Page 290 - Canine Lameness

262 16 ­Neurorogico giNciN rAectNe trucigi gim

contusive injury to the spinal cord. Unlike Type I and II IVDH, the disc material herniated during
an ANNPE is nondegenerated, highly hydrated, and gelatinous so it rapidly dissipates leaving min-
imal to no spinal cord compression. For a visual, this can be likened to a water pistol being dis-
charged towards a person’s soft abdomen, leaving a bruise.
Affected patients are frequently older, large-breed dogs. Typically, vocalization during intense
activity is reported along with a characteristic clinical presentation: peracute onset of often severe,
asymmetric neurologic deficits that are nonprogressive after the initial 24–48 hours. The clinical
signs in most cases are lateralized and while a monoparesis can occur, other limbs are commonly
affected to a lesser severity. Approximately 40% will have moderate spinal hyperesthesia on exami-
nation. Most dogs will regain complete or near-complete neurologic function with conservative
therapy. Since these are non-compressive lesions, surgery is typically not indicated.
The imaging modality of choice to diagnose ANNPE is MRI, with the following criteria used:
focal spinal cord signal changes (indicating pathology like inflammation and edema), a lesion that
is located over the IVD space and is often lateralized, reduction in size of the well-hydrated nucleus
pulposus, mild narrowing of the IVD space, and a small volume of IVD material with minimal to
no spinal cord compression.

16.3.1.3 Fibrocartilaginous Embolism
Infarction from an FCE or other vascular-related diseases (e.g. arterial embolism causing ischemic
neuromyopathy) are common causes for hemiparesis but can also produce a thoracic limb mono-
paresis if the cervical intumesce gray matter is involved. Histologically, the embolus is identical to
the nucleus pulposus of the IVD, indicating that penetration of this material into spinal vessels
causes the embolism and associated ischemia of the spinal cord (Nakamoto et al. 2008). The clini-
cal presentation, diagnostic steps, and treatment of dogs with FCE and ANNPE are very similar;
however, dogs with FCE are generally non-painful after 24 hours and therefore show spinal hyper-
esthesia less frequently on examination. Other differentiating features of ANNPE and FCE include
the following clinical features: dogs with ANNPE are significantly older and are more likely to
have history of vocalization at the onset of clinical signs. While any age and breed can be affected,
large and giant breeds seem overrepresented with FCE. Additionally, dogs with ANNPE had
lesions affecting the C1–C5 spinal cord segments more often than FCE (Fenn et al. 2016).
Differentiating these two is not necessarily of clinical importance; however, ruling out other dis-
eases (such as acute bleeding from a tumor or compressive lesion) can be important. Since it can
be difficult to differentiate lesions on CT that do not contrast enhance, MRI is the modality of
choice to diagnose both FCE and ANNPE (De Risio and Platt 2010).

16.3.1.4 Cervical Spondylomyelopathy
CSM (“Wobbler Syndrome”) is a common cause of cervical myelopathy in medium- to giant-breed
dogs, where dynamic and static compressive factors leading to a chronic progressive (typically over
weeks to months) proprioceptive ataxia, with varying degrees of cervical hyperesthesia and paresis
(Da Costa 2010). Two pathophysiologic processes have been described, with some amount of over-
lap. Osseous-associated compression is more common in young adult giant-breed dogs (e.g. Great
Danes). It typically affects the C1–C5 spinal cord region, therefore resulting in symmetric, UMN
clinical signs. Disc-associated compression commonly affects the C6–T2 spinal cord region. Middle-
aged large-breed dogs, especially Doberman Pinschers are overrepresented. Classically, these dogs
will have ventral compression from encroachment of Type II IVDH resulting in the classic sym-
metric tetraparesis with a stiff short-strided, LMN thoracic limb gait and GP/UMN pelvic limb gait.
However, rarely CSM may cause asymmetric clinical signs that could be confused with lameness.