Damage to the pyramidal tracts is necessary and sufficient for the production of the pyramidal syndrome in man

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.