Nerve Root Reimplantation in Brachial Plexus Injuries

Vanaclocha‐Vanaclocha, Vicente; Saiz-Sapena, Nieves; Ortiz-Criado, José María; Vanaclocha, Leyre

doi:10.5772/intechopen.82431

Cited by 1 publication

(1 citation statement)

References 205 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As noted previously, neuroprotective treatments given early after injury tend to protect motor neurons that would have died anyway, thereby giving them a chance to survive, sprout and re-innervate their targets [ 53 ]. There is a need to buy time in the clinic so that axotomized motor neurons can sprout and reach their targets such as muscles before they become fibrotic and degenerate too [ 54 , 55 ]. The current neuroprotective treatments, 7-nitroindazole and SP600125 given long term, did partially preserve motor neurons, ventral horn size, and hence, function.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Suppression of c-Jun and nNOS Preserves Ultrastructural Features of Lower Motor Neurons and Forelimb Function after Brachial Plexus Roots Avulsion

Liaquat

Wang

et al. 2021

Cells

View full text Add to dashboard Cite

Brachial plexus root avulsions cause debilitating upper limb paralysis. Short-term neuroprotective treatments have reported preservation of motor neurons and function in model animals while reports of long-term benefits of such treatments are scarce, especially the morphological sequelae. This morphological study investigated the long-term suppression of c-Jun- and neuronal nitric oxide synthase (nNOS) (neuroprotective treatments for one month) on the motor neuron survival, ultrastructural features of lower motor neurons, and forelimb function at six months after brachial plexus roots avulsion. Neuroprotective treatments reduced oxidative stress and preserved ventral horn motor neurons at the end of the 28-day treatment period relative to vehicle treated ones. Motor neuron sparing was associated with suppression of c-Jun, nNOS, and pro-apoptotic proteins Bim and caspases at this time point. Following 6 months of survival, neutral red staining revealed a significant loss of most of the motor neurons and ventral horn atrophy in the avulsed C6, 7, and 8 cervical segments among the vehicle-treated rats (n = 4). However, rats that received neuroprotective treatments c-Jun JNK inhibitor, SP600125 (n = 4) and a selective inhibitor of nNOS, 7-nitroindazole (n = 4), retained over half of their motor neurons in the ipsilateral avulsed side compared. Myelinated axons in the avulsed ventral horns of vehicle-treated rats were smaller but numerous compared to the intact contralateral ventral horns or neuroprotective-treated groups. In the neuroprotective treatment groups, there was the preservation of myelin thickness around large-caliber axons. Ultrastructural evaluation also confirmed the preservation of organelles including mitochondria and synapses in the two groups that received neuroprotective treatments compared with vehicle controls. Also, forelimb functional evaluation demonstrated that neuroprotective treatments improved functional abilities in the rats. In conclusion, neuroprotective treatments aimed at suppressing degenerative c-Jun and nNOS attenuated apoptosis, provided long-term preservation of motor neurons, their organelles, ventral horn size, and forelimb function.

show abstract

Section: Discussionmentioning

confidence: 99%