Is lower leg proprioception essential for triggering human automatic postural responses?

It is unknown to what extent automatic postural responses are triggered by lower leg proprioception. This issue was addressed by studying postural con trol in five carefully selected patients with subtle diabetic polyneuropath y (restricted to the lower legs) and 15 healthy subjects. All patients had bilaterally absent Achilles tendon reflexes and weak or absent patella tend on reflexes, but muscle strength was fully preserved. Subjects were tested while standing on a supporting, movable forceplate. The contribution of low er leg proprioception to automatic postural responses was investigated by r andomly exposing the subjects to either a 4 degrees 'toe-up' rotational per turbation ('normal ankle input'), a simultaneous 4-cm rearward translation and 4 degrees toe-up rotation ('enhanced ankle input'), or a simultaneous 4 -cm rearward translation and 4 degrees 'toe-down' rotation ('nulled ankle i nput'). We recorded surface EMG (stretch reflexes and balance-correcting re sponses) from leg and trunk muscles, ankle torque and angular velocities of the upper and lower legs and trunk. We argued that automatic postural resp onses that have abnormally small amplitudes in patients and are modulated i n controls with the velocity of different types of ankle rotations must rec eive a major input from lower leg proprioception. Conversely, automatic pos tural responses that are weakly modified in amplitude or onset by different ankle perturbations and are present despite nulled ankle inputs and, final ly, are unaffected in patients with distal polyneuropathy must be triggered or modulated by inputs other than from lower leg proprioception. Normal po stural synergies and strategies were maintained in patients, although withi n a given synergy the timing and amplitude of some automatic postural respo nses were abnormal. A few automatic postural responses appeared to be trigg ered or modulated by lower leg proprioception. Thus, early stretch reflexes in soleus and medial gastrocnemius were severely diminished in patients, w hile in controls these stretch reflexes were modulated by different ankle p erturbations. Furthermore, balance-correcting responses in tibialis anterio r were diminished and delayed in patients, while in controls these balance- correcting responses were modulated by different ankle perturbations. Other automatic postural responses were apparently not triggered or modulated by lower leg proprioception, but likely received a major input from more prox imal sensory systems. Thus, in both groups prominent balance-correcting res ponses were present in several muscles (soleus, gastrocnemius, quadriceps, paraspinals and trapezius) during the 'nulled ankle input' condition, where ankle position was stabilised over the first 250 ms. During the 'enhanced ankle input' condition, where prominent ankle dorsiflexion occurred during the first 200 ms, amplitudes of balance-correcting responses were only marg inally weaker in patients than in controls. We analysed body segment displa cements to unveil the potential nature of proximal triggers for automatic p ostural responses. As opposed to the 'inverted pendulum' concept of postura l control, early movement occurred in the knees, hips and trunk well before the onset of automatic postural responses. For example, during the 'nulled ankle input' condition, the lower leg moved forward with early knee flexio n, followed by knee extension. The trunk extended backwards at 80 ms, which was followed by forward flexion. The absent stretch reflex and weaker bala nce-correcting responses in patients produced changed trunk velocity profil es (mainly a reduced initial backward motion of the trunk), but lower-body segment movements showed no consistent differences between the two groups. Considering these body segment displacements, any automatic postural respon se with an onset within the first 200 ms could well be triggered by recepto rs located at the knee, hip or trunk. These results indicate that most bala nce-correcting responses are not triggered by lower leg proprioception. We speculate that lower leg inputs are mainly used to trigger some lower leg a utomatic postural responses when knee movements are small, as occurs with t he commonly used toe-up rotational perturbations. Under other circumstances , lower leg inputs act mainly to modulate automatic postural responses, onc e these have been triggered by more proximal inputs within the upper legs o r the trunk. In the absence of this modulation, trunk movements are changed .