Pyramidal weakness: Is it time to retire the term?

Pyramidal weakness, that is, the weakness that preferentially spares the antigravity muscles, is considered an integral part of the upper motor neuron syndrome. Despite its name, pyramidal weakness has very little to do with the pyramidal tract, and preeminent texts on neurology, neuroanatomy, and clinical examination differ considerably in their descriptions and localization of this enigmatic finding. Evidence from human and nonhuman primate studies demonstrates that lesions confined only to the corticospinal (pyramidal) tract cause significant deficits in fine motor control of the hand, but do not cause posturing or patterned weakness of the extremities. Lesioning of the corticofugal fibers, particularly the corticoreticular and corticopontine tracts, leads to dysbalanced output from reticulospinal, and vestibulospinal systems, which along with changes in rubrospinal tract output balance, probably accounts for the pyramidal weakness pattern. Importantly, this would delineate that pyramidal weakness could only be incited by lesions above the brainstem. It has also been suggested that the inherently greater strength of the antigravity musculature is the substrate for pyramidal weakness, independent of any preferential motor innervation. These hypotheses require further testing in myometric studies with carefully selected participants.

Automated summary

Pyramidal weakness, a key feature of the upper motor neuron syndrome, is not directly related to the pyramidal tract and may be caused by lesions in the corticofugal fibers. Lesions above the brainstem are likely to be the trigger for pyramidal weakness, and the inherently greater strength of antigravity muscles may play a role in this phenomenon. Further myometric studies are needed to test these hypotheses.