Contribution of muscle afferents to prolonged flexion withdrawal reflexes in human spinal cord injury

The contribution of force-sensitive muscular afferents to prolonged flexion withdrawal reflexes, or flexor spasms, after human spinal cord injury (SCI) was investigated. In three separate experimental conditions, flexion reflexes were triggered in subjects with SCI using trains of electrocutaneous stimuli delivered at the foot and lower leg and compared with reflexes elicited via intramuscular (i.m.) electrical stimuli. In the first experiment, flexion reflexes were elicited using i.m. stimuli to the tibialis anterior (TA) in the majority of subjects tested. The ratio of peak isometric ankle to hip torques during i.m.-triggered reflexes were proportionally similar to those evoked by electrocutaneous foot or shank stimulation, although the latency to onset and peak flexion torques were significantly longer with i.m. stimulation. In the second experiments, the amplitude and frequency of i.m. TA stimulation were varied to alter the stimulus-induced muscle torque. Peak ankle and hip torques generated during the flexion reflex responses were correlated to a greater extent with stimulus-induced muscle torques as compared with the modulated stimulus parameters. In the third experimental series, i.m. stimuli delivered to the gastrocnemius (GS) elicited flexion reflexes in approximately half of the subjects tested. The combined data indicate a potentially prominent role of the stimulus-induced muscle contraction to the magnitude and latency of flexor reflex behaviors after i.m. TA stimulation. Results after i.m. GS stimulation indicate multi-joint flexion reflexes can also be elicited, although to a lesser extent than i.m. TA stimulation.     

Modulation of flexion reflex induced by hip angle changes in human spinal cord injury

The flexion reflex can be elicited via stimulation of skin, muscle, and high-threshold afferents inducing a generalized flexion of the limb. In spinalized animal models this reflex is quite prominent and is strongly modulated by actions of hip proprioceptors. However, analogous actions on the flexion reflex in spinal cord injured (SCI) humans have not yet been examined. In this study, we investigated the effects of imposed static hip angle changes on the flexion reflex in ten motor incomplete SCI subjects when input from plantar cutaneous mechanoreceptors was also present. Flexion reflexes were elicited by low-intensity stimulation of the sural nerve at the lateral malleolus, and were recorded from the ipsilateral tibialis anterior (TA) muscle. Plantar skin stimulation was delivered through two surface electrodes placed on the metatarsals, and was initiated at different delays ranging from 3 to 90 ms. We found that non-noxious sural nerve stimulation induced two types of flexion reflexes in the TA muscle, an early, and a late response. The first was observed only in three subjects and even in these subjects, it appeared irregularly. In contrast, the second (late) flexion reflex was present uniformly in all ten subjects and was significantly modulated during hip angle changes. Flexion reflexes recorded with hip positioned at different angles were compared to the associated control reflexes recorded with hip flexed at 10°. Hip flexion (30°, 40°) depressed the late flexion reflex, while no significant effects were observed with the hip set in neutral angle (0°). Strong facilitatory effects on the late flexion reflex were observed with the hip extended to 10°. Moreover, the effects of plantar skin stimulation on the flexion reflex were also found to depend on the hip angle. The results suggest that hip proprioceptors and plantar cutaneous mechanoreceptors strongly modulate flexion reflex pathways in chronic human SCI, verifying that this type of sensory afferent feedback interact with spinal interneuronal circuits that have been considered as forerunners of stepping and locomotion. The sensory consequences of this afferent input should be considered in rehabilitation programs aimed to restore movement and sensorimotor function in these patients.     

