Ambulation in Dogs With Absent Pain Perception After Acute Thoracolumbar Spinal Cord Injury

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Abstract

Acute thoracolumbar spinal cord injury (SCI) is common in dogs frequently secondary to intervertebral disc herniation. Following severe injury, some dogs never regain sensory function to the pelvic limbs or tail and are designated chronically “deep pain negative.” Despite this, a subset of these dogs develop spontaneous motor recovery over time including some that recover sufficient function in their pelvic limbs to walk independently without assistance or weight support. This type of ambulation is commonly known as “spinal walking” and can take up to a year or more to develop. This review provides a comparative overview of locomotion and explores the physiology of locomotor recovery after severe SCI in dogs. We discuss the mechanisms by which post-injury plasticity and coordination between circuitry contained within the spinal cord, peripheral sensory feedback, and residual or recovered supraspinal connections might combine to underpin spinal walking. The clinical characteristics of spinal walking are outlined including what is known about the role of patient or injury features such as lesion location, timeframe post-injury, body size, and spasticity. The relationship between the emergence of spinal walking and electrodiagnostic and magnetic resonance imaging findings are also discussed. Finally, we review possible ways to predict or facilitate recovery of walking in chronically deep pain negative dogs. Improved understanding of the mechanisms of gait generation and plasticity of the surviving tissue after injury might pave the way for further treatment options and enhanced outcomes in severely injured dogs.

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Most cited references 111

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Chondroitinase ABC promotes functional recovery after spinal cord injury.

Elizabeth Bradbury, Lawrence D. F. Moon, Reena J Popat … (2002)

The inability of axons to regenerate after a spinal cord injury in the adult mammalian central nervous system (CNS) can lead to permanent paralysis. At sites of CNS injury, a glial scar develops, containing extracellular matrix molecules including chondroitin sulphate proteoglycans (CSPGs). CSPGs are inhibitory to axon growth in vitro, and regenerating axons stop at CSPG-rich regions in vivo. Removing CSPG glycosaminoglycan (GAG) chains attenuates CSPG inhibitory activity. To test the functional effects of degrading chondroitin sulphate (CS)-GAG after spinal cord injury, we delivered chondroitinase ABC (ChABC) to the lesioned dorsal columns of adult rats. We show that intrathecal treatment with ChABC degraded CS-GAG at the injury site, upregulated a regeneration-associated protein in injured neurons, and promoted regeneration of both ascending sensory projections and descending corticospinal tract axons. ChABC treatment also restored post-synaptic activity below the lesion after electrical stimulation of corticospinal neurons, and promoted functional recovery of locomotor and proprioceptive behaviours. Our results demonstrate that CSPGs are important inhibitory molecules in vivo and suggest that their manipulation will be useful for treatment of human spinal injuries.

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The injured spinal cord spontaneously forms a new intraspinal circuit in adult rats.

Oliver Weinmann, Martin Kerschensteiner, Thomas C. Mettenleiter … (2004)

In contrast to peripheral nerves, central axons do not regenerate. Partial injuries to the spinal cord, however, are followed by functional recovery. We investigated the anatomical basis of this recovery and found that after incomplete spinal cord injury in rats, transected hindlimb corticospinal tract (CST) axons sprouted into the cervical gray matter to contact short and long propriospinal neurons (PSNs). Over 12 weeks, contacts with long PSNs that bridged the lesion were maintained, whereas contacts with short PSNs that did not bridge the lesion were lost. In turn, long PSNs arborize on lumbar motor neurons, creating a new intraspinal circuit relaying cortical input to its original spinal targets. We confirmed the functionality of this circuit by electrophysiological and behavioral testing before and after CST re-lesion. Retrograde transynaptic tracing confirmed its integrity, and revealed changes of cortical representation. Hence, after incomplete spinal cord injury, spontaneous extensive remodeling occurs, based on axonal sprout formation and removal. Such remodeling may be crucial for rehabilitation in humans.

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Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury.

