Ueyama T, Shirataki K, Tamaki N
Department of Neurosurgery, Takasago Municipal Hospital, Japan.
No Shinkei Geka. 1996 Nov;24(11):1035-9.
We encountered a case of traumatic basilar artery dissection presenting with "locked-in" syndrome. A 46-year-old-man fell approximately 2 meters and landed in an inverted position. He was admitted to our hospital after 4 days. He was in coma on admission, and neurological examination revealed that his pupils were 2 mm in size and reactive, the corneal reflex of both sides was absent, the pharyngeal reflex was absent, and quadriplegia was present. CT and MRI showed infarction at the ventral portion of the pons. 3D-CT and CT using a bone algorithm showed fractures of the upper clivus, the left petrous bone, and the left occipital condyle. Angiography showed a pearl and string sign at the upper basilar artery. It is suggested that the cause of the infarction of the ventral portion of the pons was the occlusion of the perforating arteries due to the basilar artery dissection, and the mechanism of the basilar artery dissection was the hyperextension or hyperflexion of the basilar artery by the movement of the brain stem caused by the traumatic impact. Repeated angiography revealed gradual improvement. Eventually he freed himself from the "locked-in" syndrome.
我们遇到了一例创伤性基底动脉夹层伴“闭锁综合征”的病例。一名46岁男性从约2米高处坠落,呈倒立姿势着地。4天后他被收治入我院。入院时他处于昏迷状态,神经系统检查发现其瞳孔直径2毫米且有反应,双侧角膜反射消失,咽反射消失,存在四肢瘫痪。CT和MRI显示脑桥腹侧梗死。三维CT和采用骨算法的CT显示斜坡上部、左侧岩骨和左侧枕髁骨折。血管造影显示基底动脉上段呈“串珠样”征。提示脑桥腹侧梗死的原因是基底动脉夹层导致穿支动脉闭塞,而基底动脉夹层的机制是创伤性撞击引起脑干移动导致基底动脉过度伸展或过度屈曲。重复血管造影显示病情逐渐改善。最终他摆脱了“闭锁综合征”。