Absence of local sign withdrawal in chronic human spinal cord injury

Local sign withdrawal, a reflex to direct the limb away from noxious cutaneous stimuli, is thought to be indicative of a modular organization of the spinal cord. To assess the integrity of such an organization of the spinal cord in chronic human spinal cord injury (SCI), we tested the electromyogram (EMG) and joint torque responses to cutaneous stimuli applied to 6 locations of the leg in 10 SCI volunteers and 3 spinal-intact controls. The 6 locations included the medial arch of the foot, the second metatarsal, the dorsum, the region over the sural nerve at the lateral malleolus, and the anterior and posterior aspects of the lower leg. Although spinal-intact subjects demonstrated local sign withdrawal, the data from SCI subjects indicated that an invariant flexion response pattern was produced regardless of stimulus location. Ankle dorsiflexion and hip flexion were produced in all subjects at all locations and no difference in the ratio of hip:ankle torques could be detected for the 6 test locations. A windup-crossover test, employing a sequence of 6 stimuli at 1-s intervals was used to assess whether common neuronal pathways were responsible for the loss of modular organization. An additional 10 SCI volunteers were tested using stimuli in which the stimulus location was switched between the 2nd and 3rd stimulus of the test sequence. The response to the crossover stimulus more closely resembled the response to the 3rd stimulus of a windup sequence than a response without conditioning stimuli. These results indicate that increased excitability produced by windup at one stimulus site is maintained at the 2nd site. This observation suggests that deep dorsal horn neurons, typically associated with musculotopic mapping, may be reorganized in chronic spinal cord injury.     

Afferent mechanisms for the reflex response to imposed ankle movement in chronic spinal cord injury

We have reported earlier that externally imposed ankle movements trigger ankle and hip flexion reflexes in individuals with spinal cord injury (SCI). In order to examine the afferent mechanisms underlying these movement-triggered reflexes, controlled ankle movements were imposed in 17 SCI subjects. In 13 of these subjects, reflex torques were recorded at the hip, knee and ankle in response to 5 ankle movement ranges, and 4 movement speeds. Subjects were tested using both ankle plantarflexion and dorsiflexion movements. The principal outcome measure, peak hip flexion torque of the induced reflexes, was used for comparing the effects of movement range and speed on the reflex response. We found that movement-triggered reflexes were sensitive to the angular range of ankle deflection, but insensitive to the velocity of the movement. Movement amplitudes sufficient to trigger hip and ankle flexion were routinely associated with increases in ankle passive force, suggesting that force-sensitive receptors participated in the reflex response. However, increases in angular range also corresponded to increases in muscle length, making it difficult to distinguish whether the response was triggered by a load-sensitive receptor (e.g., Golgi tendon organ or muscle free nerve ending) or a position-sensitive receptor responsive to absolute ankle angle (e.g., muscle spindle secondary afferent). The absence of velocity dependence of the reflex suggested that spindle Ia afferents were not major contributors. These results suggest movement-triggered reflexes originate in muscle receptors that are sensitive to either absolute muscle length, to muscle force or to both. Although receptors that are sensitive to absolute muscle length cannot be excluded with certainty, the finding that reflex responses require that ankle movements elicit an increase in passive force argues for a prominent role of nonspindle mechanoreceptors, such as group III/IV muscle afferents. These afferents are activated preferentially as muscles are stretched to near maximum length, and they appear to have potent reflex effects in spinal cord injury.     

Flexor reflex responses triggered by imposed knee extension in chronic human spinal cord injury

Hypersensitivity of the flexor reflex pathways to input from force-sensitive muscle afferents may contribute to the prevalence and severity of muscle spasms in patients with spinal cord injury (SCI). In this study, we triggered flexor reflexes with constant velocity knee movements in 15 subjects with SCI. Ramp and hold knee extension perturbations were imposed on one leg while the hip and ankle were held in an isometric position using an instrumented leg brace. Knee, ankle and hip torque responses and electromyograms from six muscles of the leg were recorded following controlled knee extension at four different velocities. Tests were conducted with the hip in both flexed and extended positions. During the movement into knee extension, a velocity-dependent stretch reflex, represented by a progressively increasing knee flexion torque, was observed. In addition, another type of reflex that resembled a flexor reflex (flexion of the hip and ankle) was also triggered by the imposed knee extension. The magnitude of the ankle dorsiflexion torque responses was significantly correlated to the stretch reflex torque at the knee in 9 of the 15 subjects. We concluded that stretch reflexes initiate a muscle contraction that then can contribute to a flexor reflex response, possibly through muscle group III/IV afferent pathways. These results suggest that spasticity in SCI consists of a myriad of complex reflex responses that extend beyond stretch reflexes.     

