The effect of cortical lesions on the electromyographic response to joint displacement in the squirrel monkey forelimb

Lenz, F. A.; Tatton, W. G.; Tasker, R. R.

doi:10.1523/jneurosci.03-04-00795.1983

Cited by 35 publications

(15 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since motoneurone firing results from the summation of all inputs to the motoneurone pool, we concur with the view (Villis & Cooke, 1976;Lee & Tatton, 1982) that M2 may well be mediated by multiple pathways. The relative contribution of motor cortex may be greater for distal than proximal muscles (Marsden et al 1976;Lenz et al 1983), consistent with the greater excitatory effect of c.m. cells on motoneurones of distal muscles (Phillips, 1969).…”

mentioning

confidence: 58%

“…Indeed, the latency of M2 for different muscles increases with the distance between the muscle and the brain (Melvill-Jones & Watt, 1971;Marsden et al 1973Marsden et al , 1976. Furthermore, cortical lesions in the monkey abolish or reduce M2 ; Lenz, Tatton & Tasker, 1983) and eliminate the corresponding long-latency facilitation of the H reflex (Chofflon, Lachat & Ruegg, 1982).…”

Section: Introductionmentioning

confidence: 99%

“…Segmented peaks in the e.m.g. response of biceps and triceps to muscle stretch have been demonstrated in decerebrate as well as spinal cats and primates (Ghez & Shinoda, 1978;Tracey, Walmsley & Brinkman, 1980;Miller & Brooks, 1981;Lenz et al 1983). One plausible mechanism is suggested by the observation that muscle spindle afferents may exhibit multiple bursts in response to quick stretch of their parent muscles (Hagbarth, Young, Hagglund & Wallin, 1980;Tracey et al 1980;Hagbarth, Hagglund, Wallin & Young, 1981).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.

Cheney¹,

Fetz²

1984

The Journal of Physiology

307

155

View full text Add to dashboard Cite

SUMMARY1. To test the hypothesis that a transcortical reflex contributes to the stretch-evoked long-latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp-and-hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period.2. C.m. cells were identified by a clear post-spike facilitation in spike-triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp-and-hold wrist movements, (b) passive ramp-and-hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles.3. Muscle-lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 1 -2+2-1 ms (mean+S.D.), and the second (M2) began at 27-9 +51 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13-5 + 3-4 ms followed by a peak beginning at 33 9 + 3-0 ms.4. The responses of twenty-one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty-one c.m. cells responded at short latency (23-4 ± 8-8 ms) to torque perturbations which stretched their target muscles.5. For each c.m. cell-target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post-spike facilitation (efferent time). The mean transcortical loop time was 304+ t10-2 ms, comparable to the mean onset latency of the M2 peak (27-9 + 5 1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post-spike facilitation, overlapped the M2 e.m.g. peak. P. D. CHENEY AND E. E. FETZ6. In addition to responding to perturbations which stretched their target muscles, as predicted by the transcortical stretch reflex hypothesis, eight of eighteen c.m. cells also responded at short latency (22-0 ± 7-4 ms) to perturbations which shortened their target muscles. These excitatory responses were appropriately timed to contribute to the long-latency e.m.g. peak in their target muscles evoked by muscle-shortening perturbations. The functional consequence of the long-latency coactivation of flexors and extensors is a stiffening of the joint, to which these bidirectionally activated c.m. cells contribute.7. Seventeen ofnine...

show abstract

mentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.

Cheney¹,

Fetz²

1984

The Journal of Physiology

307

155

View full text Add to dashboard Cite

show abstract

“…There is compelling evidence that the M2 response in thenar, finger and wrist muscles is mediated, in part, by a transcortical pathway that traverses the primary motor cortex (Marsden et al 1973(Marsden et al , 1977Capaday et al 1991;Day et al 1991;Palmer and Ashby 1992;Tsuji and Rothwell 2002). There has been no evidence to date for such a transcortical loop in more proximal upper limb muscles, including the biceps (Lenz et al 1983;Cohen et al 1991;Thilmann et al 1991;Fellows et al 1996). Task-dependent modulation of the M2 in distal muscles has been shown to be smaller than the effect seen in proximal muscles (Rothwell et al 1980).…”

