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Mohammed F. Shamji Toronto Western Hospital 4 2013 34 4 Functional Imaging A5 A6 Copyright held by the American Association of Neurological Surgeons. You may not sell, republish, or systematically distribute any published materials without written permission from JNSPG. 2013 Introduction: Intervertebral disc (IVD) herniation causes radiculopathy by mechanical compression and biochemical irritation of nearby neural structures. Animal models of radiculopathy describe demyelination, slowed nerve conduction, and heightened pain sensitivity

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the non-chondrodystrophic (NCD) or “mongrel” dog that retains its population of notochordal cells (unlike humans) does not develop DDD if at all, until much later in life. Here we demonstrate that NCCM is capable of regenerating the degenerative disc in a pre-clinical animal model of DDD. Materials/Methods: We used a 26-gauge needle and image guidance to develop DDD in a pre-clinical rodent model and characterized the degenerative cascade from healthy through 10-weeks by analyzing the IVD NPs until 6-weeks post injury. Meanwhile we generated notochordal cell

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intervertebral disc (IVD) in animal models induces structural damage and leads to IVD degeneration over time. Prior rodent IVD degeneration models have involved injury to multiple IVDs, which confounds the mechanism of pain generation. This study identifies a behavioral and pain-related sensitivity phenotype after puncture of one lumbar IVD. Materials/Methods: Baseline functional assessments including static weight-bearing, gait analysis, site-specific algesia, and open field testing were done for Sprague-Dawley rats (n=36, 18 weeks old) the day before lumbar IVD