No abstract

In patients with focal hand dystonia (FHD), pathological overflow activation occurs in muscles not involved in the movement. Short intracortical inhibition (SICI) has been shown to contribute to shaping the output of primary motor cortex (M1) and to be deficient in FHD. Surround inhibition is a neural mechanism which can sharpen desired movement by inhibiting unwanted movement in adjacent muscles. To establish further the phenomenon of surround inhibition and to determine whether SICI might play a role in its genesis, single and paired pulse transcranial magnetic stimulation (TMS), and H-reflex testing were applied to evaluate the excitability of the relaxed abductor pollicis brevis muscle (APB) at various intervals during a movement of the index finger in sixteen patients with FHD and twenty age-matched healthy subjects. While control subjects showed significant inhibition of APB motor evoked potential (MEP) size during movement initiation and facilitation of APB MEP size during the maintenance phase, FHD patients did not modulate APB MEP size. In contrast, SICI was not modulated in any phase in controls, but FHD patients showed reduced SICI during movement initiation. Hmax/Mmax-ratio in control subjects increased only during movement initiation. The results provide further evidence for the presence of surround inhibition in M1, where it occurs only during movement initiation, indicating that different mechanisms underlie movement initiation and maintenance. Thus, surround inhibition is sculpted both in time and space and may be an important neural mechanism during movement initiation to counteract increased spinal excitability. SICI may contribute to its generation, since in patients with FHD, the lack of depression of APB MEP size is accompanied by a reduction in SICI.

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.

Transcranial magnetic stimulation (TMS) of the motor cortex was applied during locomotion to investigate the significance of corticospinal input upon the gait pattern. Evoked motor responses (EMR) were studied in the electromyogram (EMG) of tibialis anterior (TA), gastrocnemius (GM) and, for reference, abductor digiti minimi (AD) muscles by applying below-threshold magnetic stimuli during treadmill walking in healthy adults. Averages of 15 stimuli introduced randomly at each of 16 phases of the stride cycle were analysed. Phase-dependent amplitude modulation of EMR was present in TA and GM which did not always parallel the gait-associated modulation of the EMG activity. No variation of onset latency of the EMR was observed. The net modulatory response was calculated by comparing EMR amplitudes during gait with EMR amplitudes obtained (at corresponding background EMG activities) during tonic voluntary muscle contraction. Large net responses in both muscles occurred prior to or during phasic changes of EMG activity in the locomotor pattern. This facilitation of EMR was significantly higher in leg flexor than extensor muscles, with maxima in TA prior to and during late swing phase. A comparison of this facilitation of TA EMR prior to swing phase and prior to a phasic voluntary foot dorsiflexion revealed a similar onset but an increased amount of early facilitation in the gait condition. The modulated facilitation of EMR during locomotion could in part be explained by spinal effects which are different under dynamic and static motor conditions. However, we suggest that changes in corticospinal excitability during gait are also reflected in this facilitation. This suggestion is based on: (1) the similar onset yet dissimilar size of facilitatory effects in TA EMR prior to the swing phase of the stride cycle and during a voluntary dynamic activation, (2) the inverse variation of EMR and EMG amplitudes during this phase, and (3) the occurrence of this inversion at stimulation strengths below motor threshold (motor threshold was determined during weak tonic contraction and EMR were facilitated during gait). It is hypothesized that the facilitation is phase linked to ensure postural stability and is most effective during the phases prior to and during rhythmical activation of the leg muscles resulting in anticipatory adjustment of the locomotor pattern.

The effect of an optic flow pattern on human locomotion was studied in subjects walking on a self-driven treadmill. During walking an optic flow pattern was presented, which gave subjects the illusion of walking in a tunnel. Visual stimulation was achieved by a closed-loop system in which optic flow and treadmill velocity were automatically adjusted to the intended walking velocity (WV). Subjects were instructed to keep their WV constant. The presented optic flow velocity was sinusoidally varied relative to the WV with a cycle period of 2 min. The independent variable was the relative optic flow (rOF), ranging from -1, i.e., forward flow of equal velocity as the WV, and 3, i.e., backward flow 3 times faster than WV. All subjects were affected by rOF in a similar way. The results showed, firstly, an increase in stride-cycle variability that suggests a larger instability of the walking pattern than in treadmill walking without optic flow; and, secondly, a significant modulating effect of rOF on the self-chosen WV. Backward flow resulted in a decrease, whereas forward flow induced an increase of WV. Within the analyzed range, a linear relationship was found between rOF and WV. Thirdly, WV-related modulations in stride length (SL) and stride frequency (SF) were different from normal walking: whereas in the latter a change in WV is characterized by a stable linear relationship between SL and SF (i.e., an approximately constant SL to SF ratio), optic flow-induced changes in WV are closely related to a modulation of SL (i.e., a change of SL-SF ratio). Fourthly, this effect of rOF diminished by about 45% over the entire walking distance of 800 m. The results suggest that the adjustment of WV is the result of a summation of visual and leg-proprioceptive velocity informations. Visual information about ego-motion leads to an unintentional modulation of WV by affecting specifically the relationship between SL and SF. It is hypothesized that the space-related parameter (SL) is influenced by visually perceived motion information, whereas the temporal parameter (SF) remains stable. The adaptation over the entire walking distance suggests that a shift from visual to leg-proprioceptive control takes place.