Page 81 - Canine Lameness

4.3 The Neurologic Examination 53

an overreaching quality is noticed at the end of the swing phase, sometimes described as “soldier
marching.” If these symptoms are subtle, they may be confused with an orthopedic problem.
In many cases, by observing gait alone, the examiner can determine, not only if a patient has a
gait abnormality due to orthopedic disease or a neurologic lesion but for the latter, whether a UMN
or LMN lesion is present. However, patients with bilateral limb pain (e.g. hip disease or ruptured
cruciate ligaments) may “appear” ataxic, making the distinction challenging. Similarly, some dogs
with marked bilateral paresis due to an LMN lesion can appear uncoordinated, but as a function of
the severity of the paresis limiting the rate and range of foot placement. Gait abnormalities due to
orthopedic disease can also be difficult to differentiate from paresis, especially a monoparesis.
LMN lesions causing paresis are manifested as a gait with a shortened stride length (from inability
to support body weight) or a limb(s) that buckles under the weight of the dog and may be accom-
panied by increased fatigability and decreased muscle tone. In contrast, if the alteration of stride
phases is caused by orthopedic disease, muscle tone is maintained, and fatigability is often not
evident. Orthopedic lameness may also improve after activity, depending on the disease. To decide
if a dog is truly ataxic, using descriptions of cardiac arrhythmias as an analogy for gait can be a
helpful guide. Dogs that are ataxic will have foot placement that is irregularly irregular, implying
neurologic origin. A rhythmic, regularly irregular gait is more consistent with lameness, monopa-
resis (e.g. a nerve sheath tumor affecting the radial nerve), or symmetric paresis (e.g. an interverte-
bral disc herniation in the lumbar intumescence lesion causing paraparesis). The presence of
uneven nail wear (Figure 4.3) supports a nervous system lesion causing paresis and/or ataxia;
orthopedic conditions do not typically have uneven nail wear.

4.3.4 Cranial Nerves
Cranial nerve dysfunction, if present, is a clear indicator of neurologic disease. Of particular
importance to the patient with lameness is evaluation of the patient for evidence of Horner syn-
drome, a disruption of the sympathetic innervation of the eye. This innervation is complex and
involves several neurons. The neurons initially travel from the brainstem to the spinal cord and
synapse on LMNs in the cranial thoracic spinal cord, typically at the level of T1–T3 spinal cord seg-
ments, before redirecting and coursing cranially to provide sympathetic innervation to the eye
(Penderis 2015). Sympathetic stimulation keeps the eyeball positioned normally within the orbit,
widens the palpebral fissure, and dilates the pupils. Disruption of this pathway may result in
Horner syndrome, characterized by retraction of the eye ball (enophthalmos), pupillary constric-
tion (miosis), narrowing of the palpebral fissure (ptosis), and third eyelid protrusion; protrusion of
the third eyelid occurs passively with enophthalmos. The finding of Horner syndrome indicates an
ipsilateral lesion in the nervous system along the sympathetic pathway at any number of locations
of the sympathetic pathway. In a dog presenting with thoracic limb lameness, the finding of Horner
syndrome not only confirms a neurologic lesion but more specifically points to a lesion involving
the first to third thoracic spinal cord segments or LMNs as they exit (e.g. lateralized disc protrusion
or a brachial plexus tumor, Videos 4.1 and 16.1). Commonly, only ipsilateral miosis (i.e. partial
Horner syndrome) is seen with lesions at this level.

4.3.5 Postural Reactions

Postural reactions test the same neurologic pathways already evaluated in gait assessment, namely
the proprioceptive and motor systems. They help identify which limb or limbs is/are affected and
confirm that a nervous system disorder is present. However, since all components of both the CNS