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Myelopathy
Joan R. Coates, DVM, MS, DACVIM (Neurology)

Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO, USA

Myelopathy is a nonspecific term representing patholo- motor units of the cervical, thoracic, lumbar, sacral, and
gies that result in signs of spinal cord dysfunction. It is caudal segments. The severity of motor and sensory
important for the clinician to recognize the neurologic deficits from spinal cord disease is dependent upon the
signs of myelopathy and to differentiate from or avoid rapidity of disease onset, extent of lesion involvement,
misdiagnosis of other mimicking orthopedic and neuro- and the area within the vertebral column.
muscular (nerve, muscle, neuromuscular junction) dis- Spinal cord injury occurs through primary mechanical
orders. Signalment, history, and physical and neurologic and secondary injury mechanisms. Primary injury results
examination findings will establish presence of a mye- from extrinsic or intrinsic injury processes causing lacer-
lopathy, provide neuroanatomic localization and consid- ation, compression, contusion, ischemia, and inflamma-
eration of differentials. Ultimately, with neurodiagnostics tion of the tissue. The acute stage consists of primary
to narrow the differential diagnosis, appropriate thera- tissue effects after injury such as central hemorrhage after
pies can be selected for treatment or management of a severe compression/concussive injury. Typically, myelo-
patients with spinal cord disease. pathic changes initially involve the gray matter with cen-
trifugal spread to the white matter. Sequential hemorrhage,
edema, and neuronal necrosis depend on severity and
History type of injury. The primary injury initiates a cascade of
vascular, ionic, and biochemical events, associated with
An accurate clinical history is important in defining the ischemia that contributes to secondary spinal cord injury
cause of the myelopathy. Time of onset (sudden or insidi- processes and irreversible neuronal damage. Physical
ous), rate of progression (static, gradual or rapid), and attributes of the chronic stage subsequent to secondary
temporal relation (intermittent/episodic, stable or chronic) injury mechanisms include cavitation, presence of apop-
can be established. Acute disorders such as fibrocartilagi- tosis, and Wallerian degeneration. Neurodegenerative
nous embolism (FCE), aortic thromboemboli, trauma, diseases related to underlying inherited, metabolic or
discospondylitis, and Hansen type I intervertebral disc toxic causes result in intrinsic neuronal degeneration
herniation and meningomyelitis often present with sud- involving the cell body, axon, and/or myelin.
den onset and can be rapidly progressive (Table 76.1).
Chronic disorders such as spinal canal/spinal cord
neoplasia, degenerative lumbosacral syndrome, cervical Clinical Signs
spondylomyelopathy, degenerative myelopathy, and
Hansen type II intervertebral disc herniation cause The primary objective of the neurologic examination in
insidious signs of myelopathy (Table 76.2). spinal cord disease is to determine an accurate neuro-
anatomic localization (C1–5, C6–T2, T3–L3, L4–S3, and
caudal segments) (Table 76.3) and lesion distribution
Pathophysiology (focal, multifocal, diffuse). Careful interpretation of the
neurologic examination is essential to avoid diagnostic
The spinal cord serves as a conduit for the upper motor procedures that are inappropriate for lesion determina-
neuronal fibers, sensory pathways and the origin of the tion and potentially harmful to the patient.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical