Unusual features of this case
With regard to the location of the spinal cord lesion, our patient's clinical presentation had two unusual features. First,
in most dogs, the spinal cord lower motor neuron cell bodies supplying the femoral and part of the sciatic nerves are located
at the L3-L4 vertebral level.4 Despite the location of the hypertrophied articular processes at L3-L4, the dog in this report displayed clinical signs
consistent with general proprioceptive ataxia due to upper motor neuron dysfunction. One possibility for this apparent discrepancy
is individual anatomical variation. Another possibility relates to the nature of the lesion itself. The hypertrophied articular
processes caused mild compression of the dorsal and lateral portions of the spinal cord, regions occupied primarily by ascending
sensory tracts. The lower motor neurons in this region likely experienced minimal compression from the abnormal synovial articulation,
with most of the compression directed toward sensory proprioceptive white matter tracts.
The other unusual aspect of our patient's clinical presentation was fecal incontinence in the absence of a lesion in the region
of the sacral spinal cord segments. Fecal incontinence is commonly associated with lesions in the sacral spinal cord segments
or associated spinal nerve roots, as these structures innervate the anal sphincter musculature.4 Fecal incontinence is a recognized complication of degenerative lumbosacral stenosis in dogs and is associated with a poor
to guarded prognosis for postoperative resolution if present for more than one month.5,6
Fecal incontinence associated with upper motor neuron spinal cord lesions has recently been described in seven dogs.7 Similar to the dog in our case report, all seven dogs had lesions compressing the dorsal aspect of the spinal cord, and
all had normal perineal sensation and perineal (anal sphincter) reflexes. It is theorized that fecal incontinence associated
with upper motor neuron spinal cord lesions is due to interruption of ascending sensory information from the rectum, interruption
of descending inhibitory influence on the sacral defecation reflex, or a combination of the two.7 In the report of seven dogs with fecal incontinence, the incontinence resolved in four of the five dogs that underwent decompressive
surgery, despite a history of incontinence ranging from three months to three years.7 Although case numbers are still low, it appears that fecal incontinence associated with upper motor neuron dysfunction may
more likely resolve after surgical decompression than will fecal incontinence associated with lower motor neuron dysfunction.
Clinicians should be aware that vertebral articular process hypertrophy can cause myelopathy in dogs. In addition, fecal incontinence
can occur secondary to upper motor neuron lesions (i.e. cranial to the sacral spinal cord segments), and this incontinence may be ame na ble to surgical intervention.
This case report was provided by Curtis W. Dewey, DVM, MS, DACVIM (neurology), DACVS; Ursula Krotscheck, DVM, DACVS; Kevin
Winegardner, DVM; and Maureen Vaillancourt, DVM, Department of Clinical Sciences, College of Veterinary Medicine, Cornell
University, Ithaca, NY 14853.
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graphic, myelographic and magnetic resonance imaging investigations. Vet Rec 2005;156:601-605.
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7. Chen AV, Bagley RS, West CL, et al. Fecal incontinence and spinal cord abnormalities in seven dogs. J Am Vet Med Assoc 2005;227:1945-1951.