Department of Small Animal Medicine and Surgery, University of Veterinary Medicine, Hannover, Germany.
Epilepsia. 2013 Apr;54(4):580-8. doi: 10.1111/epi.12071. Epub 2013 Jan 7.
In humans, traumatic brain injury (TBI) is one of the most common causes of acquired (symptomatic) epilepsy, but as yet there is no treatment to prevent the development of epilepsy after TBI. Animal models of posttraumatic epilepsy (PTE) are important to characterize epileptogenic mechanisms of TBI and to identify clinically effective antiepileptogenic treatments. The prevalence and phenomenology of naturally occurring canine epilepsy are similar to those in human epilepsy. However, the risk of epilepsy after TBI has not been systemically studied in dogs. We therefore performed a large retrospective study in 1,000 dogs referred to our clinical department over a period of 11.5 years with the aim to determine the incidence of early and late seizures after head trauma in this species.
Two strategies were used: in group I (n = 392), we evaluated whether dogs referred for the treatment of a head trauma (group Ia) or other trauma (group Ib) developed seizures after the trauma, whereas in group II (n = 608) we evaluated whether dogs referred for the treatment of recurrent epileptic seizures had a history of head trauma. Data for this study were obtained from our clinical database, questionnaires sent to the dogs' owners, and owner interviews.
In group Ia, 6.6% of the dogs developed PTE, which was significantly different from group Ib (1.9%), indicating that head trauma increased the risk of developing epilepsy by a factor of 3.4. The risk of PTE increased with severity of TBI; 14.3% of the dogs with skull fracture developed PTE. In group II, 15.5% of the dogs with epilepsy had a history of head injury, which was significantly higher than the incidence of PTE determined for group Ia.
Our study indicates that head trauma in dogs is associated with a significant risk of developing epilepsy. Therefore, dogs with severe TBI are an interesting natural model of PTE that provides a novel translational platform for studies on human PTE.
在人类中，创伤性脑损伤（TBI）是获得性（症状性）癫痫最常见的原因之一，但目前尚无预防 TBI 后癫痫发生的治疗方法。创伤后癫痫（PTE）的动物模型对于确定 TBI 的致痫机制以及识别临床上有效的抗癫痫发生治疗方法非常重要。犬自然发生癫痫的患病率和表型与人类癫痫相似。然而，TBI 后癫痫的风险在犬中尚未系统研究过。因此，我们在我们的临床科室就诊的 1000 只犬中进行了一项大型回顾性研究，目的是确定这种动物头部创伤后早期和晚期发作的发生率。
我们使用了两种策略：在第 I 组（n=392）中，我们评估了因头部创伤（I 组 a）或其他创伤（I 组 b）而接受治疗的犬在创伤后是否发生癫痫发作，而在第 II 组（n=608）中，我们评估了因反复发作性癫痫而接受治疗的犬是否有头部创伤史。这项研究的数据来自我们的临床数据库、发送给犬主人的调查问卷和主人访谈。
在 I 组 a 中，6.6%的犬发生了 PTE，与 I 组 b（1.9%）相比差异显著，表明头部创伤使发生癫痫的风险增加了 3.4 倍。PTE 的风险随 TBI 的严重程度而增加；颅骨骨折的犬中 14.3%发生了 PTE。在 II 组中，15.5%的癫痫犬有头部外伤史，明显高于 I 组 a 确定的 PTE 发生率。
我们的研究表明，犬头部创伤与发生癫痫的风险显著相关。因此，患有严重 TBI 的犬是 PTE 的一个有趣的天然模型，为 PTE 的人类研究提供了一个新的转化平台。
