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.
Highlights
The majority of dogs suffering from acute spinal cord injury (SCI) will recover adequate or even normal function [1]
A proportion of permanently deep pain negative dogs demonstrate notable spontaneous motor recovery over time [2, 4, 5]. This can range from non-purposeful kicking movements of the limbs, especially following tactile stimulation below the injury level, to overground walking with minimal apparent paresis or ataxia. Ambulation exhibited by this population, typically known as “spinal walking,” is commonly considered exclusively reflexive stepping generated by the spinal cord caudal to the level of injury as described by experimental studies of SCI in dogs and other species [6,7,8,9,10,11,12,13,14]
Reorganization and adaptations that occur at all levels might influence recovery of motor function below the level of severe injury. These include regrowth of axons across the epicenter, recovery/reactivation of conduction of residually intact upper motor neurons (UMN) axons traversing the lesion epicenter, a more autonomous role for the central pattern generator (CPG), alterations in excitability of interneurons and lower motor neurons (LMN) below injury, activation of silent synapses, changes in synaptic weight, and alterations in sensory input or how afferent input is integrated at the level of the spinal cord below injury [29, 33,34,35,36,37,38]
Summary
- Sensorimotor complete injury: term used to describe functionally and/or physically complete injury in people where there is absent voluntary movement or pain perception below the injury level; synonymous with AIS-A designation using human SCI grading parameters. - Chronically paralyzed: broad, non-specific term used to capture the population of dogs with permanent neurologic impairment (motor, sensory, and/or deficits in continence) following severe SCI. Dogs in this group can exhibit paraplegia (i.e., no pelvic limb movement at all) or display varying degrees of pelvic limb movements that fall short of being useful (i.e., they remain non-ambulatory). - Spinal walking: independent ambulation in a “deep pain negative” dog typically characterized by lack of coordination between thoracic and pelvic limbs, difficulty turning, or going backward, intermittent falling (especially when changing directions), frequently intact toe knuckling response but absent hopping, and increased spasticity
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