Is hemiplegic cerebral palsy equivalent to amblyopia of the corticospinal system?
Is hemiplegic cerebral palsy equivalent to amblyopia of the corticospinal system?
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DOI：
10.1002/ana.21108
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发表时间：
2007-11-01
影响因子：
11.2
通讯作者：
Cioni, Giovanni
中科院分区：
文献类型：
--
作者：
Eyre, Janet A.;Smith, Martin;Cioni, Giovanni
目的：重度偏瘫型脑性瘫痪患者非梗死区皮质的同侧皮质脊髓投射增加。我们研究了他们的严重损伤是否可能部分是由活动依赖性引起的，来自受影响皮质的存活对侧皮质脊髓投射被来自未受影响皮质的更活跃的同侧皮质脊髓投射竞争性移位，从而加重损伤。经颅磁刺激（TMS）在32名健康儿童、14名单侧卒中儿童和25名双侧病变儿童中，在最初的2年内，每个半球的皮质脊髓束发育特征。磁共振成像和解剖研究比较皮质脊髓束生长在13例围产期中风与46名健康subject.Results：婴儿单侧病变最初有反应后TMS的受影响的皮质，这变得越来越不正常，7最终失去了。从非梗死皮质投射的同侧皮质脊髓轴突有相关的肥大。磁共振成像和解剖研究表明，肥大的皮质脊髓束从非梗死半球。卒中后不久的TMS结果不能预测损伤;随后的反应丧失和来自非梗死皮质的同侧皮质脊髓轴突肥大预测2年时的严重损伤。双侧病变的婴儿保持对TMS的反应，从两个半球与一个正常的模式development.Interpretation：而不是代表“修复可塑性”，增加同侧的预测从noninfarcted皮质复合残疾的竞争性取代幸存的对侧皮质脊髓的预测从梗死皮质。这可能为为什么偏瘫性脑瘫的体征出现较晚并且在生命的前2年内进展提供了病理生理学解释。
Objective: Subjects with severe hemiplegic cerebral palsy have increased ipsilateral corticospinal projections from their noninfarcted cortex. We investigated whether their severe impairment might, in part, be caused by activity-dependent, competitive displacement of surviving contralateral corticospinal projections from the affected cortex by more active ipsilateral corticospinal projections from the nonaffected cortex, thereby compounding the impairment.Methods: Transcranial magnetic stimulation (TMS) characterized corticospinal tract development from each hemisphere over the first 2 years in 32 healthy children, 14 children with unilateral stroke, and 25 with bilateral lesions. Magnetic resonance imaging and anatomic studies compared corticospinal tract growth in 13 patients with perinatal stroke with 46 healthy subjects.Results: Infants with unilateral lesions initially had responses after TMS of the affected cortex, which became progressively more abnormal, and seven were eventually lost. There was associated hypertrophy of the ipsilateral corticospinal axons projecting from the noninfarcted cortex. Magnetic resonance imaging and anatomic studies demonstrated hypertrophy of the corticospinal tract from the noninfarcted hemisphere. TMS findings soon after the stroke did not predict impairment; subsequent loss of responses and hypertrophy of ipsilateral corticospinal axons from the noninfarcted cortex predicted severe impairment at 2 years. Infants with bilateral lesions maintained responses to TMS from both hemispheres with a normal pattern of development.Interpretation: Rather than representing "reparative plasticity," increased ipsilateral projections from the noninfarcted cortex compound disability by competitively displacing surviving contralateral corticospinal projections from the infarcted cortex. This may provide a pathophysiological explanation for why signs of hemiplegic cerebral palsy appear late and progress over the first 2 years of life.