Bilateral paramedian thalamic infarct in the presence of an unpaired thalamic perforating artery
Bilateral paramedian thalamic infarct in the presence of an unpaired thalamic perforating artery
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DOI：
10.1007/s007010200040
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发表时间：
2002-01-01
影响因子：
2.4
通讯作者：
Alp, MS
中科院分区：
文献类型：
--
作者：
Roitberg, BZ;Tuccar, E;Alp, MS
双侧准正中丘脑梗死是罕见的。提示的机制是中央未配对的丘脑穿孔动脉闭塞，这是一种解剖变异。在少数现有的关于这种情况的报告中，诊断仅基于计算机断层扫描（CT）或磁共振成像（MRI）的发现。不排除丘脑病变的其他原因，也没有血管造影显示假定的变异动脉。我们提出一例48岁男性双侧丘脑梗死的CT和MRI表现。最初的神经学检查显示嗜睡，严重的联合运动和感觉失语症，以及轻微的向上凝视限制。患者无局灶性运动障碍。24小时后，患者更加警觉，言语更加流利，但明显出现了korsakoff型健忘症和注意力持续时间差。经过6个月的康复治疗，患者病情缓慢好转。双侧丘脑病变可由几种情况引起。其中包括硫胺素缺乏症、脑狼疮、弓形虫病、囊虫病、脑梅毒龈瘤，甚至肿瘤和真菌感染。所有这些在我们的案例中都被排除了。超选择数字减影血管造影（DSA）显示单个未配对的丘脑穿支。据我们所知，这是第一次在体内证明这种解剖变异与双侧丘脑梗死有关。
Bilateral paramedian thalamic infarction is rare. The suggested mechanism is occlusion of a central unpaired thalamic perforating artery - an anatomic variant. In the few existing reports of this condition, the diagnosis was based on computed tomography (CT) or magnetic resonance imaging (MRI) findings alone. Other causes of thalamic lesions were not ruled out, and there was no angiographic demonstration of the presumed variant artery.We present a case of a 48-year-old man with a bilateral thalamic infarction seen on CT and MRI. Initial neurological examination revealed lethargy, severe combined motor and sensory aphasia, and a mild upward gaze limitation. The patient had no focal motor deficits. After 24 hours, the patient was more alert and his speech became more fluent, but Korsakoff-type amnesia with poor attention span became apparent. The patient improved slowly over 6 months of rehabilitation.Bilateral thalamic lesions can be caused by several conditions. Among those are thiamine deficiency, cerebral lupus, toxoplasmosis, cysticercosis, cerebral syphilitic gumma, and even tumors and fungal infections. All these were ruled out in our case. Superselective digital subtraction angiography (DSA) demonstrated a single unpaired thalamic perforator. To our knowledge, this is the first time this anatomical variant has been demonstrated in vivo in association with bilateral thalamic infarction.