Search

The neural mechanisms of walking impairment after stroke are not well characterized. Specifically, there is a need for understanding the mechanisms of impaired plantarflexor power generation in late stance. Here, we investigated the association between two neurophysiologic markers, the long-latency reflex (LLR) response and dynamic facilitation of antagonist motor-evoked responses, and walking function. Fourteen individuals with chronic post-stroke hemiparesis and thirteen healthy controls performed both isometric and dynamic plantarflexion. Transcranial magnetic stimulation (TMS) assessed supraspinal drive to the tibialis anterior. LLR activity was assessed during dynamic voluntary plantarflexion and individuals post-stroke were classified as either LLR present (LLR+) or absent (LLR-). All healthy controls and nine individuals post-stroke exhibited LLRs, while five did not. LLR+ individuals revealed higher clinical scores, walking speeds, and greater ankle plantarflexor power during walking compared to LLR- individuals. LLR- individuals exhibited exaggerated responses to TMS during dynamic plantarflexion relative to healthy controls. The LLR- subset revealed dysfunctional modulation of stretch responses and antagonist supraspinal drive relative to healthy controls and the higher functioning LLR+ individuals post-stroke. These abnormal physiologic responses allow for characterization of individuals post-stroke along a dimension that is clinically relevant and provides additional information beyond standard behavioral assessments. These findings provide an opportunity to distinguish among the heterogeneity of lower extremity motor impairments present following stroke by associating them with responses at the nervous system level.

Spinal reciprocal inhibition (RI) and intracortical inhibition are important physiological mechanisms for voluntary movement control and functional recovery of voluntary movement in patients with stroke. Spasticity, which impairs motor performance, is one of the major manifestations of stroke. RI may be involved in reducing spasticity. This might allow finger extension, and, therefore, better hand function by reducing co-contraction with finger extensors. One potential mechanism of functional reorganization of the motor cortex is that pre-existing masking pathways are unmasked by decreased intracortical inhibition. The inhibitory neurotransmitter GABA plays an important role in this process. Changes in RI might be mediated through unmasking of cortical pathways through decreased inhibition, with the neurotransmitter GABA. These changes can be assessed using short-latency intracortical inhibition (SICI) and RI. Functional recovery in the chronic phase of stroke induced by rehabilitation was accompanied by SICI and spinal RI changes. Cortical reorganization and spinal plasticity might play important roles in functional recovery induced by rehabilitation, even in patients with chronic severe hemiparesis. This review aims to provide a focused overview of neuroplasticity of spinal RI and intracortical inhibition associated with functional motor recovery from stroke. [ABSTRACT FROM AUTHOR]

Spasticity is a common problem in patients with stroke that contributes to motor dysfunction. However, the pathophysiological mechanisms underlying spasticity are not fully understood. The purpose of the present study was to explain the relationship between features of spinal neural circuits assessed using electrophysiological techniques and the clinical manifestations of stroke. The participants were 71 patients with chronic hemiparetic stroke. To assess spinal neural circuits, Hmax/Mmax of the forearm flexor muscles and reciprocal inhibition (RI) between forearm extensor and flexor muscles with the H reflex conditioning-test paradigm were measured. The relationships between electrophysiological parameters and clinical variables (age, time from stroke onset, upper extremity functional scores, and spasticity) were then analyzed. It was found that the third phase of RI (RI-3) correlated with the modified Ashworth scores of the wrist and finger flexors. No other correlations were found between electrophysiological and clinical measures. These results suggest that RI-3 is associated with spasticity and may be helpful to understand the basis of post-stroke spasticity. [ABSTRACT FROM AUTHOR]

