Equine Temporohyoid Osteoarthropathy Study Guide

Overview and Clinical Importance

Temporohyoid osteoarthropathy (THO), also known as middle ear disease or stylohyoid osteoarthropathy, is a progressive condition affecting the temporohyoid joint and surrounding structures in horses. This disease is characterized by proliferative bone changes at the articulation between the stylohyoid bone and the petrous temporal bone, potentially leading to joint fusion, nerve damage, and fractures. THO represents an important differential diagnosis for horses presenting with facial nerve paralysis, vestibular dysfunction, or head-shaking and is a recognized cause of neurological disease on the NAVLE.

THO can affect horses of any age, breed, or gender, though it most commonly presents in adult horses. The condition may be unilateral or bilateral, with bilateral disease reported in a significant proportion of cases. Early recognition and appropriate treatment are essential for optimal outcomes.

Anatomy of the Hyoid Apparatus

The hyoid apparatus is a complex arrangement of bones that suspends the tongue, pharynx, and larynx from the skull. Understanding this anatomy is fundamental to comprehending the pathophysiology and clinical signs of THO.

Components of the Hyoid Apparatus

Critical Anatomic Relationships

The temporohyoid joint is in close proximity to several critical structures:

• Cranial Nerve VII (Facial): Controls facial expression, eyelid closure, ear movement, and tear production
• Cranial Nerve VIII (Vestibulocochlear): Responsible for hearing and balance/vestibular function
• Petrous temporal bone: Houses the middle and inner ear; fractures can extend into the cranial vault
• Guttural pouch: The stylohyoid bone runs through this structure, allowing endoscopic visualization
• Tympanic bulla: Located medial to the temporohyoid joint; can be affected by disease extension

Board Tip - Memory Aid: "7-8 at the Gate" - Cranial nerves VII (Facial) and VIII (Vestibulocochlear) pass through the petrous temporal bone near the temporohyoid joint. When THO causes fractures, these nerves are damaged, producing the classic presentation of facial paralysis (CN VII) and vestibular signs (CN VIII).

Etiology and Pathophysiology

The exact cause of THO remains incompletely understood. Several proposed mechanisms exist:

Proposed Etiologies

Pathophysiology

Regardless of the initiating cause, the disease process follows a predictable pattern:

• Inflammation and Proliferation: Bony proliferation develops around the temporohyoid joint and proximal stylohyoid bone
• Joint Fusion (Ankylosis): Progressive ossification leads to fusion of the temporohyoid joint, eliminating normal motion
• Mechanical Stress: Normal movements (swallowing, head turning, chewing, vocalizing) create stress through the fused joint
• Fracture: Stress fractures occur at the petrous temporal bone or stylohyoid bone
• Nerve Damage: Fractures damage CN VII and CN VIII, causing characteristic clinical signs

Clinical Signs

Clinical signs of THO vary depending on the stage of disease and whether fracture has occurred. Signs are typically unilateral but bilateral disease occurs.

Early/Pre-Fracture Signs

• Pain or sensitivity when pressure applied to the base of the ear or throatlatch region
• Head tossing or shaking
• Reluctance to accept the bit or work in a frame
• Resistance to specific head positions under saddle
• Ear rubbing
• Non-specific behavioral changes

Advanced/Post-Fracture Signs

Diagnosis

Diagnosis of THO relies on clinical signs, neurological examination, and imaging. Multiple modalities may be needed for definitive diagnosis.

Clinical Examination

• Complete neurological examination: Assess cranial nerves, particularly CN VII and CN VIII function
• Palpation: Check for pain at the base of the ear and over the basihyoid bone
• Ophthalmologic examination: Evaluate for corneal ulceration, tear production (Schirmer tear test), palpebral reflex
• Otoscopic examination: May reveal external ear canal abnormalities in some cases

Diagnostic Imaging

Treatment

Treatment of THO involves both medical and surgical approaches. Studies show that surgical intervention results in better outcomes than medical management alone.

Medical Management

Ocular Management

Corneal ulceration secondary to CN VII dysfunction requires aggressive treatment:

• Topical antibiotics for corneal ulceration
• Artificial tears/lubricants for keratoconjunctivitis sicca
• Temporary tarsorrhaphy (surgical eyelid closure) in severe cases
• Conjunctival flap or corneal graft for non-healing ulcers

Surgical Management

Surgery aims to reduce mechanical stress on the temporohyoid joint by interrupting force transmission through the hyoid apparatus. Current preferred procedure is ceratohyoidectomy.

Prognosis

Prognostic Factors

• Early diagnosis and treatment: Key to positive outcomes
• Severity of neurological signs at presentation: More severe signs = worse prognosis
• Age: Older horses at diagnosis have reduced survival
• Bilateral disease: May require bilateral surgery; more guarded prognosis
• Corneal ulceration: Complicates management but typically resolves with treatment
• Hearing loss: Permanent; does not improve with treatment

Differential Diagnosis

When evaluating a horse with facial nerve paralysis and/or vestibular signs, consider: