Long-latency Reflex Research Articles

Excitatory actions of experimental muscle pain on early and late components of human jaw stretch reflexes

It has recently been shown that a slow stretch evokes a short-latency (probably monosynaptic) and a long-latency (polysynaptic) reflex response in human jaw-closing muscles. The effect of nociceptive muscle input on the fusimotor system has not been investigated in detail. In order to investigate the effect of sustained muscle pain on the jaw stretch reflex, two main experiments were performed. Stretch reflex responses were evoked in the masseter and temporalis muscles by slow stretches (1-mm displacement, 40-ms ramp time) before, during and 15 min after a period of experimentally induced muscle pain. In experiment I, a dose of 1.0 M hypertonic or 154 mM isotonic (control) saline was infused in random order into the left masseter for up to 15 min ( n=12). The level of excitation of the left masseter at 15% maximal voluntary contraction was controlled by visual feedback of the surface EMG (sEMG). In experiment II, a dose of 1.0 M saline was infused into the left masseter but with feedback from the sEMG of the right masseter ( n=12). In a control experiment, both sEMG and intramuscular EMG (imEMG) were recorded from the left and right masseters; the feedback was from imEMG of the left masseter ( n=12). The early (onset: 9–10 ms) and late (duration from 25 to 40 ms) reflex components were recorded and analysed in all experiments. Infusion of 1.0 M saline caused moderate pain (mean score on a Visual Analogue Pain Scale: 4.9–5.0 cm). The peak-to-peak amplitude of the early reflex component in the painful masseter normalized to the pre-stimulus EMG activity was significantly higher during the pain than the pre- and post-infusion conditions in all experiments. The normalized area of the late reflex component in the painful masseter was significantly larger than in the pre-infusion condition in all experiments. Isotonic saline had no significant effect on the jaw stretch reflexes. These results indicate that experimental jaw-muscle pain in humans facilitates the early as well as the late component of the jaw stretch reflex response as revealed by both sEMG and imEMG. This effect appears to be independent of the level of excitation of the muscle and not related to volume effects of the injected saline. A change in the sensitivity of the fusimotor system during muscle pain is suggested as an explanation.

Long-latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex

Objective: The cortical relay time (CRT) for V2 of long-latency reflexes (LLRs) in the contracted thenar and short toe flexor muscles was studied. Methods: LLRs and somatosensory evoked potentials (SEPs) were studied by electrical stimulation of the median or posterior tibial nerve. The CRT for V2 was calculated by subtracting the onset latency of cortical potentials in SEPs and that of motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) from the onset latency of V2 in eight healthy subjects. Results: The CRT for the thenar muscles was 11.4±0.9 ms (mean±SD), as the onset latency was 48.8±1.4 ms for V2, 16.0±1.2 ms for N20 and 21.3±1.1 ms for MEP, respectively. The CRT for the short toe flexor muscles was 3.0±1.3 ms, as the onset latency was 80.5±4.5 ms for V2, 35.3±1.8 ms for P38 and 42.2±2.0 ms for MEP, respectively. Conclusion: Significantly longer CRT for V2 for the thenar muscles ( P<0.001, paired Student's t test) may indicate more synaptic relays as compared to that for the short toe flexor muscles.

Changes of forearm EMG and cerebral evoked potentials following sudden muscle stretch in patients with Huntington's disease

