37A.Q. Rana, J.A. Morren, Neurological Emergencies in Clinical Practice, DOI 10.1007/978-1-4471-5191-3_4, © Springer-Verlag London 2013

Bell’s palsy is an idiopathic facial paralysis that results from acquired cranial nerve VII (facial nerve) dysfunction. It usually presents with a sudden onset unilateral inability to move facial muscles on the affected side, although it is mostly self-limiting.

Peripheral facial nerve dysfunction presents as facial muscle paralysis, with or without loss of taste sensation on the anterior two-thirds of the tongue. It may be progressive, reaching its most debilitating state within 3 weeks from the onset. The diagnosis of Bell’s palsy becomes unlikely if even minute levels of facial function do not return in 3 to 4 months. About 80–85 % of patients have spontaneous and complete recovery within 3 months, with a variable degree of residual de fi cits in the rest [ 1 ] .

Stabilize the Patient

ABCs

1. Assess the airway and breathing rate, and look for signs of respiratory distress. Most patients will be stable.

2. Check the vital signs and assess if the patient is hemodynamically stable. Place the patient on a cardiac monitor and pulse oximeter. Most patients will be stable.

Chapter 4 Facial Weakness (Bell’s Palsy)

38 Chapter 4. Facial Weakness (Bell’s Palsy)

Focused History

1. Ask about the presenting symptoms, time of onset, and if progressive or not. There may be no antecedent symptoms of a viral syndrome like an upper respiratory tract infection.

2. Ask questions to rule out any other causes of the presenting symptoms especially other de fi cits suggestive of stroke.

Focused Exam

1. Assess language function. Check for naming, repetition, fl uency, and comprehension.

2. Evaluate cranial nerve function including visual fi elds, lifting eyebrows and frowning, and nasolabial fold symmetry. Assess ability to blow cheeks out, seal lips, and whistle. Check strength of eyelid closure and assess hearing. Patients have ipsilateral eyebrow sagging or inability to generate wrinkles, inability to close eyes completely, and loss of nasolabial fold with drooping (and/or drooling) at corner of the mouth. Depending on the severity and extent of the lesion, patients may have hyperacusis ipsilaterally. A key fi nding is weak-ness affecting the upper face (including forehead) which is usually spared in an upper motor neuron-type facial palsy.

Identify the Underlying Cause

Take Further History

Ask about any additional symptoms, such as reduction in lacrimation, hyperacusis, and loss of taste sensation or recent history of head trauma (a rare cause). Decreased lacrimation, hyperacusis, and loss of taste on anterior two-thirds of tongue may be associated symptoms which provide information on the severity of the illness including the degree of proximal extension of the facial nerve lesion.

39Treat the Underlying Cause

Do Further Examination

A complete neurological examination should be done. This includes testing mental status, other cranial nerves, muscle tone and power, muscle bulk and adventitious movements, deep tendon re fl exes, plantar responses, coordination with station and gait assessment, as well as sensory examination of all modalities. Other non-cranial nerve deficits may indicate a central etiology like stroke.

Do Investigations

1. Usually no investigations are necessary if the clinical pic-ture is consistent with diagnosis of Bell’s palsy.

2. Electrodiagnostic tests such as NCS/EMG including blink re fl ex testing can help to con fi rm the diagnosis and indi-cate severity but are usually not required. Imaging studies are not required either. They can sometimes help to rule out other causes such as stroke, acoustic neuromas, or other focal mass lesions if the diagnosis is questionable. As most cases are self-limiting, further advanced diagnostic tests are usually unnecessary.

Treat the Underlying Cause

Treatment varies, depending on the individual and the severity of the illness. Mild cases may not require treatment as they sub-side generally within 2 weeks. In other cases, treatment include: 1. Prednisone (60 mg daily for 5 days, then decreased by

10 mg daily for a total of 10 days of treatment) can help to reduce in fl ammation. In diabetics, prednisone may be dosed at 30 mg/day for 2–3 days. Steroid usage is now a level A recommendation [ 2 ] .

2. Acyclovir (400 mg three times daily for 5 days) can be pre-scribed for possible viral causes, but its added bene fi t is uncertain [ 2, 3 ] .

40 Chapter 4. Facial Weakness (Bell’s Palsy)

3. Arti fi cial eye drops (Lacri-lube ® ) can used to maintain lubrication during the day, and an eye patch can be applied at night time to avoid corneal ulceration, a dreaded complication.

Discussion

A serious complication to be wary of is corneal damage because of excessive dryness resulting in corneal ulceration due to inability to completely close the eye on the affected side. As such, proper eye care is an important part of treatment.

References

1. Finsterer J. Management of peripheral facial nerve palsy. Eur Arch Otorhinolaryngol. 2008;265(7):743–52.

2. Gronseth GS, Paduga R, American Academy of Neurology. Evidence-based guideline update: steroids and antivirals for Bell palsy: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2012;79(22):2209–13.

3. Lampert L, Wong YJ. Combined antiviral-corticosteroid therapy for Bell palsy yields inconclusive bene fi t. J Am Dent Assoc. 2012;143(1):57–8.