Facial paralysis is inability to move the muscles of facial expression (eyelids, lips, ears, nose, etc), caused by a lesion of the motor component of the facial nerve (cranial nerve 7). Diagnosis is based on clinical features and tests to identify the specific cause. Treatment is directed at the underlying cause.
The lower motor neuron cell bodies in animals are in the facial motor nucleus, located in the rostral aspect of the medulla oblongata of the brainstem. The facial nerve (cranial nerve 7) exits the brainstem near the vestibulocochlear nerve (cranial nerve 8), passes through the petrous temporal bone, and then exits the skull through the stylomastoid foramen, splitting into auricular, palpebral, and buccal branches.
In the horse, after exiting the skull, the facial nerve runs across the lateral wall of the guttural pouch. Then the nerve and its branches run through the thin subcutaneous tissues of the face and across the bony supraorbital ridge, making the nerve susceptible to damage from even minor trauma.
Although the facial nerve provides motor innervation to the face, sensation to the face is primarily supplied by the trigeminal nerve (cranial nerve 5), and includes sensation to the cornea and eyelids (ophthalmic branch of cranial nerve 5), the upper lips (maxillary branch), and the lower lips (mandibular branch). The mandibular branch also provides motor innervation to the muscles of mastication (masseter, temporalis, and digastricus muscles).
Etiology of Facial Paralysis
Facial paralysis can occur with a variety of underlying lesions (see the table ).
Causes of Facial Paralysis in Dogs, Cats, and Horses
Cause | Dog | Cat | Horse |
|---|---|---|---|
Infection | Otitis media | Otitis media | Otitis media, guttural pouch infection |
Nasopharyngeal polyp | Rare | Common | NA |
Trauma | Ear surgery | Ear surgery | Recumbency, kicks, falls |
Metabolic | Hypothyroidism | NA | NA |
Idiopathic | Common | Uncommon | Rare |
Degenerative | NA | NA | Temporohyoid osteoarthropathy |
Neoplastic | Ceruminous gland adenocarcinoma, cholesteatoma | Squamous cell carcinoma | Lymphoma |
Brainstem lesions | Encephalitis (immune mediated, infectious), neoplasia, stroke | Encephalitis (FIP), neoplasia | Equine protozoal encephalomyelitis |
Abbreviations: FIP, feline infectious peritonitis; NA, not a cause of facial paralysis in this species. | |||
Otitis media is a common cause of facial paralysis, especially in dogs and cats.
In cats, nasopharyngeal polyps often extend into the tympanic bullae, resulting in facial paralysis.
Temporohyoid osteoarthropathy and guttural pouch infections can cause facial paralysis in horses.
Trauma is a common cause of facial paralysis, especially in large animals. In horses, halter injuries and prolonged lateral recumbency can injure the buccal branches of the facial nerve on the side of the jaw and cause unilateral or bilateral paresis or paralysis of the lips and nostrils. Cattle that struggle in stanchions can injure the palpebral branch of the facial nerve as it crosses the zygomatic arch, causing unilateral or bilateral paresis or paralysis of the eyelid(s).
In dogs and cats, the facial nerve can be damaged during surgery, such as total ear canal ablation or removal of tumors in the facial nerve region.
Hypothyroidism in dogs can affect various cranial nerves, including the facial nerve.
Idiopathic facial neuritis is common in dogs. This poorly understood syndrome may be similar to facial nerve palsy (Bell palsy) in humans. It develops in middle-aged to older dogs as a sudden onset of unilateral or, less frequently, bilateral facial paralysis with no other clinical signs.
Primary neoplasia of the facial nerve is rare; however, neoplasms in the region of the middle ear can affect the nerve. Squamous cell carcinoma and ceruminous gland adenocarcinoma of the middle ear are most common in dogs and cats.
Brainstem lesions that can cause facial paralysis include encephalitis, neoplasia, and stroke. Specific causes of encephalitis include immune-mediated meningoencephalitis in dogs, feline infectious peritonitis in cats, and equine protozoal myeloencephalitis in horses.
Clinical Findings and Lesions of Facial Paralysis
Clinical signs of facial paralysis vary with the location, severity, and chronicity of the underlying lesion:
A unilateral lesion of the facial nucleus or proximal portion of the facial nerve causes paresis or paralysis of the eyelids, ears, lips, and nostrils.
A lesion of the auriculopalpebral branch of the facial nerve, near the zygomatic arch, results in paresis or paralysis of the eyelids and ear only.
A lesion of the palpebral branch of the facial nerve, crossing the zygomatic arch, results in paresis or paralysis of the eyelids only.
A lesion of the buccal branch of the facial nerve, as it courses along the surface of the masseter muscles, results in paresis or paralysis of the lips and nostrils only.
The most consistent clinical sign of facial paralysis is an inability to blink. There is also a loss of the palpebral reflex and menace response (see ). Instead of closing the eyelids, affected patients will retract the globe, which causes passive elevation of the third eyelid.
Pearls & Pitfalls
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In acute lesions, the ear carriage is often lower on the side of the lesion (the ipsilateral side). The patient's lips on the paralyzed side may hang loosely, exposing mucosa. When the animal eats or drinks, food and/or fluids may fall from the lips. The animal may drool excessively, and food may collect between the lips and teeth.
With unilateral lesions, the nose deviates away from the side of the lesion. In horses, the affected nostril is unable to dilate. (See .)
Right facial paralysis in a horse, causing deviation of the muzzle to the left, dropping of the right ear, and ptosis of the right upper eyelid.
Courtesy of Dr. Carla Sommardahl.