Various investigators have reported that the late-reflex electromyographic (EMG) activity following muscle stretch is decreased in Huntington's disease. To explore the basis of this decreased activity, we recorded the late EMG responses together with associated cerebral responses following muscle stretch in patients with Huntington's disease. Five patients and seven controls voluntarily participated in two sets of experiments in which they grasped a handle attached to a torque motor and maintained the wrist isometrically against a constant flexor force of 2.3 newtons (N). The force was changed unpredictably (first set of experiments) or predictably (second set) to 10.4 N, causing a stretch of wrist extensors or flexors. Rectified surface EMG from the extensor and flexor carpi radialis muscles was integrated for the M2 and M3 components of the late responses. Cerebral responses were recorded from F3, F4, C3, C4, and Cz and averaged separately depending upon condition. The late muscle responses to unpredictable muscle stretch were decreased or absent in patients with Huntington's disease. The cerebral responses recorded at Cz differed markedly between patients and controls, beginning approximately 15 ms prior to the onset of the late M2 muscle response. Although the initial positivity was similar in amplitude, all other cerebral components were markedly reduced in the patient group. Both controls and patients showed a markedly attenuated cerebral response when the muscle stretch was predictable. The electrocerebral response to muscle stretch is thus altered prior to the onset of M2 in patients with Huntington's disease, suggesting that the long-latency reflex involves transcerebral pathways that are affected in this disease.

Changes in long-latency reflexes onset latencies across full-wave rectified and non-rectified recordings

Electrically elicited long-latency reflexes (LLRs) were obtained from thenar muscles by either fully rectified or non-rectified raw recordings in 10 healthy volunteers. The LLR II onset latencies were significantly (P<0.0001) delayed on rectified (mean±SD: 49.8±2.9 ms) compared to raw (45.3±2.3 ms) recordings, with a mean difference of 4.4 ms. These data show that, according to the recording technique employed, the LLR II onset latencies can change considerably. The possible implications on cortical relay time (CRT) calculation and the understanding of the intracortical connections physiology are discussed.

Modulation of exteroceptive suppression periods in human jaw-closing muscles by local and remote experimental muscle pain

The exteroceptive suppression periods (ES) in human jaw-closing muscles can be conditioned by a wide range of somatosensory stimuli and cognitive states. The aim of this study was to examine the effects of tonic experimental jaw-muscle pain versus remote muscle pain on the short-latency (ES1) and long-latency (ES2) reflex in the jaw-closing muscles. Twelve healthy subjects participated in the first experiment with jaw-muscle pain. In random order 5% hypertonic or 0.9% isotonic saline was infused into the left masseter muscle for 15 min. The pain intensity was scored continuously by the subjects on a 10-cm visual analogue scale (VAS). Electromyographic (EMG) activity was recorded bilaterally from the masseter and temporalis muscles during the pre-infusion, early phase of infusion (from 120 to 480 s), late phase of infusion (from 540 to 900 s) and post-infusion. An electrical stimulus was delivered to the skin above the left mental nerve (ipsilateral to the painful muscle) to evoke the ES in the contracting jaw-closing muscles. Ten healthy subjects participated in experiment 2 which was as identical to experiment 1 except that the electrical stimulus was delivered to the right mental nerve (contralateral to the painful muscle). Nine healthy subjects participated experiment 3 where remote muscle pain was induced in the left tibialis anterior muscle. In experiment 1 painful infusion of hypertonic saline caused a significantly later onset latency of ES2 in the left masseter muscle during the late phase of infusion compared to pre-infusion values ( P<0.05). The duration of ES2 in the same muscle was significantly shorter during the late infusion phase compared to pre- and post-infusion values ( P<0.05) and the degree of suppression was significantly reduced during the early infusion compared to the pre-infusion values ( P<0.05). Isotonic saline did not influence the ES1 or ES2. In experiment 2, similar significant inhibitory changes were found in the ES2 on the painful side. In experiment 3, no significant effects on ES1 and ES2 were observed during painful infusion of hypertonic saline into the leg muscle. These results indicate that the effects of tonic jaw-muscle pain on ES2 can be distinguished from a generalized effect of muscle pain. Furthermore, there seems to be a differential and lateralized effect of jaw-muscle pain on the brain stem reflex circuits involved in the generation of ES1 and ES2 probably through a presynaptic mechanism.

Reflex excitability of facial motoneurons at onset of muscle reinnervation after facial nerve palsy.