Recent studies have shown that afferents arising from muscle receptors located on one side can affect the activity of muscles on the contralateral side. In animal preparations, evidence supports that afferent pathways originating from one limb converge onto interneurons mediating disynaptic reciprocal Ia inhibition of the opposite limb. This study was designed to investigate whether this pathway is similar in humans to that described in animals. Thirteen healthy volunteers participated in one of two experiments. In experiment 1, the effects of ipsilateral posterior tibial nerve (iPTN) stimulation were assessed on the reciprocal Ia inhibition of the contralateral soleus (cSOL) motoneuronal pool ( n = 8). Across all participants, iPTN stimulation intensity was 1.69 ± 0.3 × Motor Threshold (MT) and contralateral common peroneal (cCPN) stimulation intensity was 0.86 ± 0.16 × MT. iPTN and cCPN stimulation were delivered separately or in combination and changes in the ongoing electromyography (EMG) quantified. In experiment 2, the amplitude of a test SOL H-reflex elicited by contralateral PTN (cPTN) stimulation was quantified following iPTN, cCPN or iPTN + cCPN nerve stimulation ( n = 5). Intensities used during the H-reflex conditioning experiment were 1.79 ± 0.4 × MT for the iPTN stimulation and 0.88 ± 0.16 × MT for cCPN stimulation. Across all participants, the onset of the cSOL EMG suppression was 42 ± 4, 44 ± 3 and 44 ± 3 ms for iPTN, cCPN and iPTN + cCPN conditions, respectively. The inhibition from the combined iPTN and cCPN stimulation was significantly greater compared to the algebraic sum of their separate effects. When conditioning the cSOL H-reflex, the ISI between the test cPTN and the iPTN or cCPN stimulus was 5.4 ± 0.5 and 2.6 ± 0.5, respectively. The combined stimulation induced a significantly greater inhibition compared to their separate effects. These data provide evidence of convergence on common inhibitory interneurons by muscle afferents activated by iPTN and cCPN stimulation during sitting. Since the inhibition elicited by cCPN stimulation is known to be mediated by the disynaptic Ia inhibitory pathway, this suggests that the crossed inhibition of cSOL motoneurones elicited by muscle afferents from the ipsilateral plantarflexor muscles is at least partly mediated by Ia inhibitory interneurons in the contralateral human spinal cord. This is similar to what has been observed in the cat. [ABSTRACT FROM AUTHOR]

Rotation of an upper limb joint produces excitatory stretch reflex peaks M1 and M2 in the stretched muscles and simultaneous decrease in electromyographic (EMG) activity in the shortened muscles. The objective of this study was to examine whether the decreased activity in the antagonists (rINHIB) is purely from unloading of the spindles or receives active inhibition involving inhibitory interneurons. If rINHIB is due only to unloading, then the termination of rINHIB should vary with the duration of perturbation used to elicit stretch reflex, namely shorter stretches should result in shorter values of decreased periods of EMG. To examine this question, rectangular pulses, ranging in duration from 25 to 150 ms, were used to stretch wrist flexors or extensors with a torque motor. These rectangular pulses resulted in joint rotations which peaked at times ( T) ranging from approximately 75-160 ms. As shown by previous authors, when the duration of rotation was shortened, the magnitude of M1 did not change, while the magnitude of M2 decreased. However, termination time of rINHIB in the shortened muscles did not change with change in T, implying thereby that unloading of spindles of the antagonist muscles is not the only mechanism for the reduction in activity and that inhibitory reflex pathways most likely contribute. Possible sources of inhibition are discussed for the short- and long-latency inhibition. [ABSTRACT FROM AUTHOR]

If reduced reciprocal inhibition plays a causal role in the pathophysiology of spasticity as has been suggested in several studies, the inhibition is expected to be impaired in spastic, but not in normal muscles. Patients with neurolathyrism offer a possibility of testing this prediction since the spastic symptoms in these patients are restricted to the lower extremities only. Three patients with neurolathyrism were tested. Their data were compared with 15 age-matched healthy subjects. All patients showed signs of spasticity in the legs. Two patients had normal voluntary muscle force in the lower extremities and one had decreased force. No clinical abnormalities were found in the upper extremities. Reciprocal inhibition between ankle dorsiflexor and plantarflexor muscles was absent in all patients, whereas the inhibition between wrist extensor and flexor muscles was present and of normal size and latency. These findings are consistent with the hypothesis that reduced reciprocal inhibition plays a causal role in the pathophysiology of spasticity. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate short-term effects of walking with functional electrical stimulation (FES) on inhibitory and excitatory spinal reflexes in healthy subjects. The FES was applied to the common peroneal (CP) nerve during the swing phase of the step cycle when the ankle flexors are active. We have previously shown that corticospinal excitability for the tibialis anterior (TA) muscle increased after 30 min of FES-assisted walking. An increase of corticospinal excitability could be due to the changes in spinal and/or cortical excitability. Thus, we wished to examine whether a short-term application of FES would increase spinal motoneuronal excitability. Changes could also result from effects on inhibitory as well as excitatory pathways, but to our knowledge no studies have investigated short-term effects of FES on spinal inhibitory pathways. Therefore, we measured reciprocal and presynaptic inhibition, as well as reflex excitability, before and after FES-assisted walking. As controls, effects of FES-like stimulation at rest and walking without stimulation were tested in separate sessions. The TA H-reflex amplitude did not increase after FES in any of the conditions tested, so we have no evidence that FES increases spinal excitability for the TA. The soleus H-reflex decreased slightly (10%) after FES-assisted walking, and remained decreased for at least 30 min. However, the control experiment indicated that this decrease was associated with walking and not with stimulation. Thirty minutes of FES did not produce any significant effects on spinal inhibitory pathways examined in the present study. In conclusion, the soleus H-reflex showed a small but consistent decrease and no spinal circuits examined showed an increase, as was observed in the corticospinal excitability. Thus, we suggest that a short-term application of FES increases the excitability of the cortex or its connections to the spinal cord more effectively than that of spinal pathways. [ABSTRACT FROM AUTHOR]