A lesion of the facial nerve proximal to the stylomastoid foramen can damage parasympathetic fibers that travel with the nerve to the lacrimal and nasal glands. This causes neurogenic keratoconjunctivitis sicca (KCS) and/or dryness and hyperkeratosis of the nasal planum (xeromycteria). Decreased tearing with eyelid paresis can lead to corneal ulceration, especially in horses. A Schirmer tear test is indicated to assess tearing in any patient with facial paralysis.
Once facial nerve dysfunction is recognized, it is important to determine whether the lesion is in the brainstem or the peripheral nerve:
Brainstem lesions typically are associated with additional deficits, such as ipsilateral limb paresis or deficits in proprioceptive positioning, other cranial nerve deficits, or altered mentation.
Ipsilateral head tilt with vestibular and/or ipsilateral Horner syndrome (ptosis, miosis, and enophthalmos) with normal mentation and limb function indicates the lesion is in the middle or inner ear, where the facial nerve and parasympathetic innervation to the face travel.
Isolated facial nerve paralysis with no other deficits indicates the lesion is in the peripheral nerve.
Horses with temporohyoid osteoarthropathy (THO) often have unilateral or bilateral facial paralysis or vestibular dysfunction. THO is characterized by bony proliferation of the articulation of the stylohyoid bone with the petrous temporal bone. The etiology is poorly understood but could be a primary degenerative joint disease; however, spread of infection from the middle ear or guttural pouch has also been proposed as a cause (2).
Enlargement of the proximal portion of a stylohyoid bone can compress the facial nerve, causing facial paralysis, head shaking, and behavior changes. The temporohyoid joint can eventually fuse, predisposing to fracture of the petrous temporal bone resulting in acute neurological signs, including vestibular dysfunction and seizures.
Clinical signs of THO include head shaking, cribbing, facial nerve paralysis, corneal ulcer, and vestibular dysfunction (ataxia, head tilt, abnormal nystagmus). Less common are seizures, which can be fatal in some cases.
Diagnosis of Facial Paralysis
History and physical examination
Otoscopic examination, ophthalmic examination, or neurological examination
Thyroid function testing (in dogs)
Endoscopic examination of the guttural pouch (in horses)
Radiography and advanced imaging (CT or MRI)
In cases of facial paralysis, diagnostic testing is directed at identifying the underlying cause.
Diagnosis of otitis media is based on otoscopic examination with cytological evaluation and culture. In some cases, skull radiography or advanced imaging (CT or MRI) is helpful to evaluate the middle ear (see ).
The bone of the left tympanic bulla of a dog is thickened, with increased density within the bulla.
Dr, William B. Thomas
Nasopharyngeal polyps are often visible on otoscopic examination or by elevating the soft palate to visualize the nasopharynx; this typically requires general anesthesia.
In horses with suspected THO, endoscopy of the guttural pouch identifies enlargement of the proximal stylohyoid bone and abnormalities of the temporohyoid joint. Radiography or standing CT can be used to evaluate the bony articulation and impinging bony proliferation.
Diagnosis of trauma is based on history and clinical signs.
Diagnosis of hypothyroidism is based on testing of thyroid function and response to treatment.
In idiopathic facial neuritis, diagnostic testing results are normal, other than MRI, which often shows abnormal enhancement of the facial nerve.
In cases of primary neoplasia of the facial nerve, biopsy of affected tissue is necessary for definitive diagnosis. CT or MRI is helpful to determine the extent of the lesion when surgery is a consideration.
MRI allows visualization of the facial nerve and in indicated when the lesion localizes to the brainstem. CSF analysis and titers for infectious causes can also help reach a diagnosis.
Treatment and Prognosis of Facial Paralysis
Management of underlying cause
Supportive therapy (eg, ophthalmic lubrication)
Surgery in cases refractory to medical therapy
Treatment of facial paralysis is directed at the underlying cause, if possible.
Administration of artificial tears is helpful, especially if tear production is decreased. Corneal ulceration must be watched for and treated promptly.
Horses with collapsing nostrils can require corrective surgery.
Species that use the lips for drinking and prehension of food must be given deep water containers and wet, bulky mashes.
The prognosis is variable, depending on the underlying cause. Early treatment of infections increases the chance of neurological recovery; however, in many cases, permanent paresis results. Facial paralysis associated with hypothyroidism typically improves within 6–8 weeks after starting thyroid hormone supplementation (1). With idiopathic facial paralysis, partial or complete improvement can occur over several weeks to months; however, in some cases the contralateral side becomes affected.
If nerve function does not return, permanent muscle contracture can occur secondary to chronic paralysis and fibrosis. Contracture of affected muscles might be mistaken for improvement because the muscles no longer droop or sag. With facial muscle contracture, the lip on the affected side can be higher than on the normal side, the nose deviates toward the lesion, and the base of the pinna is positioned abnormally high on the head.
Pearls & Pitfalls
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Supportive treatment of horses with temporohyoid osteoarthropathy involves administration of NSAIDs and broad-spectrum antimicrobials.
Surgery, such as partial stylohyoidectomy, ceratohyoidectomy, or basihyoid-ceratohyoid disarticulation, can help in cases refractory to medical therapy.
Key Points
Diagnosis of facial paralysis is based mainly on clinical signs.
The underlying cause of facial paralysis must be treated, if possible.
The prognosis for neurological recovery is guarded in many cases; however, isolated facial paralysis is rarely debilitating.
For More Information
References
Jaggy A, Oliver JE, Ferguson DC, Mahaffey EA, Glaus T Jr. Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs. J Vet Intern Med. 1994;8(5):328-336. doi:10.1111/j.1939-1676.1994.tb03245.x
Blythe LL. Otitis media and interna and temporohyoid osteoarthropathy. Vet Clin North Am Equine Pract. 1997;13(1):21-42. doi:10.1016/S0749-0739(17)30253-5
