Introduction

• Intermittent facial spasms or uni- or bilateral facial paralysis or paresis.
• Cause: can be immune mediated, or due to inflammation, eg otitis media/interna, infection, myasthenia gravis, toxins, eg botulism, trauma, neoplasia, (both extracranial and intracranial), toxic (hypersensitivity associated with potentiated sulfonamides), idiopathic, <75% of cases in 1 study.
• Also seen in conjunction with polyradiculoneuropathy, polyneuropathy, and hypothyroidism.
• Signs: drooping and inability to move the ear and lip, drooling, widened palpebral fissure, absent abduction of nostril during inspiration, deviation of nose towards normal side, absent spontaneous or provoked blinking.
• Diagnosis: signs, EMG, nerve conduction studies, brainstem auditory evoked responses (BAER), MRI, CT scan, autoscopic examination.
• Treatment: symptomatic for the facial nerve paralysis, specific treatment for the primary disease may reverse the facial neuropathy.
• Prognosis: guarded for the complete return of function.

Pathogenesis

Etiology

• Active degeneration of large and small caliber myelinated nerve fibers without inflammation.
• The inciting cause is unknown.
• Most common cause in dogs (75%).
• Appears analogous to Bell's Palsy in humans.

Facial paralysis

• Trauma, eg ear trauma or peripheral facial trauma.
• Iatrogenic following bulla osteotomy Bulla osteotomy.
• Otitis media Otitis media /interna Bulla osteotomy.
• Polyneuropathy.
• Acquired myasthenia gravis Myasthenia gravis.
• Botulism Clostridium botulinum.
• Neoplasia (both extracranial and intracranial).
• Hypothyroid neuropathy Hypothyroidism.
• Brain stem inflammation.
• Polyradiculopathies.
• Toxic (hypersensitivity associated with potentiated sulfonamides).
• Tick paralysis Neurology: tick paralysis.

Predisposing factors

• Head/face trauma.

Specific

• Previous otitis externa Skin: otitis externa.
• Total ear canal ablation Ear: total ear canal ablation /lateral bulla osteotomy (13-36% of procedures).

• Hypothyroidism.

Pathophysiology

• Degeneration of facial nerve.
• The facial canal that is adjacent to the tympanic cavity lacks a bony wall for a very short distance as it runs in the petrosal portion of the temporal bone. This leaves the facial nerve exposed to the cavity and therefore to disease processes affecting the middle ear.

• Otitis media/interna → damage to facial nerve as it passes between middle and inner ear → loss of function → unilateral paralysis of facial muscles or hemifacial spasm.
• Other causes of damage to facial nerve anywhere along its course → axonal damage especially of large-diameter myelinated fibers → loss of function of facial muscles or facial spasm.
• A primary irritation of the facial nerve nucleus or increased excitability of the facial nucleus by upper motor neuron dysfunction can also cause hemifacial spasm.

Timecourse

• Most times onset of facial neuropathy is acute.
• Most cases have severe paresis and paralysis of the facial nerve which remains static.

Diagnosis

Treatment

Prevention

Outcomes