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N Petersen

Publications and source records attributed to N Petersen.

At least 37 records · Page 2Linked to original sources
PubMed1999

Bradykinin induces interleukin-6 expression in astrocytes through activation of nuclear factor-kappaB.

Bradykinin, a mediator of inflammation, is produced in the brain during trauma and stroke. It is thought to open the blood-brain barrier, although the mechanism is unclear. We have investigated, therefore, the effect of bradykinin on the expression of interleukin-6 (IL-6), a putative modulator of the blood-brain barrier, in astrocytes. IL-6 gene transcription was evaluated by transient transfection of the human IL-6 promoter linked to the luciferase gene. In murine astrocytes, bradykinin stimulated IL-6 secretion and gene transcription. The effect of bradykinin was blocked by KN-93, an inhibitor of Ca2+/calmodulin-dependent protein kinases, and by bisindolylmaleimide I, an inhibitor of protein kinase C, suggesting the involvement of these protein kinases. Mutations in the multiple response element and the binding site for nuclear factor-kappaB (NF-kappaB), but not in other known elements of the IL-6 promoter, interfered with induction of IL-6 transcription. The involvement of NF-kappaB was supported further by the finding that overexpression of nmIkappaB alpha, a stable inhibitor of NF-kappaB, inhibited the induction of IL-6 by bradykinin. Bradykinin activated NF-kappaB in primary astrocytes as shown by increased DNA binding of NF-kappaB. These data demonstrate that bradykinin stimulates IL-6 expression through activation of NF-kappaB, which may explain several inflammatory effects of bradykinin.

Animals↗
PubMed1998

The effect of transcranial magnetic stimulation on the soleus H reflex during human walking.

1. The effect of transcranial magnetic stimulation (TMS) on the soleus H reflex was investigated in the stance phase of walking in seventeen human subjects. For comparison, measurements were also made during quiet standing, matched tonic plantar flexion and matched dynamic plantar flexion. 2. During walking and dynamic plantar flexion subliminal (0.95 times threshold for a motor response in the soleus muscle) TMS evoked a large short-latency facilitation (onset at conditioning-test interval: -5 to -1 ms) of the H reflex followed by a later (onset at conditioning-test interval: 3-16 ms) long-lasting inhibition. In contrast, during standing and tonic plantar flexion the short-latency facilitation was either absent or small and the late inhibition was replaced by a long-lasting facilitation. 3. When grading the intensity of TMS it was found that the short-latency facilitation had a lower threshold during walking than during standing and tonic plantar flexion. Regardless of the stimulus intensity the late facilitation was never seen during walking and dynamic plantar flexion and the late inhibition was not seen, except for one subject, during standing and tonic plantar flexion. 4. A similar difference in the threshold of the short-latency facilitation between walking and standing was not observed when the magnetic stimulation was replaced by transcranial electrical stimulation. 5. The lower threshold of the short-latency facilitation evoked by magnetic but not electrical transcranial stimulation during walking compared with standing suggests that cortical cells with direct motoneuronal connections increase their excitability in relation to human walking. The significance of the differences in the late facilitatory and inhibitory effects during the different tasks is unclear.

Cerebral Cortex↗
PubMed1998

Evaluation of reciprocal inhibition of the soleus H-reflex during tonic plantar flexion in man.

Changes in reciprocal inhibition from ankle dorsiflexors to ankle plantar flexors were evaluated at increasing levels of tonic plantar flexion in 11 healthy subjects. Stimulation of the common peroneal nerve (CPN) evoked a short-latency depression of the rectified and averaged soleus electromyogram (average latency of depression: 40 ms) and a short-latency inhibition of the soleus H-reflex (conditioning-test interval: 2-3 ms). When the intensity of the CPN stimulation was below approximately 1.2 x motor threshold (x MT) the inhibition of both the soleus EMG (expressed as the amount of EMG during the inhibition as percentage of the background EMG) and the soleus H-reflex (expressed as the size of the conditioned reflex as percentage of the control H-reflex size) were seen to decrease with increasing levels of plantar flexion. At intensities of stimulation higher than approximately 1.2 x MT the inhibition of the EMG and the H-reflex was very strong and was not modulated with contraction. It is suggested that the decrease of reciprocal inhibition with increasing levels of plantar flexion is due to a decreased excitability of the Ia inhibitory interneurones which are responsible for the inhibition. It is emphasized that submaximal stimulation is necessary to demonstrate this modulation of inhibition and that the functional contribution of reciprocal inhibition to motor performance cannot be revealed from the amount of inhibition evoked by artificial electrical stimulation of a peripheral nerve.

Adult↗
PubMed1998

Evidence that a transcortical pathway contributes to stretch reflexes in the tibialis anterior muscle in man.

1. In human subjects, stretch applied to ankle dorsiflexors elicited three bursts of reflex activity in the tibialis anterior (TA) muscle (labelled M1, M2 and M3) at mean onset latencies of 44, 69 and 95 ms, respectively. The possibility that the later of these reflex bursts is mediated by a transcortical pathway was investigated. 2. The stretch evoked a cerebral potential recorded from the somatosensory cortex at a mean onset latency of 47 ms in nine subjects. In the same subjects a compound motor-evoked potential (MEP) in the TA muscle, evoked by magnetic stimulation of the motor cortex, had a mean onset latency of 32 ms. The M1 and the M2 reflexes thus had too short a latency to be caused by a transcortical pathway (minimum latency, 79 ms (47 + 32)), whereas the later part of the M2 and all of the M3 reflex had a sufficiently long latency. 3. When the transcranial magnetic stimulation was timed so that the MEP arrived in the TA muscle at the same time as the M1 or M2 reflexes, no extra increase in the potential was observed. However, when the MEP arrived at the same time as the M3 reflex a significant (P < 0.01) extra-facilitation was observed in all twelve subjects investigated. 4. Peaks evoked by transcranial magnetic stimulation in the post-stimulus time histogram of the discharge probability of single TA motor units (n = 28) were strongly facilitated when they occurred at the same time as the M3 response. This was not the case for the first peaks evoked by electrical transcranial stimulation in any of nine units investigated. 5. We suggest that these findings are explained by an increased cortical excitability following TA stretch and that this supports the hypothesis that the M3 response in the TA muscle is - at least partly - mediated by a transcortical reflex.

Adult↗
PubMed1998

Gating of somatosensory evoked potentials during voluntary movement of the lower limb in man.

Somatosensory evoked potentials (SEPs) evoked by stimulation of the tibial nerve (TN) in the popliteal fossa, the sural nerve (Sur) at the lateral malleole, and an Achilles tendon (Achilles) tap were recorded before and during voluntary plantarflexion, dorsiflexion, and cocontraction of the ipsi- and contralateral foot in normal subjects. Suppression (gating) of the TN-SEP began around 60 ms before the onset of electromyographic activity (EMG), and became maximal 50-100 ms after the onset of EMG. Similar gating was observed for the SEP evoked by activation of muscle afferents (Achilles) and cutaneous afferents (Sur). The TN-SEP was similarly depressed at the onset of a plantarflexion as at the onset of dorsiflexion. A depression, although much smaller, was also observed at the onset of movement of the contralateral limb. The depression of the TN-SEP after the onset of EMG decreased when fast-conducting afferents were blocked by ischemia below the knee joint. The TN-SEP was equally depressed during tonic dorsiflexion, plantar-flexion, and cocontraction of dorsi- and plantarflexors. The TN-SEP was depressed for up to 300 ms when preceded by stimulation of Sur or a biceps femoris tendon tap. Gating of lower limb SEPs thus appears to have both central and peripheral components of which neither seems to be specific for the muscle being contracted or the sensory afferents being stimulated. We encourage that caution is taken when drawing functional conclusions regarding movement-specific modulation of afferent inflow to the somatosensory cortex based on observations of gating of lower limb SEP.

Adult↗
PubMed1998

Flexor reflex afferents reset the step cycle during fictive locomotion in the cat.

The generation of locomotor-like spinal rhythms has been proposed to involve two neural centres with mutual reciprocal inhibition (Graham Brown's "half-centre" hypothesis). Much later a particular set of segmental flexor reflex pathways were described as being organized in accordance with this half-centre hypothesis. As these pathways became operative following injection of monoaminoxidase inhibitors and L-3,4-dihydroxyphenylalanine (L-dopa), i.e. under the same conditions under which a spontaneous locomotor activity may develop, it was assumed that these particular pathways and spinal rhythm generators involve the same neuronal networks. In order to give further evidence to this hypothesis, we investigated whether short trains to "flexor reflex afferents" (FRA) reset the spinal locomotor rhythm, i.e. shorten or lengthen the stimulated cycle after which the regular rhythm is resumed with step cycles of the original duration. The experiments were performed in anaemically decapitated, high-spinal curarized cats. A steady locomotor rhythm was induced by injection of nialamide and L-dopa and the influence of electrical stimulation (trains of 50-1000 ms) of FRA (joint, cutaneous, and group II and III muscle afferents) onto this rhythm was tested. Stimulation of FRA induced a clear resetting of the locomotor rhythm, which was mainly characterized by a flexion reflex pattern: during the extension phase the extensor activity was interrupted and a flexion phase was initiated; during the late flexion phase mainly a prolongation of that phase with a variable change of the following extension phase was induced. In addition to this prevailing pattern, stimulation of some nerves (in particular nerves to more distal extensors and the sural nerve) could often prolong extension, when stimulated during the late extension, or terminate the flexor burst and initiate a new extension phase, when stimulated during the late flexion phase. This pattern is probably due to the concomitant stimulation of group I afferents in the case of the muscle nerves and to separate non-FRA pathways in the case of the sural nerve. The results demonstrate that the interneurones of the FRA pathways, which are operative during L-dopa-induced locomotion in spinal animals, can be considered as neuronal elements of the rhythm-generating network for locomotion.

Animals↗
PubMed1998

Pharmacologically evoked fictive motor patterns in the acutely spinalized marmoset monkey (Callithrix jacchus).

The existence of a spinal network capable of generating rhythmic alternating activity resembling locomotion still has not been firmly established in primates, including man, although evidence for one is accumulating. The present study investigated whether it is possible to activate such a network by administration of a variety of pharmacological agents to acutely spinalized marmoset monkeys (Callithrix jacchus) in the absence of phasic afferent input to the spinal cord. Fourteen marmoset monkeys were decerebrated, spinalized, and paralyzed. The nerves supplying both hindlimbs were cut and recorded from. In 5 monkeys the effect of electrical stimulation of the brainstem was investigated before spinalization. In 3 of these monkeys, rhythmic activity alternating between extensors and flexor nerves was seen. In the 2 other monkeys only synchronized activity was elicited. In acutely spinalized monkeys, administration of L-3,4-dihydroxyphenylalanine (L-dopa; 3-4 h after treatment with nialamide) failed to evoke any rhythmic alternating activity. In contrast, administration of clonidine elicited alternating activity in all of 8 monkeys tested. In 4 of these monkeys, the activity was restricted to alternation between ipsilateral and contralateral flexor nerves, whereas alternating activity between ipsilateral flexors and extensors was also seen in the other 4 monkeys. Administration of excitatory amino acids (NMDA or NMA) also elicited rhythmic alternating activity in 7 of 10 spinalized monkeys. In 4, rhythmic alternating activity was seen between extensors and flexors on one limb as well as between ipsilateral and contralateral flexors. In 3 monkeys NMDA/NMA produced alternation between extensors and flexors of one limb without alternation between the ipsilateral and contralateral sides. Administration of noradrenaline failed to elicit any rhythmic activity, but rather completely depressed already existing activity. Administration of serotonin (5-HT) was ineffective in facilitating alternating activity in 6 of 8 monkeys and was facilitatory to rhythmic activity in the other 2. We suggest that these data provide further evidence of a network capable of eliciting rhythmic alternating activity resembling locomotion in the primate spinal cord. The network, however, seems to be more difficult to activate pharmacologically in those conditions than in other mammals. This may especially be the case in higher primates, including man.

