Facial paralysis is paralysis of the muscles affecting facial expression (eyelids, lips, ears, nose, etc). It can be caused by a lesion of the peripheral portion of the facial nerve or the facial nucleus in the brain stem. Diagnosis is based on clinical signs and use of tests to identify the specific cause. Treatment is directed at the underlying etiology.
The nucleus of the facial nerve is located in the rostral medulla oblongata of the brain stem. The facial nerve (cranial nerve 7) exits the brain stem near the vestibulocochlear nerve, passes through the petrous temporal bone, and then exits the skull through the stylomastoid foramen, splitting into auricular, palpebral, and buccal branches.
Clinical Findings and Lesions of Facial Paralysis in Animals
Clinical signs of facial paralysis vary with the location, severity, and chronicity of the 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 is an inability to blink. There is a loss of the palpebral reflex and menace response. Instead of closing the eyelids, affected patients will retract the globe, which causes the third eyelid to passively elevate. In acute denervation, the ear carriage is often lower on the side of the lesion (the ipsilateral side). The 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.
If the parasympathetic portion of the facial nerve is affected, there is reduced tear and saliva production on the side of the lesion. The reduced tearing and eyelid paresis can lead to corneal ulceration, especially in horses. A Schirmer tear test is indicated in any patient with facial paralysis to assess tear production.
The presence or absence of other neurologic deficits helps to localize the lesion. Limb paresis, postural reaction deficits, or altered mentation indicates the facial paralysis is likely caused by a lesion in the brain stem. Ipsilateral head tilt and/or ipsilateral Horner syndrome (ptosis, miosis, and enophthalmos ) with normal mentation and limb function indicates the lesion is in the middle/inner ear; this is because the facial nerve and parasympathetic innervation to the face travel near the middle and inner ear. Horses with temporohyoid osteoarthropathy often present with ipsilateral facial paralysis and vestibular dysfunction.
Diagnosis of Facial Paralysis in Animals
History and physical (including neurologic) examination
Otoscopic examination should also be performed in dogs and cats
Thyroid function testing is indicated in dogs
Endoscopic examination of the guttural pouch should be performed in horses
Ophthalmic examination may also be necessary
Otitis media is a common cause of facial paralysis, especially in dogs and cats. Diagnosis is based on otoscopic examination with cytology and culture. In some cases, skull radiographs, CT, or MRI examinations are necessary. In cats, nasopharyngeal polyps often extend into the tympanic bullae, resulting in facial paralysis. Polyps are often visible on otoscopic examination or by elevating the soft palate to visualize the nasopharynx; this typically requires general anesthesia.
Trauma is a common cause of facial paralysis, especially in large animals. In horses, halter injuries and prolonged lateral recumbency may 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 may 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 small animals (ie, dogs, cats), the facial nerve can be damaged during surgery, such as total ear canal ablation or removal of tumors in the facial nerve region.
Guttural pouch infections can cause facial paralysis in horses. Lesions of the facial nerve nucleus can result in facial nerve paralysis due to equine protozoal myeloencephalitis (EPM). CSF analysis and measurement of titers for EPM are essential for diagnosis and institution of appropriate treatment.
Hypothyroidism in dogs can affect various cranial nerves, including the facial nerve. Diagnosis is based on testing of thyroid function and, if indicated, response to treatment.
Idiopathic facial neuritis is common in dogs. This poorly understood syndrome may be similar to Bell's palsy in humans. It presents in middle-aged to older dogs as a sudden onset of unilateral or, less frequently, bilateral facial paralysis with no other clinical signs. All diagnostic testing typically returns normal results.
Primary neoplasia of the facial nerve is rare, but 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. Biopsy analysis of affected tissue is necessary for definitive diagnosis. A CT or MRI test is helpful to determine the extent of the lesion when surgery is a consideration.
Treatment and Prognosis of Facial Paralysis in Animals
Treatment is directed at the underlying cause, if possible. Installation of artificial tears to the eyes is helpful, especially if tear production is decreased. Corneal ulceration must be watched for and treated promptly. Horses with collapsing nostrils may require corrective surgery. Species that use the lips for drinking and prehension of food must be given deep water containers and wet, bulky mashes.
Prognosis is variable depending on the etiology. Early treatment of infections increases the chance of neurologic recovery; however, in many cases there is permanent paresis. Facial paralysis associated with hypothyroidism typically improves within 6–8 weeks of thyroid supplementation. 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 contracture may occur secondary to chronic muscle paralysis and fibrosis. Contracture of affected muscles may be mistaken for improvement because the muscles no longer droop or sag. With facial muscle contracture, the lip on the affected side may 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.
Key Points
Diagnosis of facial paralysis is based mainly on clinical signs.
The underlying cause must be treated, if possible.
Prognosis for neurologic recovery is guarded in many cases; however, isolated facial paralysis is rarely debilitating.