The present studies are designed to further characterise the interneuronal pathway mediating the disynaptic reciprocal group I inhibition between flexors and extensors at the wrist and the elbow levels in humans. In the first series of experiments, we compared the electrical threshold of the reciprocal group I inhibition at the wrist and the elbow level after a prolonged vibration aimed at raising the electrical threshold of the antagonistic activated Ia afferents. Prolonged vibration to the ‘conditioning’ tendon, which raised significantly the electrical threshold of the inhibition at the elbow level, did not alter it at the wrist level. These results suggest that the dominant input to the relevant interneurones is Ia in origin at the elbow level but Ib in origin at the wrist level. In the second series of experiments, using the spatial facilitation method, we compared the effects on the post-stimulus time histograms of single voluntarily activated motor units of two volleys delivered both separately and together to group I afferents in the nerves supplying the homonymous and antagonistic muscles. At the wrist, but not at the elbow level, the peak of homonymous monosynaptic group I excitation was reduced on combined stimulation, although the antagonistic IPSP was just at the threshold. Because the suppression did not involve the initial bins of the peak, it is argued that the suppression is not due to presynaptic inhibition of Ia terminals, but probably reflects convergence between the homonymous and antagonistic volleys onto the interneurones mediating the disynaptic inhibition. Taken together with the previously reported effects of recurrent inhibition on reciprocal inhibition, these results suggest that inhibition between flexors and extensors is differently organised at the elbow (reciprocal Ia inhibition) and the wrist (non-reciprocal group I inhibition) levels. It is argued that the particular connectivity at the wrist level might correspond to some functional requirements at this ball joint. [ABSTRACT FROM AUTHOR]

Repetitive transcranial magnetic stimulation (rTMS) has been shown to induce adaptations in cortical neuronal circuitries. In the present study we investigated whether rTMS, through its effect on corticospinal pathways, also produces adaptations at the spinal level, and what the neuronal mechanisms involved in such changes are. rTMS (15 trains of 20 pulses at 5 Hz) was applied over the leg motor cortical area in ten healthy human subjects. At rest motor evoked potentials (MEPs) in the soleus and tibialis anterior muscles were facilitated by rTMS (at 1.2×MEP threshold). In contrast, the soleus H-reflex was depressed for 1 s at stimulus intensities from 0.92 to 1.2×MEP threshold. rTMS increased the size of the long-latency depression of the soleus H-reflex evoked by common peroneal nerve stimulation and decreased the femoral nerve facilitation of the soleus H-reflex. These observations suggest that the depression of the H-reflex by rTMS can be explained, at least partly, by an increased presynaptic inhibition of soleus Ia afferents. In contrast, rTMS had no effect on disynaptic reciprocal Ia inhibition from ankle dorsiflexors to plantarflexors. We conclude that a train of rTMS may modulate transmission in specific spinal circuitries through changes in corticospinal drive. This may be of relevance for future therapeutic strategies in patients with spasticity. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the contribution of reciprocal inhibition to muscle tone by examining the transmission in the reciprocal inhibitory pathway in patients with a known defect in the glycine receptor. The study was performed in eight patients with hereditary hyperekplexia, six with the major form and two with the minor form of the disease. A mutation in the α1-subunit of the glycine receptor had been demonstrated in the patients with the major form, whereas no mutation was seen in the patients with the minor form. Disynaptic reciprocal inhibition, which is presumed to be mediated by glycine, was not seen in the patients with the major form of the disease, while it could be evoked in the patients with the minor form of the disease. Presynaptic inhibition, which is presumed to be mediated by GABA, was seen in both types of patients. It is concluded that the major form of hereditary hyperekplexia is associated with impaired transmission in glycinergic reciprocal inhibitory pathways. The findings demonstrate the importance of reciprocal inhibition for the muscle tone in man, and it is suggested that the impaired reciprocal inhibition seen in patients with a defect in the glycine receptor may contribute to the increased muscle stiffness that is observed in these patients. [ABSTRACT FROM AUTHOR]