Animals↗
PubMed1998

Sensitivity of H-reflexes and stretch reflexes to presynaptic inhibition in humans.

The sensitivity of soleus H-reflexes, T-reflexes, and short-latency stretch reflexes (M1) to presynaptic inhibition evoked by a weak tap applied to the biceps femoris tendon or stimulation of the common peroneal nerve (CPN) was compared in 17 healthy human subjects. The H-reflex was strongly depressed for a period lasting up to 300-400 ms (depression to 48 +/- 23%, mean +/- SD, of control at a conditioning test interval of 70 ms) by the biceps femoris tendon tap. In contrast, the short-latency soleus stretch reflex elicited by a quick passive dorsiflexion of the ankle joint was not depressed. The soleus T-reflex elicited by an Achilles tendon tap was only weakly depressed (92 +/- 8%). The H-reflex was also significantly more depressed than the T-reflex at long intervals (>15 ms) after stimulation of CPN (H-reflex 63 +/- 14%, T-reflex 91 +/- 13%; P < 0. 01). However, the short-latency (2 ms) disynaptic reciprocal Ia inhibition evoked by stimulation of CPN was equally strong for H- and T-reflexes (H-reflex 72 +/- 10%, T-reflex 67 +/- 13%; P = 0.07). Peaks in the poststimulus time histogram (PSTH) of the discharge probability of single soleus motor units (n = 53) elicited by an Achilles tendon tap had a longer duration than peaks evoked by electrical stimulation of the tibial nerve (on average 5.0 ms as compared with 2.7 ms). All parts of the electrically evoked peaks were depressed by the conditioning biceps femoris tendon tap (average depression to 55 +/- 27% of control; P < 0.001). A similar depression was observed for the initial 2 ms of the peaks evoked by the Achilles tendon tap (69 +/- 48%; P < 0.001), but the last 2 ms were not depressed. Conditioning stimulation of the CPN at long intervals (>15 ms) also depressed all parts of the electrically evoked PSTH peaks (n = 34; average 65%; P < 0.001) but had only a significant effect on the initial 2 ms of the peaks evoked by the Achilles tendon tap (85%; P < 0.001). We suggest that the different sensitivity of mechanically and electrically evoked reflexes to presynaptic inhibition is caused by a difference in the shape and composition of the excitatory postsynaptic potentials underlying the two reflexes. This difference may be explained by a different composition and/or temporal dispersion of the afferent volleys evoked by electrical and mechanical stimuli. We conclude that it is not straightforward to predict the modulation of stretch reflexes based on observations of H-reflex modulation.

Adult↗
PubMed1997

Evidence suggesting a transcortical pathway from cutaneous foot afferents to tibialis anterior motoneurones in man.

1. Stimulation of the superficial peroneal or the sural nerve (3 shocks, 3 ms interval, 1 ms duration, 2.5 x perception threshold) evoked a reflex activation of the tibialis anterior muscle at a latency of approximately 70-95 ms in all of nine healthy human subjects. Stimulation of the medial plantar nerve only rarely produced similar effects. The possibility that a transcortical pathway contributes to these late reflex responses was investigated by combining the cutaneous stimulations and a transcranial magnetic stimulation of the contralateral motor cortex. 2. A significant facilitation of short-latency peaks in the post-stimulus time histogram of single tibialis anterior motor units evoked by the transcortical magnetic stimulation was observed in eight out of nine subjects following stimulation of the superficial peroneal or sural nerves at the latency of the long-latency reflex. In contrast such a facilitation was only rarely seen when the medial plantar nerve was stimulated. 3. With the same timing for the stimuli, the superficial peroneal and sural nerve stimulations also produced a significant increase in the short-latency, presumed monosynaptic, facilitation of the tibialis anterior H reflex produced by the brain stimulation. 4. Similar facilitatory effects of the cutaneous stimuli could not be demonstrated when the magnetic stimulation of the cortex was replaced with electrical stimulation, implying that cortical excitability is affected by a conditioning cutaneous stimulation. 5. It is suggested that the long-latency reflexes in the tibialis anterior muscle evoked by activation of cutaneous afferents from the human foot are, at least partly, mediated by a transcortical pathway.

