450 Canine Sports Medicine and Rehabilitation
ROM was compared at the levels of C3–C4,
C4–C5, and C5–C6. For injuries (1) and (2), for
about 2 weeks the ROM was increased com
pared with the sham procedure. For injury (3),
the ROM was actually decreased for about 6–8
weeks. The differences in ROM were only
appreciated during the healing phase, but were
significant. At 25 weeks, all animals exhibited
the same ROM as the sham control. This study
provides some guideline as to when to expect
complete recovery as well as the ROM changes
as the animals heal and return to presurgical
limits. A similar study concluded that ROM
returns to presurgical levels in all injury studies
when evaluating flexion–extension, lateral
movement, and rotation after 6 months of heal
ing (Crisco et al., 1990). ROM does not equate
with strength but return of strength in the face
of full ROM might mean that spinal surgery
may not limit a canine athlete’s ability to com
pete. More scientific information on how to get
the best return to normal function is sorely
needed.
Conservative therapy
Very little scientific evidence is available about
the treatment or prevention of spinal injuries in
the canine athlete.
Cage confinement with spinal injuries treated
conservatively is still very popular but has
changed dramatically from the 12 weeks com
mon in the 1970s to the 2–4 weeks currently rec
ommended. This kind of extreme confinement
is very often successful when the patient is
recovering from an acute episode of spinal
discomfort. Pain medication is used judiciously
and walks are for defecation and urination only.
Many physical therapists believe that cage con
finement is likely to be detrimental because
experience in people suggests that early ther
apy works best. Animals whose spinal cords
have been experimentally transected make the
best recovery when rehabilitation is immediate
(Chau et al., 1998). Whether there is a best mid
dle ground for these two extremes is currently
unexplored territory. Anecdotal recommenda
tions abound.
Once dogs are beyond the acute phase, indi
vidual patients take to their exercise programs
differently. Usually by week 8, patients can
start training for their particular event. The goal
is to keep the exercises below full exertion for at
least 12 weeks. There is no standard protocol
for retraining, as often we do not know whether
the back pain is from bone, disc, muscle, joint,
or ligament.
This really is no different than the standard
treatment for sciatica in people. The specific
cause of this particular condition is poorly
understood, yet stretching and strengthening
done slowly usually works. These conservative
therapies are usually applied after the acute
episode subsides.New approaches to spinal cord
rehabilitationIt has been known for almost half century that
non‐primates are less dependent than primates
on intracranial centers to walk (Grillner, 1975;
Kiehn, 2006). The typical hemiplegia seen in
severe intracranial stroke victims is virtually
unheard of in dogs. There is significant evi
dence that the dog does not have separate right
brain and left brain functions as occurs in
humans (Springer & Deutsch, 2001). With
extensive hemispheric damage, the dog quickly
learns to compensate. The locomotion genera
tors that are located within the spinal cord to
pattern each limb specifically and in concert
with the other limbs are well developed in the
dog (Handa et al., 1986). The reflex arcs so elo
quently described by Sherrington modify this
locomotion so that it is appropriate to the envi
ronment without having to draw much cortical
attention. Grillner (1975) has extensively
reviewed the history of these discoveries. An
animal with a complete spinal cord transection
at T13 not only walks very well on the treadmill
but can adjust its speed to that of the changing
treadmill. This animal has formed new connec
tions within its spinal cord. Afferent neurons
that originally were part of the reflex pathway
now initiate movement by way of new connec
tions to the pattern generators (Cote & Gossard,
2004). Turbes (1997) showed that virtually any
neural information that spans the gap of a spi
nal cord defect could initiate good movement.
These discoveries are not new but the massive
locomotion literature has had very little impact
on the way we treat the canine spinal patient.