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.
Balancing exercises on instable bases (sensorimotor training [SMT]) are often used in the rehabilitation process of an injured athlete to restore joint function. Recently it was shown that SMT was able to enhance rate of force development (RFD) in a maximal voluntary muscle contraction. The purpose of this study was to compare adaptations on strength capacity following ballistic strength training (BST) with those following an SMT during a training period of 1 microcycle (4 weeks). Maximum voluntary isometric strength (MVC), maximum RFD (RFDmax) and the corresponding neural activation of M. soleus (SOL), M. gastrocnemius (GAS), and M. tibialis anterior (TIB) were measured during plantar flexion in 33 healthy subjects. The subjects were randomly assigned to a SMT, BST, or control group. RFDmax increased significantly stronger following BST (48 +/- 16%; p < 0.01) compared to SMT (14 +/- 5%; p < 0.05), whereas MVC remained unchanged in both groups. Median frequencies of the electromyographic power spectrum during the first 200 ms of contraction for GAS increased following both BST (45 +/- 21%; p < 0.05) and SMT (45 +/- 22%; p < 0.05), but median frequencies for SOL increased only after SMT (13 +/- 4%; p < 0.05). Additionally, mean amplitude voltage increased following BST for SOL (38 +/- 12%; p < 0.01) and for GAS (73 +/- 23%; p < 0.01) during the first 100 ms, whereas it remained unchanged after SMT. It is concluded that BST and SMT may induce different neural adaptations that specifically affect recruitment and discharge rates of motor units at the beginning of voluntary contraction. Specific neural adaptations indicate that SMT might be used complementarily to BST, especially in sports that require contractile explosive properties in situations with high postural demands, e.g., during jumps in ball sports.
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.
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