2016
DOI: 10.1016/j.spinee.2015.09.018
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Longitudinal extension of myelomalacia by intramedullary and subdural hemorrhage in a canine model of spinal cord injury

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Cited by 33 publications
(65 citation statements)
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“…In cases with severe tissue destruction in the center, the spinal cord tissue was replaced by an amorphous mixture of spinal cord tissue debris, macrophages, and blood. In those dogs, this hemorrhagic necrotic material was also found inside or dorsal to the central canal, or both in spinal cord segments distant from the center of the lesion in otherwise mildly damaged spinal cord tissue as described previously . Gliosis and vascular proliferation were present in chronic cases.…”
Section: Resultssupporting
confidence: 66%
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“…In cases with severe tissue destruction in the center, the spinal cord tissue was replaced by an amorphous mixture of spinal cord tissue debris, macrophages, and blood. In those dogs, this hemorrhagic necrotic material was also found inside or dorsal to the central canal, or both in spinal cord segments distant from the center of the lesion in otherwise mildly damaged spinal cord tissue as described previously . Gliosis and vascular proliferation were present in chronic cases.…”
Section: Resultssupporting
confidence: 66%
“…To evaluate the longitudinal extension of the lesion, the presence of myelomalacia, defined as complete loss of structural integrity of spinal cord parenchyma, was assessed on all sections of each animal, thus including the center, adjacent and more remote spinal cord segments. The longitudinal extension was categorized as grade 0 (no malacia), grade 1 (focal malacia at the center), and grade 2 (ADMM from the center across at least 3 spinal cord segments) as previously described and illustrated …”
Section: Methodsmentioning
confidence: 99%
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“…Severity of neurologic injury spans a spectrum up to and including sensorimotor complete injury, with predictable patterns of recovery across different severities (Olby et al, 2003, 2004; Bergknut et al, 2012). Primary and secondary mechanisms of SCI in dogs are consistent with those observed in humans, and include central gray matter hemorrhage, necrosis, cavitation, sparing of subpial axons, axonal degeneration, and variable degrees of demyelination (Smith and Jeffery, 2006; Moore and Oglesbee, 2014; Henke et al, 2014, 2015). Accordingly, clinical dog models can serve as a “bridge” between rodent models of SCI and human patients because they address many translational issues.…”
Section: Introductionsupporting
confidence: 59%