Non-Compressive Myelopathies

Spinal cord diseases without compression of the spinal cord or/and the meninges are referred as non-compressive myelopathies, and can be ischaemic (fibrocartilaginous embolism), inflammatory/infectious (meningomyelitis of unknown aetiology, discospondylitis, distemper myelitis, toxoplasmosis/neosporosis), traumatic (acute non-compressive nucleus pulposus extrusion, spinal cord concussion), congenital/hereditary (e.g. spinocerebellar ataxia of Jack Russel Terriers), neoplastic (intramedullary infiltrative neoplasia e.g. lymphoma) and degenerative (degenerative myelopathy). Fibrinocartilaginous embolism (FCE) is a peracute non-progressive non-painful usually asymmetric myelopathy commonly seen in T3-L3 spinal cord and in non-chondrodystrophic breeds. Meningomyelitis of Unknown Aetiology (MUA) is an acute/chronic progressive painful symmetric myelopathy, most frequently seen in C1-T2 spinal cord. Discospondylitis has similar manifestation, however it is more commonly seen in L4-S3 spinal cord and is accompanied by systemic signs and/or urinary tract infection (that may be the cause of it). Distemper myelitis should be considered in dogs with no/partial vaccination history. Toxoplasmosis/Neosporosis can cause myelitis (focal or diffuse); with neosporosis giving a characteristic pelvic limbs rigidity in puppies. Trauma or intense exercise can be the cause of spinal cord concussion/contusion (without accompanied bone fractures/subluxations) or traumatic disc disease (acute non-compressive nucleus pulposus extrusion, ANNPE). Both of them manifest as peracute non-progressive usually painful symmetric/asymmetric myelopathies. Spinal tumours usually cause compression of the spinal cord and/or the meninges, however intramedullary infiltrative neoplasias such as lymphoma can cause chronic, rarely acute, progressive non-painful symmetric/asymmetric myelopathy. The latter is difficult to be distinguished, even from a diagnostic imaging point of view, from a spinal cord inflammation, contusion/concussion, oedema or myelomalacia. At last, degenerative myelopathy is a chronic progressive non-painful symmetric/asymmetric myelopathy of the middle-aged/elderly dogs with a variety of manifestations (from paraparesis to tetraplegia). Similar symptomatology, apart from the compressive myelopathies, can be given by syringomyelia, pharmacological causes of paraparesis/ataxia (phenobarbital, bromide, gabapentin), steroid responsive meningitis-arteritis (SRMA), ischemic neuromyopathy due to aortic thromboembolism, but also diffuse neuromuscular disease (neuropathies, junctionopathies, myopathies). In conclusion, knowing the characteristics of each myelopathy is very important ('six-finger' rule: signalment, onset, progress, pain, symmetry, neurolocalisation) for spinal disease differential diagnosis, but also for the prognosis especially when the general practitioner cannot proceed on further laboratory or diagnostic imaging investigations or even when the specialist, even after an MRI, has reached a diagnostic dead end