Reflex Response to Imposed Bilateral Hip Oscillations in Human Spinal Cord Injury

2007 ◽  
Vol 98 (4) ◽  
pp. 1849-1861 ◽  
Author(s):  
Tanya Onushko ◽  
Brian D. Schmit
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Afferent Input ◽  
Reflex Response ◽  
Neural Pathways ◽  
Joint Torques ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Hip Flexion ◽  
Surface Electromyograms

In human spinal cord injury (SCI), imposed unilateral hip movements trigger multijoint, coordinated reflexes that might incorporate interneuronal circuitry involved in normal motor control, such as neural pathways associated with the reflex control of locomotion. To further investigate the complexity of these hip-triggered reflexes, we measured the effects of kinematics of the contralateral hip on this type of spastic reflex activity in 11 chronic SCI subjects. A novel servomotor drive system was constructed to impose bilateral hip oscillations while the knees and ankles were held stationary in instrumented leg braces. Surface electromyograms (EMGs) and joint torques were recorded during the imposed hip oscillations. Tests were conducted at two different frequencies to test for velocity dependence of the reflexes and the following four paradigms were used to examine the effects of contralateral hip afferents on hip-triggered spastic reflexes: 1) bilateral alternating, 2) bilateral synchronous, 3) unilateral leg oscillation with the contralateral leg held stationary in hip extension, and 4) unilateral leg oscillation with the contralateral leg held stationary in hip flexion. The response to bilateral alternating movements resulted in a significantly larger reflex magnitude compared with the bilateral synchronous movements ( P < 0.001). Unilateral leg perturbations yielded reflex patterns that were consistent with the reflex patterns observed during alternating and synchronous hip oscillations. These observations suggest that spastic reflex excitability is modulated through afferent input from the contralateral hip in a manner that is generally consistent with locomotion.

Absence of Local Sign Withdrawal in Chronic Human Spinal Cord Injury

2003 ◽  
Vol 90 (5) ◽  
pp. 3232-3241 ◽  
Author(s):  
Brian D. Schmit ◽  
T. George Hornby ◽  
Vicki M. Tysseling-Mattiace ◽  
Ela N. Benz
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stimulus Location ◽  
Joint Torque ◽  
Test Sequence ◽  
Modular Organization ◽  
Human Spinal Cord ◽  
Local Sign ◽  
Cord Injury ◽  
Hip Flexion

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

Spastic Reflexes Triggered by Ankle Load Release in Human Spinal Cord Injury

2006 ◽  
Vol 96 (6) ◽  
pp. 2941-2950 ◽  
Author(s):  
Ming Wu ◽  
Brian D. Schmit
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Human Movement ◽  
Knee Extension ◽  
Muscle Afferents ◽  
Spinal Reflex ◽  
Joint Torques ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Load Release

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

Windup of Flexion Reflexes in Chronic Human Spinal Cord Injury: A Marker for Neuronal Plateau Potentials?

2003 ◽  
Vol 89 (1) ◽  
pp. 416-426 ◽  
Author(s):  
T. G. Hornby ◽  
W. Z. Rymer ◽  
E. N. Benz ◽  
B. D. Schmit
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Reflex Response ◽  
Electromyographic Activity ◽  
Plateau Potentials ◽  
Physiological Basis ◽  
Human Spinal Cord ◽  
Reflex Responses ◽  
Flexion Reflex ◽  
Cord Injury

The physiological basis of flexion spasms in individuals after spinal cord injury (SCI) may involve alterations in the properties of spinal neurons in the flexion reflex pathways. We hypothesize that these changes would be manifested as progressive increases in reflex response with repetitive stimulus application (i.e., “windup”) of the flexion reflexes. We investigated the windup of flexion reflex responses in 12 individuals with complete chronic SCI. Flexion reflexes were triggered using trains of electrical stimulation of plantar skin at variable intensities and inter-stimulus intervals. For threshold and suprathreshold stimulation, windup of both peak ankle and hip flexion torques and of integrated tibialis anterior electromyographic activity was observed consistently in all patients at inter-stimulus intervals ≤3 s. For subthreshold stimuli, facilitation of reflexes occurred only at intervals ≤1 s. Similarly, the latency of flexion reflexes decreased significantly at intervals ≤1 s. Patients that were receiving anti-spasticity medications (e.g., baclofen) had surprisingly larger windup of reflex responses than those who did not take such medications, although this difference may be related to differences of spasm frequency between the groups of subjects. The results indicate that the increase in spinal neuronal excitability following a train of electrical stimuli lasts for ≤3 s, similar to previous studies of nociceptive processing. Such long-lasting increases in flexion reflex responses suggest that cellular mechanisms such as plateau potentials in spinal motoneurons, interneurons, or both, may partially mediate spinal cord hyperexcitability in the absence of descending modulatory input.

