A prospective study was performed to delineate the pathologic processe
s occurring in the degradation of muscle function with the onset of sp
asticity. Sixteen adult patients with spasticity secondary to traumati
c brain injury (TBI) were evaluated clinically and histologically. Sho
rt-term patients showed even distribution of mild, moderate, and sever
e spasticity, while moderate spasticity predominated in the chronic gr
oup. Motor control was predominately selective with pattern overlay in
both groups. Muscles with spasticity of less than 6 months duration s
howed nonspecific histologic changes. Muscles with spasticity of durat
ion longer than 1 year demonstrated neurogenic atrophy, some also show
ed signs of denervation followed by reinnervation. No evidence of comp
artment syndrome was found in the spastic muscles studied. Transient h
igh elevation of intramuscular pressure was noted in some patients dur
ing muscle stretch or activity. Muscles that become spastic following
TBI demonstrate neurogenic degeneration, generally apparent greater th
an 1 year after the injury. Prior to this, spastic muscles demonstrate
nonspecific atrophic changes.