We studied 18 patients with complete unilateral denervation of the facial muscles after idiopathic facial nerve palsy to determine whether motoneuronal excitability is enhanced in the few motor units that are active at onset of muscle reinnervation. The study was carried out between 75 and 90 days after the facial nerve lesion. We used two needle electrodes to record simultaneously the spontaneous and voluntary activity of the orbicularis oris (OOris) and orbicularis oculi (OOculi) muscles, as well as the responses to ipsilateral and contralateral facial and supraorbital nerve stimuli. All patients showed involuntary firing of motor unit action potentials (MUAPs) in at least one of the muscles. Synkinetic activation of motor units in the OOris was induced by spontaneous blinking in all patients, and by inhalation and swallowing in some. Electrical stimulation of the ipsilateral facial nerve induced a direct M response in only 4 patients. In contrast, long-latency reflex responses were induced in both muscles by electrical stimulation of ipsilateral and contralateral facial and supraorbital nerves in all patients, at latencies ranging between 44 and 132 ms. The shape of such MUAP reflex responses was the same as that of the MUAPs seen to fire at rest. These findings provide evidence of enhanced excitability of facial motoneurons in our patients. Such hyperexcitability may be partly responsible for the postparalytic motor dysfunction syndrome that occurs after facial palsy with severe axonal damage.

Postural reflexes in patients with HIV-1 infection

Objective: We studied whether medium latency (ML) and long latency (LL) postural reflexes, which are abnormal in a number of neurological conditions including basal ganglia disorders, provide an early marker of CNS involvement in HIV-positive patients. Methods: Leg reflexes were elicited in 9 neurologically normal HIV-positive patients and 10 healthy controls who were standing upright, using toe-up forceplate rotations of varying amplitude (4° and 10°) and predictability (serial and random). Results: For predictable amplitude perturbations, posturally destabilizing ML and stabilizing LL responses in HIV-seropositives did not differ from controls. However, for unpredictable amplitude perturbations, HIV-positive patients inappropriately manifested a mid-size default LL response, in contrast to healthy subjects who showed a maximum size default response. Conclusions: These results suggest that impaired modulation of LL reflex processing occurs in early stages of HIV infection, prior to the onset of clinical postural instability, and this dysregulation may be influenced by cognitive factors.

Long latency responses in pure sensory stroke due to thalamic infarction.

Our study was designed to clarify the role of the thalamus in the generation of the electrically elicited long-latency reflexes (LLR) in voluntarily activated hand muscles. EMG responses of the thenar muscles were evoked by electrical stimulation of the median nerve at the wrist at motor threshold intensity in 10 patients with acute pure sensory stroke due to thalamic infarction. Concomitant recording of somatosensory evoked potentials (SEPs) was performed. The subjects were asked to steadily abduct the thumb at 20-30% of maximal force against a force transducer. Rectified and averaged EMG activities were recorded. The LLR II was missing completely or significantly attenuated in the majority of the patients (9 of 10), of whom 3 also had delayed latency. Abnormal SEPs were documented in 7 patients (7 of 10). In the follow-up, 5 patients had partial reversal of LLR II. LLR II was still pathological in 1 fully recovered patient. Our results further confirm the transcortical generation of LLR II and imply that a thalamic relay is present in the afferent limb of the LLR.

The pathophysiology of primary dystonia.