Flexion reflex modulation during stepping in human spinal cord injury

The flexion reflex modulation pattern was investigated in nine people with a chronic spinal cord injury during stepping using body weight support on a treadmill and manual assistance by therapists. Body weight support was provided by an upper body harness and was adjusted for each subject to promote the best stepping pattern with the least manual assistance required by the therapists. The flexion reflex was elicited by sural nerve stimulation with a 30 ms pulse train at 1.2–2 times the tibialis anterior reflex threshold. During stepping, stimuli were randomly dispersed across the gait cycle which was divided into 16 equal bins. A long latency (>110 ms) flexion reflex was present in all subjects, while a short (>30 ms) and a medium latency (>70 ms) flexion reflex were present only in three subjects. For each response, the non-stimulated EMG was subtracted from the stimulated EMG at identical time windows and bins, normalized to the maximal corresponding EMG, and significant differences were established with a Wilcoxon rank-sum test. The long latency flexion reflex was facilitated at late stance and during the swing-to-stance transition phase. A reflex depression was present from heel strike until mid-stance and during the swing-to-stance transition phase. The short and medium latency flexion reflexes were depressed during mid-stance followed by facilitation during the stance-to-swing transition phase. Regardless of the latency, facilitatory flexion responses during the swing phase coincided with decreased activity of ipsilateral ankle extensors. The flexion reflex was modulated in a phase dependent manner, a behavior that was absent for the soleus H-reflex in most of these patients (Knikou et al. in Exp Brain Res 193:397–407, 2009). We propose that training should selectively target spinal reflex circuits in which extensor muscles and reflexes are involved in order to maximize sensorimotor recovery in these patients.     

The intralimb coordination of the flexor reflex response is altered in chronic human spinal cord injury

The current study compared the intralimb coordination of flexor reflex responses in spinal intact and complete chronic spinal cord injured (SCI) individuals. Noxious electrocutaneous stimulation was applied at the apex of the medial arch of the foot (50 mA, 500 Hz, 1 ms pulse width, 20 ms) in 21 complete chronic SCI and 19 spinal intact volunteers and the flexor reflex response was quantified by measuring the isometric joint torques at the ankle, knee and hip. The results showed that SCI individuals had significantly smaller peak knee and hip joint flexion torques, often exhibited a net knee extension torque, and produced a much smaller hip joint flexion torque during the flexor reflex response in contrast to the spinal intact individuals. The latency of the reflex response, measured from the tibialis anterior electromyogram, was comparable in both test populations. These findings indicate that the intralimb coordination of the flexor reflex response of chronic complete SCI individuals is altered, possibly reflecting a functional reorganization of the flexion pathways of the spinal cord.     

Spastic reflexes triggered by ankle load release in human spinal cord injury

The rapid decrease in firing of load-sensitive group Ib muscle afferents during unloading may be particularly important in triggering the swing phase of gait. However, it still remains unclear whether load-sensitive muscle afferents modulate reflex activity in human spinal cord injury (SCI), as suggested by studies in the cat. The right hip of 12 individuals with chronic SCI was subjected to ramp (60 degrees /s) and hold (10 s) movements over a range from 40 degrees flexion to 0-10 degrees extension using a custom servomotor system. An ankle dorsiflexion load was imposed and released after the hip reached a targeted position using a custom-designed pneumatic motor system. Isometric joint torques of the hip and knee, reaction torque of the ankle, and surface electromyograms (EMGs) from eight muscles of the leg were recorded following the imposed hip movement and ankle load release. Reflexes, characterized by hip flexion torque, knee extension, and coactivation of ankle flexors and extensors, were triggered by ankle load release when the hip was in an extended position. The ankle load release was observed to enhance the reflexes triggered by hip extension itself, suggesting that ankle load afferents play an important role in spastic reflexes in human SCI and that the reflex pathways associated with ankle load afferents have important implications in the spinal reflex regulation of human movement. Such muscle behaviors emphasize the role of ankle load afferents and hip proprioceptors on locomotion. This knowledge may be especially helpful in the treatment of spasms and in identifying rehabilitation strategies for producing functional movements in human SCI.     

