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CASE DESCRIPTION 3 dogs were examined because of a sudden onset of signs of pain (1 dog) or paraparesis (2 dogs). CLINICAL FINDINGS Neurologic findings consisted of myelopathy affecting the lumbar intumescence (1 dog) and T3-L3 myelopathy (2 dogs). In all dogs, MRI revealed spinal cord compression caused by L3-4 disk herniation. All dogs underwent routine surgical decompression of the intervertebral disk herniation. During MRI and decompressive surgery, physiologic variables were monitored. Immediately after surgery, all dogs were paraplegic with pelvic limb neurologic dysfunction consistent with myelopathy affecting the L4 through caudal spinal cord segments. TREATMENT AND OUTCOME Within 24 hours after surgery, repeated MRI in all dogs revealed hyperintensity in the spinal cord gray matter of the lumbar intumescence on T2-weighted images. In the absence of neurologic improvement, dogs were euthanized at 3, 91, and 34 days after surgery. Postmortem microscopic examination of each dog's spinal cord at the lumbar intumescence revealed necrosis of the gray matter with relative white matter preservation suggestive of an ischemic injury. CLINICAL RELEVANCE Dramatic neurologic deterioration following decompressive surgery for intervertebral disk herniation in dogs may be associated with the development of poliomyelomalacia secondary to ischemia. In these 3 dogs, ischemia developed despite probable maintenance of normal spinal cord blood flow and perfusion during anesthesia. To exclude other causes, such as compression or hemorrhage, MRI was repeated and revealed hyperintensity of the spinal cord gray matter on T2-weighted images, which microscopically corresponded with ischemic neurons and neuronal loss.

Acute spinal cord injury consists of a primary, traumatic event followed by a cascade of secondary events resulting in ongoing cell damage and death. There is great interest in prevention of these secondary effects to reduce permanent long-term neurologic deficits. One such target includes reactive oxygen species released following injury, which can be enzymatically converted into less harmful molecules by superoxide dismutase and catalase. Canine intervertebral disc herniation has been suggested as a naturally occurring model for acute spinal cord injury and its secondary effects in people. The aims of this study were to test the safety of a novel antioxidant delivery system in four healthy dogs and to indirectly test effect of delivery via cytokine measurement. All dogs experienced adverse events to some degree, with two experiencing adverse events considered to be severe. The clinical signs, including combinations of bradycardia, hypotension, hypersalivation, pale gums, and involuntary urination, were consistent with complement activation-related pseudoallergy (CARPA). CARPA is a well-known phenomenon that has been reported to occur with nanoparticle-based drug delivery, among other documented causes. Two dogs also had mild to moderate changes in their blood cell count and chemistry, including elevated alanine transferase, and thrombocytopenia, which both returned to normal by day 7 post-administration. Cytokine levels trended downwards over the first 3 days, but many were elevated at measurement on day 7. Intradermal testing suggested catalase as a potential cause for reactions. No long-term clinical signs were observed, and necropsy results revealed no concerning pathology. Additional evaluation of this product, including further characterization of reactions to catalase containing components, dose-escalation, and desensitization should be performed before evaluation in clinically affected dogs.