Adult↗
PubMed1995

Evidence favouring different descending pathways to soleus motoneurones activated by magnetic brain stimulation in man.

1. In resting subjects low-intensity magnetic stimulation of the brain evoked an inhibition of the soleus H reflex at short latency (conditioning-test interval, -2 to +1 ms) followed approximately 10 ms later by a period of facilitation. During voluntary dynamic or tonic plantar flexion the same stimulus evoked a facilitation with a shorter latency than the inhibition (conditioning-test interval, -5 to -1 ms). 2. At the onset of ramp-and-hold plantar flexion the short-latency facilitation was seen at lower intensities of stimulation than the long-latency facilitation in six of seven subjects. At rest and/or during tonic plantar flexion the opposite was observed in four of the subjects, whereas the two facilitations had approximately the same threshold in the remaining subjects. 3. The short-latency facilitation decreased approximately 100 ms after the onset of ramp-and-hold plantar flexion in all of eight subjects. The long-latency facilitation, in contrast, either had the same size throughout the ramp phase or even increased around the end of the ramp phase. 4. The short-latency facilitation of the reflex was significantly larger at the onset of a fast ramp-and-hold plantar flexion (10 N m (150 ms)-1) than at the onset of a slow contraction (10 N m (600 ms)-1), whereas the opposite was the case for the long-latency facilitation. 5. As the short- and long-latency facilitations had different thresholds and were differently regulated during voluntary movement, it is suggested that they are caused by activation of different descending pathways by the magnetic stimulus.

Adult↗
PubMed1995

Changes in the effect of magnetic brain stimulation accompanying voluntary dynamic contraction in man.

1. The soleus (Sol) H reflex was conditioned by magnetic stimulation of the contralateral motor cortex at rest and during voluntary contraction in healthy human subjects. The intensity of the magnetic stimulus was adjusted so as to have no effect on the H reflex at rest. During tonic voluntary contraction the same magnetic stimulus produced a facilitation with a short latency and a long duration, thus reflecting an increased excitation of Sol motoneurones by the magnetic stimulus during voluntary contraction. 2. The amount of reflex facilitation produced by brain stimulation within the initial 0.5-1 ms after its onset was investigated at different times during dynamic ramp-and-hold plantar flexion. The facilitation was largest at the onset of voluntary activity in the Sol muscle. It then decreased abruptly within 100 ms after the onset of the voluntary contraction. Neither the voluntary Sol activity nor the control H reflex decreased at this time. 3. Electrical stimulation of the brain with the anode placed lateral to the vertex produced a facilitation of the H reflex, which preceded the facilitation evoked by magnetic stimulation by 1-2 ms. The facilitation produced by the magnetic stimulus occurred or increased at the onset of contraction in relation to rest in all experiments. However, this was the case in only two out of eight experiments, when the brain was stimulated electrically. 4. The size of the reflex facilitation measured at the onset of contraction was larger the faster the contraction. Positive correlations were found between the size of the facilitation and the peak of the first and second derivative of the torque and the peak Sol EMG activity. 5. It is suggested that the observed changes in the size of the short-latency reflex facilitation produced by magnetic brain stimulation mainly reflects changes in the excitability of corticospinal cells, since similar changes were not observed in the size of the unconditioned Sol H reflex or in the short-latency reflex facilitation produced by electrical brain stimulation. The data support the hypothesis that fast conducting corticospinal fibres with monosynaptic projections to spinal motoneurones are involved in the initiation of voluntary movement in man.

Adult↗
PubMed1995

Latency of effects evoked by electrical and magnetic brain stimulation in lower limb motoneurones in man.

1. The latency of effects in the tibialis anterior (TA) and soleus (Sol) muscles evoked by electrical and magnetic stimulation of the motor cortex was evaluated in human subjects by H reflex testing. Post-stimulus time histograms (PSTHs) were established for the discharge of single voluntarily activated motor units and motor-evoked potentials (MEPs) in the surface electromyogram. 2. At rest both electrical and magnetic stimulation evoked an inhibition of the Sol H reflex at the lowest intensities of stimulation. In some subjects a facilitation with an earlier onset was seen when increasing the stimulation strength. When the anode for the electrical stimulation was placed at the vertex directly above the leg motor area, the inhibition or facilitation often had the same latency as when evoked by magnetic stimulation. However, when the anode was placed 2-3 cm lateral to the vertex, effects evoked by the electrical stimulus often occurred 1-2 ms earlier. 3. Short-latency peaks in the PSTH of the discharges of single TA motor units also tended to occur earlier when evoked by electrical stimulation with the anode lateral to the vertex than when evoked by magnetic stimulation or electrical stimulation with the anode at the vertex. 4. In one subject, near-maximal electrical stimulation evoked MEPs with a latency corresponding to that seen following stimulation of the brainstem by electrodes placed bilaterally over the mastoid processes approximately 16 cm more distal. Maximal magnetic stimulation, in contrast, never resulted in responses with a latency shorter than that seen with the weakest electrical stimuli at the vertex. 5. The initial facilitation of the Sol H reflex evoked by magnetic stimulation and by electrical anodal stimulation at the vertex increased when the subject performed a voluntary plantarflexion. In contrast, the earlier facilitation evoked by electrical anodal stimulation 2-3 cm lateral to the vertex had the same size both at rest and during contraction. 6. We suggest that magnetic stimulation and electrical anodal stimulation at the vertex may preferentially activate descending cortical cells at, or close to, the cell soma. The initial responses evoked by these two stimuli may therefore be influenced by the excitability of the cortical cells. On the other hand, electrical stimulation with the anode 2-3 cm lateral to the vertex seems to often activate the axons at a deeper level. The initial responses evoked by this type of stimulation may therefore not be influenced by the excitability of the cortical cells.

Adult↗
PubMed1995

Changes in transmission across synapses of Ia afferents in spastic patients.

The transmission across synapses of Ia afferents on spinal motor neurons was investigated in 30 healthy subjects and 25 spastic multiple sclerosis patients. Slow passive stretch (17 degrees/s of the soleus muscle evoked a pronounced depression of the soleus Hoffmann reflex (H-reflex) lasting for more than 10 s in the healthy subjects. This depression was less pronounced and had a shorter duration in the spastic patients. A tap applied to the biceps femoris tendon also produced an inhibition of the soleus H-reflex, which was larger in the healthy subjects than in the spastic patients. This inhibition only lasted for 300-400 ms. Finally, stimulation of the femoral nerve (FN) produced a facilitation of the soleus H-reflex, which was larger in the spastic patients than in the healthy subjects. The inhibition of the H-reflex evoked by the biceps femoris tendon tap is known to be caused by presynaptic inhibition of the Ia afferents, which mediate the reflex. The facilitation of the soleus H-reflex produced by FN stimulation has also been shown to be influenced by changes in presynaptic inhibition. The increased facilitation from the FN and the decreased inhibition from the biceps femoris tendon tap onto the soleus H-reflex in spastic patients are thus both compatible with a deficient presynaptic inhibition in these subjects. The long lasting depression of the reflex evoked by a previous slow stretch of the soleus muscle is most likely caused by a decrease of the probability of transmitter release from the Ia afferents. The decrease of this depression in spastic patients suggests that mechanisms other than presynaptic inhibition may contribute to changes in the efficiency of transmission across the synapses of Ia afferents in spastic patients and thus contribute to the exaggeration of stretch reflexes seen in these patients.