Bingbing Song, H. Herrmann, Hui Zhong … (2007)

Spinal cord injuries (SCIs) in humans and experimental animals are often associated with varying degrees of spontaneous functional recovery during the first months after injury. Such recovery is widely attributed to axons spared from injury that descend from the brain and bypass incomplete lesions, but its mechanisms are uncertain. To investigate the neural basis of spontaneous recovery, we used kinematic, physiological and anatomical analyses to evaluate mice with various combinations of spatially and temporally separated lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons. We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice. Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections. Targeting interventions toward augmenting the remodeling of relay connections may provide new therapeutic strategies to bypass lesions and restore function after SCI and in other conditions such as stroke and multiple sclerosis.

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Author and article information

Contributors

Melissa J. Lewis: URI : http://loop.frontiersin.org/people/839549/overview

Nick D. Jeffery: URI : http://loop.frontiersin.org/people/930974/overview

Natasha J. Olby: URI : http://loop.frontiersin.org/people/808262/overview

Journal

Journal ID (nlm-ta): Front Vet Sci

Journal ID (iso-abbrev): Front Vet Sci

Journal ID (publisher-id): Front. Vet. Sci.

Title: Frontiers in Veterinary Science

Publisher: Frontiers Media S.A.

ISSN (Electronic): 2297-1769

Publication date (Electronic): 26 August 2020

Publication date Collection: 2020

Volume: 7

Electronic Location Identifier: 560

Affiliations

Author Affiliations: DACVIM-Neurology, Associate Professor, Neurology and Neurosurgery, Department of Veterinary Clinical Sciences, The Ohio State University College of Veterinary Medicine, Columbus, OH, United States; DACVIM-Neurology, Professor of Neurology/Neurosurgery; Distinguished Chair of Gerontology, Department of Clinical Sciences, North Carolina State University College of Veterinary Medicine, Raleigh, NC, United States; DACVIM-Neurology Professor; Chair, and Head, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, United States; DAVCIM (Neurology), Assistant Professor of Neurology, Purdue University College of Veterinary Medicine, Department of Veterinary Clinical Sciences, West Lafayette, IN, United States; Professor Neurology & Neurosurgery; Professor in Small Animal Clinical Sciences, College of Veterinary Medicine, Texas A&M University, College Station, TX, United States; ACVIM - Neurology Professor and Service Head, Neurology and Neurosurgery, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH, United States; Department of Clinical Sciences, Colorado State University, Fort Collins, CO, United States; Department of Clinical Science and Services, Royal Veterinary College, Hatfield, United Kingdom; The Royal Veterinary College, University of London, Hatfield, United Kingdom & CVS Referrals, Bristol Veterinary Specialists at Highcroft, Bristol, United Kingdom; Institute of Veterinary Pathology, Faculty of Veterinary Medicine, Leipzig University, Leipzig, Germany; Division of Clinical Neurology, Department for Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland; Department Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany/Europe; Neurology and Neurosurgery, Department of Veterinary Medicine and Surgery, University of Missouri, 900 E. Campus Dr., MU Veterinary Health Center, University of Missouri, Columbia, MO, United States; Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany/Europe

[1] ¹Department of Veterinary Clinical Sciences, Purdue University College of Veterinary Medicine , West Lafayette, IN, United States

[2] ²Department of Small Animal Clinical Sciences, Texas a & M College of Veterinary Medicine and Biomedical Sciences , College Station, TX, United States

[3] ³Department of Clinical Sciences, North Carolina State University , Raleigh, NC, United States

Author notes

Edited by: Luisa De Risio, Animal Health Trust, United Kingdom

Reviewed by: Franck Forterre, University of Bern, Switzerland; Massimo Baroni, Valdinievole Veterinary Clinic, Italy

*Correspondence: Melissa J. Lewis lewis444@ 123456purdue.edu

This article was submitted to Veterinary Neurology and Neurosurgery, a section of the journal Frontiers in Veterinary Science

Article

DOI: 10.3389/fvets.2020.00560

PMC ID: 7479830

PubMed ID: 33062648

SO-VID: e470170c-ab1c-4fe2-90de-56b081121be3

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This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 05 June 2020

Date accepted : 14 July 2020

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Figures: 0, Tables: 0, Equations: 0, References: 117, Pages: 11, Words: 9511

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Ambulation in Dogs With Absent Pain Perception After Acute Thoracolumbar Spinal Cord Injury

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Most cited references 111

Chondroitinase ABC promotes functional recovery after spinal cord injury.

The injured spinal cord spontaneously forms a new intraspinal circuit in adult rats.

Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury.

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Cited by 9

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