamazepine（CBZ）in the treatment of trigeminal neuralgia（TN）-associated dizziness. METHODS：129 patients diagnosed as primary TN of our hospital were studies retrospectively;21 patients were not treated with CBZ;74 treated with CBZ with daily dose〈600 mg;34 treated with CBZ with daily dose ≥600 mg.MRI and MRTA were used to detect insufficiency of cerebral blood supply and surrounding vascular structures of the exit zone of the trigeminal nerve root,and investigate the relationship of CBZ amount,different states of cerebral blood supply insufficiency,vascular structures of different trigeminal nerve root with CBZ-associated dizziness. RESULTS：There was no significant difference in the incidence of dizziness among patients without CBZ therapy,receiving CBZ with daily dose ≥600 mg or 〈 600 mg（P〉0.05）. The incidence of dizziness in patients without insufficiency of cerebral blood supply was decreased significantly in patients with insufficiency of cerebral blood supply and cerebral infarction（P〈0.05）. There was no statistical significance in the incidence of dizziness in patients with cerebral infarction and those with insufficiency of cerebral blood supply（P〉0.05）. There was no significant difference in the incidence of dizziness among patients without vascular close to never,those with vascular close to never but without neurovascular compression and those with neurovascular compression（P〉0.05）. CONCLUSIONS：Insufficiency of cerebral blood supply is a possible pathogenesis of CBZ in the treatment of TN-associated dizziness,but there is no significant relationship of drug dosage and nerve vascular structures with CBZ in the treatment of TN-associated dizziness.