Rebound responses to prolonged flexor reflex stimuli in human spinal cord injury

The purpose of this study was to examine the reflex effects of electrical stimulation applied to the thigh using skin electrodes, targeting the sensory fibers of the rectus femoris and sartorius, in people with spinal cord injury (SCI). Thirteen individuals with SCI were recruited to participate in experiments using prolonged electrical stimuli on the right medial thigh over the regions of the sartorius and rectus femoris muscles. Three stimuli, spaced 20 s apart, were applied at 30 Hz for 1 s at four different intensities (15–60 mA) while subjects rested in a seated position. Isometric joint torques of the hip, knee and ankle, and electromyograms (EMGs) from six muscles of the leg were recorded during the stimulation. Early in the stimulation, a flexion response was observed at the hip and ankle, analogous to a flexor reflex; however, this response was usually followed by a “rebound” response consisting of hip extension, knee flexion and ankle plantarflexion, occurring in 10/13 subjects. Stimuli applied in a more lateral (mid thigh) electrode position (i.e. over the rectus femoris) were less effective in producing the response than medial placement, despite vigorous quadriceps activation. This complex reflex response is consistent with activation of a coordinating spinal circuit that could play a role in motor function. The reversal of the reflex pattern emphasizes the potential connection between skin/muscle afferents of the thigh, possibly including sartorius muscle afferents and locomotor reflex centers. This knowledge may be helpful in identifying rehabilitation strategies for enhancing gait training in human SCI.     

Altered activation patterns by triceps surae stretch reflex pathways in acute and chronic spinal cord injury

Spinal reflexes are modified by spinal cord injury (SCI) due the loss of excitatory inputs from supraspinal structures and changes within the spinal cord. The stretch reflex is one of the simplest pathways of the central nervous system and was used presently to evaluate how inputs from primary and secondary muscle spindles interact with spinal circuits before and after spinal transection (i.e., spinalization) in 12 adult decerebrate cats. Seven cats were spinalized and allowed to recover for 1 mo (i.e., chronic spinal state), whereas 5 cats were evaluated before (i.e., intact state) and after acute spinalization (i.e., acute spinal state). Stretch reflexes were evoked by stretching the left triceps surae (TS) muscles. The force evoked by TS muscles was recorded along with the activity of several hindlimb muscles. Stretch reflexes were abolished in the acute spinal state due to an inability to activate TS muscles, such as soleus (Sol) and lateral gastrocnemius (LG). In chronic spinal cats, reflex force had partly recovered but Sol and LG activity remained considerably depressed, despite the fact that injecting clonidine could recruit these muscles during locomotor-like activity. In contrast, other muscles not recruited in the intact state, most notably semitendinosus and sartorius, were strongly activated by stretching TS muscles in chronic spinal cats. Therefore, stretch reflex pathways from TS muscles to multiple hindlimb muscles undergo functional reorganization following spinalization, both acute and chronic. Altered activation patterns by stretch reflex pathways could explain some sensorimotor deficits observed during locomotion and postural corrections after SCI.     

Neurophysiological examination of the corticospinal system and voluntary motor control in motor-incomplete human spinal cord injury