Activation of a motoneuron pool is often accompanied by inhibition of the antagonistic pool through a system of reciprocal inhibition between the two parts of the neuronal network controlling the antagonistic pools. In the present study, we describe the activity of such a system in the isolated spinal cord of the lamprey, when a tonic motor output is evoked by extracellular stimulation (0.5–1 s train of pulses, 20 Hz) of either end of the spinal cord. With two electrodes symmetrically positioned in relation to the midline, stimulation with either of them separately elicited prolonged (1–5 s) ipsilateral ventral root activity. Activity could be abolished by stronger, simultaneously applied, stimulation of the contralateral side of the cord, suggesting that reciprocal inhibition between hemisegments operates when a tonic motor output is generated. Simultaneous stimulation of both sides of the spinal cord with a single electrode with a large tip (300–400 µm in diameter), positioned over the anatomical midline, elicited inconsistent right-side, left-side, or bilateral ventral root responses. A minor displacement (10–20 µm) to the left or right from the midline resulted in activation of ipsilateral motoneurons, whereas the contralateral motoneurons were silent. These findings indicate that a small asymmetry in the excitatory drive to the left and right spinal hemisegments can be further amplified by reciprocal inhibition between the hemisegments. Longitudinal splitting of the spinal cord along the midline resulted in reduced reciprocal inhibition between the hemisegments separated by the lesion. The reduction was proportional to the extent of the split. The inhibition was abolished when the split reached nine segments in length. From these experiments, the longitudinal distribution of the commissural axons responsible for inhibition of contralateral motor output could be estimated. [ABSTRACT FROM AUTHOR]

The question of whether Ia reciprocal inhibition might depend on the motor task and on the type of motor unit activated was investigated in the human extensor carpi radialis muscles. Ia reciprocal inhibition induced by stimulating the median nerve (conditioning stimulation) was estimated by measuring the changes in the firing probability of 37 extensor motor units in response to the radial nerve stimulation (100 test stimuli) delivered 1 ms after the conditioning stimulation. Six subjects were asked to perform a task consisting of either selectively contracting their wrist extensor muscles or co-activating their wrist and finger antagonist muscles by clenching their hand around a manipulandum. In the control recordings (test stimulation alone), the mean response probability of the 37 motor units was found to be greater during hand clenching. The motor units were identified on the basis of their force thresholds, their macro-potentials, and their twitch contraction times. The data obtained in the control recordings were consistent with the size principle. In the recordings where the responses were conditioned by applying median nerve stimulation, the response probability of the motor units with low force thresholds, small macro-potential areas, and long twitch contraction times tended to decrease, in line with the presence of Ia reciprocal inhibition, whereas the response probability of the motor units with higher force thresholds, larger macro-potential areas, and shorter twitch contraction times tended to increase. The median nerve stimulation may therefore have altered the efficiency with which the extensor Ia inputs recruited the homonymous motoneurones in the pool. The flexor group I afferents activated while the median nerve was stimulated had inhibitory effects on the slow contracting motor units, and facilitatory effects mainly on the fast contracting motor units. Both of these effects were stronger during hand clenching, in which the numerous cutaneous receptors of the palm and fingertips are liable to be activated. Besides their own effects on the excitability of the various types of motor units, cutaneous inputs are known to potentiate the Ib interneurones. In addition, the effects of the conditioning stimulation were superimposed on the tonic activity of the Ia and Ib afferents from the flexor wrist and finger muscles. This may explain why both the inhibitory and facilitatory effects of the median nerve stimulation were enhanced during hand clenching. [ABSTRACT FROM AUTHOR]

