Vg. Macefield et al., THE CONTRIBUTION OF TRANSCORTICAL PATHWAYS TO LONG-LATENCY STRETCH AND TACTILE REFLEXES IN HUMAN HAND MUSCLES, Experimental Brain Research, 108(1), 1996, pp. 147-154
Long-latency electromyographic (EMG) responses can be evoked in the fi
rst dorsal interosseous muscle (FDI) by unexpected slips of an object
(skin stretch) held between the index and thumb, or by forcible adduct
ion of the metacarpophalangeal joint (muscle stretch). The former type
of response is due to stimulation of tactile afferents in the skin of
the digits, whereas the latter also activates muscle receptors. Previ
ous studies have provided good evidence that long-latency reflex respo
nses to stretch of distal muscles involve activity in a transcortical
reflex pathway. The present experiments examined whether cutaneous ref
lexes also utilise a transcortical route. Transcranial magnetic or ele
ctrical stimuli were given over the motor cortex to evoke EMG activity
during the period of the long-latency reflex response. When evoked by
muscle stretch the responses to magnetic stimulation were facilitated
more than those to electric stimulation. In contrast, facilitation wa
s equal during the long-latency reflex elicited by cutaneous stimulati
on. Because of the different ways in which electrical and magnetic sti
muli are believed to activate the motor cortex, we interpret these res
ults to mean that the long-latency response to skin stretch is not med
iated by a transcortical mechanism in the majority of subjects, wherea
s that following muscle stretch is. However, these are average data. I
n a few individual subjects, the opposite results were obtained. We su
ggest that there may be differences between subjects in the transcorti
cal contribution to long-latency reflex responses. The implication is
that, under normal circumstances, several pathways may contribute to t
hese responses. If so, the relative roles of the pathways may change d
uring different tasks, and in pathological states lesions in one syste
m may well be accompanied by compensatory changes in other systems.