This study employed neurophysiological methods to relate the condition of the corticospinal system with the voluntary control of lower-limb muscles in persons with motor-incomplete spinal cord injury. It consisted of two phases. In a group of ten healthy subjects, single and paired transcranial magnetic stimulation (TMS) of the motor cortex was used to study the behavior of the resulting motor evoked potentials (MEP) in lower-limb muscles. Interstimulus intervals (ISIs) of 15–100 ms were examined for augmentation of test MEPs by threshold or subthreshold conditioning stimuli. The second phase of this study examined eight incomplete spinal cord injured (iSCI) subjects, American Spinal Injury Association Impairment Scale C (n =5) and D (n =3) in whom voluntary motor control was quantified using the surface EMG (sEMG) based Voluntary Response Index (VRI). The VRI is calculated to characterize relative output patterns across ten lower-limb muscles recorded during a standard protocol of elementary voluntary motor tasks. VRI components were calculated by comparing the distribution of sEMG in iSCI subjects with prototype patterns collected from 15 healthy subjects using the same rigidly administered protocol, The resulting similarity index (SI) and magnitude values provided the measure of voluntary motor control. Corticospinal system connections were characterized by the thresholds for MEPs in key muscles. Key muscles were those that function as the prime-movers, or agonists for the voluntary movements from which the VRI data were calculated. Results include healthy-subject data that showed significant increases in conditioned MEP responses with paired stimuli of 15–50 ms ISI. Stimulus pairs of 75 and 100 ms showed no increase in MEP peak amplitude over that of the single-pulse conditioning stimulus alone, usually no response. For the iSCI subjects, 42% of the agonists responded to single-pulse TMS and 25% required paired-pulse TMS to produce an MEP. American Spinal Injury Association Impairment Scale component motor scores for agonist muscles, Quadriceps, Tibialis Anterior, and Triceps Surae, were significantly lower where MEPs could not be obtained (p <0.05). VRI values were also significantly lower for motor tasks with agonists that had no resting MEP (p <0.01). Therefore, the presence of a demonstrable connection between the motor cortex and spinal motor neurons in persons with SCI was related to the quality of post-injury voluntary motor control as assessed by the VRI.     

Some features of the stretch reflex after spinal cord injury

The object of the investigation was to study correlation between the state of the spinal reflex apparatus in spinal patients and the presence or absence of clonus. The magnitude of the electrical response of the soleus muscle to passive dorsiflexion of the angle at different speeds was studied. Clonus took place in 10 patients (group 1) and was absent in another 12 patients (group 2). Ten healthy subjects served as the control group. A considerable difference was found in the curves of distribution of magnitude of the responses for the different groups of subjects. Characteristically the patients of group 1 showed a shift of the model to the right, but the patients of group 2 showed a shift to the left compared with the mode to healthy subjects. The same pattern was found regardless of the angular velocity studied. The threshold velocity in the patients of group 2 was significantly higher than normal, whereas in the patients of group 1 it was close to normal. Activity in the calf muscles and ability to move about or even to walk were observed in most patients of group 1 but in only a few patients of group 2. It is suggested that the presence of clonus corresponds to a more normal state of the spinal reflex apparatus and to better clinical indices than in patients without clonus.Institute for Problems in Information Transmission, Academy of Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR, V. S. Rusinov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 3, pp. 207–209, March, 1979.     

The tonic stretch reflex and spastic hypertonia after spinal cord injury

The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is not equivalent and care should be taken in generalizing results between them.     

Locomotor and reflex adaptation after partial denervation of ankle extensors in chronic spinal cats

This work investigates the capacity of the spinal cord to generate locomotion after a complete spinal section and its ability to adapt its locomotor pattern after a peripheral nerve lesion. To study this intrinsic adaptive capacity, the left lateral gastrocnemius-soleus (LGS) nerve was sectioned in three cats that expressed a stable locomotion following a complete spinal transection. The electromyograph (EMG) of multiple hindlimb muscles and reflexes, evoked by stimulating the left tibial (Tib) nerve at the ankle, were recorded before and after denervation during treadmill locomotion. Following denervation, the mean amplitude of EMG bursts of multiple hindlimb muscles increased during locomotion, similar to what is found after an identical denervation in otherwise intact cats. Reflex changes were noted in ipsilateral flexors, such as semitendinosus and tibialis anterior, but not in the ipsilateral knee extensor vastus lateralis following denervation. The present results demonstrate that the spinal cord possesses the circuitry necessary to mediate increased EMG activity in multiple hindlimb muscles and also to produce changes in reflex pathways after a muscle denervation. The similarity of changes following LGS denervation in cats with an intact and transected spinal cord suggests that spinal mechanisms play a major role in the locomotor adaptation.     

