Front Matter

444 Canine Sports Medicine and Rehabilitation

fibrocartilaginous embolization (FCE). Although
the origin of the fibrocartilage is unknown, it is
suspected that the source is the nucleus pulposus.
More than 40 years after this condition was first
described, we still do not have a clear understand­
ing of how the material gets into the arterial vas­
culature of the spinal cord (Zaki & Prata, 1976).
Dogs with suspected FCE usually recover ade­
quate function so autopsy material is very uncom­
mon (Figure 17.25). The hallmark of this disease
is an acute onset of spinal cord dysfunction,
usually during activity. The signs are often asym­
metrical, rapidly progressive, and usually not
associated with hyperpathia (De Risio & Platt,
2010). Transient hyperalgesia at the onset of the
signs is common but short in duration. Most dogs
return to normal function over a 6–8‐week period
dependent upon the amount and location of the
ischemic damage. Intact pain sensation and signs
of motor recovery within 2 weeks after onset of
signs indicate a favorable outcome.

Degenerative conditions of the
spinal cord

Sporadic and rare degenerative conditions of
the spinal cord have been recorded over many
decades. Consideration should be given to
these disorders based on clinical signs, typical
young age of onset, and breed predilection.
The  classification scheme for the degenerative
spinal cord disorders of animals is further

described in Table  17.1. Breed predispositions

suggest that many of these disorders have an

inherited basis. Initial clinical signs often are

worse in the pelvic limbs but then progress to

involve the thoracic limbs and possibly the

brainstem and forebrain. Definitive diagnosis

of these diseases is usually determined

by  histopathology of the affected tissues.

Degenerative spinal cord disorders involving

myelinopathy and axonopathy are classified

based on their histopathological features.

Canine degenerative myelopathy, the most

common degenerative spinal cord disorder, is

covered in the next section. A more extensive

list of these degenerative conditions and the

breeds they affect can be found in the Handbook

of Veterinary Neurology (Lornez et al., 2010).

Degenerative myelopathy

History, signalment, and epidemiology

Canine degenerative myelopathy (DM) was

first described by Averill in 1973 as an insidi­

ous, progressive, general proprioceptive ataxia

and upper motor neuron (UMN) spastic paresis

of the pelvic limbs ultimately leading to para­

plegia and necessitating euthanasia. The earli­

est clinical signs begin when dogs are at least 8

years or older with a mean age of onset at 9

years. There is no sex predilection. The patho­

logical features of DM include axonal dege­

neration with secondary demyelination and

astroglial proliferation (sclerosis) in all spinal

cord funiculi, but consistently most severe in

the dorsal portion of the lateral funiculus and in

the dorsal columns of the middle to lower tho­

racic region (Averill, 1973; Griffiths & Duncan,

1975; Braund & Vandevelde, 1978; March et al.,

2009). Neuronal cell body degeneration or loss

in the ventral horn of the spinal cord is not a

prominent histopathological finding but does

occur in terminal disease (Ogawa et al., 2014).

In 1975, Griffiths and Duncan published a

series of cases with similar clinical signs and

histological changes in the white matter. They

also reported hyporeflexia and nerve root

involvement, and they termed the condition

chronic degenerative radiculomyelopathy.

Recent histopathological studies of dogs in the

late disease stage with lower motor neuron

(LMN) signs have documented denervation

Figure 17.25 Tissue section from a dog’s spinal cord
showing gray matter destruction from a fibrocartilaginous
embolus. The area with a diffuse light pattern has been
damaged by a lack of perfusion.