scholarly journals The Effect of Diazepam on Presynaptic Inhibition in Patients with Complete and Incomplete Spinal Cord Lesions

1975 ◽  
Vol 2 (3) ◽  
pp. 179-184 ◽  
Author(s):  
M. Verrier ◽  
S. MacLeod ◽  
P. Ashby
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
H Reflex ◽  
Inhibitory Mechanism ◽  
Spinal Cord Lesions ◽  
Spinal Lesions

SUMMARY:The effect of diazepam on presynaptic inhibition in man has been examined in 5 patients with complete spinal transections and 7 patients with incomplete lesions. The inhibition of the H reflex by vibration applied to the tendo Achilles was used to assess presynaptic inhibition of the la monosynaptic pathway. Diazepam increased this inhibition in the patients with incomplete lesions, but had no significant effect on the inhibition in the patients with complete spinal transections.Evidently diazepam can enhance presynaptic inhibition in man. The effect, however, cannot be demonstrated in patients with longstanding complete spinal lesions possibly because of some alteration in the segmental presynaptic inhibitory mechanism in this group.

scholarly journals Neurophysiological Changes Following Spinal Cord Lesions in Man

1975 ◽  
Vol 2 (2) ◽  
pp. 91-100 ◽  
Author(s):  
P. Ashby ◽  
M. Verrier
Keyword(s):  
Spinal Cord ◽  
Achilles Tendon ◽  
Clinical Features ◽  
Presynaptic Inhibition ◽  
Spinal Cord Lesions ◽  
Tonic Vibration Reflex ◽  
Spinal Lesions ◽  
Spinal Lesion ◽  
Tendon Reflex ◽  
Normal Transmission

SUMMARY:A study has been made of the neurophysiological changes that follow spinal cord lesions in man. The Achilles tendon reflex (ATR) is used to estimate transmission in the la monosynaptic pathway, and the tonic vibration reflex (TVR) to estimate transmission in the la polysynaptic pathway to motoneurons. The inhibition of the H reflex by vibration is used as an estimate of presynaptic inhibition of the la monosynaptic pathway. Immediately following a complete lesion of the spinal cord presynaptic inhibition of the la monosynaptic pathway appears to be greatly increased. This enhanced inhibition may last several months but it eventually declines and in some instances becomes less than normal. Transmission in the la polysynaptic pathway is permanently abolished by a complete spinal lesion. A hypothesis is developed from these findings to explain the evolution of some of the clinical features that follow complete spinal lesions in man. Distinct differences are observed when the spinal lesion is incomplete. Transmission in the la polysynaptic pathway may be preserved and there may be no increase in presynaptic inhibition. These differences may depend upon the integrity of certain spinal long tracts which cannot be tested clinically.

scholarly journals Presynaptic and Postsynaptic Effects of the Anesthetics Sevoflurane and Nitrous Oxide in the Human Spinal Cord

2007 ◽  
Vol 107 (4) ◽  
pp. 553-562 ◽  
Author(s):  
Jan H. Baars ◽  
Michael Benzke ◽  
Falk von Dincklage ◽  
Josephine Reiche ◽  
Peter Schlattmann ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nitrous Oxide ◽  
Presynaptic Inhibition ◽  
Femoral Nerve ◽  
Volatile Anesthetic ◽  
H Reflex ◽  
Receptor Subtype ◽  
Gamma Aminobutyric Acid ◽  
Human Spinal Cord ◽  
Two Parameters

Background Reduced spinal excitability contributes to the suppression of movement responses to noxious stimuli during the anesthetic state. This study examines and compares presynaptic and postsynaptic effects of two anesthetics in the human spinal cord. Methods The authors tested two parameters during the administration of 0.8 vol% sevoflurane or 40 vol% nitrous oxide compared with control states before and after drug administration: (1) the size of the soleus H reflex (integrating presynaptic and postsynaptic effects) at increasing stimulus intensities (recruitment curve) and (2) the amount of presynaptic inhibition on Ia afferents of the quadriceps femoris, evaluated by the heteronymous facilitation of the soleus H reflex caused by a conditioning stimulation of the femoral nerve. The study was performed in 10 subjects for each drug. Results At the chosen concentrations, the maximum H reflex was reduced by 26.3 +/- 8.4% (mean +/- SD) during sevoflurane and by 33.5 +/- 15.6% during nitrous oxide administration. The averaged recruitment curves were similarly depressed under the influence of the two drugs. The reduction of H-reflex facilitation was significantly stronger for sevoflurane (28.8 +/- 20.0%) than for nitrous oxide administration (6.2 +/- 26.4%). Conclusions These results demonstrate in humans presynaptic effects of the volatile anesthetic sevoflurane but not of nitrous oxide. A possible explanation for this difference may be the different potency of the respective drugs in enhancing gamma-aminobutyric acid type A receptor-mediated inhibition, because presynaptic inhibition in the spinal cord involves this receptor subtype.

Locomotor training improves premotoneuronal control after chronic spinal cord injury

2014 ◽  
Vol 111 (11) ◽  
pp. 2264-2275 ◽  
Author(s):  
Maria Knikou ◽  
Chaithanya K. Mummidisetty
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Presynaptic Inhibition ◽  
H Reflex ◽  
Locomotor Training ◽  
Dependent Manner ◽  
Step Cycle ◽  
Cord Injury ◽  
Spinal Inhibition ◽  
Presynaptic Facilitation

Spinal inhibition is significantly reduced after spinal cord injury (SCI) in humans. In this work, we examined if locomotor training can improve spinal inhibition exerted at a presynaptic level. Sixteen people with chronic SCI received an average of 45 training sessions, 5 days/wk, 1 h/day. The soleus H-reflex depression in response to low-frequency stimulation, presynaptic inhibition of soleus Ia afferent terminals following stimulation of the common peroneal nerve, and bilateral EMG recovery patterns were assessed before and after locomotor training. The soleus H reflexes evoked at 1.0, 0.33, 0.20, 0.14, and 0.11 Hz were normalized to the H reflex evoked at 0.09 Hz. Conditioned H reflexes were normalized to the associated unconditioned H reflex evoked with subjects seated, while during stepping both H reflexes were normalized to the maximal M wave evoked after the test H reflex at each bin of the step cycle. Locomotor training potentiated homosynaptic depression in all participants regardless the type of the SCI. Presynaptic facilitation of soleus Ia afferents remained unaltered in motor complete SCI patients. In motor incomplete SCIs, locomotor training either reduced presynaptic facilitation or replaced presynaptic facilitation with presynaptic inhibition at rest. During stepping, presynaptic inhibition was modulated in a phase-dependent manner. Locomotor training changed the amplitude of locomotor EMG excitability, promoted intralimb and interlimb coordination, and altered cocontraction between knee and ankle antagonistic muscles differently in the more impaired leg compared with the less impaired leg. The results provide strong evidence that locomotor training improves premotoneuronal control after SCI in humans at rest and during walking.

Alterations in group Ia projections to motoneurons following spinal lesions in humans

1990 ◽  
Vol 64 (2) ◽  
pp. 637-647 ◽  
Author(s):  
A. Mailis ◽  
P. Ashby
Keyword(s):  
Spinal Cord ◽  
Normal Subjects ◽  
Muscle Afferents ◽  
Short Latency ◽  
Spinal Cord Lesions ◽  
Stretch Reflexes ◽  
Spinal Lesions ◽  
Group I ◽  
Ia Epsp ◽  
Stimulation Of