Reciprocal inhibition of the voluntarily contracting wrist extensor (extensor carpi radialis, ECR) evoked by proprioceptive afferent input from the flexor (flexor carpi radialis, FCR), was studied in healthy human subjects. Vibration of the FCR tendon was used to elicit Ia-dominated afferent discharge whilst inhibition of ECR was assessed as the reduction in asynchronous, on-going EMG. A small early phase of inhibition (I1) was evident in 25% of trials. The latency (ca. 25 ms) of this component suggested that it was mediated by an Ia oligosynaptic, possibly 'classical' disynaptic, inhibitory pathway. A later and apparently separate phase of reduced activity (12, ca. 40 ms) was, however, far more consistently observed (96% of trials) and of greater magnitude. The 12 component was usually followed, some 20 ms later, by a phase of elevated activity (El, 72% trials). Reductions in simultaneously recorded net extensor torque commenced at about 60 ms following the onset of flexor tendon vibration, i.e. some 20 ms after the main I2 EMG component. These mechanical responses must have almost exclusively resulted from reciprocal inhibition of extensor EMG since vibration of the relaxed FCR evoked minimal excitatory flexor activity. The reflex pattern, in any individual subject, was relatively unaffected by altering the duration of the vibration train between one and nineteen cycles (125 Hz). This suggests that the entire response complex resulted largely from the initial afferent volley. The sizes of both the I1 and I2 reductions in ECR activity increased with increasing voluntary extensor contraction so that their depths remained constant proportions of background EMG. Very similar results were obtained when reciprocal inhibition of FCR was produced by vibration of the belly of ECR. Thus, reciprocal inhibition between wrist muscles is mainly expressed as a rather stereotyped, short duration reduction in EMG whose depth is determined by the pre-existing level of motor activity. Some functional implications of this form of reflex behaviour are discussed. [ABSTRACT FROM AUTHOR]

A long lasting inhibition (> 8 s) of the soleus Hoffmann reflex (H-reflex) was evoked by a preceding soleus H-reflex, by a brief voluntary ankle flexor or extensor muscle contraction or by a tap applied to the Achilles tendon. The time course of this long lasting inhibition was similar in all these cases, suggesting that the same spinal mechanism is involved. Furthermore, it was shown that the post-activation depression may interfere with the determination of inhibitory or facilitatory effects on the H-reflex. It is stressed that when the onset of inhibitory or facilitatory effects on the soleus H-reflex is to be determined in relation to start of an ankle movement, either very long stimulus intervals (> 8 s) must be used, or the onset must be determined in relation to a reference value of the soleus H-reflex, which may be influenced by the long lasting inhibitory effect, but not yet by the succeeding muscle contraction. [ABSTRACT FROM AUTHOR]

Variations of presynaptic inhibition in heteronymous Ia fibres projecting to soleus motoneurones were studied during the first 250 ms of phasic voluntary isometric contractions of the antagonist tibialis anterior muscle in human subjects. During the first 60-80 ms of TA e.m.g activity, presynaptic inhibition was often more marked than at rest, but not in all experimental sessions. After 60-80 ms, presynaptic inhibition was always increased compared to rest and to the onset of TA e.m.g. activity. A 'rebound' in femoral nerve induced Ia facilitation was often observed between 90-150 ms. The early increase in presynaptic inhibition was widespread and non specific since it was observed at the onset of extensor carpi radialis contractions of maximal strength. The 'rebound' in heteronymous Ia facilitation was interpreted as a relative decrease in presynaptic inhibition to which nonspecific suprasegmental and cutaneous effects contributed. The late increase in presynaptic inhibition in Ia fibers to soleus motoneurones was considered as reciprocally inhibiting the Sol H-reflex, thus counteracting the phasic stretch of the antagonist muscle during TA contraction. [ABSTRACT FROM AUTHOR]

Changes in the firing probability of single motor units in response to electrical stimulation of muscle nerves and to tendon taps were used to derive the projections of large muscle afferents to the motoneurons of various thigh muscles in man. Homonymous facilitation was demonstrated to virtually all of the sampled motor units of biceps (BI), semitendinosus (ST), vastus lateralis (VL) and vastus medialis (VM). Heteronymous facilitation was readily demonstrated between VM and VL but was never obtained from ST to BI and never unequivocally obtained from BI to ST. Reciprocal inhibition was demonstrated from femoral nerve afferents to all of the sampled units of BI, and ST but reciprocal inhibition of VM or VL was never obtained from BI afferents and infrequently from ST afferents. These projections of group I afferents in man show certain specific differences from those of the cat and baboon that may reflect the normal function of the limb. [ABSTRACT FROM AUTHOR]