Co-contraction and overflow of EMG activity of inappropriate muscles are typical features of all dystonic movements whether voluntary or involuntary. Voluntary movements are slow and more variable than normal, and there is particular difficulty switching between component movements of a complex task. Reduced spinal cord and brainstem inhibition is common to many reflex studies (long-latency reflexes, cranial reflexes and reciprocal inhibition). These reflex abnormalities may contribute to the difficulties in voluntary movements but cannot be causal as they can occur outside the clinically involved territory. Clinical and neurophysiological studies have emphasized the possible role of sensory feedback in the generation of dystonic movements. Abnormalities of cortical and basal ganglia function have been described in functional imaging and neurophysiological studies of patients with dystonia and in animal models of primary dystonia. Studies of cortical function have shown reduced preparatory activity in the EEG before the onset of voluntary movements, whilst magnetic brain stimulation has revealed changes in motor cortical excitability. Functional imaging of the brain in primary dystonia has suggested reduced pallidal inhibition of the thalamus with consequent overactivity of medial and prefrontal cortical areas and underactivity of the primary motor cortex during movements. These findings are supported by preliminary neuronal recordings from the globus pallidus and the thalamus at the time of stereotaxic surgery in patients with dystonia. All this evidence suggests that primary dystonia results from a functional disturbance of the basal ganglia, particularly in the striatal control of the globus pallidus (and substantia nigra pars reticulata). This causes altered thalamic control of cortical motor planning and executive areas, and abnormal regulation of brainstem and spinal cord inhibitory interneuronal mechanisms.

Effects of RPR 100893, a potent NK1 antagonist, on the jaw-opening reflex in the guinea pig

RPR 100893 appears as a new potent NK1 selective non-peptide antagonist both in vitro and in vivo, and exhibits high affinity for guinea pig and human NK1 receptor [M. Tabart, J.-F. Peyronel, Synthesis of RPR 100893, prototype of a new series of potent and selective non-peptide NK1 antagonists: the triarylperhydroisoindolols, Bioorg. Med. Chem. Lett., 4 (1994) 673–676.]. Intra-oral administration of RPR 100893 (3, 15, 10, 30 mg/kg) was performed in freely moving guinea pigs during recording of the short- (6–10 ms) and long-latency (18–26 ms) jaw-opening reflex (JOR) elicited by electrical stimulation (0.5 Hz) of the lower incisor tooth pulp. RPR 100893 induced a noticeable and dose-dependent increase of the long-latency reflex thresholds ( P<0.001) but was ineffective on the short-latency responses ( P=0.14). The results suggest that, in guinea pigs, the long-latency JOR requires activation of NK1 receptors, while the earlier reflex component, elicited by activation of periodontal afferents, does not. These NK1 receptors could be located either on JOR interneurons activated by tooth pulp afferents or on digastric motoneurons, receiving the tooth pulp input through a polysynaptic pathway.

Central mechanisms in human enhanced physiological tremor

The sites of the central nervous structures involved in enhanced physiological tremor (EPT) are still unclear. The syndrome of persistent mirror movements (PMM) is characterized by abnormal bilateral corticospinal projections. If a supraspinal mechanism is involved in EPT, the activity of EPT should be coherent between both sides in subjects with this abnormality. We investigated three PMM subjects and three normal controls. Focal transcranial magnetic stimulation (TMS) resulted in contralateral hand muscle responses in the controls. The PMM subjects, in contrast, had bilateral responses. Similarly, long-latency reflexes (LLR) in PMM could be recorded bilaterally, while the control subjects showed responses only on the stimulated side. EPT was evoked by intravenous salbutamol. EMG time series were recorded bilaterally from the wrist extensor muscles and cross spectra were calculated. If there was a significant right-left-coherence, phase analysis was performed. No control subject showed a significant right-left-coherence of tremor activity. In contrast, a significant coherence was found in PMM between 8 and 12 Hz. When the mechanical tremor frequency of one hand was reduced by loading, coherences and phase spectra of the EMGs remained unchanged. By comparing the results from TMS, LLR and cross spectral analysis we come to the conclusion, that the 8 to 12 Hz component of EPT is transmitted transcortically, most likely originating from two separate generators for both sides.

