Bell Palsy Clinical Presentation

Updated: Jul 12, 2017
  • Author: Danette C Taylor, DO, MS, FACN; Chief Editor: Selim R Benbadis, MD  more...
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Presentation

History

The diagnosis of Bell palsy must be made on the basis of a thorough history and physical examination, as well as the use of diagnostic testing when necessary. Bell palsy is a diagnosis of exclusion. Clinical features of the disorder that may help to distinguish it from other causes of facial paralysis include the sudden onset of unilateral facial paralysis and the absence of signs and symptoms of CNS, ear, and cerebellopontine angle disease.

Symptoms of Bell palsy include the following:

  • Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)
  • Posterior auricular pain
  • Decreased tearing
  • Hyperacusis
  • Taste disturbances
  • Otalgia

Early symptoms include the following:

  • Weakness of the facial muscles
  • Poor eyelid closure
  • Aching of the ear or mastoid (60%)
  • Alteration of taste (57%)
  • Hyperacusis (30%)
  • Tingling or numbness of the cheek/mouth
  • Epiphora
  • Ocular pain
  • Blurred vision

Onset

The onset of Bell palsy is typically sudden, and symptoms tend to peak in less than 48 hours. This sudden onset can be frightening for patients, who often fear they have had a stroke or have a tumor and that the distortion of their facial appearance will be permanent.

Because the condition appears so rapidly, patients with Bell palsy frequently present to the emergency department (ED) before seeing any other health care professional. More people first notice paresis in the morning. Because the symptoms require several hours to become evident, most cases of paresis likely begin during sleep.

Facial paralysis

The paralysis must include the forehead and lower aspect of the face. The patient may report the inability to close the eye or smile on the affected side. He or she also may report increased salivation on the side of the paralysis. If the paralysis involves only the lower portion of the face, a central cause should be suspected (ie, supranuclear). If the patient complains of contralateral weakness or diplopia in conjunction with the supranuclear facial palsy, a stroke or intracerebral lesion should be strongly suspected.

If a patient has gradual onset of facial paralysis, weakness of the contralateral side, or a history of trauma or infection, other causes of facial paralysis must be strongly considered. Progression of the paresis is possible, but it usually does not progress beyond 7–10 days. A progression beyond this point suggests a different diagnosis. Patients who have bilateral facial palsy must be evaluated for Guillain-Barré syndrome, Lyme disease, and meningitis.

Many patients report numbness on the side of the paralysis. Some authors believe that this is secondary to involvement of the trigeminal nerve, whereas other authors argue that this symptom is probably from lack of mobility of the facial muscles and not lack of sensation.

Ocular manifestations

Early ocular complications include the following:

  • Lagophthalmos (inability to close the eye completely)
  • Paralytic ectropion of the lower lid
  • Corneal exposure
  • Brow droop
  • Upper eyelid retraction
  • Decreased tear output/poor tear distribution
  • Loss of the nasolabial fold
  • Corneal erosion, infection, and ulceration (rare)

Late ocular manifestations include the following:

  • Mild, generalized mass contracture of the facial muscles, rendering the affected palpebral fissure narrower than the opposite one (after several months)
  • Aberrant regeneration of the facial nerve with motor synkinesis
  • Reversed jaw winking (ie, contracture of the facial muscles with twitching of the corner of the mouth or dimpling of the chin occurring simultaneously with each blink)
  • Autonomic synkinesis (ie, crocodile tears—tearing with chewing)
  • Permanent, disfiguring facial paralysis (rare)

Two thirds of patients complain about tear flow. [10] This results from the reduced function of the orbicularis oculi in transporting the tears. Fewer tears arrive at the lacrimal sac, and overflow occurs. The production of tears is not accelerated.

Posterior auricular pain

Half of the patients affected with Bell palsy may complain of posterior auricular pain. [10] The pain frequently occurs simultaneously with the paresis, but pain precedes the paresis by 2-3 days in about 25% of patients. Ask the patient if he or she has experienced trauma, which may account for the pain and facial paralysis.

One third of patients may experience hyperacusis in the ear ipsilateral to the paralysis, which is secondary to weakness of the stapedius muscle.

Taste disorders

While only one third of patients report taste disorders, [10] 80% of patients show a reduced sense of taste. Patients may fail to note reduced taste, because of normal sensation in the uninvolved side of the tongue. Early recovery of the sense of taste suggests that the patient will experience a complete recovery.

Facial spasm

Facial spasm, a very rare complication of Bell palsy, occurs as tonic contraction of 1 side of the face. Spasms are more likely to occur during times of stress or fatigue and may be present during sleep. This condition may occur secondary to compression of the root of the seventh nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root.

Facial spasm occurs most commonly in patients in the fifth and sixth decades of life. Sometimes the etiology is not found. The presence of progressive facial hemispasm with other cranial nerve findings indicates the possibility of a brainstem lesion.

Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It may be mild and result in slight movement of the mouth or chin when the patient blinks or in eye closure with smiling. Crocodile tears can be observed; patients shed tears while they eat.

Cranial neuropathies

Some believe that other cranial neuropathies may also be present in Bell palsy; however, this is not uniformly accepted. The symptoms in question include the following:

  • Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves
  • Dysfunction of the vestibular nerve
  • Hyperesthesia of the cervical sensory nerves
  • Vagal or trigeminal motor weakness
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Physical Examination

Weakness and/or paralysis from involvement of the facial nerve affects the entire face (upper and lower) on the affected side. A careful examination of the head, ears, eyes, nose, and throat must be carried out in all patients with facial paralysis. Time must also be taken to examine the patient’s skin for signs of squamous cell carcinoma, which can invade the facial nerve, and parotid gland disease.

Focus attention on the voluntary movement of the upper part of the face on the affected side; in supranuclear lesions, such as occur in a cortical stroke (upper motor neuron; above the facial nucleus in the pons), the upper third of the face is spared in the majority of cases, while the lower two thirds are paralyzed. The orbicularis, frontalis, and corrugator muscles are innervated bilaterally at the level of the brainstem, which explains the pattern of facial paralysis in these cases. [31]

Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the side affected by the palsy. When the patient is asked to raise his or her eyebrows, the side of the forehead with the palsy will remain flat. When the patient is asked to smile, the face will become distorted and lateralize to the side opposite the palsy.

Otologic examination

An otologic examination includes pneumatic otoscopy and tuning fork examination. An otologic cause should be considered if the history or physical examination demonstrates evidence of acute or chronic otitis media, including a tympanic membrane perforation, otorrhea, cholesteatoma, or granulation tissue, or if a history of ear surgery is noted. Concurrent rash or vesicles along the ear canal, pinna, and mouth should raise the suspicion for Ramsay Hunt syndrome (herpes zoster oticus).

The external auditory canal must be inspected for vesicles, injection or erythema, infection, or trauma. The patient may have decreased sensation to pinprick in the posterior auricular area. Tympanic membranes should be normal; the presence of inflammation, vesicles, or other signs of infection raises the possibility of complicated otitis media.

The patient who has paralysis of the stapedius muscle will report hyperacusis. This can be tested clinically using the stethoscope loudness test. In this, the patient wears a stethoscope, and an activated tuning fork is placed at its bell. The loud sound will lateralize to the side of the paralyzed stapedius muscle.

Ocular examination

With weakness/paralysis of the orbicularis oculi muscle (facial nerve innervation) and normal function of the levator muscle (oculomotor nerve innervation) and Mueller muscle (sympathetic innervation), the patient frequently is not able to close the eye completely on the affected side. On attempted eye closure, the eye rolls upward and inward on the affected side. (This is known as Bell phenomenon and is considered a normal response to eye closure.) In addition, the tear reflex is absent in many cases of Bell palsy.

For these reasons, the patient may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye. The patient may appear to have loss of corneal reflex on the affected side; however, the contralateral eye blinks when testing the corneal reflex on the affected side.

Oral examination

A careful oral examination must be performed. Taste and salivation are affected in many patients with Bell palsy. Taste may be assessed by holding the tongue with gauze and testing each side of the tongue independently with salt, sugar, and vinegar. The mouth must be washed after testing with different substances. The affected side has decreased taste compared with the normal side.

Neurologic examination

Careful neurologic examination is necessary in patients with facial paralysis. This includes complete examination of all of the cranial nerves, sensory and motor testing, and cerebellar testing. A neurologic abnormality warrants neurologic referral and further testing, such as MRI of the brain, lumbar puncture, and EMG where appropriate.

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Grading

The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI. [3, 4, 5] Grade I is normal facial function.

Grade II is mild dysfunction. Characteristics include the following:

  • Slight weakness is noted on close inspection
  • Slight synkinesis may be present
  • Normal symmetry and tone are noted at rest
  • Forehead motion is moderate to good
  • Complete eye closure is achieved with minimal effort
  • Slight mouth asymmetry is noted

Grade III is moderate dysfunction. The following characteristics are found:

  • An obvious, but not disfiguring, difference is noted between the 2 sides
  • A noticeable, but not severe, synkinesis, contracture, or hemifacial spasm is present
  • Normal symmetry and tone are noted at rest
  • Forehead movement is slight to moderate
  • Complete eye closure is achieved with effort
  • A slightly weak mouth movement is noted with maximal effort

Grade IV is moderately severe dysfunction. Signs include the following:

  • An obvious weakness and/or disfiguring asymmetry is noted
  • Symmetry and tone are normal at rest
  • No forehead motion is observed
  • Eye closure is incomplete
  • An asymmetrical mouth is noted with maximal effort

Grade V is severe dysfunction. Characteristics include the following:

  • Only a barely perceptible motion is noted
  • Asymmetry is noted at rest
  • No forehead motion is observed
  • Eye closure is incomplete
  • Mouth movement is only slight.

Grade VI is total paralysis. The following are noted:

  • Gross asymmetry
  • No movement

In this system, grades I and II are considered good outcomes, grades III and IV represent moderate dysfunction, and grades V and VI describe poor results. Grade VI is defined as complete facial paralysis; all of the other grades are defined as incomplete. An incomplete facial paralysis denotes an anatomically and, to some degree, functionally intact nerve. The degree of facial nerve function should be noted in the chart at the patient’s initial visit.

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