Quantification of spinal ataxia in dogs with thoracolumbar spinal cord injury

The clinical sign of ataxia is related to several neurological diseases and is seen in conjunction with paresis in dogs with spinal cord injury (SCI). Endeavours to objectify canine spinal ataxia in SCI remain limited. The aim of this clinical study was to determine and quantify differences between gait characteristics of ataxic dogs with thoracolumbar myelopathy and healthy control dogs using a computer-and treadmill-based gait analysis system. Five dogs with spinal ataxia and six healthy dogs underwent video-and computer-assisted gait analysis while walking on a four-ground reaction force plate treadmill system (maximum speed of 0.7 m/s). Spatio-temporal and kinetic gait characteristics regarding the dogs' locomotion were analysed with a focus on the individual coefficient of variation (CV), as a potential measure for quantification of the level of ataxia. Ataxic dogs with thoracolumbar SCI showed no effect on symmetry indices but higher variability in spatio-temporal and kinetic gait parameters mainly in the pelvic, but also in the thoracic limbs. Double support phase of the individual limb was prolonged in SCI dogs at the cost of the single support and swing phase. Reduced peaks of ground reaction forces (GRF) could potentially be explained by reduction of muscle strength, as a strategy of avoiding falling by taking enthusiastic steps, or by alteration of the rhythmogenic spinal circuits between the pelvic and thoracic limb pattern generators.

Automated summary

This clinical study aimed to determine and quantify the differences in gait characteristics between dogs with spinal ataxia and healthy control dogs using a computer-and treadmill-based gait analysis system. Dogs with thoracolumbar myelopathy showed higher variability in spatio-temporal and kinetic gait parameters mainly in the pelvic and thoracic limbs, but no effect on symmetry indices. Reduced peaks of ground reaction forces could potentially be explained by reduction of muscle strength or alteration of the rhythmogenic spinal circuits.