Page 1111 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1086 CHAPTER 10

VetBooks.ir of feed between teeth and cheeks. It is important to butazone, 2–4 mg/kg i/v or p/o q12 h, or flunixin
Treatment consists of either NSAIDS (phenyl-
determine the site of the lesion, as it determines the
prognosis. Full facial paralysis occurs if the facial
nerve is injured proximal to the vertical ramus of meglumine, 1.1 mg/kg i/v or p/o q12 h for 3–5 days) or
corticosteroids (dexamethasone, 0.05–0.1 mg/kg i/v,
the mandible. These injuries are seen with fractures i/m or p/o q24 h for 48–72 hours). The use of a topi-
of the vertical ramus of the mandible, the stylohyoid cal anti-inflammatory cream, such as 1% diclofenac
bone or the petrous temporal bone. Other causes of sodium, may also be indicated to control inflamma-
unilateral facial paralysis without direct injury to tion associated with the facial nerve. The prognosis
the facial nerve are medullary lesions involving the for the return of facial nerve function depends on
facial nucleus, polyneuritis equi, idiopathic facial the site and severity of the lesion. Without severe
paralysis, haemorrhage into the middle or inner skin laceration, the prognosis for horses with periph-
ear, guttural pouch mycosis and parotid lymph- eral facial paralysis is good, although recovery may
node abscessation. Distal facial nerve damage is take several weeks to months. If there is section of
most commonly caused by direct injury from exter- the nerve and the ends can be identified, immediate
nal trauma, head entrapment or prolonged lateral surgical repair is indicated.
recumbency (Fig. 10.38). A frequent site of dam-
age is where the nerve, or its branches, cross(es) the SPINAL CORD TRAUMA
mandible or zygomatic arch.
Definition/overview
Suspected spinal cord trauma is one of the most
10.38 common neurological disorders presented to equine
practitioners. Musculoskeletal and/or neurological
abnormalities may be encountered.

Aetiology/pathophysiology
Injury to the spinal cord can be considered to hap-
pen in two stages: the primary mechanical insult to
neurons, axons and the microvasculature; and the
secondary injury which is related to the cascade of
events associated with ischaemia, oxidative stress,
excitotoxicity and inflammation. The pathology
associated with the secondary phase of injury may
play an important role in determining prognosis,
perhaps more so than the original physical injury.
Given its greater vascularity and oxygen demand, it
is thought that the grey matter is more susceptible to
mechanical damage than the white matter in spinal
cord trauma.
Many cases of vertebral trauma with, or without,
neurological signs have been reported. Spinal cord
trauma typically occurs following a traumatic inci-
dent (e.g. a fall) and may, or may not, be associated
with vertebral trauma. Fractures occasionally occur
secondary to other pathology such as neoplasia. The
cervical vertebrae are common sites for vertebral
Fig. 10.38 Skull fracture causing trauma to the left fractures, especially the occipitoatlantoaxial region
facial nerve. Note the muzzle deviation to the right. in foals, and the cranial cervical site in rotational or