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.

Modulation of presynaptic inhibition of Ia afferents projecting monosynaptically to soleus motoneurones was investigated during human gait. Changes in presynaptic inhibition of Ia afferents were deduced from alterations in the amount of heteronymous soleus H-reflex facilitation evoked by a constant femoral nerve stimulation. It has been shown that this facilitation is mediated through a monosynaptic Ia pathway and that during its first 0.5 ms it is still uncontaminated by any polysynaptic effect and can be used to assess ongoing presynaptic inhibition of Ia terminals to soleus motoneurones. During gait, heteronymous facilitation was reduced with respect to its control value (rest during sitting) and modulated during the step cycle: it reached its maximum at mid-stance and decreased to near zero by the end of stance. At the same time the H-reflex amplitude was to some extent similarly modulated. It is argued that this decrease in heteronymous Ia facilitation and in H-reflex amplitude reflects an increased, ongoing presynaptic inhibition of Ia terminals projecting onto soleus motoneurones, which could be from central and/or peripheral origin. D1 inhibition, i.e. the late and long-lasting inhibition of the soleus H-reflex evoked by a train of stimuli to the common peroneal nerve, was used as another method to assess presynaptic inhibition. This D1 inhibition was decreased during gait, and it is argued that this decrease might reflect an occlusion in presynaptic pathways or increased presynaptic inhibition of pathways mediating the conditioning volley.

The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with L-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and L-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean +/- SD age 48.1 +/- 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 +/- 2.4 years, mean stimulation time 15.4 +/- 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of L-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. L-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received L-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with L-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.

After injuries to the anterior cruciate ligament (ACL) a functional instability is frequently observed which has been attributed to a disturbed sensorimotor function. In light of the clinical importance of ACL injuries and the resulting functional instability, it is of enormous clinical interest to elucidate the role of sensorimotor pathways that involve the ACL. In animals and humans a direct reflex pathway between the ACL and the hamstrings has been shown. The onset latencies of responses reported after ventral tibia translation were around 40-50 ms (range 17.9-65) and were regarded as medium latency responses (MLR). However, ventral tibia translation should also induce a stretch of the hamstring muscles and evoke a short latency response (SLR). Before any muscle response after ventral tibia translation can be ascribed to anatomical structures, it is crucial to analyze the obtained muscle responses carefully. The aim of the present study was the development of an algorithm to differentiate SLR and MLR responses after ventral tibia translation. In ten healthy subjects reflex responses of the hamstrings after anterior tibia translation and after tendon taps on the biceps femoris tendon were evaluated. To investigate the influence of skin afferents, control experiments were performed after lidocain injection of the dorsal calf. The mean onset latency of the tendon jerk reflex was 21.9 +/- 3.1 ms (range 17.3 - 28.7 ms). Both SLR responses (mean onset latency: 20.3 +/- 3.5 ms; range 15.4 - 25.8) and MLR responses (mean onset latency: 38.9 +/- 4.2 ms; range 32.9 - 46.7) were obtained in all subjects. Skin afferents from the calf do not play a major role. The development of an evaluation algorithm is presented that allows a safe differentiation between these partly superimposed SLR and MLR components. It is demonstrated that by measuring the first part of the SLR from the onset to the first peak the end of the SLR can be predicted and that the onset latency of the MLR component can be assessed reliably. Possible reasons are discussed why previous studies only reported responses at MLR latencies. The fact that both SLR and MLR components can be observed after anterior tibia translation underlines the necessity to differentiate the responses before they can be ascribed to any anatomical structures. As a basis for future work the algorithm presented may become a useful tool to differentiate which afferent pathways play a role in initiating hamstring activity.