de Oliveira-Souza Ricardo
D'Or Institute for Research & Education (IDOR), Brazil; Federal University of the State of Rio de Janeiro, Brazil.
Med Hypotheses. 2015 Jul;85(1):99-110. doi: 10.1016/j.mehy.2015.04.007. Epub 2015 Apr 29.
The causal role played by damage to the pyramidal tracts in the production of spastic hemiplegia in man has been hotly debated over the past hundred years. Two broad streams of thought have emerged from this dispute. The first, which is grounded on the clinicopathological schools of Jean-Martin Charcot (1825-1893) and Paul Flechsig (1847-1929), claimed that the four cardinal signs of hemiplegia, namely (i) paralysis, (ii) spasticity, (iii) hyperactive phasic muscle reflexes ("tendon jerks") and (iv) the sign of Babinski, are caused by injury or dysfunction of the pyramidal tracts. The second school, championed by John Farquhar Fulton (1899-1960) and Derek Denny-Brown (1901-1981), reflects the increasing influence of experimental neurology on clinicopathological concepts after World War II. According to this school, most elements of the pyramidal syndrome are caused by the added release or injury of extrapyramidal structures at different levels of the forebrain and brainstem. Most symptoms of spastic hemiplegia were thus interpreted as signs of extrapyramidal (e.g., reticulospinal) release or damage. However, consensus on which symptoms of spastic hemiplegia were due to pyramidal or extrapyramidal changes was never reached. To add to this uncertainty, a number of clinicopathological cases that supported the old view were sporadically published over the same period. The purpose of the present essay is to provide clinicoanatomic perspective to the neurological literature in support of the hypothesis that damage to the pyramidal tracts is a necessary and sufficient condition for the production of the complete pyramidal syndrome in man.
在过去的一百年里，锥体束损伤在人类痉挛性偏瘫产生中所起的因果作用一直备受激烈争论。这场争论产生了两种主要的思想流派。第一种流派以让 - 马丁·夏科（1825 - 1893）和保罗·弗莱施西格（1847 - 1929）的临床病理学流派为基础，声称偏瘫的四个主要体征，即（i）瘫痪，（ii）痉挛，（iii）阶段性肌肉反射亢进（“腱反射”）和（iv）巴宾斯基征，是由锥体束损伤或功能障碍引起的。第二种流派由约翰·法夸尔·富尔顿（1899 - 1960）和德里克·丹尼 - 布朗（1901 - 1981）倡导，反映了第二次世界大战后实验神经学对临床病理学概念的影响日益增加。根据这一流派，锥体束综合征的大多数要素是由前脑和脑干不同水平的锥体外系结构的额外释放或损伤引起的。因此，痉挛性偏瘫的大多数症状被解释为锥体外系（如网状脊髓束）释放或损伤的体征。然而，对于痉挛性偏瘫的哪些症状归因于锥体束或锥体外系变化，从未达成共识。更增加这种不确定性的是，同一时期偶尔会发表一些支持旧观点的临床病理病例。本文的目的是为神经学文献提供临床解剖学视角，以支持锥体束损伤是人类产生完整锥体束综合征的必要和充分条件这一假设。
