Task-related changes in propriospinal excitation from hand muscles to human flexor carpi radialis motoneurones.

This study addresses whether there is excitation from human hand muscles to flexor carpi radialis (FCR) motoneurones mediated through propriospinal circuits and, if so, whether it is used in specific motor tasks. Electrical stimuli to the ulnar nerve at wrist level produced an excitation in FCR motoneurones with characteristics typical of a propriospinally mediated effect: low threshold (0.6 x motor threshold (MT)), a group I effect that was not reproduced by purely cutaneous stimuli, long central delay (4.

Mediation of late excitation from human hand muscles via parallel group II spinal and group I transcortical pathways.

This study addresses the question of the origin of the long-latency responses evoked in flexors in the forearm by afferents from human hand muscles. The effects of electrical stimuli to the ulnar nerve at wrist level were assessed in healthy subjects using post-stimulus time histograms for flexor digitorum superficialis and flexor carpi radialis (FCR) single motor units (eight subjects) and the modulation of the ongoing rectified FCR EMG (19 subjects). Ulnar stimulation evoked four successive peaks of heteronymous excitation that were not produced by purely cutaneous stimuli: a monosynaptic Ia excitation, a second group I excitation attributable to a propriospinally mediated effect, and two late peaks.

Increase in group II excitation from ankle muscles to thigh motoneurones during human standing.

In standing subjects, we investigated the excitation of quadriceps (Q) motoneurones by muscle afferents from tibialis anterior (TA) and the excitation of semitendinosus (ST) motoneurones by muscle afferents from gastrocnemius medialis (GM). Standing with a backward lean stretches the anterior muscle pair (TA and Q) and they must be co-contracted to maintain balance. Equally, forward lean stretches the posterior muscle pair (GM and ST) and they must be co-contracted.

Changes in propriospinally mediated excitation of upper limb motoneurons in stroke patients.

It has been argued that, in humans, a part of the descending command to upper limb motoneurons is transmitted through cervical propriospinal pre-motoneurons. We explored whether excitation of these putative propriospinal neurons projecting onto extensor carpi radialis (ECR) motoneurons was modified in patients recovering from stroke. Suppression of the voluntary on-going ECR EMG activity by stimulation of cutaneous afferents in the superficial radial nerve was used to estimate the component of the descending command passing through the propriospinal relay.

Excitability of human muscle afferents studied using threshold tracking of the H reflex.

In human peripheral nerves, physiological evidence has been presented for a number of biophysical differences between cutaneous afferents and alpha motor axons. The differences in strength-duration properties for cutaneous afferents and motor axons in the median nerve have been attributed to greater expression of a persistent Na(+) conductance (I(Na,P)) on cutaneous afferents. However, it is unclear whether the biophysical properties of human group Ia afferents differ from those of cutaneous afferents.

Propriospinal transmission of part of the corticospinal excitation in humans.

In humans a substantial part of corticospinal excitation to upper limb motoneurons is mediated through cervical premotoneurons located rostral to motoneurons, analogous to the feline system of C3-C4 propriospinal neurons. The indirect (disynaptic) component of the corticospinal command passing through the propriospinal relay may be updated by the extensive convergence at this level of afferent inputs (both excitatory and inhibitory) from the moving limb. Propriospinal neurons are potently inhibited by feedback inhibitory interneurons facilitated from the motor cortex, and this explains why artificial volleys delivered to the pyramidal system by itself have failed to demonstrate this indirect corticospinal projection.

A cervical propriospinal system in man.

Peripheral stimuli facilitate, at a pre-motoneuronal level, the responses elicited in human upper limb motoneurons (MNs) by transcranial magnetic stimulation over the motor cortex (TMS). Several features indicate that the relevant premotoneurones are distinct from segmental interneurones and located rostral to MNs. Thus, corticospinal volleys would have an indirect (propriospinal) pathway to upper limb MNs, in addition to the direct cortico-motoneuronal pathway.

Suppression of the H reflex in humans by disynaptic autogenetic inhibitory pathways activated by the test volley.

The present studies were designed to increase an existing limitation on the size of the H reflex by accentuating an inhibitory effect of group I afferents in the test volley. They were precipitated by the observation that, during strong voluntary contractions of quadriceps (Q), the late deep peroneal (DP) facilitation of the Q H reflex was suppressed but the facilitation of the ongoing EMG was not. The effects of conditioning stimuli to DP, superficial peroneal (SP) and articular afferents on the excitation of Q motoneurones (MNs) produced by femoral nerve (FN) stimulation were assessed in 11 healthy human subjects using the H reflex of vastus intermedius or the peak of group I excitation in post-stimulus time histograms (PSTHs) of single motor units (MUs) in vastus lateralis.

Excitability changes in human peripheral nerve axons in a paradigm mimicking paired-pulse transcranial magnetic stimulation.

A peripheral nerve model was developed to determine whether changes in axonal excitability could affect the findings in studies of cortical processes using paired-pulse transcranial magnetic stimulation (TMS). The recovery of axonal excitability from a conditioning stimulus smaller than the test stimulus was qualitatively similar to that with suprathreshold conditioning stimuli. There was an initial decrease in excitability, equivalent to refractoriness at conditioning-test intervals < 4 ms, an increase in excitability, equivalent to supernormality, at intervals of 5-20 ms and a second phase of decreased excitability, equivalent to late subnormality at intervals > 30 ms.