THE CONTRIBUTION OF TRANSCORTICAL PATHWAYS TO LONG-LATENCY STRETCH AND TACTILE REFLEXES IN HUMAN HAND MUSCLES

Citation
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
Citations number
39
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144819
Volume
108
Issue
1
Year of publication
1996
Pages
147 - 154
Database
ISI
SICI code
0014-4819(1996)108:1<147:TCOTPT>2.0.ZU;2-B
Abstract
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.