1. The hypothesis that the exaggerated tendon jerks and stretch reflexes that follow chronic spinal cord lesions in humans result from alterations in transmission from group I muscle afferents to motoneurons was tested by making observations on nine normal subjects and 25 patients with spinal cord lesions. All the patients had increased tendon jerks, one-third of them had both increased tendon jerks and increased, velocity-dependent stretch reflexes (i.e.g spasticity). 2. Changes in the firing probability of single, voluntary-activated soleus or tibialis anterior motor units during stimulation of the muscle nerve below the threshold of the alpha-motoneuron axons were used to derive the characteristics of the postsynaptic potentials produced by group I volleys in single motoneurons. Paired stimuli were used to test how multiple volleys in group I muscle afferents were transmitted to motoneurons. 3. Stimulation of the posterior tibial nerve produced a short-latency period of increased firing probability representing the homonymous composite Ia excitatory postsynaptic potential (EPSP) in all soleus motoneurons tested. There was no detectable alteration in the magnitude, duration, or profile of the short-latency facilitation in the patients with spinal lesions when compared with normal subjects. 4. In patients with traumatic spinal cord lesions less than 8 wk in duration the magnitude of the facilitation representing the composite Ia EPSP was significantly larger than normal, although only one out of the four patients in this group had spasticity. 5. In the patients with the greatest spasticity, group I volleys produced a second period of facilitation 11-15 ms after the facilitation representing the composite Ia EPSP. This is presumed to represent enhanced transmission through polysynaptic pathways from group I afferents to motoneurons. 6. In normal subjects the facilitation of motoneurons produced by the second of two group I volleys is greater 5 and 10 ms after the first volley and less 20, 30, and 50 ms after the first volley. These changes involve at least two factors: 1) changes in excitability of peripheral nerves and 2) changes in transmission at the Ia-motoneuron synapse. 7. In patients with spinal lesions the facilitation produced by the second of two muscle-afferent volleys was less depressed at the 30-ms interstimulus interval. 8. Thus two separate abnormalities have been uncovered in human subjects with chronic spinal lesions: 1) a change in the transmission of multiple volleys from muscle afferents to motoneurons and 2) an increase in transmission through polysynaptic pathways from Ia afferents to motoneurons. Both could contribute to the increased tendon jerks and exaggerated stretch reflexes.

Differential effects of a flexor nerve input on the human soleus H-reflex during standing versus walking

1995 ◽  
Vol 73 (4) ◽  
pp. 436-449 ◽  
Author(s):  
C. Capaday ◽  
B. A. Lavoie ◽  
F. Comeau
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
Stance Phase ◽  
Conditioning Stimulus ◽  
Background Level ◽  
H Reflex ◽  
Emg Activity ◽  
Group I ◽  
The Difference

A conditioning (C) stimulus at group I strength was delivered during standing to the common peroneal (CP) nerve before a test (T) stimulus at several C–T intervals ranging from 0 to 150 ms. At sufficiently long C–T intervals (100–120 ms) the soleus H-reflex was strongly inhibited despite little, or no change, in the background level of EMG activity. This finding indicates that a significant portion of the inhibition occurs at a premotoneuronal level, likely via presynaptic inhibition of the Ia-afferent terminals. During standing, at C–T intervals of 100–120 ms (optimal C–T interval) a conditioning stimulus to the CP nerve of 1.5 times motor threshold (MT) intensity reduced the soleus H-reflex by an average of 45.8% (n = 14 subjects). The conditioning stimulus always produced a clear inhibition of the H-reflex during standing at these C–T intervals. The effects of this conditioning stimulus on the soleus H-reflex were then determined in the early part of the stance phase of walking. In contrast to standing, the conditioning stimulus produced little or no inhibition during the early part of the stance phase of walking (average inhibition 45.8 vs. 11.6%, n = 14 subjects). The soleus background EMG, and the soleus and tibialis anterior M-waves were essentially the same during standing and walking. Furthermore, there was no shift of the optimal C–T interval during walking. The difference in the effects of the conditioning stimulus was not due to differences in the size of the test H-reflex in each task. It appears to be due to a genuine task-dependent change in the input–output properties of the underlying spinal cord circuits. There are at least two, mutually compatible, explanations of these results. Firstly, during walking the intraspinal terminals of the afferent fibres (group Ia and Ib) conducting the conditioning volley may be presynaptically inhibited, or their input gated at the interneuronal level. Secondly, on the assumption that the conditioning stimulus is acting via the presynaptic inhibitory network in the spinal cord, it is possible that during walking this network is saturated as a result of increased central or peripheral synaptic inputs. Finally, it seems unlikely that differences in the refractoriness of the CP nerve between the tasks may be involved; the reasons for this are presented in the discussion.Key words: Ia afferents, motoneurons, presynaptic inhibition, EMG, posture, locomotion, spinal cord.

scholarly journals Hypothesis: Hughlings Jackson and presynaptic inhibition: is there a big picture?

