A patient presents to your office with unilateral tearing, foreign body sensation, and inability to close their eye or smile on one side. You notice that half of the patient’s face is drooping. The first thought is “did this patient have a stroke and do I need to get them to the ER?” You take a breath, recall neuroanatomy, and begin your detective work.
In this article we’ll discuss the clinical presentation of Bell’s palsy and review the pathophysiology, management, and treatment options available. We’ll also review the neuroanatomy to differentiate Bell’s palsy from other etiologies (eg. stroke, neoplasm).
Making a diagnosis
Begin with a patient history, trying to ascertain the timing of onset and associated symptoms. Do they have pain in or behind their ear, dysgeusia, and/or hyperacusis? Are they experiencing weakness/paralysis/numbness in their extremities? Are they having trouble walking, speaking, swallowing?
Your first physical assessment (as it is for all patients) should be of the patient’s face and adnexa looking for asymmetry or abnormalities. You notice drooping of one side of the face with flattening of nasolabial fold, corner of the mouth, and lower eyelid. You also notice diminished wrinkling of the forehead on the affected side.
Next, test the facial muscles. Ask the patient to lift their eyebrows as if they are surprised, squeeze their eyes shut, puff out their cheeks, and smile. Look for flattening of the nasolabial fold and inability to bury eyelashes when closing eyes tightly - as these are signs of mild facial weakness.
Typically, when patients have complete paralysis to one side of the face, including the forehead and eyebrows, the diagnosis of Bell’s palsy should be among your top differentials. In cases when the forehead and eyebrow are spared, intracranial pathology should be high among your differentials (eg. stroke).
In Bell’s palsy, symptoms arise over hours to days with maximum severity of symptoms at 3 days. The median age of onset is 40. Sometimes a patient may wake up with symptoms making it difficult to ascertain exactly how quickly they came on.
Males and females are affected equally. There are no racial or ethnic predilections. It can occur at any age, although Bell’s palsy tends to affect those in mid to later life more often. Incidence is higher in those with pregnancy (especially with preeclampsia) immunocompromised states, recent upper respiratory viral infection, diabetes, and hypertension.
Left: The innervation to the muscles of the upper face originates on both sides of the brain, whereas the innervation to the muscles of the lower face comes from the opposite side of the brain only. Middle: When the cortex is injured, there’s weakness in the contralateral lower face only. Right: When the facial nerve is injured, there’s weakness in the ipsilateral upper and lower face.
The upper portion of the face (forehead and eyes) receives innervation from both sides of the brain. The lower half (cheeks, mouth) receive only contralateral innervation from the central nervous system (motor cortex).
If the patient has a complete facial paralysis on one side of the face, this is a peripheral or “lower motor” neuron lesion, meaning the lesion occurred at or after where the facial nerve leaves the brainstem. Since the lesion occurred after innervation crossing, it affects all ipsilateral nerve fibers that have reached that side of the face. The most common peripheral cause of acute facial palsy is Bell’s palsy.
If the patient is able to wrinkle their forehead and has equal eyelid apertures, but has paralysis of the lower portion of one side of the face, this is a central or “upper motor” neuron lesion, meaning the lesion initiated from the central nervous system. The most common cause of acute facial paralysis from a central lesion is an ischemic stroke. Due to the bilateral innervation to the upper face, they are still able to control this part of their face. Acute ischemic stroke is caused by an occlusion of a blood vessel supplying the brain. The onset of symptoms occurs over a few seconds to minutes and tends to occur in patients age 60 and older. These patients may also have other concomitant neurological symptoms including numbness/tingling of extremities, slurred speech, or transient loss of other senses like sight (double vision) or smell.
If an ischemic stroke occurs at the level of the brainstem, it may affect the upper face and mimic a Bell’s palsy. However, since ischemia will occur in a region of the brain, not only to one nerve, there will likely also be other associated symptoms. Testing nearby cranial and motor nerves can help give an indication of whether this is truly an isolated nerve paralysis.
- CN I/olfactory: ask pt if any trouble smelling
- CN II/optic: test BCVA and examine nerve appearance-look for pallor/edema. Also, check pupil responses and rule out an afferent defect.
- CN III, IV, VI/oculomotor, trochlear, abducens: EOMs-check for diplopia or palsy in 9 positions of gaze
- CN V/trigeminal: test facial sensation by having the patient close their eyes and gently rub the end of a tissue along each side of their forehead, cheeks, and chin to ensure they can feel it equally on each side; CNV also controls the muscles of mastication. A cotton-tipped applicator or tissue can be used to assess facial sensation.
- CN VII/facial: taste on anterior 2/3 of the tongue, somatosensory information from the ear (ask about pain in or behind the ear), muscles of facial expression: ask pt to raise their eyebrows, squeeze their eyes shut and check for burying of lashes or try to pull lids apart (orbicularis oculi), puff out their cheeks (buccinators) and smile widely (orbicularis oris).
- CN VIII/vestibulocochlear: hearing (hyperacusis), balance
- CN IX/X/glossopharyngeal/vagus: swallowing, coughing
- CN XI/spinal accessory nerve: turn head to each side, shrug shoulders
- CN XII/hypoglossal: sticking out tongue
Bell’s palsy accounts for 75-90% of CN VII palsies. The remaining causes of CNVII palsy include infection (Lyme or TB), granulomatous disorders (sarcoidosis), trauma, inflammation, autoimmune diseases, facial diplegia, vasculitis, viruses (coxsackievirus, cytomegalovirus, adenovirus, mumps, rubella, influenza B, Epstein-Barr), iatrogenic and neoplastic.
Neoplasms are responsible for 5% of all CNVII palsies; with the most common benign neoplasm being facial nerve schwannoma and the most common malignant neoplasm being squamous cell carcinoma. A slowly progressive facial palsy should raise immediate suspicion of neoplastic origin. If the patient cannot recall the day of onset, send for emergent CT/MRI. Based on history and exam, relevant lab tests should be ordered to rule out other causes. This may be best co-managed with the patient’s primary care provider.
Onset of facial paralysis and likely cause
|Hours, <3 days||Bell’s Palsy|
Management of ocular sequelae
Your job after determining the patient has Bell’s palsy is to manage the cornea to avoid exposure keratopathy which can have serious effects. Start the patient on preservative-free artificial tears hourly, lubricating ointment, and taping lids closed before bed. Check that the patient has intact Bell’s phenomenon, an upward rolling of the eyes when eyes close. If so, this will protect somewhat against exposure keratopathy. Consider Eyeseals Hydrating Sleep Mask (Eye Eco) for overnight protection and moisturizing. Patients may also consider moisture/swim goggles for showering.
Tx: Although most cases of Bell’s palsy are self-limiting and resolve within several weeks without pharmacologic intervention, various treatment options do exist. Some practitioners may consider oral steroids dosed at 60mg/day (divided dose) for 5 days, followed by a 5-day taper reducing the dosage by 10mg/day to hasten recovery. Steroids have the most effect when started within 72 hours of the onset of symptoms. Anti-viral treatment remains controversial as does the potential implication for Herpes Simplex reactivation in the cause of Bell’s. Physical therapy may also be beneficial for some patients in their recovery of idiopathic facial palsy.
85% of patients with Bell’s Palsy will have some recovery in the first 3 weeks and most recover to near-complete levels after several months and up to one year. Resolution is better in those who are younger with partial paralysis versus older with complete paralysis. If no resolution is seen after a few months, consider alternate causes and investigate further.
Bell’s Palsy is a diagnosis of exclusion. To differentiate it from other more serious causes of facial nerve palsy, get a detailed history to determine the timing of onset, examine facial muscles and associated cranial muscles, and motor symptoms. History of acute unilateral facial paralysis over 72 hrs without other neurologic symptoms is sufficient to make a diagnosis of Bell’s Palsy without labs or imaging required. Your role is to manage the ocular sequelae and make appropriate referrals if other neurological symptoms are found or reported.
While a complete facial paralysis typically will appear worse than it really is, it is our job as primary eye care providers to counsel our patients and reassure them of prognosis and recovery. Explaining that symptoms may take several weeks or more to resolve helps to properly set the patient’s expectations. By recalling your neuroanatomy, and after a thorough clinical assessment of the patient, you can rest assured in your diagnosis.