Long-Loop Reflexes in Small Hand Muscles Studied in Normal Subjects and in Patients With Huntington's Disease

Abstract

Long-latency electromyographic (EMG) responses of the first dorsal interosseus muscle were evoked by short displacements of the index finger in healthy subjects and in patients with Huntington's disease (HD). In all 20 healthy subjects the early spinal response (mean latency 31.5 ms) was followed by a reproducible later reflex response with a mean latency of 56.5 ms. The activity pattern of single motor units of the stretched muscle was similar to that of the surface EMG. Thus all single motor units tested could be active during either the first or second response phase, but never in both in a given trial. Of the 50 patients with HD, the late EMG response was missing completely in all but 7, but the early spinal component was almost identical to that of the control group. Double stretches at an interval of 25 ms evoked two similar EMG responses in these patients, proving that the motoneuron pool is still excitable during the time at which the second response would have appeared in healthy subjects. The reflex responses of the thenar muscles evoked by electrical stimulation of the median nerve were examined during a voluntary opposing contraction of the thumb in both groups of subjects. In normal subjects, two EMG responses could be distinguished with latencies similar to those of the mechanically elicited responses. Patients with HD again lacked the second response, although the first spinal response was always present. The results are discussed with respect to different proposals concerning the origin of long-latency responses in human muscles. At least for distal hand muscles, the results suggest that the long-latency responses are long-loop reflexes.

Different mechanisms underlie the long‐latency stretch reflex response of active human muscle at different joints.

“…That this is unlikely to be the case is indicated by the extremely poor correlation between the magnitude of the increase of the MI response and of the reduction of the M2 response in the HD patients. Furthermore, in an earlier study (Noth et al 1985) in which small perturbations of the finger were made, the FDI-M1 response of HD patients and normal subjects was identical, but the FDI-M2 response was nevertheless absent or residual in HD patients. The increase in the MI component does not, therefore, explain the loss of M2 in the FDI in HD patients.…”

“…Minor involvement of a transcortical pathway in the M2 response of upper arm muscles cannot, therefore be ruled out. In an earlier study of the wrist flexor muscles of HD patients, Thompson and his co-workers (Thompson, Berardelli, Rothwell, Day, Dick, Benecke & Marsden, 1988) noted that M2 responses were present in a far higher proportion (88 %) of patients than the M2 of hand muscles (40 % for flexor pollicis longus; also 30 % for FDI (Noth et al 1985)). The magnitude of the wrist flexor M2 was reduced, when present, to 50 % of the normal value, a finding confirmed by a more recent study (Abbruzzese, Dall'Agata, Morena, Spadavecchia, Ratto & Favale, 1990).…”

“…It is widely accepted that the loss of the later reflex component following mechanical (Noth et al 1985) or electrical (Deuschl, Liicking & Schenck, 1989) stimulation of the hand muscles in HD patients occurs as the result of disruption of a long-loop, possible transcortical, reflex pathway. Thus HD represents a useful model to test the universality of the long-loop theory as a mechanism for the M2 responses of other muscles.…”

“…But, as Marsden and his co-workers have pointed out (Marsden, Rothwell & Day, 1983), given the wide functional requirements made of different joints and their muscles, there is no intrinsic reason why only one mechanism should apply for all muscles, or even why a mixture of mechanisms might not be responsible for any given M2 response; while a transcortical reflex loop might be expected in muscles, such as those of the hand, which are predominantly under direct cortical control during much of their behavioural repertoire, it is possible that long-loop reflexes in muscles normally engaged in more automatic movements, such as stance and gait, would have reflex mechanisms which reflect the greater involvement of peripheral circuitry in their control. Indeed, much of the conflicting evidence that has fuelled the debate has been obtained from different muscles and further confusion has arisen from the application of 'long-latency' to a variety of electromyogram (EMG) (Noth, Podoll & Friedemann, 1985). Closely associated with this loss of the FDI M2 is a reduction in the early somatosensory-evoked cortical potentials arising from stimulation of peripheral nerves in both the upper and lower limbs (Noth, Engel, M2 STRETCH REFLEX MECHANISMS IN MAN Friedemann & Lange, 1984;Bollen, Arts, Roos, Van der Velde & Buruma, 1985).…”

Control of manipulative forces during unimanual and bimanual tasks in patients with Huntington’s disease

“…Alternatively, a reduced efficiency of sensorimotor processing may induce an increased force specification. Disturbed sensorimotor activity in HD has been suggested because of a total suppression or reduced activity of the reactive EMG response (Fellows et al 1997;Noth et al 1985), an abnormal (sub)cortical activation during passive sensory stimulation (Boecker et al 1999), changes in somatosensory evoked potentials (Noth et al 1984;Töpper et al 1993) and deficits in feedback control when external perturbations are introduced during reaching movements (Smith et al 2000).…”