2016 ◽  
Vol 116 (1) ◽  
pp. 41-50 ◽  
Author(s):  
Alan J. McComas
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
Voluntary Movement ◽  
Inhibitory Mechanism ◽  
Sensory Data ◽  
Cutaneous Reflex ◽  
Tonic Level ◽  
Big Picture ◽  
The One ◽  
Sensory Fibers

Presynaptic inhibition is a very powerful inhibitory mechanism and, despite many detailed studies, its purpose is still only partially understood. One accepted function is that, by reducing afferent inflow to the spinal cord and brainstem, the tonic level of presynaptic inhibition prevents sensory systems from being overloaded. A corollary of this function is that much of the incoming sensory data from peripheral receptors must be redundant, and this conclusion is reinforced by observations on patients with sensory neuropathies or congenital obstetric palsy in whom normal sensation may be preserved despite loss of sensory fibers. The modulation of incoming signals by presynaptic inhibition has a further function in operating a “gate” in the dorsal horn, thereby determining whether peripheral stimuli are likely to be perceived as painful. On the motor side, the finding that even minimal voluntary movement of a single toe is associated with widespread inhibition in the lumbosacral cord points to another function for presynaptic inhibition: to prevent reflex perturbations from interfering with motor commands. This last function, together with the normal suppression of muscle and cutaneous reflex activity at rest, is consistent with Hughlings Jackson's concept of evolving neural hierarchies, with each level inhibiting the one below it.

Effect of Rhythmic Arm Movement on Reflexes in the Legs: Modulation of Soleus H-Reflexes and Somatosensory Conditioning

2004 ◽  
Vol 91 (4) ◽  
pp. 1516-1523 ◽  
Author(s):  
Alain Frigon ◽  
David F. Collins ◽  
E. Paul Zehr
Keyword(s):  
Spinal Cord ◽  
Nerve Stimulation ◽  
Presynaptic Inhibition ◽  
Arm Movement ◽  
Common Peroneal Nerve ◽  
H Reflex ◽  
Reflex Amplitude ◽  
Lumbosacral Spinal Cord ◽  
Arm Cycling ◽  
Shoulder Flexion

During locomotor tasks such as walking, running, and swimming, the arms move rhythmically with the legs. It has been suggested that connections between the cervical and lumbosacral spinal cord may mediate some of this interlimb coordination. However, it is unclear how these interlimb pathways modulate reflex excitability during movement. We hypothesized that rhythmic arm movement would alter the gain of reflex pathways in the stationary leg. Soleus H-reflexes recorded during arm cycling were compared with those recorded at similar positions with the arms stationary. Nerve stimulation was delivered with the right arm at approximately 70° shoulder flexion or 10° shoulder extension. H-reflexes were evoked alone (unconditioned) or with sural or common peroneal nerve (CP) conditioning to decrease or increase soleus IA presynaptic inhibition, respectively. Both conditioning stimuli were also delivered with no H-reflex stimulation. H-reflex amplitudes were compared at similar M-wave amplitudes and activation levels of the soleus. Arm cycling significantly reduced ( P < 0.05) unconditioned soleus H-reflexes at shoulder flexion by 21.7% and at shoulder extension by 8.8% compared with static controls. The results demonstrate a task-dependent modulation of soleus H-reflexes between arm cycling and stationary trials. Sural nerve stimulation facilitated H-reflexes at shoulder extension but not at shoulder flexion during static and cycling trials. CP nerve stimulation significantly reduced H-reflex amplitude in all conditions. Reflexes in soleus when sural and CP nerve stimulation were delivered alone, were not different between cycling and static trials; thus the task-dependent change in H reflex amplitude was not due to changes in motoneuron excitability. Therefore modulation occurred at a pre-motoneuronal level, probably by presynaptic inhibition of the IA afferent volley. Results indicate that neural networks coupling the cervical and lumbosacral spinal cord in humans are activated during rhythmic arm movement. It is proposed that activation of these networks may assist in reflex linkages between the arms and legs during locomotor tasks.

