Staaf Gert, Geijer Bo, Lindgren Arne, Norrving Bo
Department of Neurology, Lund University Hospital,SE-221 85, Sweden.
Cerebrovasc Dis. 2004;17(1):1-8. doi: 10.1159/000073891. Epub 2003 Oct 3.
The 'capsular warning syndrome' (CWS) of recurrent stereotyped episodes of motor or sensory dysfunction is clinically well recognized, and is associated with a high risk of imminent lacunar infarction with permanent deficits resembling those of CWS. However, the pathophysiology of CWS has not been well characterized. We report a clinicoanatomic correlation with MR imaging studies in the acute and chronic phases in patients with CWS.
Between April 1997 and March 2001, we prospectively studied 8 patients, mean age 73.3 years, presenting with 4-17 motor or sensorimotor transient ischemic attacks (TIAs; duration 2-90 min) up to 3 days after onset of the first episode. Four patients were free of symptoms between the attacks and had no residua, whereas 4 patients developed a pure motor or sensorimotor stroke within 1-3 days after symptom onset. Diffusion-weighted echoplanar MRI (DWI) and T(2)-weighted MRI studies were performed within 1 week after symptom onset and were repeated 1-2 months later.
Seven of the 8 patients had an appropriate lesion on DWI in the acute phase. DWI abnormalities in the 3 patients with TIAs were 4-10 mm in diameter and confined to the lateral thalamus or medial globus pallidus without involving the internal capsule, whereas 4 patients who developed a stroke had abnormalities localized to the putamen extending to corona radiata (3 patients), or the pontomesencephalic junction (1 patient). All 6 patients who underwent follow-up MRI had an infarct on T(2)-weighted images corresponding to, but usually smaller than, the acute phase DWI abnormality.
Small infarcts in the basal ganglia or the pons, close to central motor pathways, appear to be the primary lesion in CWS. The pathophysiology of CWS is complex, and may involve hemodynamic mechanisms in penetrating arterial territories, as well as molecular mechanisms, such as peri-infarct depolarizations affecting adjacent motor pathways.
复发性刻板运动或感觉功能障碍发作的“囊膜警告综合征”（CWS）在临床上已得到充分认识，且与即将发生腔隙性梗死的高风险相关，其永久性缺损类似于CWS。然而，CWS的病理生理学尚未得到很好的描述。我们报告了CWS患者急性期和慢性期与磁共振成像研究的临床解剖学相关性。
1997年4月至2001年3月期间，我们前瞻性研究了8例患者，平均年龄73.3岁，在首次发作后3天内出现4 - 17次运动或感觉运动性短暂性脑缺血发作（TIAs；持续时间2 - 90分钟）。4例患者在发作间期无症状且无残留症状，而4例患者在症状发作后1 - 3天内发生了纯运动或感觉运动性卒中。在症状发作后1周内进行扩散加权回波平面磁共振成像（DWI）和T2加权磁共振成像研究，并在1 - 2个月后重复进行。
8例患者中有7例在急性期DWI上有合适的病变。3例TIA患者的DWI异常直径为4 - 10毫米，局限于外侧丘脑或内侧苍白球，未累及内囊，而4例发生卒中的患者异常位于壳核并延伸至放射冠（3例）或脑桥中脑交界处（1例）。所有6例接受随访磁共振成像的患者在T2加权图像上有梗死灶，对应于急性期DWI异常，但通常小于急性期DWI异常。
基底节或脑桥靠近中央运动通路的小梗死灶似乎是CWS的主要病变。CWS的病理生理学很复杂，可能涉及穿通动脉区域的血流动力学机制以及分子机制，如影响相邻运动通路的梗死周围去极化。
