Equine Vestibular Disease Study Guide

Overview and Clinical Importance

Vestibular disease in horses represents a significant category of neurological disorders affecting balance, coordination, and spatial orientation. The vestibular system is responsible for maintaining equilibrium and coordinating eye movements with head position. Dysfunction of this system produces characteristic clinical signs that are commonly tested on the NAVLE examination.

The two most common causes of vestibular disease in horses are temporohyoid osteoarthropathy (THO) and head trauma (basilar skull fractures). Understanding the anatomical basis, clinical presentation, diagnostic approach, and treatment options is essential for accurate diagnosis and effective case management.

Anatomy of the Vestibular System

Peripheral Vestibular System

The peripheral vestibular system consists of receptor organs within the inner ear and the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII). The inner ear is housed within the petrous temporal bone and contains the membranous labyrinth, which is filled with endolymph.

Key Structures

• Semicircular Canals (3): Anterior, posterior, and lateral canals detect angular acceleration (rotational head movement). The canals are oriented at approximately 90 degrees to each other.
• Utricle: Detects linear horizontal acceleration (forward-backward movement)
• Saccule: Detects linear vertical acceleration (up-down movement) and gravity
• Hair Cells: Mechanoreceptors that convert head movement into nerve signals via deflection of stereocilia
• Vestibulocochlear Nerve (CN VIII): Transmits vestibular and auditory signals to the brainstem

Central Vestibular System

The central vestibular system includes the four vestibular nuclei in the rostral medulla oblongata and the flocculonodular lobes of the cerebellum. These structures process vestibular input and coordinate the vestibulo-ocular and vestibulospinal reflexes that maintain balance and gaze stability.

Guttural Pouch Anatomy and Clinical Relevance

The guttural pouches are diverticula of the auditory tubes unique to equids. They are divided into medial and lateral compartments by the stylohyoid bone. Several critical neurovascular structures pass through or adjacent to the guttural pouches, making endoscopic examination essential for diagnosing vestibular disease.

Structures Within the Guttural Pouch

Differentiating Peripheral vs Central Vestibular Disease

Accurate localization of vestibular lesions is critical for determining etiology, guiding diagnostic workup, and establishing prognosis. Clinical examination findings allow differentiation between peripheral and central vestibular disease in most cases.

Temporohyoid Osteoarthropathy (THO)

Pathophysiology

Temporohyoid osteoarthropathy is a chronic progressive condition characterized by bony proliferation of the stylohyoid bone and petrous temporal bone, leading to eventual ankylosis (fusion) of the temporohyoid joint. The exact etiology remains unclear, with proposed mechanisms including:

• Extension of middle/inner ear infection (otitis media/interna): Low-grade infection spreads from the tympanic bulla to the temporohyoid joint
• Primary degenerative osteoarthropathy: Age-related joint degeneration without infectious etiology
• Trauma: Direct or repetitive injury to the hyoid apparatus
• Crib-biting behavior: Studies in Japanese Thoroughbreds show significant association (12x higher odds) with THO

Once the temporohyoid joint becomes ankylosed, normal movements such as chewing, swallowing, and head movement place excessive stress on the fused joint, predisposing to stress fracture of the petrous temporal bone. The prevalence of temporal bone fractures is high in horses with severe THO.

Clinical Signs

THO typically affects adult horses with a median age of 10-11 years, though it can occur at any age. No sex or breed predisposition has been definitively established. Clinical signs vary based on disease stage:

Early Signs (Pre-fracture)

• Pain or sensitivity when pressure applied to base of ear
• Head shaking or head tossing
• Ear rubbing against fixed objects
• Resistance to the bit; difficulty working in a frame
• Behavioral changes; bridling problems

Acute Signs (Post-fracture)

• Vestibular signs: Head tilt, ataxia, circling, falling toward the affected side
• Facial nerve paralysis: Ear droop, lip deviation away from lesion, absent menace response, absent palpebral reflex, nostril collapse
• Corneal ulceration: Secondary to decreased tear production and inability to blink
• Nystagmus: Horizontal, with fast phase away from lesion
• Ventrolateral strabismus: Best observed when head is elevated and extended

Diagnosis

• Complete Neurological Examination: Confirm vestibular dysfunction; assess cranial nerve function; differentiate peripheral from central disease
• Guttural Pouch Endoscopy: Primary diagnostic method. Look for thickening/proliferation of the proximal stylohyoid bone. ALWAYS examine both sides as bilateral disease occurs.
• Skull Radiographs: Lateral and ventrodorsal views may reveal osseous proliferation. Limited by superimposition and difficulty positioning ataxic horses.
• Computed Tomography (CT): Gold standard imaging. Provides detailed evaluation of temporohyoid joint, stylohyoid bone, tympanic bullae, and fractures. Requires general anesthesia.
• MRI: Useful for soft tissue evaluation and inner/middle ear structures. Less commonly used due to anesthesia requirements in ataxic horses.