Modulation of Coordinated Muscle Activity During Imposed Sinusoidal Hip Movements in Human Spinal Cord Injury

2004 ◽  
Vol 92 (2) ◽  
pp. 673-685 ◽  
Author(s):  
Robert E. Steldt ◽  
Brian D. Schmit
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Muscle Activity ◽  
Sagittal Plane ◽  
Afferent Feedback ◽  
Vastus Medialis ◽  
Joint Torques ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Hip Extension

Individuals with chronic spinal cord injury (SCI) often demonstrate multijoint reflex activity that is clinically classified as an extensor spasm. These responses are commonly observed in conjunction with an imposed extension movement of the hips, such as movement from a sit to a supine position. Coincidentally, afferent feedback from hip proprioceptors has also been implicated in the control of locomotion in the spinalized cat. Because of this concurrence, we postulated that extensor spasms that are triggered by hip extension might involve activation of organized interneuronal circuits that also have a role in locomotion. If true, imposed oscillations of the hip would be expected to produce activity of the leg musculature in a locomotor pattern. Furthermore, this muscle activity would be entrained to the hip movement. The right hip joints of 10 individuals with chronic SCI, consisting of both complete [American Spinal Injury Association (ASIA) A] and incomplete (ASIA B,C) injuries, were subjected to ramp and hold (10 s) movements at 60°/s and sinusoidal oscillations at 1.2, 1.88, and 2.2 rad/s over ranges from 40 to –15° (±5°) using a custom servomotor system. Surface EMG from seven lower extremity muscles and sagittal-plane joint torques were recorded to characterize the response. Ramp and hold perturbations produced coactivation at the hip, knee, and ankle joints, with a long duration (5–10 s). Sinusoidal perturbations yielded consistent muscle timing patterns that resulted in alternating flexor and extensor joint torques. EMG and joint torques were commonly entrained to the frequency of movement, with rectus femoris, vastus medialis, and soleus activity coinciding with hip extension and medial hamstrings activity occurring during hip flexion. Individual muscle timing patterns were consistent with hip position during normal gait, except for the vastus medialis. These results suggest that reflexes associated with extensor spasms may occur through organized interneuronal pathways, such as spinal centers for locomotion.

scholarly journals Impaired Organization of Paired-Pulse TMS-Induced I-Waves After Human Spinal Cord Injury

2015 ◽  
Vol 26 (5) ◽  
pp. 2167-2177 ◽  
Author(s):  
John Cirillo ◽  
Finnegan J. Calabro ◽  
Monica A. Perez
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Paired Pulse ◽  
Human Spinal Cord ◽  
Cord Injury

The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight Loss ◽  
Ganglioside Gm1 ◽  
Rat Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

scholarly journals Safety and Feasibility of Autologous Olfactory Ensheathing Cell and Bone Marrow Mesenchymal Stem Cell Co-transplantation in Chronic Human Spinal Cord Injury: A Clinical Trial

2021 ◽  
Author(s):  
Homa Zamani ◽  
Mina Soufizomorrod ◽  
Saeed Oraee-Yazdani ◽  
Dariush Naviafar ◽  
Mohammadhosein Akhlaghpasand ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Bone Marrow ◽  
Spinal Cord Injury ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Safety Issue ◽  
Functional Evaluation ◽  
Olfactory Ensheathing Cell ◽  
Human Spinal Cord ◽  
Cord Injury

Abstract Cell-based therapies are considered as promising strategies for spinal cord regeneration. However, a combinatorial cell therapeutic approach seems more beneficial as it can target various aspects of the injury. Here, we assessed the safety and feasibility of autologous mucosal Olfactory Ensheathing Cell (OEC) and bone marrow Mesenchymal Stem Cell (MSC) co-transplantation in patients with chronic, complete (American Spinal Injury Association (ASIA) classification A) Spinal Cord Injury (SCI). Three patients with the traumatic SCI of the thoracic level were enrolled. They received autologous OEC and MSC combination through the lumbar puncture. All adverse events and possible functional outcomes were documented performing pre- and post-operative general clinical examination, Magnetic Resonance Imaging (MRI), neurological assessment based on the International Standard of Neurological Classification for SCI (ISNCSCI), and functional evaluation using Spinal Cord Independence Measure version III (SCIM III). No serious safety issue was recorded during the two years of follow-up. MRI findings remained unchanged with no neoplastic tissue formation. ASIA impairment scale improved from A to B in one of the participants. SCIM III evaluation also showed some degrees of progress in this patient's quality of life. The two other patients had negligible or no improvement in their sensory scores without any changes in the ASIA impairment scale and SCIM III scores. No motor recovery was observed in any of the participants. Overall, this two-year trial was not associated with any adverse findings, which may suggest the safety of autologous OEC and bone marrow MSC combination for the treatment of human SCI.This study was registered at the Iranian Registry of Clinical Trials (IRCT registration number: IRCT20160110025930N2/ registration date: 2018-09-29).

scholarly journals Motoneuron Death after Human Spinal Cord Injury

2017 ◽  
Vol 34 (3) ◽  
pp. 581-590 ◽  
Author(s):  
Robert M. Grumbles ◽  
Christine K. Thomas
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Human Spinal Cord ◽  
Cord Injury
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