Fatigue properties of human thenar motor units paralysed by chronic spinal cord injury

Human muscles paralysed chronically by spinal cord injury (SCI) fatigue excessively. Whether these reductions in force reflect a decrease in the fatigue resistance of the motor units is unknown. Our aim was to determine the fatigability of thenar motor units paralysed chronically (10 ± 2 years) by cervical SCI. Surface electromyographic activity (EMG) and force were recorded from 17 paralysed motor units ( n = 7 subjects) in response to intraneural motor axon stimulation (13 pulses at 40 Hz, 1 s⁻¹ for 2 min). Unit force decreased progressively, reaching 8–60% of initial after 2 min, whereas both the amplitude and area of the first EMG potentials in the trains increased significantly (both P < 0.05). Thus, transmission of neural signals to the sarcolemma was effective and the reduction in force must reflect impaired processes in the muscle fibres. The median fatigue index for paralysed units (0.31), the ratio of the force at 2 min compared to the initial force, was significantly lower than that for units from control subjects (0.85, P < 0.05), but the distribution of fatigue indices for each population had a similar shape (ranges: 0.08–0.60 and 0.41–0.95, respectively). Hence, chronic paralysis did not limit the range of fatigability typically found for thenar units, only its magnitude. These findings suggest that all paralysed units underwent similar reductions in fatigue resistance. After fatigue, paralysed unit forces were reduced at all frequencies (1–100 Hz, P < 0.05). Twitch contraction and half-relaxation times were increased, as was the frequency needed to produce half maximal force ( P < 0.05). Thus, stimulation protocols used to produce functional movements in paralysed muscles need to accommodate the significant and rapid fatigue of the motor units.     

Motor unit firing during and after voluntary contractions of human thenar muscles weakened by spinal cord injury

Spinal cord injury may change both the distribution and the strength of the synaptic input within a motoneuron pool and therefore alter force gradation. Here, we have studied the relative contributions of motor unit recruitment and rate modulation to force gradation during voluntary contractions of thenar muscles performed by five individuals with chronic (>1 yr) cervical spinal cord injury. Mean +/- SD thenar unit firing rates were low during both steady-level 25% (8.3 +/- 2.2 Hz, n = 27 units) and 100% maximal voluntary contractions (MVCs, 9.2 +/- 3.1 Hz, n = 23 units). Thus modest rate modulation, or a lack of it in some units, was seen despite an average fourfold increase in integrated surface electromyographic activity and force. During ramp contractions, units were recruited at 5.7 +/- 2.5 Hz, but still only reached maximal firing rates of 12.8 +/- 4.9 Hz. Motor units were recruited up to 85% of the maximal force achieved (14.6 +/- 5.6 N). In contrast, unit recruitment in control hand muscles is largely complete by 30% MVC. Thus, during voluntary contractions of thenar muscles weakened by cervical spinal cord injury, motor unit rate modulation was limited and recruitment occurred over a wider than usual force range. Those motor units that were stopped voluntarily had significantly lower derecruitment versus recruitment thresholds. However, 8 units (24%) continued to fire long after the signal to end the voluntary contraction at a mean frequency of 5.9 +/- 0.8 Hz. The forces generated by this prolonged unit activity ranged from 0.3 to 7.2% maximum. Subjects were unable to stop this involuntary unit activity even with the help of feedback. The mechanisms that underlie this prolonged motor unit firing need to be explored further.     

Response characteristics of spinal cord dorsal horn neurons in chronic allodynic rats after spinal cord injury

The physiological mechanisms of chronic pain in patients with spinal cord injury (SCI) are poorly understood. In the present study, we explored response characteristics of dorsal horn neurons of spinally injured rats exhibiting chronic pain (pain-like response to innocuous mechanical and cold stimulation). Several abnormalities were found in the distribution and response characteristics of dorsal horn neurons in chronic allodynic rats. First, 17% of the recorded neurons (vs. 0% in control animals) had no receptive field. Most of these units were located at or close to the lesioned spinal segment, and they discharged spontaneously at high frequencies. Allodynic rats also showed a significant decrease in the proportion of low-threshold (LT) neurons and an increase in the proportion of wide dynamic range (WDR) neurons. The rate of spontaneous activity of high-threshold (HT) neurons was significantly higher in allodynic compared with control rats. Moreover, HT neurons in allodynic animals showed increased neuronal responses to mechanical stimulation. WDR neurons responded with higher discharge rates to innocuous von Frey hair stimulation in allodynic compared with control rats. The percentage of WDR and HT neurons showing afterdischarges to noxious pinch was also significantly increased in the allodynic rats. The proportion of WDR and HT neurons responding to innocuous cold stimulation respectively increased from 53 and 25% in control rats to 91 and 75% in allodynic animals. These results suggest that the chronic pain-like behaviors in spinally injured rats may be generated and maintained by abnormalities in dorsal horn neurons.     