Reciprocal inhibition from the anterior tibial muscle onto antagonist motoneurones of the soleus muscle was studied in normal man under control conditions and after low intensity stimulation of cutaneous afferent fibres from the sole and dorsal region of the ipsilateral and contralateral foot. Ipsilateral cutaneous stimulation increased the reciprocal inhibition to the soleus motoneurones, without qualitative differences between the effect from the sole and that from the dorsal region of the foot. Stimulation of cutaneous afferent fibres from the contralateral foot produced the reverse effect, i.e., depression of the Ia reciprocal inhibition from the tibialis anterior to the soleus motoneurones. No effects could be observed when cutaneous areas other than those of the foot were stimulated. The effects of cutaneous stimulation on the reciprocal inhibition became evident only when this inhibition approached its maximum and, thus, they most strongly influenced its recovery phase. Since cutaneous stimulation does not modify the test reflex when given alone, it is likely that there must be convergence on common premotoneuronal interneurones. Indirect evaluation of central delay suggests that the cutaneous afferent fibres from the foot have oligosynaptic spinal connections with interneurones belonging to the group I pathways to the antagonists. Our findings furnish additional evidence that short-latency inhibition of soleus motoneurones after a single conditioning stimulation of group I afferents from the tibialis anterior muscle constitutes a true example of disynaptic Ia reciprocal inhibition in man. [ABSTRACT FROM AUTHOR]

Reciprocal innervation of the soleus motoneurones upon initiation of voluntary ankle dorsiflexion was investigated in eight patients with Parkinson's disease. H-reflex and visually guided step tracking methods were used for testing moto-neurone excitability and for controlling the timing of movement initiation, respectively. While reciprocal inhibition appeared almost simultaneously with the agonist electromyographic (EMG) onset in normal subjects (Kagamihara and Tanaka 1985), facilitation appeared in the majority of patients under the same onset condition. It increased slowly, reaching a maximum at about 100 ms after the EMG onset. It then subsided slowly at around 200-300 ms, and was replaced thereafter by an inhibitory effect. No coactivation of the soleus muscle was detected electromyographically. The facilitation between the EMG onset and the onset of mechanical contraction was attributed to the direct effect of the descending command from the brain, suggesting a certain disorder in controlling the system for reciprocal innervation. [ABSTRACT FROM AUTHOR]

We studied the potential contribution of postsynaptic mechanisms to the depression of reflex excitability which occurs immediately after a voluntary release from tonic muscle contraction. The excitability of the Soleus (Sol) motor pool was tested at rest and after voluntary muscle relaxation. In both cases the Sol H-reflex was conditioned by 1. a single shock to the peroneal nerve, in order to activate the Ia interneurones (INs) mediating the reciprocal inhibition via a peripheral input, or by 2. a short-lasting voluntary contraction of the Tibialis Anterior (TA) muscle, to activate the Ia INs via a central command. Changes in excitability of Renshaw cells were also tested at rest and after release, to assess the role of recurrent inhibition in the release-induced inhibition of the Sol H-reflex. It was demonstrated that: 1. the excitability of the INs mediating the reciprocal inhibition was only slightly enhanced in comparison with resting conditions; 2. the H-reflex of the antagonist muscle (TA) evoked after Sol release was not consistently facilitated with respect to rest; 3. the command to contract the TA muscle reduced the H-reflex of the Sol muscle during rest but not after Sol release; 4. recurrent inhibition did not increase its effect in the post-release period. Such features suggest that recurrent and reciprocal post-synaptic inhibitions do not play a major role in reducing the reflex excitability of a relaxing muscle; rather, the command to release prevents the reciprocal inhibitory effect which accompanies the contraction of the antagonist muscle. The findings support the concept that release-induced reflex depression is mediated mainly by presynaptic inhibition of autogenetic spindle afferences (Schieppati and Crenna 1984). [ABSTRACT FROM AUTHOR]

The aim of the study was to examine the supraspinal control during voluntary movements of the foot in man, of the Ia inhibitory interneurones activated from the anterior tibial muscle and projecting to the soleus α-motoneurones. Previous studies have reported an increased inhibition of the soleus α-motoneurones by a constant conditioning stimulus to the common peroneal nerve during dorsiflexion of the foot. This was interpreted as a sign of supraspinal facilitation of the Ia inhibitory interneurones. However, these results could not be reproduced in the present study. The contradictory results can probably be explained by some important methodological differences in the use of the H-reflex technique. [ABSTRACT FROM AUTHOR]

