No abstract

Transcranial direct current stimulation (tDCS) of the human motor cortex at an intensity of 1 mA has been shown to be efficacious in increasing (via anodal tDCS) or decreasing (via cathodal tDCS) the excitability of corticospinal projections to muscles of the hand. In this study, we examined whether tDCS at currents of 2 mA could effect similar changes in the excitability of deeper cortical structures that innervate muscles of the lower leg. Similar to the hand area, 10 min of stimulation with the anode over the leg area of the motor cortex increased the excitability of corticospinal tract projections to the tibialis anterior (TA) muscle, as reflected by an increase in the amplitude of the motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation. MEP amplitudes recorded at rest and during a background contraction were increased following anodal tDCS and remained elevated at 60 min compared to baseline values by 59 and 35%, respectively. However, in contrast to the hand, hyperpolarizing cathodal stimulation at equivalent currents had minimal effect on the amplitude of the MEPs recorded at rest or during background contraction of the TA muscle. These results suggest that it is more difficult to suppress the excitability of the leg motor cortex with cathodal tDCS than the hand area of the motor cortex.

. Changes in cortically related intermuscular coherence accompanying improvements in locomotor skills in incomplete spinal cord injury. J Neurophysiol 95: 2580 -2589, 2006. First published January 11, 2006 doi:10.1152/jn.01289.2005. In human spinal cord injury, the neuronal mechanisms mediating the improvement of locomotor function in response to intensive treadmill training are not well understood. In this study, we examined if such recovery is mediated, in part, by increases in residual corticospinal drive to muscles of the leg during walking. To do this, we measured the coherence of electromyogram (EMG) activity between two antagonist muscles (intermuscular coherence), specifically at frequencies between 24 and 40 Hz, which is thought to indicate common drive to two muscles from corticospinal inputs. In 12 subjects with incomplete spinal cord injury, intermuscular coherence was measured between hamstrings and vastus lateralis EMG that was activated during walking on a motorized treadmill. Before training, appreciable coherence in the 24 -40 Hz frequency band was only present in subjects with moderate volitional motor strength in their leg muscles (n ϭ 8 subjects) compared with subjects with little or no leg muscle strength (n ϭ 4 subjects), reconfirming that 24 -40 Hz frequency coherence is likely mediated by common supraspinal inputs. After training, increases in 24 -40 Hz coherence only occurred in the eight subjects with moderate leg muscle strength who also exhibited improvements in locomotor recovery as assessed by the 21 point WISCI II scale (termed responders). In contrast, development of intermuscular coherence in the 24 -40 Hz frequency band did not occur in the four subjects with absent or weak muscle strength. These subjects also did not improve in their locomotor ability as reflected in unchanging WISCI II scores (termed nonresponders). Lower-frequency coherence (5-18 Hz), which is thought to contain common drive from spinal inputs, did not change in either group. In a subset of subjects that were previously assessed with transcranial magnetic stimulation (TMS) before and after training (n ϭ 5 responders and 3 nonresponders), there was a significant and positive relationship between increases in 24 -40 Hz coherence and increases in evoked muscle responses to TMS of the primary motor cortex. Taken together, increases in higher-frequency EMG coherence in subjects with residual voluntary muscle strength and its parallel relation to changes in TMS-evoked responses provides further evidence that improvements in locomotor function from treadmill training are mediated, in part, by increases in corticospinal drive to muscles of the leg during walking.

The ODFS was perceived by the users to be of considerable benefit. A comprehensive clinical follow-up service is essential to achieve the maximum continuing benefit from FES-based orthoses.

Following spinal cord injury (SCI), prolonged muscle spasms are readily triggered by brief sensory stimuli. Animal and indirect human studies have shown that a substantial portion of the depolarization of motoneurons during a muscle spasm comes from the activation of persistent inward currents (PICs). The brief (single pulse) sensory stimuli that trigger the PICs and muscle spasms in chronically spinalized animals evoke excitatory post-synaptic potentials (EPSPs) that are broadened to more than 500 ms, the duration of depolarization required to activate a PIC in the motoneuron. Thus, in humans, we investigated if post-synaptic potentials (PSPs) evoked from brief (<20 ms) sensory stimulation are changed after SCI and if they are broadened to > or =500 ms to more readily activate motoneuron PICs and muscle spasms. To estimate both the shape and duration of PSPs in human subjects we used peristimulus frequencygrams (PSFs), which are plots of the instantaneous firing frequency of tonically active single motor units that are time-locked to the occurrence of the sensory stimulus. PSFs in response to cutaneomuscular stimulation of the medial arch or toe of the foot, a sensory stimulus that readily triggers muscle spasms, were compared between non-injured control subjects and in spastic subjects with chronic (>1 year), incomplete SCI. In non-injured controls, a single shock or brief (<20 ms) train of cutaneomuscular stimulation produced PSFs consisting of a 300 ms increase in firing rate above baseline with an interposed period of reduced firing. Parallel intracellular experiments in motoneurons of adult rats revealed that a 300 ms EPSP with a fast intervening inhibitory PSP (IPSP) reproduced the PSF recorded in non-injured subjects. In contrast, the same brief sensory stimulation in subjects with chronic SCI produced PSFs of comparatively long duration (1200 ms) with no evidence for IPSP activation, as reflected by a lack of reduced firing rates after the onset of the PSF. Thus, unlike non-injured controls, the motoneurons of subjects with chronic SCI are activated by very long periods of pure depolarization from brief sensory activation. It is likely that these second-long EPSPs securely recruit slowly activating PICs in motoneurons that are known to mediate, in large part, the many seconds-long activation of motoneurons during involuntary muscle spasms.