Pantano P, Formisano R, Ricci M, Di Piero V, Sabatini U, Barbanti P, Fiorelli M, Bozzao L, Lenzi G L
Department of Neurological Sciences, University of Rome La Sapienza, Italy.
Brain. 1995 Oct;118 ( Pt 5):1329-38. doi: 10.1093/brain/118.5.1329.
Patients with a motor deficit due to ischaemic stroke usually develop muscular spasticity, but in some cases they may remain with a prolonged muscular flaccidity which impairs their recovery. Little is known about the causes of these two different functional outcomes. We correlated CT/MRI and 99mTc HM-PAO SPECT with clinical findings in 42 patients at a mean time interval of 3 months after stroke. The patients were divided into two cohorts with either flaccid (prolonged muscular flaccidity) or spastic (muscular spasticity) hemiparesis. Although patients with prolonged muscular flaccidity had a greater motor deficit, the mean structural volume of the ischaemic lesion was similar to that of the muscular spasticity cohort. There was a significantly higher prevalence of structural involvement of the lentiform nucleus in prolonged muscular flaccidity cases. Relative perfusion in the lentiform nucleus, thalamus and contralateral cerebellar hemisphere was significantly lower in prolonged muscular flaccidity than in muscular spasticity patients. A subgroup with only subcortical structural lesions also showed significantly lower relative perfusion in the ipsilateral frontal association areas. A primary involvement of the lentiform nucleus by the structural lesion seems to be crucial for the persistence of flaccidity after stroke. However, cerebral blood flow (CBF) changes in other structurally intact regions indicate their additional role. It is likely that both subcortical-cortical loops involved in motor control, i.e. cortex-basal ganglia-thalamus-cortex and cortex-pons-cerebellum-thalamus-cortex, are more widely and more severely affected in patients with prolonged muscular flaccidity.
因缺血性中风导致运动功能缺损的患者通常会出现肌肉痉挛，但在某些情况下，他们可能会长期存在肌肉松弛，这会影响其康复。对于这两种不同功能结果的原因知之甚少。我们将42例患者在中风后平均3个月的时间间隔内进行的CT/MRI和99mTc HM-PAO SPECT检查结果与临床发现进行了相关性分析。这些患者被分为两个队列，分别是弛缓性（长期肌肉松弛）或痉挛性（肌肉痉挛）偏瘫患者。虽然长期肌肉松弛的患者运动功能缺损更严重，但缺血性病变的平均结构体积与肌肉痉挛队列相似。在长期肌肉松弛的病例中，豆状核结构受累的患病率显著更高。长期肌肉松弛患者的豆状核、丘脑和对侧小脑半球的相对灌注明显低于肌肉痉挛患者。仅存在皮质下结构病变的亚组在同侧额叶联合区的相对灌注也明显较低。结构性病变对豆状核的原发性累及似乎是中风后弛缓持续存在的关键。然而，其他结构完整区域的脑血流量（CBF）变化表明了它们的额外作用。很可能参与运动控制的皮质下-皮质环路，即皮质-基底神经节-丘脑-皮质和皮质-脑桥-小脑-丘脑-皮质，在长期肌肉松弛的患者中受到更广泛、更严重的影响。
