6 Vestibular Disease in Horses

Vestibular Disease in Horses

• Two common causes include Temporohyoid osteoarthropathy (THO) and skull trauma.

Peripheral Vestibular Disease

• Head tilt occurs with the poll toward the lesion.
• Nystagmus is horizontal, exhibiting a fast phase away from the lesion.
• Falling, with the horse lying on the side of the lesion or leaning toward it.
• Circling is a clinical sign.
• Asymmetric ataxia is present, but strength is preserved.
• Loss of hearing can occur.

Central Vestibular Disease

• Presents with similar clinical signs.
• Nystagmus can be horizontal, rotary, or vertical.
• Altered mentation is observed.
• Proprioceptive deficits are present.
• Weakness is a clinical sign.
• Multiple cranial nerve (CN) deficits are seen.

Temporohyoid Osteoarthropathy (THO) Pathophysiology

• Related to degenerative joint disease of the temporohyoid joint.
• Bony proliferation occurs at the stylohyoid bone articulation with the petrous temporal bone, leading to temporohyoid joint fusion.
• Predisposes horses to stress fractures.
• Activities leading to fracture include: eating, vocalization, any activity involving tongue movement, and iatrogenic causes, such as passage of a nasogastric tube or dental procedures.
• Previously considered an extension of otitis media-interna.

THO Clinical Signs

• Prior to stress fracture: head shaking, painful chewing/eating, resistance to the bit, ear rubbing, resentment of head/ear manipulation, and exudate from the external ear canal (otitis media-interna).
• After stress fracture: commonly see CN 7 and CN 8 abnormalities.
• #1 differential for both CN 7 and 8 abnormalities.
• CN 7 (facial nerve paralysis) signs: ear droop, ptosis, muzzle deviation/droop, and decreased tear production.
• CN 8 (vestibulocochlear) signs: head tilt, nystagmus, falling/leaning, circling, ataxia, and hearing loss.
• Less common signs if the fracture extends include dysphagia, seizures, bacterial meningitis, and death.

THO Diagnosis

• Endoscopy reveals proliferation/thickening of the stylohyoid bone in the guttural pouch.
• Skull radiographs show periosteal proliferation and sclerosis of the stylohyoid bone and petrous temporal bone; fracture lines are difficult to identify.
• CT is sensitive for detecting inflammation, bony proliferation, and fracture.
• Other diagnostics include CSF analysis (cytology and culture if bacterial meningitis is suspected) and brainstem auditory evoked response (BAER) testing to assess hearing.

THO Treatment Goals

• Stabilization of the horse with decreased inflammation near the fracture site.
• Treatment involves broad-spectrum antibiotics.
• Keratitis and decreased tear production are treated if present.
• Surgery is performed to remove pressure on the temporohyoid articulation and decrease the likelihood of repeated petrous temporal bone fracture.
• Partial stylohyoid ostectomy involves removal of a 2-3 cm segment of the stylohyoid bone leading to fibrous nonunion, possible complications include laceration of the lingual artery, injury to the hypoglossal or facial nerve, and regrowth of the stylohyoid ostectomy site.
• Ceratohyoidectomy is technically easier with fewer complications.

THO Prognosis

• Fair to good if the horse survives the immediate fracture episode.
• Up to 2 years of neurologic improvement can be seen.
• Long-term, permanent deficits such as facial nerve paralysis and hearing loss are possible.
• Potential exists for acute onset of severe neurologic signs due to re-fracture, and surgery decreases this risk.

Head Trauma Injuries

• Two basic types: direct frontal blow and flip over backwards.

Skull Fractures

• Can affect bones associated with the calvarium, including the petrous temporal bone.
• Fractures can result from strong traction forces of rectus capitis ventralis muscles, especially the basilar, basisphenoid, and basioccipital bones.
• Basioccipital-basisphenoidal suture fractures are more common in horses less than 5 years old since it doesn't fuse.
• Avulsion fractures can occur.

Head Trauma Clinical Signs

• Hemorrhage or CSF leakage from the ears can be seen.
• Epistaxis is a sign.
• Neurologic signs depend on the location of the trauma, commonly including vestibular and/or facial nerve signs, blindness, respiratory distress, depression to coma, seizures, and increased intracranial pressure.
• Increased intracranial pressure can result in a worsening of mental status, abnormal pupillary size or inequality, and the development of paresis.

Head Trauma Diagnostics

• Radiographs can be used.
• CT is sensitive for detecting bony abnormalities
• Endoscopy can be performed.
• CSF analysis may be performed if increased intracranial pressure is not suspected, as AO tap is contraindicated if increased intracranial pressure is present due to risk of herniation through the foramen magnum.

Head Trauma Treatment

• Treatment of life-threatening injuries involves establishing an airway, venous access, IV fluids, hemostasis.
• Anti-inflammatories, such as corticosteroids, NSAIDs, DMSO, and Vitamin E,may be used.
• Intracranial pressure can be decreased with hypertonic saline, mannitol, and furosemide
• Diazepam, midazolam, phenobarbital, and pentobarbital can be used to control seizures.

Head Trauma Prognosis

• Depends on the severity of the injury.
• Better prognosis if early treatment and response is noted.
• Basilar bone fractures have a poorer prognosis compared to other types of head trauma.
• Poor prognostic indicators: bilateral pupil dilation with no response to light, apneustic or erratic breathing patterns, recumbency (>4 hours), tetraparesis, and severe dementia, all of which indicate a poor to grave prognosis.