Preserved ambulation in a puppy with severe thoracolumbar myelodysplasia

A 19-week-old female Blue Heeler puppy presented with pelvic limb ataxia lasting for at least 3 months. She was much smaller than her littermates and considered deaf. There was no evidence of trauma on previous radiographs. Serology for canine distemper virus and Neospora caninum was negative. The puppy was ambulatory with obvious pelvic limb ataxia, moderate paraparesis and a ‘bunny-hopping’ gait when moving faster. Postural reactions, apart from the digit knuckling test, were severely delayed/absent bilaterally. Spinal reflexes were intact and easily elicited. The cutaneous trunci muscle reflex was absent caudal to T10 bilaterally. Pain perception, assessed using haemostats, was absent in the digits of both pelvic limbs but intact in the tail. The puppy appeared continent, demonstrated by posturing to urinate in appropriate areas. Magnetic resonance imaging of the thoracolumbar spine (Siemens Verio 3.0T) revealed scoliosis and a large fluid-filled space primarily involving the dorsal part of the spinal cord from T2 to L3 vertebral levels. Within the most severely affected region (T9–T11), more than 90% of the spinal cord parenchyma was obliterated. There was mild T2/STIR hyperintensity within the parenchyma from T7 to T8 (Fig 1). Differential diagnoses for the image appearance included extensive syringomyelia resulting from trauma, although a congenital aetiology (i.e. myelodysplasia) was more strongly suspected. Myelodysplasia of the spinal cord includes a group of developmental anomalies, including inherited spinal dysraphism in Weimaraners, resulting from defects during embryologic closure of the neural tube. The occurrence in this Blue Heeler suggests possible similar genetic susceptibility in this breed, although other teratogenic agents should also be considered. Surprisingly, this puppy remained strongly ambulatory and apparently continent, despite marked spinal cord parenchymal deficit. The increased flexor reflexes in the pelvic limbs were presumed secondary to increased ‘gain’ in the reflex pathway, consistent with plastic changes associated with severe loss of thoracolumbar spinal cord integrity.