Long-latency spinal reflex in man after flexor reflex afferent stimulation

A Roby-Brami, B Bussel
Brain 1987, 110: 707-25
Electromyographic (EMG) flexor muscle responses evoked by electrical stimulation of ipsilateral peripheral nerves were studied in 16 patients with clinically complete spinal cord transection. Stimuli were applied either to a cutaneous nerve (sural) or to a mixed nerve (tibial) and muscle responses were recorded from tibialis anterior, biceps femoris and rectus femoris. EMG recordings after both sural and tibial nerve stimulation showed that distinct early and late ipsilateral flexor muscle responses could be elicited. This distinction was more evident for tibialis anterior. The latency of the early responses averaged approximately 100 ms with sural and 75 ms with tibial nerve stimulation. This corresponds to the latency of the flexion withdrawal reflex previously described in normal man. After sural stimulation, the early reflex appeared in biceps femoris at a threshold intensity not significantly different from that in normal man given the same stimulation parameters. Late responses appeared after a longer latency (130 ms) and at a lower threshold than the early flexor reflex. In all patients a striking feature of the late response was that its latency increased with increasing stimulus intensity, the maximum latency being as long as 450 ms. This increase also occurred with increasing duration of high intensity stimulus trains. Neither the appearance of a late response nor its latency increase could be explained by a peripheral loop due to a preceding muscle contraction (from either motor axon stimulation or motoneuronal discharge corresponding to the early flexion reflex). It was therefore concluded that both were directly elicited by the afferent volley set up by electrical stimulation. The low threshold of the late reflex corresponded to the excitation of relatively rapidly conducting afferents and its central spinal delay was more than 100 ms. The late reflexes were compared with those described by Andén et al. (1964) in the acute spinal cat injected with DOPA and were found to have similar characteristics. The mechanism for the increase in latency of the late response is discussed in relation to the interpretation of Lundberg (1979).

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