Motor unit discharge characteristics during voluntary contraction in patients with incomplete spinal cord injury

Synchronisation of motor unit discharges is commonly seen in hand muscles of normal man but is absent following neurologically complete spinal cord injury and reduced after stroke. These findings support the notion that some corticospinal inputs to motoneurones are shared and contribute to the observed synchrony of discharge. In this study we have examined motor unit discharge in hand muscles below the level of an incomplete spinal cord injury in an attempt to relate strength of synchrony to the integrity of the corticospinal tract. Eight patients with incomplete spinal cord injury (neurological level C3-C7) and eight control subjects took part in the study. The patients had sustained injury 14-191 weeks prior to the recordings and had since regained good motor function in their hands. Two concentric needle electrodes were inserted into the first dorsal interosseus muscle which subjects were instructed to contract weakly so that potentials from individual motor units could be reliably identified on both recordings. Synchrony was detected by constructing cross-correlograms between the discharges of pairs of individual motor units. The amount of synchronous firing was determined from the magnitude of any peak in the cross-correlogram, as the probability above chance (XP) of one motor unit firing with respect to the other and vice versa. The degree of synchrony was lower (P < 0.05) in the patient group (mean XP 0.06) than in the control group (mean XP 0.09). The incidence of significant synchrony was lower in the patient group (41.8 %) than in the control group (92.9 %). The mean (+/- S.E.M.) frequency of motor unit discharge was slightly lower (P < 0.05) in patients (9.7 +/- 0.4 impulses s-1) than controls (10.8 +/- 0.5 impulses s-1). The mean width of synchrony peaks was narrower (P < 0.05) in patients (11.4 +/- 1.1 ms) than controls (13.2 +/- 0.6 ms). We conclude that the weaker synchrony of motor unit discharge in incomplete spinal cord injury may reflect permanent damage to some corticospinal axons.     

Mental stress inhibits pain perception and heart rate variability but not a nociceptive withdrawal reflex

AIM: Do distraction from- or attention to sural nerve stimulation affect pain, heart rate variability, and a spinal withdrawal reflex? MATERIAL AND METHODS: In 26 male volunteers, electrical stimulation at the distal cutaneous receptive field of the sural nerve elicited pain and a nociceptive withdrawal reflex. Intensity of pain was rated on a numeric rating scale. Electromyographic reflex responses were measured from biceps femoris muscle. Cardiac autonomic function was estimated by heart rate variability measures and was expressed in the time domain as mean of RR-intervals for normal heart beats (mean-RR) and standard deviation of all normal RR-intervals (SD-NN) and, in the frequency domain, where pure vagal activity was assessed by high frequency power (0.15-0.4 Hz). Low frequency power (0.04-0.15 Hz) reflects both parasympathetic and sympathetic control. Effect parameters were recorded before and during random distraction and attention. Distraction from sural nerve stimulation was induced by a mental arithmetic test, paced auditory serial addition task (PASAT), while attention was induced by concentrating on painful foot stimulation. RESULTS: Paced auditory serial addition task decreased mean-RR and SD-NN, frequency domain parameters, as well as pain (P<0.001). In contrast, PASAT did not change the spinal withdrawal reflex. Attention did not affect any effect parameter. CONCLUSION: Distraction by PASAT altered autonomic activity and inhibited pain but failed to affect withdrawal reflex responses, while attention had no effect on either parameter. Psychological distraction and attention may have different effects on noxious evoked pain perception and autonomic activity. Pain relief during PASAT probably involves supraspinal mechanisms.