Poster abstracts

Poster number 85 submitted by Timothy Faw

Mid-thoracic Spinal Cord Injury Results in Morphological Changes and Neuronal Hyperactivity in the Locomotor Networks of the Remote Lumbar Spinal Cord

Timothy D. Faw, PT, DPT, NCS (Neuroscience Graduate Studies Program, The Ohio State University), Christopher N. Hansen, Ph.D. (Center for Brain and Spinal Cord Repair, The Ohio State University), Lesley C. Fisher (School of Health and Rehabilitation Sciences, The Ohio State University), Samantha D. Kerr (School of Health and Rehabilitation Sciences, The Ohio State University), John Buford, PT, Ph.D. (School of Health and Rehabilitation Sciences, The Ohio State University), D. Michele Basso, PT, Ed.D. (School of Health and Rehabilitation Sciences, The Ohio State University)

Abstract:
Spasticity is clinically defined as a velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks and is a common sequela of spinal cord injury (SCI). Spasticity occurs in up to 75% of individuals with SCI with most reporting that it negatively impacts quality of life. While the pathophysiology of spasticity is largely unknown, one possible mechanism involves dysfunction of the spinal interneurons (Neilson 2004). Previously we showed an inability of the remote lumbar spinal cord to learn an instrumental task at chronic time points following mid-thoracic transection (TX). Here, we examined interneurons of the lumbar cord for morphological changes as key players in this known deficit. We used Golgi’s staining technique combined with neuron tracing software to quantify dendritic spines of interneurons located in laminas VI and VII after different injury severities. We looked at acute (7d) and chronic (42d) time points in both complete and incomplete injuries as a model of reactive plasticity following SCI as well as to examine the effects of sparing on this response. This experiment is compelling as it is the first to attempt quantification of plasticity in the lumbar locomotor networks that likely contribute to spasticity in humans. Preliminary data showed an increase in the number of dendritic spines following transection suggesting a potentially maladaptive response. Additionally, these interneurons had smaller cell body size compared to those of naïve animals. Consistent with the noted morphological changes, data acquired from sister groups showed a decrease in stimulation amplitude required to produce a predetermined ankle flexion force of 0.4-0.5N in the tibialis anterior muscle after chronic transection injury (n=5; Mean Stim = 0.64mA +/- 0.19) compared to naïve (n=8; Mean Stim = 2.30 +/- 0.10; p<.001). Together, these findings show that morphological changes of lumbar interneurons appear to produce greater neuronal excitability, which would be consistent with hyperreflexia and spasticity. They also provide a novel target for interventions designed to reduce spasticity and promote functional recovery following spinal cord injury.

References:
1) Neilson et al (2007) Acta Physiol 189(2):171-80.
2) Roy and Edgerton (2012) Exp Neurol 235(1):116-22.
3) Hansen et al (2014) Submitted.

Keywords: Spinal Cord Injury, Plasticity, Spasticity