Gait abnormalities in tibial nerve paralysis: A biomechanical study

Gastrocnemius-soleus dysfunction is a frequent result of cauda equina lesions and peripheral neuropathies and of stroke and brain injury. Temporary tibial nerve paralysis constitutes a comparable laboratory condition which allows the controlled examination of aspects of these disabilities. The biomechanical effects of temporary tibial nerve paralysis in six normal young adult volunteers were examined to quantitatively define the gait abnormalities resulting from gastrocnemius-soleus paralysis and to provide a basis for the assessment of the effectiveness of different orthotic designs in restoring a normal gait pattern. The motion of the right lower extremity, ground reactive forces acting on the right lower extremity, timing of gait events and step length were recorded, first during normal ambulation and then during ambulation after a right tibial nerve block. Step length was reduced bilaterally after the nerve block (p<0.005); the reduction was greater for the left (unblocked) step than for the right (blocked) step (p<0.005). Right heeloff was delayed until the time of left heelstrike in all subjects after the right tibial block. Right heeloff occurred later (p<0.005) while left heelstrike occurred earlier than normal (p<0.005). The shorter left step length and earlier left heelstrike resulted from a reduction in the forward progression of the right hip (p<0.001). When subjects were deprived of the plantar flexion activity necessary to counteract dorsiflexion moments at the ankle, they delayed the forward progression of the center of pressure (p<0.001) to avoid the unstable collapse of the foot into dorsiflexion. The delay in the forward movement of the center of pressure resulted in a decreased ankle dorsiflexion moment (p<0.001). With the lag of forward movement of the center of pressure the ground reactive force line was located more posterior to the knee center, increasing the knee flexion moment (p<0.05) and rendering the knee unstable. These findings suggest that restoration of the gait pattern toward normal in tibial nerve paralysis would require an orthotic device which prevents excessive dorsiflexion at the ankle, thus allowing more normal advancement of the center of pressure with the resultant adequate forward movement of the hip and pelvis.