The role of gingival mechanoreceptors in the reflex control of human jaw-closing muscles

Electromyographic (EMG) experiments were undertaken to investigate the jaw reflexes evoked by activation of gingival receptors in 12 humans. EMG recordings were made from an active masseter muscle whilst ramp–plateau mechanical stimuli were applied to the gingiva. Stimuli with a constant rate of rise (0.2 N/msec) and a variable plateau force (up to 2 N), evoked a complex set of short- and long-latency inhibitory and excitatory responses. These occurred as a sequence of inhibition–excitation–inhibition–excitation, although not all of these elements were seen on every occasion. The median thresholds of these four responses ranged from 0.5 to 1 N but overall there were no significant differences between them ( p>0.05, Friedman’s ANOVA). In other experiments, the same reflexes were recorded in response to application to the gingiva of 1 N ramp–plateau stimuli (5 msec rise time) and 1 N tap stimuli applied to the adjacent tooth. The application of a local anaesthetic agent to the stimulated gingiva produced reductions in the mean magnitude of almost all the responses but these were significant ( p<0.05; ANOVA) only for the long-latency inhibitions evoked by ramping the gingiva and the long-latency excitations evoked by either stimulus. It is concluded that mechanoreceptors in the gingiva can mediate long-latency inhibitory and excitatory jaw reflexes, and that these receptors may also contribute to long-latency reflexes evoked by tapping teeth. The scarcity of effects of gingival anaesthesia on the short-latency reflexes may be due to such responses being mediated by receptors deeper in the periodontium.

Short- and long-latency reflex responses during different motor tasks in elbow flexor muscles.

Stretch reflex responses in three elbow flexor muscles - the brachioradialis and the short and long heads of the biceps brachii - were studied during different motor tasks. The motor tasks were iso-velocity (8 deg/s) elbow flexion movements in which the muscles performed shortening or lengthening contractions, or were isometric contractions. Care was taken to maintain constant background electromyographic (EMG) activity in the brachoradialis muscle at a 50-deg elbow angle across the tasks by changing the magnitude of the initial load. During each task, mechanical perturbations (duration 170 ms) were applied at pseudorandom intervals when the elbow angle was 50 deg. The magnitude of the perturbation was varied across tasks in order to induce an elbow extension velocity of 80 deg/s over the first 50 ms after the onset of perturbation. The stretch reflex EMG responses in all muscles varied across the three tasks, despite a constant EMG level and similar perturbation-induced angular velocity in the direction of elbow extension. In particular, both the short- and long-latency reflex EMG components were reduced during the lengthening contractions. Further, the task-dependent variations in the early (M2) and the late (M3) components of the long-latency reflex were different, i.e., the magnitude of M3 was considerably enhanced during the shortening task as compared with that of M2. These findings suggest that central modification was responsible for the task-dependent modulation of late EMG responses.

Symmetric force response of human masticatory muscles to stretch and unloading.

During chewing, the force exerted by the jaw-closing muscles must constantly adapt to changing resistances between the teeth, as the food is broken down. In the present study, the changes in biting force resulting from small, controlled displacements imposed on isometrically contracting jaw-closing muscles were measured. We found that the force changes resulting from small loading and unloading movements were normally highly symmetrical. The initial force change was linear, and preceded the onset of reflex changes in muscle activity. Later changes in force were the result of both short- and long-latency reflexes in the jaw-closing muscles, the long-latency component being quantitatively greater. The long-latency unloading reflex in the jaw-closing muscles has not been described hitherto. The symmetry of force increase with loading and decrease with unloading was absent in one subject with atypical stretch and H-reflexes.

Disturbances of precision grip in Huntington's disease

Disturbed motor control of the fingers, as revealed by the response to unexpected loading of an object held in a precision grip, or to finger perturbation during isometric holding, has been studied in patients with Huntington's disease (HD) and in normal subjects. In normal subjects unexpected loading elicited a reflex response (mean latency 73 ms) in the first dorsal interosseus muscle (FDI). This was accompanied by a clear increase in grip force, reaching a maximum at 200 ms, which stabilised block position. Index finger perturbation led to a long-latency reflex response in the FDI of all normal subjects. No such response was seen in the HD patients. The response to object loading, in contrast, was present, but significantly delayed (mean onset 95 ms; P=0.0135). The response was qualitatively normal, with grip force reaching a maximum at 220–230 ms. It is suggested that the absence of the long-latency stretch reflex and the delay in the response to loading in HD patients may represent a reduction in somatosensory input to the cortex caused by disruption of basal ganglia structures.

