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

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.

2004 ◽  
Vol 162 (2) ◽  
pp. 239-249 ◽  
Author(s):  
Ming Wu ◽  
T. George Hornby ◽  
Jennifer Hilb ◽  
Brian D. Schmit

2004 ◽  
Vol 92 (6) ◽  
pp. 3375-3384 ◽  
Author(s):  
T. G. Hornby ◽  
V. M. Tysseling-Mattiace ◽  
E. N. Benz ◽  
B. D. Schmit

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


2007 ◽  
Vol 98 (4) ◽  
pp. 1849-1861 ◽  
Author(s):  
Tanya Onushko ◽  
Brian D. Schmit

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.


2004 ◽  
Vol 92 (2) ◽  
pp. 673-685 ◽  
Author(s):  
Robert E. Steldt ◽  
Brian D. Schmit

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.


2005 ◽  
Vol 168 (4) ◽  
pp. 566-576 ◽  
Author(s):  
Ming Wu ◽  
T. George. Hornby ◽  
Jennifer H. Kahn ◽  
Brian D. Schmit

2015 ◽  
Vol 26 (5) ◽  
pp. 2167-2177 ◽  
Author(s):  
John Cirillo ◽  
Finnegan J. Calabro ◽  
Monica A. Perez

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young

✓ 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.


2021 ◽  
Author(s):  
Homa Zamani ◽  
Mina Soufizomorrod ◽  
Saeed Oraee-Yazdani ◽  
Dariush Naviafar ◽  
Mohammadhosein Akhlaghpasand ◽  
...  

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).


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