The antigravity soleus muscle (Sol) is crucial for compensation of stance perturbation. A corticospinal contribution to the compensatory response of the Sol is under debate. The present study assessed spinal, corticospinal, and cortical excitability at the peaks of short- (SLR), medium- (MLR), and long-latency responses (LLR) after posterior translation of the feet. Transcranial magnetic stimulation (TMS) and peripheral nerve stimulation were individually adjusted so that the peaks of either motor evoked potential (MEP) or H reflex coincided with peaks of SLR, MLR, and LLR, respectively. The influence of specific, presumably direct, corticospinal pathways was investigated by H-reflex conditioning. When TMS was triggered so that the MEP arrived in the Sol at the same time as the peaks of SLR and MLR, EMG remained unaffected. Enhanced EMG was observed when the MEP coincided with the LLR peak (P < 0.001). Similarly, conditioning of the H reflex by subthreshold TMS facilitated H reflexes only at LLR (P < 0.001). The earliest facilitation after perturbation occurred after 86 ms. The TMS-induced H-reflex facilitation at LLR suggests that increased cortical excitability contributes to the augmentation of the LLR peaks. This provides evidence that the LLR in the Sol muscle is at least partly transcortical, involving direct corticospinal pathways. Additionally, these results demonstrate that approximately 86 ms after perturbation, postural compensatory responses are cortically mediated.

Soleus H-reflex facilitation evoked by a supramaximal conditioning stimulation to the femoral nerve was investigated in 28 healthy control subjects and 35 spastic patients of whom 17 were paraplegics with bilateral spinal cord lesion and 18 were hemiplegics with unilateral cerebral lesion. Heteronymous facilitation from quadriceps to soleus was measured 0.4 ms after onset, while the monosynaptic Ia excitation is still uncontaminated by any non-monosynaptic effect and can be used to assess ongoing presynaptic inhibition on Ia terminals to soleus motor neurons. In paralegics, this heteronymous Ia facilitation was significantly larger than in control subjects (all individual results in these patients being above the mean observed in controls). This must reflect a decrease in presynaptic inhibition of Ia terminals in the paraplegics explored here. There was no correlation between this decreased presynaptic inhibition of Ia terminals and the degree of spasticity measured by Ashworth's scale. Surprisingly, the amount of heteronymous Ia facilitation in hemiplegics was the same as in normal subjects. This indicates that presynaptic inhibition of Ia terminals is unchanged in these patients and disagrees with the usual interpretation of reduced vibratory inhibition of the soleus H-reflex in hemiplegics. It is argued that this disagreement is due to the fact that vibratory inhibition of the reflex also depends on post-activation depression following repetitive synaptic transmission.

The decrease in MEP- and Hcond-facilitation implies reduced corticospinal and cortical excitability at the transcortically mediated LLR. Changes in cortical excitability were directly related to improvements in stance stability as shown by correlation of these parameters. The absence of such a correlation between Hmax/Mmax ratios and stance stability suggests that mainly supraspinal adaptations contributed to improved balance performance following training.

Postural instability is one of the most incapacitating factors in Parkinson's disease (PD). The underlying deficits and the effects of treatment are still not well understood. The aims of the present study were: (i) to identify abnormalities of postural control in PD patients during unperturbed stance and externally perturbed stance (anterior-posterior tilts of the support surface and of the visual scene); (ii) to assess the effects of L-dopa medication and subthalamic nucleus (STN) stimulation on posture control; and (iii) to characterize potential differential or additive effects of both treatments. Eight PD patients under chronic STN stimulation were investigated and compared with 10 normal controls. The assessment was performed in a crossover design (+/- STN stimulation, +/- L-dopa). During unperturbed stance, we recorded measures of spontaneous sway in terms of displacement, velocity and frequency of the centre of pressure (COP), lower body (LB) and upper body (UB) excursions. In addition, inter-segmental UB-LB coupling was investigated as a measure of axial stiffness. All these measures were abnormally large in patients OFF treatment. Under L-dopa treatment, the velocity, frequency and coupling measures were reduced, whereas sway amplitude increased. Very similar effects were obtained under STN stimulation, and these effects became more pronounced in the combined treatment condition. In these data, reduction of inter-segmental coupling correlated with increase in sway amplitude. The finding suggests that axial stiffness reduction under treatment revealed a treatment- resistant deficit in the sensorimotor postural control loop. However, these two effects did not correlate with the motor subscores of the unified Parkinson's disease rating scale (UPDRS), which indicates that they are of minor functional relevance for posture control. A frequency peak in the COP excursions at 0.7-1.1 Hz, which we take to indicate a resonance behaviour of the postural control loop, became reduced under therapy. The reduction of this peak did correlate with most improvements in the UPDRS under therapy. Support surface tilt revealed that an UB righting on the LB segment, which is present in normal controls, is missing in the patients. The postural responses to visual tilt were abnormally large in patients, independent of whether the support was stable or slightly moving, while the control subjects clearly profited from a stable support. This finding suggests that PD patients lack the ability of normal subjects to use sensory or cognitive information when suppressing the destabilizing effect of visual tilt. These abnormal tilt reactions of the patients were resistant to treatment with L-dopa, STN stimulation and a combination of the two. Overall, the effects of STN stimulation on posture control essentially paralleled those of L-dopa during both unperturbed and externally perturbed stance.

The aim of this study was to investigate the role of presumably direct corticospinal pathways in long-term training of the lower limb in humans. It was hypothesized that corticospinal projections are affected in a training-specific manner. To assess specificity, balance training was compared to training of explosive strength of the shank muscles and to a nontraining group. Both trainings comprised 16 1-h sessions within 4 weeks. Before and after training, the maximum rate of force development was monitored to display changes in motor performance. Neurophysiological assessment was performed during rest and two active tasks, each of which was similar to one type of training. Hence, both training groups were tested in a trained and a nontrained task. H-reflexes in soleus (SOL) muscle were tested in order to detect changes at the spinal level. Corticospinal adaptations were assessed by colliding subthreshold transcranial magnetic stimulation to condition the SOL H-reflex. The short-latency facilitation of the conditioned H-reflex was diminished in the trained task and enhanced in the nontrained task. This was observable in the active state only. On a functional level, training increased the rate of force development suggesting that corticospinal projections play a role in adaptation of leg motor control. In conclusion, long-term training of shank muscles affected fast corticospinal projections. The significant interaction of task and training indicates context specificity of training effects. The findings suggest reduced motor cortical influence during the trained task but involvement of direct corticospinal control for new leg motor tasks in humans.