Section: Generalizability Across Joints and Motor Tasksmentioning

confidence: 99%

The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle

2006

View full text Add to dashboard Cite

There is controversy within the literature regarding the influence of task instruction on the size of the long-latency stretch reflex (M2) elicited by a joint displacement. The aim of this study was to investigate if the previously reported task-dependent modulation of the M2 is specific to the M2 or can be explained by an early release of the intended voluntary response. We took advantage of the fact that the M2 is absent when the duration of the applied perturbation is less than a critical time period. This allowed us to examine modulation of muscle activity with and without the contribution of the M2. In addition, we applied transcranial magnetic stimulation (TMS) over the primary motor cortex to examine the modulation of corticomotor excitability with task instruction. Elbow joint extension displacements were used to elicit a stretch reflex in the biceps muscle. Subjects were instructed to "do not intervene" (DNI) with the applied perturbation, or to oppose the perturbation by activating the elbow flexors in response to the perturbation (FLEX). Electromyographic (EMG) activity in the time period corresponding to the M2 was significantly facilitated in the FLEX task instruction both with and without the presence of the M2. Motor evoked potentials (MEPs) elicited by TMS were also facilitated during the FLEX condition in the absence of the M2. EMG and MEP responses were not facilitated until immediately prior to the onset of the M2. Paired-pulse TMS revealed a significant reduction in short-interval intracortical inhibition (SICI) during the M2 response, but the level of SICI was not altered by the task instruction. We conclude that the taskdependent modulation of the biceps M2 results, at least in part, from an early release of the prepared movement and is accompanied by an increase in corticospinal excitability that is not specific to the M2 pathway. Task-dependent modulation of the response cannot be explained by an alteration in the excitability of intracortical inhibitory circuits.

show abstract

“…Such proximodistal differences have recently been analzyed in the squirrel monkey forelimb, where a motor cortical lesion eliminated or decreased M2 activity in distal flexors, but not in proximal flexor muscles (Lenz et al, 1983b), in parallel with the finding that the predominance of the M2 segment in the normal limb increased from proximal to distal musculature (Lenz et al, 1983a). A clear understanding of the physiological basis of these responses is of crucial importance for: (1) the choice of an appropriate species for investigating a given aspect of motor control, (2) defining the pathophysiological events leading to movement disorders in man, and (3) quantitating the effectiveness of therapeutic regimens designed to ameliorate such disorders.…”

Section: Discussionmentioning

confidence: 99%

Electromyographic and motor cortical responses to imposed displacements of the cat elbow: disparities and homologies with those of the primate wrist

Tatton¹,

North²,

Bruce³

et al. 1983

J. Neurosci.

Self Cite

View full text Add to dashboard Cite

The present "loop analysis" study was undertaken to determine the extent to which the segmented electromyographic (EMG) responses of cat triceps brachii to imposed elbow displacements can be used as a model for those occurring in primate wrist musculature under similar input conditions, since previous workers have assumed homology between the two systems. To this end, the response properties of the EMG peaks and the range of latencies available to a "transcortical loop" were determined in the cat and compared with previous findings from primates.During chronic experiments, simultaneous recordings were made from motor cortical neurons (MCNs) and triceps EMG in response to step loads imposing flexion on the elbow joint. Subsequent acute experiments in the same animals used intraspinal microstimulation to determine the antidromic latencies to the area of cortex containing responsive MCNs, and orthodromic latencies to triceps EMG activation from the same loci.Following displacements imposed from flexed initial joint angles, the EMG was segmented into two or more peaks while, from extended angles, a single segment was followed by a "silent interval" and tonic activity. Segmentation into three peaks was only observed under limited conditions. Peak 1 showed a constant latency (8 to 12 msec) and resembled the primate Ml segment. A "silent interval," not present in primate wrist muscles, followed peak 1, and its duration varied with the average velocity of the imposed displacement. Peak 2 followed the "silent interval" at variable latency (34 to 52 msec), in contrast to the constant and shorter latency shown by the primate wrist M2. Peak 3 was variable in appearance and latency (69 to 85 msec when distinguishable) and its homologies remain unclear. Peak 1 was monotonically graded with average velocity of displacement, whereas peaks 2 and 3 showed variable responses.Summation of the afferent and efferent latencies for the "receiving zone" of the motor cortex gave modal values of 19 to 23 and 23 to 27 msec for the expected time of occurrence of EMG activity dependent upon MCNs responding to the imposed displacement as part of a "transcortical loop." This activity would therefore occur during the "silent interval," in contrast to the M2 segment in primate wrist muscles, where MCN activity seems to be appropriately timed to contribute to this segment.It is concluded that the cat triceps brachii EMG responses, together with the related motor cortical responses to imposed elbow displacements, cannot be utilized as a model to study the mechanisms underlying the longer latency EMG segments observed at the primate wrist.Invasive methods, including lesioning, microstimulaneural circuits underlying mammalian motor control. In tion, and single neuron recording techniques, carried out attempts to determine whether similar circuitry operates in the cat and in a few subhuman primate species have in man, one approach has been to compare electromyprovided information essential to the understanding of ographic (EMG) activity durin...

show abstract

The effect of cortical lesions on the electromyographic response to joint displacement in the squirrel monkey forelimb

Cited by 35 publications

References 9 publications

Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.

Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.

The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle

Electromyographic and motor cortical responses to imposed displacements of the cat elbow: disparities and homologies with those of the primate wrist

Contact Info

Product

Resources

About