Cross-correlations between stimuli delivered to peripheral nerves and the discharges of single, voluntarily activated, motor units can provide information about facilitatory and inhibitory projections to single spinal motoneurons in man. The projection frequency, under the given circumstances, of a facilitatory or inhibitory pathway can be obtained from the proportion of the sampled motor units of a given muscle showing the facilitatory or inhibitory effect. Deductions about the shape and relative amplitude of the underlying post-synaptic potentials can be made from the profile of the changes in firing probability. This technique has been used to explore the projections of low threshold muscle afferents to motoneurons of various leg muscles in man. Homonymous facilitation was demonstrated to all the sampled motor units of soleus (SOL), medial gastrocnemius (MG), tibialis anterior (TA) and vastus medialis (VM) and is presumed to represent the effects of the composite muscle spindle group Ia EPSP. Heteronymous facilitation was demonstrated between certain synergists. The projection frequency was less and the magnitude of the change in firing probability was smaller than for homonymous facilitation. SOL motoneurons, however, were not facilitated from low threshold afferents in the medial gastrocnemius nerve. Reciprocal inhibition was demonstrated between certain antagonists. The majority of the sampled motor units of SOL, however, were facilitated from low threshold afferents in the common peroneal nerve. The threshold for this facilitation was higher than for the homonymous facilitation elicited from this nerve and thus a different class of afferents and/or intercalated interneurons may be involved. There are projections across the knee joint in man. Motor units in vastus medialis (VM) were facilitated from low threshold afferents in the common peroneal nerve. It is likely that these reflex connections, which differ from those in other species, reflect the functional relationships between various lower limb muscles in man. [ABSTRACT FROM AUTHOR]

The effects of ramp stretches applied to triceps surae muscle on the discharge patterns of single Ia inhibitory interneurones, monosynaptically invaded from various nerves, were studied in either decerebrate or anesthetized cats. Interneurones which received direct excitatory Ia input from the stretched muscle exhibited augmented activity both during the dynamic and static phase of stretch, which was, however, interrupted by a transient inhibitory influence during the dynamic phase of stretch. The influences on Ia inhibitory interneurones, monosynaptically invaded from hamstring or tibial nerve, were exclusively inhibitory. These stretch-induced inhibitions were better demonstrable in decerebrate than in anesthetized preparations. The timing of the discharge patterns of additionally recorded Renshaw cells during stretch, and the disappearance or reduction of the above described inhibitory effects after administration of DHE, strongly support the idea that these inhibitory actions are caused by Renshaw inhibition. In Ia inhibitory interneurones, monosynaptically activated from the antagonistic peroneal nerve, stretch induced also pronounced inhibitory effects, which were most probably caused by mutual inhibition between Ia inhibitory interneurones. The suppression of agonistic Ia inhibitory interneurone activity below the tonic resting activity corresponded to an enhancement of the monosynaptic reflex amplitude of the antagonistic motoneurone pool. The findings suggest that normal orthodromic activation of Renshaw cells, and consequently the recurrent inhibition of the Ia inhibitory interneurones, is predominantly linked with rapid phasic, rather than slow tonic, motoneuronal firing. The functional role of this mechanism for the performance of rapidly alternating movements and the damping of ballistic agonist contractions is discussed. [ABSTRACT FROM AUTHOR]

Experiments were done on nine cats anaesthetized with pentobarbitone to determine whether motor cortical zones controlling antagonistic muscles are synaptically interconnected. Motor cortical zones controlling wrist flexors, or extensors, were identified by microstimulation and intramuscular electromyographic recordings (microstimulation: 11 pulses at 333 pulses/s, current 10–40 μA). The position of each zone of interest was marked by a small ink spot on the surface of the cortex and on a scaled drawing of the cortical surface (cruciate region). Following the identification of wrist flexor and extensor zones the anterograde tracer biocytin was injected into one, or two, wrist extensor zones at three depths (400, 800 and 1500 μm) from the cortical surface. A small injection of horseradish peroxidase (HRP) – producing a dark brown spot of approximately 300–500 μm – was made in layer II–III of one or more wrist flexor zones. Similar HRP injections were made in the deep layers of wrist extensor zones that were not labelled by biocytin. The HRP injections served to mark the position of potential targets of biocytin-labelled fibres. In some experiments the biocytin was injected into a wrist flexor zone and HRP was deposited in one or more wrist extensor zones. Biocytin-labelled fibres (blue) were found throughout the expanse of the forelimb representation zone, as has been previously reported. More specifically, in all animals biocytin-labelled fibres were found in identified cortical zones controlling the same muscle(s) as well as in zones controlling an antagonist(s). Club-like swellings, indicative of synaptic boutons, were observed on these fibres. The density of labelled fibres was greater in the upper cortical layers (II–III), but a large number of terminals were also present in the lower cortical layers (V–VI). We conclude that there exist intracortical circuits linking motor cortical zones controlling antagonistic muscles. Elucidating the nature and function of these circuits is likely to be important for understanding the mode of operation of the motor cortex. [ABSTRACT FROM AUTHOR]

