Dataset Information

Quantification of deficits in lateral paw positioning after spinal cord injury in dogs.

ABSTRACT:

Background

Previous analysis of the behavioural effects of spinal cord injury has focussed on coordination in the sagittal plane of movement between joints, limb girdle pairs or thoracic and pelvic limb pairs. In this study we extend the functional analysis of the consequences of clinical thoracolumbar spinal cord injury in dogs to quantify the well-recognised deficits in lateral stability during locomotion. Dogs have a high centre of mass thereby facilitating recognition of lateral instability.

Results

We confirm that errors in lateral positioning of the pelvic limb paws can be quantified and that there is a highly significant difference in variability of foot placement between normal and spinal cord injured dogs. In this study there was no detectable difference in lateral paw positioning variability between complete and incomplete injuries, but it appears that intergirdle limb coordination and appropriate lateral paw placement recover independently from one another.

Conclusion

Analysis of lateral paw position in the dog provides an additional tier of analysis of outcome after spinal cord injury that will be of great value in interpreting the effects of putative therapeutic interventions.

SUBMITTER: Hamilton L

PROVIDER: S-EPMC2631515 | biostudies-literature | 2008 Nov

REPOSITORIES: biostudies-literature

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Publications

Quantification of deficits in lateral paw positioning after spinal cord injury in dogs.

Hamilton Lindsay L Franklin Robin J M RJ Jeffery Nicholas D ND

BMC veterinary research 20081125

<h4>Background</h4>Previous analysis of the behavioural effects of spinal cord injury has focussed on coordination in the sagittal plane of movement between joints, limb girdle pairs or thoracic and pelvic limb pairs. In this study we extend the functional analysis of the consequences of clinical thoracolumbar spinal cord injury in dogs to quantify the well-recognised deficits in lateral stability during locomotion. Dogs have a high centre of mass thereby facilitating recognition of lateral inst ...[more]

PMID: 19032742

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Project description:Spinal cord injury disrupts the communication between the brain and the spinal circuits that orchestrate movement. To bypass the lesion, brain-computer interfaces have directly linked cortical activity to electrical stimulation of muscles, and have thus restored grasping abilities after hand paralysis. Theoretically, this strategy could also restore control over leg muscle activity for walking. However, replicating the complex sequence of individual muscle activation patterns underlying natural and adaptive locomotor movements poses formidable conceptual and technological challenges. Recently, it was shown in rats that epidural electrical stimulation of the lumbar spinal cord can reproduce the natural activation of synergistic muscle groups producing locomotion. Here we interface leg motor cortex activity with epidural electrical stimulation protocols to establish a brain-spine interface that alleviated gait deficits after a spinal cord injury in non-human primates. Rhesus monkeys (Macaca mulatta) were implanted with an intracortical microelectrode array in the leg area of the motor cortex and with a spinal cord stimulation system composed of a spatially selective epidural implant and a pulse generator with real-time triggering capabilities. We designed and implemented wireless control systems that linked online neural decoding of extension and flexion motor states with stimulation protocols promoting these movements. These systems allowed the monkeys to behave freely without any restrictions or constraining tethered electronics. After validation of the brain-spine interface in intact (uninjured) monkeys, we performed a unilateral corticospinal tract lesion at the thoracic level. As early as six days post-injury and without prior training of the monkeys, the brain-spine interface restored weight-bearing locomotion of the paralysed leg on a treadmill and overground. The implantable components integrated in the brain-spine interface have all been approved for investigational applications in similar human research, suggesting a practical translational pathway for proof-of-concept studies in people with spinal cord injury.

Project description:BackgroundGlyburide (also known as glibenclamide) is effective in reducing the severity of tissue destruction and improving functional outcome after experimental spinal cord injury in rodents and so has promise as a therapy in humans. There are many important differences between spinal cord injury in experimental animals and in human clinical cases, making it difficult to introduce new therapies into clinical practice. Spinal cord injury is also common in pet dogs and requires new effective therapies, meaning that they can act as a translational model for the human condition while also deriving direct benefits from such research. In this study we investigated the pharmacokinetics and safety of glyburide in dogs with clinical spinal cord injury.MethodsWe recruited dogs that had incurred an acute thoracolumbar spinal cord injury within the previous 72 h. These had become acutely non-ambulatory on the pelvic limbs and were admitted to our veterinary hospitals to undergo anesthesia, cross sectional diagnostic imaging, and surgical decompression. Oral glyburide was given to each dog at a dose of 75 mcg/kg. In five dogs, we measured blood glucose concentrations for 10 h after a single oral dose. In six dogs, we measured serum glyburide and glucose concentrations for 24 h and estimated pharmacokinetic parameters to estimate a suitable dose for use in a subsequent clinical trial in similarly affected dogs.ResultsNo detrimental effects of glyburide administration were detected in any participating dog. Peak serum concentrations of glyburide were attained at a mean of 13 h after dosing, and mean apparent elimination half-life was approximately 7 h. Observed mean maximum plasma concentration was 31 ng/mL. At the glyburide dose administered there was no observable association between glyburide and glucose concentrations in blood.DiscussionOur data suggest that glyburide can be safely administered to dogs that are undergoing anesthesia, imaging and surgery for treatment of their acute spinal cord injury and can attain clinically-relevant serum concentrations without developing hazardous hypoglycemia. Serum glyburide concentrations achieved in this study suggest that a loading dose of 150 mcg/kg followed by repeat doses of 75 mcg/kg at 8-hourly intervals would lead to serum glyburide concentrations of 25-50 ng/mL within an acceptably short enough period after oral administration to be appropriate for a clinical trial in canine spinal cord injury.

Dataset Information

Quantification of deficits in lateral paw positioning after spinal cord injury in dogs.

Background

Results

Conclusion

Publications

Quantification of deficits in lateral paw positioning after spinal cord injury in dogs.

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