scholarly journals MRI of the Entire Spinal Cord—Worth the While or Waste of Time? A Retrospective Study of 74 Patients with Multiple Sclerosis

Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1424
Author(s):  
Esben Nyborg Poulsen ◽  
Anna Olsson ◽  
Stefan Gustavsen ◽  
Annika Reynberg Langkilde ◽  
Annette Bang Oturai ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Brain Mri ◽  
Anatomical Location ◽  
Spinal Cord Lesions ◽  
Chi Square ◽  
Exact Test ◽  
Mcdonald Criteria ◽  
Chi Square Test

Spinal cord lesions are included in the diagnosis of multiple sclerosis (MS), yet spinal cord MRI is not mandatory for diagnosis according to the latest revisions of the McDonald Criteria. We investigated the distribution of spinal cord lesions in MS patients and examined how it influences the fulfillment of the 2017 McDonald Criteria. Seventy-four patients with relapsing-remitting MS were examined with brain and entire spinal cord MRI. Sixty-five patients received contrast. The number and anatomical location of MS lesions were assessed along with the Expanded Disability Status Scale (EDSS). A Chi-square test, Fischer’s exact test, and one-sided McNemar’s test were used to test distributions. MS lesions were distributed throughout the spinal cord. Diagnosis of dissemination in space (DIS) was increased from 58/74 (78.4%) to 67/74 (90.5%) when adding cervical spinal cord MRI to brain MRI alone (p = 0.004). Diagnosis of dissemination in time (DIT) was not significantly increased when adding entire spinal cord MRI to brain MRI alone (p = 0.04). There was no association between the number of spinal cord lesions and the EDSS score (p = 0.71). MS lesions are present throughout the spinal cord, and spinal cord MRI may play an important role in the diagnosis and follow-up of MS patients.

scholarly journals Descending propriospinal neurons mediate restoration of locomotor function following spinal cord injury

2017 ◽  
Vol 117 (1) ◽  
pp. 215-229 ◽  
Author(s):  
Katelyn N. Benthall ◽  
Ryan A. Hough ◽  
Andrew D. McClellan
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Regeneration ◽  
Central Pattern Generators ◽  
Burst Activity ◽  
Compensatory Mechanism ◽  
Spinal Lesions ◽  
Cord Injury ◽  
Recovery Times ◽  
Indirect Activation

Following spinal cord injury (SCI) in the lamprey, there is virtually complete recovery of locomotion within a few weeks, but interestingly, axonal regeneration of reticulospinal (RS) neurons is mostly limited to short distances caudal to the injury site. To explain this situation, we hypothesize that descending propriospinal (PS) neurons relay descending drive from RS neurons to indirectly activate spinal central pattern generators (CPGs). In the present study, the contributions of PS neurons to locomotor recovery were tested in the lamprey following SCI. First, long RS neuron projections were interrupted by staggered spinal hemitransections on the right side at 10% body length (BL; normalized from the tip of the oral hood) and on the left side at 30% BL. For acute recovery conditions (≤1 wk) and before axonal regeneration, swimming muscle burst activity was relatively normal, but with some deficits in coordination. Second, lampreys received two spaced complete spinal transections, one at 10% BL and one at 30% BL, to interrupt long-axon RS neuron projections. At short recovery times (3–5 wk), RS and PS neurons will have regenerated their axons for short distances and potentially established a polysynaptic descending command pathway. At these short recovery times, swimming muscle burst activity had only minor coordination deficits. A computer model that incorporated either of the two spinal lesions could mimic many aspects of the experimental data. In conclusion, descending PS neurons are a viable mechanism for indirect activation of spinal locomotor CPGs, although there can be coordination deficits of locomotor activity. NEW & NOTEWORTHY In the lamprey following spinal lesion-mediated interruption of long axonal projections of reticulospinal (RS) neurons, sensory stimulation still elicited relatively normal locomotor muscle burst activity, but with some coordination deficits. Computer models incorporating the spinal lesions could mimic many aspects of the experimental results. Thus, after disruption of long-axon projections from RS neurons in the lamprey, descending propriospinal (PS) neurons appear to be a viable compensatory mechanism for indirect activation of spinal locomotor networks.

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