Some features of the stretch reflex after spinal cord injury

1979 ◽  
Vol 87 (3) ◽  
pp. 191-193 ◽  
Author(s):  
T. N. Nesmeyanova
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stretch Reflex ◽  
Cord Injury

The tonic stretch reflex and spastic hypertonia after spinal cord injury

2006 ◽  
Vol 174 (2) ◽  
pp. 386-396 ◽  
Author(s):  
Adam J. Woolacott ◽  
John A. Burne
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stretch Reflex ◽  
Cord Injury

scholarly journals Altered activation patterns by triceps surae stretch reflex pathways in acute and chronic spinal cord injury

2011 ◽  
Vol 106 (4) ◽  
pp. 1669-1678 ◽  
Author(s):  
Alain Frigon ◽  
Michael D. Johnson ◽  
C. J. Heckman
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stretch Reflex ◽  
Triceps Surae ◽  
Stretch Reflexes ◽  
Activation Patterns ◽  
Intact State ◽  
Hindlimb Muscles ◽  
Reflex Pathways ◽  
Cord Injury

Spinal reflexes are modified by spinal cord injury (SCI) due the loss of excitatory inputs from supraspinal structures and changes within the spinal cord. The stretch reflex is one of the simplest pathways of the central nervous system and was used presently to evaluate how inputs from primary and secondary muscle spindles interact with spinal circuits before and after spinal transection (i.e., spinalization) in 12 adult decerebrate cats. Seven cats were spinalized and allowed to recover for 1 mo (i.e., chronic spinal state), whereas 5 cats were evaluated before (i.e., intact state) and after acute spinalization (i.e., acute spinal state). Stretch reflexes were evoked by stretching the left triceps surae (TS) muscles. The force evoked by TS muscles was recorded along with the activity of several hindlimb muscles. Stretch reflexes were abolished in the acute spinal state due to an inability to activate TS muscles, such as soleus (Sol) and lateral gastrocnemius (LG). In chronic spinal cats, reflex force had partly recovered but Sol and LG activity remained considerably depressed, despite the fact that injecting clonidine could recruit these muscles during locomotor-like activity. In contrast, other muscles not recruited in the intact state, most notably semitendinosus and sartorius, were strongly activated by stretching TS muscles in chronic spinal cats. Therefore, stretch reflex pathways from TS muscles to multiple hindlimb muscles undergo functional reorganization following spinalization, both acute and chronic. Altered activation patterns by stretch reflex pathways could explain some sensorimotor deficits observed during locomotion and postural corrections after SCI.

Effect of spinal cord injury and its lesion level on stretch reflex modulation by cold stimulation in humans

2011 ◽  
Vol 122 (1) ◽  
pp. 163-170 ◽  
Author(s):  
H. Ogata ◽  
D.G. Sayenko ◽  
E. Yamamoto ◽  
T. Kitamura ◽  
S. Yamamoto ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stretch Reflex ◽  
Reflex Modulation ◽  
Cold Stimulation ◽  
Cord Injury ◽  
Lesion Level

scholarly journals 5-HT1D receptors inhibit the monosynaptic stretch reflex by modulating C-fiber activity

2019 ◽  
Vol 121 (5) ◽  
pp. 1591-1608 ◽  
Author(s):  
Ana M. Lucas-Osma ◽  
Yaqing Li ◽  
Katie Murray ◽  
Shihao Lin ◽  
Sophie Black ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stretch Reflex ◽  
Spinal Transection ◽  
Dorsal Rhizotomy ◽  
C Fibers ◽  
Cord Injury ◽  
C Fiber ◽  
Receptor Plasticity ◽  
Highly Correlated

The monosynaptic stretch reflex (MSR) plays an important role in feedback control of movement and posture but can also lead to unstable oscillations associated with tremor and clonus, especially when increased with spinal cord injury (SCI). To control the MSR and clonus after SCI, we examined how serotonin regulates the MSR in the sacrocaudal spinal cord of rats with and without a chronic spinal transection. In chronic spinal rats, numerous 5-HT receptor agonists, including zolmitriptan, methylergonovine, and 5-HT, inhibited the MSR with a potency highly correlated to their binding affinity to 5-HT1D receptors and not other 5-HT receptors. Selective 5-HT1D receptor antagonists blocked this agonist-induced inhibition, although antagonists alone had no action, indicating a lack of endogenous or constitutive receptor activity. In normal uninjured rats, the MSR was likewise inhibited by 5-HT, but at much higher doses, indicating a supersensitivity after SCI. This supersensitivity resulted from the loss of the serotonin transporter SERT with spinal transection, because normal and injured rats were equally sensitive to 5-HT after SERT was blocked or to agonists not transported by SERT (zolmitriptan). Immunolabeling revealed that the 5-HT1D receptor was confined to superficial lamina of the dorsal horn, colocalized with CGRP-positive C-fibers, and eliminated by dorsal rhizotomy. 5-HT1D receptor labeling was not found on large proprioceptive afferents or α-motoneurons of the MSR. Thus serotonergic inhibition of the MSR acts indirectly by modulating C-fiber activity, opening up new possibilities for modulating reflex function and clonus via pain-related pathways. NEW & NOTEWORTHY Brain stem-derived serotonin potently inhibits afferent transmission in the monosynaptic stretch reflex. We show that serotonin produces this inhibition exclusively via 5-HT1D receptors, and yet these receptors are paradoxically mostly confined to C-fibers. This suggests that serotonin acts by gating of C-fiber activity, which in turn modulates afferent transmission to motoneurons. We also show that the classic supersensitivity to 5-HT after spinal cord injury results from a loss of SERT, and not 5-HT1D receptor plasticity.

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