Treatment

Prognosis

• Surgical treatment: Good to excellent prognosis; 80% of horses treated surgically return to previous activity level
• Medical management alone: Fair prognosis; improvement seen in 1-2 months but full recovery may take up to 2 years
• Persistent deficits: Mild facial nerve paralysis (21%) and head tilt (43%) may persist but are typically not functionally limiting
• Hearing loss: Permanent if cochlear damage has occurred

Basilar Skull Fractures

Mechanism of Injury

Basilar skull fractures are the most common traumatic cause of vestibular disease in horses. These fractures typically occur when horses rear over backwards and strike the poll on the ground. The hyperextension of the head causes contraction of the rectus capitis ventralis muscles, which insert at the junction of the basisphenoid and basioccipital bones, resulting in avulsion or fracture at this junction.

Common Fracture Locations

• Basisphenoid-basioccipital suture: Most common; this suture remains open until 2-5 years of age, making young horses more susceptible
• Petrous temporal bone: Causes vestibular and facial nerve signs; CSF leakage from ears indicates fracture at this location
• Basioccipital bone: May be associated with brainstem damage

Clinical Signs

• Loss of consciousness: Minutes to hours; some horses never regain consciousness
• Hemorrhage: Epistaxis (from nostrils) or otorrhagia (from ears)
• CSF leakage: From ears or nostrils indicates fracture of petrous temporal bones
• Vestibular dysfunction: Head tilt, nystagmus, ataxia
• Facial nerve paralysis: If petrous temporal bone involved
• Depression to coma: Depending on severity of brain injury
• Seizures: May occur with severe brain injury
• Bilateral mydriasis: Poor prognostic indicator suggesting severe midbrain injury

Diagnosis and Treatment

Diagnosis: Often made based on history of trauma. Skull radiographs may reveal fracture lines, though non-displaced fractures can be difficult to detect. Endoscopy of guttural pouches may show blood in the pharynx or pouches. CT provides the best imaging but requires general anesthesia.

Treatment: Immediate management within the first 8 hours focuses on prevention/treatment of brain edema:

• Corticosteroids (dexamethasone) to reduce brain edema
• Hypertonic saline or mannitol for intracranial pressure
• Anticonvulsants if seizures present
• Broad-spectrum antibiotics to prevent secondary infection
• Supportive care: IV fluids, protection from self-trauma

Prognosis: Guarded to grave. Fair to good if the horse survives the initial fracture episode. Maximum neurologic improvement may take up to 2 years. Long-term deficits possible. Refracture risk exists.

Other Causes of Vestibular Disease

Equine Protozoal Myeloencephalitis (EPM)

EPM, caused primarily by Sarcocystis neurona and less commonly by Neospora hughesi, can affect any part of the CNS including the vestibular system. When cranial nerves VII and VIII nuclei or nerves are affected, horses may present with facial paralysis or vestibular signs.

Key Points for EPM

• Definitive host: Virginia opossum (Didelphis virginiana)
• Transmission: Horses ingest sporocysts in contaminated feed/water
• Classic presentation: Asymmetric ataxia with muscle atrophy
• Diagnosis: Serum and CSF antibody titers; intrathecal antibody production
• Treatment: Ponazuril (5 mg/kg PO q24h for 28 days), Diclazuril (1 mg/kg PO q24h for 28 days), or Sulfadiazine/pyrimethamine combination

Viral Encephalitides

West Nile Virus (WNV) and Eastern/Western Equine Encephalitis (EEE/WEE) can cause vestibular signs as part of a more generalized encephalomyelitis. Key differentiating features include:

• Fever (often present early in course)
• Muscle fasciculations (especially with WNV)
• Multiple neurological deficits (not isolated vestibular)
• Seasonal occurrence (mosquito transmission)
• Prevention: Core vaccination recommended by AAEP

Idiopathic Vestibular Syndrome

Recently described in horses, idiopathic vestibular syndrome presents with unilateral peripheral vestibular signs without identifiable cause. Similar to 'old dog vestibular disease' in canines. Horses typically make a full recovery, often within weeks, with or without anti-inflammatory treatment.

Differential Diagnosis Summary