Page 288 - Canine Lameness

260 16 ­Neurorogico giNciN rAectNe trucigi gim

two-engine gait. The presence of a two-engine gait is localizing to the cervical intumescence (C6–
T2 spinal cord or caudal cervical myelopathy).
If only the C6–T2 nerve roots are injured (i.e. a radiculopathy), a thoracic limb root signature
lameness and/or monoparesis usually results and the pelvic limbs will be normal. Whether lame-
ness or monoparesis predominates in a radiculopathy depends on the pathologic involvement of
the dorsal or ventral rootlets, respectively. This distinction is far less important than realizing that
both lameness and/or monoparesis can occur with a radiculopathy.
Differential etiologic diagnoses causing caudal cervical myelopathies and radiculopathies are
outlined below and summarized in Table 16.1. An etiologic diagnosis is established based on sig-
nalment, history, clinical signs, and results of diagnostic tests, where available. Advanced imaging
modalities such as computed tomography (CT), or preferably magnetic resonance imaging (MRI)
in most cases, combined with cerebrospinal fluid (CSF) analysis most accurately confirms the neu-
rologic cause, establishes the anatomic diagnosis, and many times, determines an etiologic cause.
Treatment and prognosis are highly variable depending on severity and cause, ranging from
emergency surgical intervention to conservative management. In general, conditions that are
acute, severe, and/or progressive typically warrant more definitive therapy. For example, decom-
pressive surgery for a Type I IVD extrusion and recovery may be more complete. Whereas, condi-
tions that are chronic, mild, and/or slowly progressive can often be managed with conservative
therapy. However, recovery tends to be incomplete with residual neurologic deficits. Judicious use
of corticosteroids is important as they can falsely alter test results (e.g. MRI and CSF) and poten-
tially affect future prognosis if an animal is being undertreated (e.g. meningomyelitis or lym-
phoma) or incorrectly treated (e.g. discospondylitis).

16.3.1.1 Degenerative Intervertebral Disc Disease and Herniation
Degenerative changes of the IVD and subsequent herniation is one of the most common neuro-
logic disorders in dogs (Brisson 2010). IVD degeneration is known to predispose to intervertebral
disc herniation (IVDH), as either extrusion or protrusion of disc material. However, IVD degenera-
tion must not be thought of as synonymous with IVD herniation, as it is also a common incidental
finding in dogs without clinical signs.
The pathophysiology of IVD degeneration can be divided into chondroid metaplasia causing a
Hansen Type I IVD extrusion and fibrous metaplasia causing Hansen Type II IVD protrusion.
Chondroid metaplasia describes the process of premature degeneration frequently seen in young
chondrodystrophic breeds but medium- to large-breed dogs can also be affected. Type I IVD
extrusion is a common cause for a root signature lameness or monoparesis. The extruded disc
material can be lateralized in the vertebral canal and/or extend into the intervertebral foramen,
causing unilateral compression of the C6–T2 spinal cord and/or nerve roots, respectively.
Alternatively, a short-strided, choppy thoracic limb gait (i.e. LMN paresis) can occur with a
midline IVD Type I extrusion or Type II protrusion. Fibrous metaplasia describes the process of
natural degeneration frequently seen in middle-aged dogs; as such, symptoms are more likely to
be slowly progressive.
Dogs with a Type I IVD extrusion tend to present more acutely and have more spinal hyperes-
thesia compared to dogs affected by Type II IVD protrusions. Dogs with Type I IVD more often
show lateralized symptoms deficits although symmetrical symptoms are also common. A more
insidious onset and slow progression (days to several months) with various degrees of spinal
hyperesthesia is seen with Type II IVD protrusions and cervical spondylomyelopathy (CSM; see
Section 16.3.1.4). However, Type II IVD protrusions can have sudden worsening of the otherwise
slowly progressive signs.