The upper motor neurons that innervate the face (corticobulbar tract) originate from the primary motor cortex in the frontal lobe and travel through corona radiata and genu of the internal capsule, entering the brainstem through the cerebral peduncle and descending to the pons where they cross to synapse on the facial motor nucleus. The portion of the facial motor nucleus that elevates the forehead receives bilateral corticobulbar innervation, but the remainder of the facial motor nucleus, which controls the lower face, receives only contralateral corticobulbar innervation. This important, and clinically useful, anatomic feature means that a corticobulbar lesion on one side of the brain will cause contralateral facial weakness of the lower face, but preserved ability to elevate the forehead due to intact innervation from the ipsilateral corticobulbar tract. This defines the so-called “central” seventh nerve palsy. When present, brain imaging with magnetic resonance imaging (MRI) should be performed to identify the underlying lesion.
Unilateral facial weakness that involves both the lower and upper face (i.e., including the inability to elevate the forehead) is frequently referred to as a “peripheral” seventh nerve palsy, implying a lesion to the facial nerve after exiting the brainstem. Bell’s palsy is the prototypical example. Note, however, that a “peripheral” seventh nerve palsy can in fact be seen with brainstem lesions that involve the ipsilateral facial motor nucleus or the axons of the facial nerve prior to exiting the brainstem (the fascicle). Given its compact organization, brainstem lesions that cause “peripheral” facial weakness are almost always associated with additional focal neurologic findings, such as hemiparesis or eye movement abnormalities.
All nerve roots and cranial nerves except for the olfactory nerve travel through the subarachnoid space. Therefore, any process causing inflammation in the cerebrospinal fluid contained within the subarachnoid space can lead to multiple cranial neuropathies and/or radiculopathies. Examples include infections such as Lyme disease, autoimmune diseases such as sarcoidosis, and carcinomatous meningitis. Diagnosis is made by lumbar puncture and analysis of cerebrospinal fluid.
Bell’s palsy is an acute idiopathic peripheral facial palsy, and is by far the most common cause of peripheral facial weakness. The weakness typically develops over hours to one day. A slower onset of symptoms or continued worsening beyond 3 weeks is inconsistent with Bell’s palsy and should prompt brain MRI. Infrequently, an identifiable cause of facial palsy may be found in patients with a presentations otherwise consistent with Bell’s palsy. These include varicella zoster infection, Lyme disease, human immunodeficiency virus (HIV) seroconversion, syphilis, and autoimmune conditions such as sarcoidosis or Sjögren syndrome. Laboratory testing for these should be considered in the appropriate clinical scenario (see sections E and F). Acute peripheral facial palsy should be treated empirically with prednisone 60 mg daily for 5 days followed by a taper of 10 mg/day for 5 days, starting as soon as possible and ideally within 3 days of symptom onset to increase the likelihood of complete facial recovery and reduce the time to recovery. Treatment should not be delayed while awaiting any laboratory tests for known causes of an acute peripheral facial palsy. Antivirals (acyclovir and valacyclovir) do not appear to improve outcome and, unless there is suspicion for zoster, should be avoided. One consequence of peripheral facial weakness is difficulty closing the affected eye, which can lead to corneal injury. Eye care should include artificial tears and ointments at night as needed and protective glasses or a patch for patients without full eye closure.
Ramsay Hunt syndrome is the combination of an acute peripheral facial palsy, ear pain, and a vesicular rash on the ear, in the external auditory canal, or in the oropharynx due to zoster. Treatment is valacyclovir 1000 mg three times daily for 10 days in addition to prednisone as with Bell palsy.
Lyme disease can cause acute facial palsy and is an important consideration in endemic areas. Patients should be asked about tick exposure and rash, and Lyme testing done when appropriate. Provided neurologic involvement is limited to facial palsy, treatment with oral doxycycline for 14 days is reasonable.
Substantial, though not always complete, early improvement is seen in the vast majority of patients with Bell’s palsy. If there is no improvement in the facial weakness on follow-up 4 months after onset, consider the possibility of a mass lesion and perform brain MRI.
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