Non-technical summaryNeural activity in parts of the cerebral cortex related to movement oscillates at frequencies around 20 Hz. These oscillations are correlated with similar rhythms in contracting muscles on the opposite side of the body. In this work, we used an analysis method called directed coherence to investigate the direction of oscillatory coupling. We find that oscillations travel not only from cortex to muscle (as expected for a motor command), but also back from muscle to cortex (reflecting sensory input). This oscillatory loop may allow the cortex to measure features of the limb state, integrating sensory inflow with the motor command.

EEG recordings from sensorimotor cortex show oscillations around 10 and 20 Hz. These modulate with task performance, and are strongest during periods of steady contraction. The 20 Hz oscillations are coherent with contralateral EMG. Computer modelling suggests that oscillations arising within the cortex may be especially dependent on inhibitory systems. The benzodiazepine diazepam enhances the size of GABAA IPSPs; its effects are reversed by the antagonist flumazenil. We tested the effect of these drugs on spectral measures of EEG and EMG, whilst eight healthy human subjects performed a precision grip task containing both holding and movement phases. Either an auxotonic or isometric load was used. EEG changes following electrical stimulation of the contralateral median nerve were also assessed. The EEG power showed similar changes in all task/stimulation protocols used. Power around 20 Hz doubled at the highest dose of diazepam used (5 mg), and returned to control levels following flumazenil. EEG power at 10 Hz was by contrast little altered. The peak frequency of EEG power in both bands was not changed by diazepam. Corticomuscular coherence at ca 20 Hz was reduced following diazepam injection, but the magnitude of this effect was small (mean coherence during steady holding in the auxotonic task was 0.062 in control recordings, 0.051 after 2.5 mg and 5 mg doses of diazepam). These results imply that 20 Hz oscillations in the sensorimotor cortex are at least partially produced by local cortical circuits reliant on GABAA‐mediated intracortical inhibition, whereas 10 Hz rhythms arise by a different mechanism. Rhythms generated during different tasks, or following nerve stimulation, are likely to arise from similar mechanisms. By examining the formulae used to calculate coherence, we show that if cortical oscillations are simply transmitted to the periphery, corticomuscular coherence should increase in parallel with the ratio of EEG to EMG power. The relative constancy of coherence even when the amplitude of cortical oscillations is perturbed suggests that corticomuscular coherence itself may have a functional role in motor control.

In motor neuron disease, the focus of therapy is to prevent or slow neuronal degeneration with neuroprotective pharmacological agents; early diagnosis and treatment are thus essential. Incorporation of needle electromyographic evidence of lower motor neuron degeneration into diagnostic criteria has undoubtedly advanced diagnosis, but even earlier diagnosis might be possible by including tests of subclinical upper motor neuron disease. We hypothesized that beta-band (15–30 Hz) intermuscular coherence could be used as an electrophysiological marker of upper motor neuron integrity in such patients. We measured intermuscular coherence in eight patients who conformed to established diagnostic criteria for primary lateral sclerosis and six patients with progressive muscular atrophy, together with 16 age-matched controls. In the primary lateral sclerosis variant of motor neuron disease, there is selective destruction of motor cortical layer V pyramidal neurons and degeneration of the corticospinal tract, without involvement of anterior horn cells. In progressive muscular atrophy, there is selective degeneration of anterior horn cells but a normal corticospinal tract. All patients with primary lateral sclerosis had abnormal motor-evoked potentials as assessed using transcranial magnetic stimulation, whereas these were similar to controls in progressive muscular atrophy. Upper and lower limb intermuscular coherence was measured during a precision grip and an ankle dorsiflexion task, respectively. Significant beta-band coherence was observed in all control subjects and all patients with progressive muscular atrophy tested, but not in the patients with primary lateral sclerosis. We conclude that intermuscular coherence in the 15–30 Hz range is dependent on an intact corticospinal tract but persists in the face of selective anterior horn cell destruction. Based on the distributions of coherence values measured from patients with primary lateral sclerosis and control subjects, we estimated the likelihood that a given measurement reflects corticospinal tract degeneration. Therefore, intermuscular coherence has potential as a quantitative test of subclinical upper motor neuron involvement in motor neuron disease.

Background. Recent evidence from both monkey and human studies suggests that the reticulospinal tract may contribute to recovery of arm and hand function after stroke. In this study, we evaluated a marker of reticulospinal output in stroke survivors with varying degrees of motor recovery. Methods. We recruited 95 consecutive stroke patients presenting 6 months to 12 years after their index stroke, and 19 heathy control subjects. Subjects were asked to respond to a light flash with a rapid wrist flexion; at random, the flash was paired with either a quiet or loud (startling) sound. The mean difference in electromyogram response time after flash with quiet sound compared with flash with loud sound measured the StartReact effect. Upper limb function was assessed by the Action Research Arm Test (ARAT), spasticity was graded using the Modified Ashworth Scale (MAS) and active wrist angular movement using an electrogoniometer. Results. StartReact was significantly larger in stroke patients than healthy participants (78.4 vs 45.0 ms, P < .005). StartReact showed a significant negative correlation with the ARAT score and degree of active wrist movement. The StartReact effect was significantly larger in patients with higher spasticity scores. Conclusion. We speculate that in some patients with severe damage to their corticospinal tract, recovery led to strengthening of reticulospinal connections and an enhanced StartReact effect, but this did not occur for patients with milder impairment who could use surviving corticospinal connections to mediate recovery.

ObjectiveTo investigate the efficacy of magnetic stimulation over the posterior fossa (PF) as a non-invasive assessment of cerebellar function in man.MethodsWe replicated a previously reported conditioning-test paradigm in 11 healthy subjects. Transcranial magnetic stimulation (TMS) at varying intensities was applied to the PF and motor cortex with a 3, 5 or 7 ms interstimulus interval (ISI), chosen randomly for each trial. Surface electromyogram (EMG) activity was recorded from two intrinsic hand muscles and two forearm muscles. Responses were averaged and rectified, and MEP amplitudes were compared to assess whether suppression of the motor output occurred as a result of the PF conditioning pulse.ResultsCortical MEPs were suppressed following conditioning-test ISIs of 5 or 7 ms. No suppression occurred with an ISI of 3 ms. PF stimuli alone also produced EMG responses, suggesting direct activation of the corticospinal tract (CST).ConclusionsCST collaterals are known to contact cortical inhibitory interneurones; antidromic CST activation could therefore contribute to the observed suppression of cortical MEPs.SignificancePF stimulation probably activates multiple pathways; even at low intensities it should not be regarded as a selective assessment of cerebellar function unless stringent controls can confirm the absence of confounding activity in other pathways.