The amplitude of the Hoffmann reflex (H-reflex) of the human soleus muscle is modulated in a cyclical way during walking. This paper addresses two questions associated with the neural mechanisms that might generate this modulation: (1) Does the amplitude of the H-reflex simply rise and fall as a function of the background excitability of the soleus motoneuron pool? (2) Is the modulation of the H-reflex dependent on events associated with activation of the antagonist muscle? The amplitude of the soleus H-reflex was compared under three conditions: natural walking, walking without activating the tibialis anterior muscle, and walking with activation of the soleus muscle in the swing phase. Human subjects were able to perform these three tasks with minimal training. The results indicated that the soleus H-reflex remained very depressed in the swing phase of walking, even when a voluntary contraction of the soleus muscle was superimposed during this time. Moreover, the presence of tibialis anterior activity had a very minor effect on the amplitude of the soleus H-reflex during walking. It is concluded that modulation of the soleus H-reflex is not simply a reflection of the background excitability of the motoneuron pool, and the modulation is not dependent on activation of the antagonist muscle. Other more powerful mechanisms are acting to modulate the reflex, most likely presynaptic inhibition of the primary afferents. [ABSTRACT FROM AUTHOR]

Recent studies have reported that no increase of the disynaptic reciprocal inhibition can be observed during tonic voluntary dorsiflexion of the foot as compared to rest, when the size of the control H-reflex is kept constant. Other studies have, however, shown that a voluntary contraction evokes a strong and long-lasting depression of the synaptic transmission from Ia afferents to motoneurones, most likely secondary to activation of these afferents during the contraction (post-activation depression). It was thought that this effect could also interfere with the demonstration of a central facilitation of the reciprocal inhibition during movement. The amount of disynaptic Ia reciprocal inhibition from the pretibial flexors to the soleus H-reflex was therefore estimated in normal human subjects at rest and during voluntary tonic dorsiflexion before, during and after blocking the peripheral feedback from the investigated muscles. It was observed that the reciprocal inhibition measured during dorsiflexion increased during occlusion of the blood supply to the leg, reaching a maximum of inhibition after 30 min of ischaemia. After release of the ischaemia the inhibition gradually decreased to its pre-ischaemic level. It is therefore suggested that the brain facilitates transmission in the Ia disynaptic reciprocal pathway during tonic voluntary dorsiflexion of the foot, but that this facilitation is normally not observed due to a post-activation depression following the peripheral feedback activation during the movement. [ABSTRACT FROM AUTHOR]

Spinal reciprocal inhibition (RI) and intracortical inhibition are important physiological mechanisms for voluntary movement control and functional recovery of voluntary movement in patients with stroke. Spasticity, which impairs motor performance, is one of the major manifestations of stroke. RI may be involved in reducing spasticity. This might allow finger extension, and, therefore, better hand function by reducing co-contraction with finger extensors. One potential mechanism of functional reorganization of the motor cortex is that pre-existing masking pathways are unmasked by decreased intracortical inhibition. The inhibitory neurotransmitter GABA plays an important role in this process. Changes in RI might be mediated through unmasking of cortical pathways through decreased inhibition, with the neurotransmitter GABA. These changes can be assessed using short-latency intracortical inhibition (SICI) and RI. Functional recovery in the chronic phase of stroke induced by rehabilitation was accompanied by SICI and spinal RI changes. Cortical reorganization and spinal plasticity might play important roles in functional recovery induced by rehabilitation, even in patients with chronic severe hemiparesis. This review aims to provide a focused overview of neuroplasticity of spinal RI and intracortical inhibition associated with functional motor recovery from stroke.

Reciprocal inhibition of soleus motoneurones in man was studied during voluntary contraction of soleus or its antagonist. Inhibition was strongest during antagonist contraction or at rest and weak during contraction of soleus itself. Possible explanations for these changes are discussed. [ABSTRACT FROM AUTHOR]