Facial nerve neuropathies

Facial nerve neuritides

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  • 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.


Clinical signs

  • Drooping ear.
  • Paralyzed lip commissure.
  • Build-up of food in the cheek on the paralyzed side.
  • Deviation of the nose away from the paralyzed side, in acute disease.
  • Deviation of the nose towards affected side with chronic disease (due to facial muscle contraction or fibrosis), or with hemifacial spasm.
  • Menace deficit with normal visual placing.
  • Absence of palpebral/corneal reflex. (Can result in corneal pathology due to decreased tear production and lack of a mechanism to spread tears across exposed cornea.)
  • Other accompanying neurologic signs:
    • Ipsilateral hemiparesis, trigeminal nerve involvement, and/or signs of central vestibular disease [Vestibulocochlear neuritides] , indicate brainstem disease.
    • Ipsilateral Horner's syndrome and signs of peripheral vestibular disease indicate middle/inner ear disease.
  • Intermittent facial or hemifacial spasm.
  • Bilateral facial paralysis.
    Muscle twitching is commonly either muscle or CNS in origin. Facial spasm is not a usual a sign of facial neuropathy.
  • Facial spasm has been reported early in the course of middle ear diseases and preceding facial paralysis in some cases, with chronic otitis media, and in two dogs with intracranial mass (causing increased excitability of facial nucleus by upper motor neuron dysfunction or primary irritation of facial nerve nucleus).
  • Dysfunction of the parasympathetic supply of lacrimal gland produces neurogenic keratoconjunctivitis sicca. This is mainly seen with lesions of the portion of the facial nerve located between the medulla and the middle ear. Lesions distal to the facial canal in the temporal bone will not affect the parasympathetic division of the facial nerve.

Differential diagnosis

Causes of facial or hemifacial spasm



  • Guarded for full return of function to the facial nerve.
  • Chronic lip paralysis may lead to permanent contracture.
  • Most facial nerve paralysis following total ear canal ablation/lateral bulla osteotomy is temporary and fully resolves within several weeks.
  • In general if facial nerve paralysis is present before surgery, improvement after surgery is unlikely.
  • MRI revealing lack of contrast enhancement of the intratemporal part of the facial nerve may be associated with a better outcome in dogs with idiopathic facial paralysis.

Expected response to treatment

  • Improvement may take place in a few weeks or months, or not at all.
  • Chronicity may result in muscle contracture and deform the facial expression permanently.
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