Long-latency reflexes of hand muscles in idiopathic focal dystonia and their modification by botulinum toxin.

Long-latency reflexes (LLR) in thenar muscles were elicited by electrical median nerve stimulation in 34 patients with idiopathic focal dystonia and 20 healthy control subjects. Twenty-seven patients had cervical dystonia and seven patients had upper limb dystonia. In about one-quarter of all patients the early LLR (LLR 1, occurring at approximately 40 ms) was abnormal with either increased amplitudes or only unilateral occurrence, mostly on the clinically affected side. Later responses (LLR 2, occurring at approximately 50 ms) were obtained bilaterally in all controls but were reduced or absent in some patients, mostly on the clinically affected side. In 12 dystonia patients, LLR studies were also performed after clinically effective injection of botulinum toxin. Following botulinum toxin treatment there was a significant reduction of LLR 2 amplitudes on the clinically affected side. Our findings suggest a differential involvement of LLR generators in idiopathic dystonia with an antagonism between LLR 1 and LLR 2 on the affected sides. We propose that the reduction of the LLR 2 response may arise from overactivity of the supplementary motor area, confirming the current concept that dystonia results from cortical overflow due to disinhibited thalamocortical pathways projecting to the supplementary motor area. In addition, the dystonic motor pattern seems open to afferent modifications induced by peripheral botulinum toxin treatment.

Silent period evoked by transcranial magnetic stimulation in unilateral thalamic infarcts

We studied 9 patients with isolated, unilateral thalamic infarcts of different location and size imaged by MRI and (in one case) by CCT. The cortical silent period (c-SP) of thenar muscles evoked by transcranial magnetic stimulation was evaluated on both sides with low (c-SP1) and high (c-SP2) stimulus intensity. Additionally, the motor-evoked thenar potentials by transcranial magnetic stimulation (MEP) and the central motor conduction time (CMT), the silent period of thenar muscles evoked by electrical median nerve stimulation (p-SP), electrically evoked short- (HR) and long-latency reflexes (LLR) of the thenar and somatosensory evoked potentials of the median nerve were investigated bilaterally. The c-SP1 was prolonged contralateral to the thalamic infarcts in 7 patients and c-SP2 in all 9 patients. Prolongation of c-SP did not correlate with location and size of the infarct, clinical symptoms or with the other parameters, which are based on pyramidal motor system (MEP, CMT), thalamocortical circuits (SEP, LLR), or spinal excitability level (p-SP, HR). These results suggest the central pathways of the c-SP to be independent from those of the remaining parameters and indicate the c-SP as a sensitive parameter reflecting thalamocortical modulation of cortical inhibition.

P401 Silent period, long-latency reflexes, and rigidity in patients with Parkinson's disease

P401 Silent period, long-latency reflexes, and rigidity in patients with Parkinson's disease

Mechanical actions of heterogenic reflexes among ankle stabilizers and their interactions with plantarflexors of the cat hindlimb.

1. The stretch-evoked reflex organization of muscles whose major action is to abduct [peroneus brevis (PB); peroneus longus (PL)] and adduct [tibialis posterior (TP); flexor digitorum longus (FDL); flexor hallucis longus (FHL)] the ankle, and their interactions with the hindlimb extensors gastrocnemius (G) and soleus (S), were studied in 27 unanesthetized decerebrate cats. Ramp-hold-release stretches of physiological amplitudes were applied to muscle tendons detached from their bony insertion, and muscle force output was measured in response to these perturbations. Flexion and crossed-extension reflexes were used to modulate baseline force. 2. PB and TP shared strong, length-dependent, short-latency inhibitory reflexes prominent when the muscles were either actively generating force or quiescent. The mechanical characteristics of this reflex suggest Ia reciprocal inhibition as the underlying mechanism. Just as reciprocal inhibition between S and tibialis anterior stiffens the ankle joint against sagittal perturbations, we propose that reciprocal inhibition between PB and TP stiffens the ankle joint against nonsagittal perturbations. 3. In all preparations (n = 7) and under all conditions examined, PB and PL shared well-demonstrated mutual excitation. The reflex responses were asymmetric (favoring excitation of PL), length dependent, and occurred simultaneously with the stretch reflex at a latency of 16-18 ms. Mutual monosynaptic projections previously described between these two muscles explain all of the above findings. Our data further demonstrate that, under certain conditions, the ensemble activity of this reflex interaction has a powerful effect on the mechanical behavior of the muscle. 4. The heterogenic reflex organization of the ankle adductors was as follows: FDL evoked a modest excitation on TP, whereas FHL evoked weak inhibition. Latency of the excitation from FDL onto TP (24 ms) was greater than expected if the reflex were mediated by heteronymous Ia afferents. In all preparations examined (n = 3), TP contributed no significant reflexes onto either FDL or FHL. 5. Mutual, asymmetric inhibition characterized interactions between PB and the plantarflexors S and G. Most remarkable was a novel, long-latency (72-74 ms) reflex inhibition evoked on both S and G by stretch of PB. When this inhibition occurred, it dramatically decreased the S (or G) stretch response. Longer PB lengths evoked greater inhibition of isometric S; regression analysis indicated that the model best predicting this inhibition contained muscle force and stiffness terms. No long-latency reflexes were noted from either G or S onto PB. The mechanism underlying long-latency inhibition is presently unknown; however, features of this interaction suggest interneurons receive either group II or group III afferent input. 6. G and TP shared short latency, mutually inhibitory, asymmetric reflexes favoring inhibition of TP. No long-latency interactions were noted, nor were there any mechanically significant interactions between S and TP. 7. Reflex interactions across the abduction/adduction axis thus favored inhibition of plantarflexion and adduction torques while emphasizing abduction torques: PB/S (or PB/G) interactions were mutual, asymmetric, and favored inhibition of G and S; TP/G interactions were mutual, asymmetric, and favored inhibition of TP; TP/PB interactions were approximately balanced. The overall mechanical outcome of these inhibitory interactions may partly underlie the global corrective strategy seen in intact cats subjected to linear perturbations. 8. No significant reflex interactions were demonstrated between PL and TP, G, or S, nor were any long-latency reflexes noted. Thus, whereas reflex interactions between the stereotypically activated PB and other stereotypically activated muscles (including TP, G, and S) were strong and well-demonstrated, interactions between the variably activated PL and these same muscles were far weaker.

Stretch reflexes of the proximal arm in a patient with mirror movements: absence of bilateral long-latency components

The stretch reflex responses evoked by unilateral limb displacement in distal (first dorsal interosseus (FDI)) and in proximal (biceps brachii (Bb)) arm muscles were studied during matched bilateral contractions in a patient with congenital mirror movements. In this patient unilateral transcortical magnetic stimulation (TMS) elicited not only the normal contralateral EMG response but also a clear ipsilateral component in the EMG of both proximal and distal arm muscles. As expected from previous studies, the ipsilateral FDI muscle responded to stretch of the index finger with short- (M1) and long-latency (M2) reflex components. In addition, the FDI contralateral to displacement exhibited an abnormal mirrored response corresponding to the M2 interval. In contrast, whereas the ipsilateral Bb responded to imposed elbow extension with a marked M1/M2 reflex response, no mirroring of either reflex component was apparent in the contralateral Bb EMG. If the mirroring of the M2 in the FDI is accepted as evidence for the transcortical nature of the M2 reflex response, then it follows that the absence of such mirroring in the Bb indicates that a transcortical mechanisms cannot play a major role in the generation of long-latency stretch reflex responses in proximal arm muscles.