Adult↗
PubMed1994

Is presynaptic inhibition distributed to corticospinal fibres in man?

1. A tendon tap of the biceps femoris tendon was found to evoke a depression of the soleus and tibialis anterior H reflexes with a duration of 300-400 ms and with an onset at a conditioning-test interval of 20-30 ms. It is suggested that the depression is caused by presynaptic inhibition of the terminals of the Ia afferents mediating the reflexes. 2. This possibility was tested by a method in which the H reflex is facilitated by a monosynaptic Ia volley from the quadriceps muscle. The attenuation of this facilitation when another pathway is stimulated is probably caused by presynaptic inhibition of Ia afferents. It was shown that the biceps femoris tendon tap depressed the size of the femoral nerve-induced facilitation of the soleus and tibialis anterior H reflexes. This suggests that the depression of the reflexes by the tendon tap was indeed caused by presynaptic inhibition. 3. To investigate whether the terminals of descending fibres were similarly susceptible to presynaptic inhibition, the stimulation of the femoral nerve was replaced by magnetic stimulation of the contralateral motor cortex. This stimulation has been shown to evoke a facilitation of the tibialis anterior and soleus H reflexes which (within its initial 0.5-1 ms) is probably caused exclusively by direct monosynaptic projections from the cortex to the motoneurones. In contrast to the facilitation evoked by Ia afferents, the descending facilitation was not influenced by the biceps tendon tap. 4. Similarly, the monosynaptic peak in the post-stimulus time histogram (PSTH) of single voluntarily activated tibialis anterior motor units evoked by stimulation of the common peroneal nerve was depressed by the tendon tap, whereas this was not the case for the presumed monosynaptic peak evoked by brain stimulation. 5. It is suggested that the tendon tap evoked presynaptic inhibition of the terminals of flexor as well as extensor Ia afferents terminating on both soleus and tibialis anterior motoneurones. In contrast, the tap failed to elicit any presynaptic inhibition of the terminals of descending fibres on the motoneurones. We suggest that descending pathways in general are free from the presynaptic control which attenuates peripheral input to motoneurones. Through modulation of presynaptic inhibition the brain may thus selectively hinder the access of peripheral feedback mechanisms to the motoneurones, while still maintaining control of the output from the spinal cord through direct and indirect projections to the motoneurones.

Adult↗
PubMed1994

Disynaptic reciprocal inhibition of ankle extensors in spastic patients.

The soleus Hoffmann-reflex (H-reflex) was conditioned by a preceding stimulation of the common peroneal nerve in 74 healthy control subjects and 39 patients with spasticity in the lower extremities due to multiple sclerosis. At a conditioning-test interval of 1-3 ms a decrease of the size of the soleus H-reflex was seen in the healthy subjects. The decrease was most likely caused by disynaptic reciprocal Ia inhibition (Crone et al., 1987). In the spastic patients a similar short-latency inhibition was rarely seen. On the contrary, in several patients a facilitation was seen at a conditioning-test interval of 3-4 ms. A short-latency inhibition as pronounced as in healthy subjects was seen in four patients. These four patients did not differ from the other patients regarding the degree of spasticity or any other clinical parameter. However, they all used an external peroneal nerve stimulator daily as a walking aid. It is suggested that the lack of short-latency reciprocal inhibition reflects a deficient control of the interneurons which mediate this inhibitory spinal mechanism between antagonistic muscles in man. This might contribute to the pathophysiology of spasticity and it might be related to the frequent occurrence of co-contraction of functionally antagonistic muscles during gait in spastic patients. The existence of a pronounced reciprocal inhibition in patients receiving frequent stimulation of the peroneal nerve may suggest that regular activation of peripheral nerves is of importance for the maintenance of the activity in spinal pathways.

Adult↗