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Brainstem transient ischemic attacks due to compression of pons from a persistent primitive trigeminal artery

机译:由于持续性原始三叉动脉对脑桥的压迫导致脑干短暂性脑缺血发作

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Sir, Persistent primitive trigeminal artery (PPTA) is the most common type of persistent carotid-basilar arterial anastomosis.[1] Most cases have been incidentally detected1121 but can present with brainstem symptoms.^1 Possible mechanisms of brain-stem ischaemia are low perfusion pressure in the vertebrobasilar system and embolisation from the stenotic carotid lesions.121 Hemodynamic factors and dysautoregulation could also play a part in the pathogenesis of vertebrobasilar territory ischaemic attacks.A 17-year old girl noted sudden onset numbness of right side of her face and left hand for 15 min. Two months later she had a similar episode; this time it was associated with difficulty in walking, slipping of footwear from left foot which lasted for 45 min. On admission, neurological examination was essentially normal. Blood biochemistry and complete blood picture were normal. Brain magnetic resonance imaging (MRI) revealed indentation of the right ventral pons by an anomalous vessel [Figure la]. Magnetic resonance angiography (MRA) showed right PPTA (Saltzman type 1) with hypoplastic ipsilateral vertebral artery and basilar artery below PPTA [Figure lb and c]. The postrerigL communicating arteries were absent bilaterally. The posterior fossa circulation was almost independent from circle of Willis. Cerebral digital subtraction angiography (DSA) and therapeutic interventions were refused by the patient's relatives. She was treated with clopidogrel plus aspirin. She did not suffer from any transient ischemic attacks (TIAs) or stroke at 3-months follow-up.
机译:主席先生,持久性三叉戟原始动脉(PPTA)是持续性颈动脉-基底动脉吻合术的最常见类型。[1]大多数病例已被偶然发现1121,但可能出现脑干症状。^ 1脑干缺血的可能机制是椎基底动脉系统灌注压力低和颈动脉狭窄引起的栓塞。121椎基底动脉区域缺血性发作的发病机制。一个17岁的女孩注意到面部右侧和左手突然麻木15分钟。两个月后,她也发生了类似的发作。这次与步行困难有关,鞋类从左脚滑落持续了45分钟。入院时,神经系统检查基本正常。血液生化和全血图像正常。脑磁共振成像(MRI)显示异常血管使右腹桥凹入[图1a]。磁共振血管造影(MRA)显示右侧PPTA(Saltzman 1型),其发育不良的同侧椎动脉和基底动脉位于PPTA下方[图1b和c]。复习后的双边交流动脉均不存在。颅后窝循环几乎独立于威利斯环。患者的亲属拒绝进行脑数字减影血管造影(DSA)和治疗干预。她接受了氯吡格雷加阿司匹林的治疗。在3个月的随访中,她没有遭受任何短暂性脑缺血发作(TIA)或中风。

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