Contents
Paralysis of any structures innervated by the facial nerve.
- M/C cause: Bell’s palsy
Neuroanatomy
Facial nerve anatomy:
Etiology
Idiopathic/Bell Palsy (70%)
Most commonly, the cause for facial nerve palsy remains unknown and has the name ‘Bell palsy.’ Bell palsy has an incidence of 10 to 40 per 100000.[2] It is a diagnosis of exclusion.
- Commonly a lower motor neuron (LMN) lesion with total unilateral palsy
Infection:
- Ramsay Hunt Syndrome/Herpes zoster oticus: Due to reactivation of herpes zoster in the geniculate ganglion
- LMN lesion of the facial nerve, deafness, vertigo, and pain
- Otitis media
- Lyme disease
Temporal bone fracture (10 to 23%):
Fractures involving the petrous part of the temporal bone and facial wounds transecting the branches of the facial nerve can cause facial nerve palsies. It takes an incredibly large force to fracture the temporal bone, and the clinician must look for signs such as hemotympanum, battles sign, and nystagmus. Temporal bone fractures usually occur unilaterally and are classified according to the plane of fracture along the petrous ridge (i.e., longitudinal vs. transverse
- Transverse fractures (40-50% chance of paralysis)
- Longitudinal fracture (20% chance of paralysis
Neoplasia (2-5%):
Slowly progressing onset of facial palsy should raise the suspicion of malignancy and prompt a full and thorough head and neck examination.
- Facial neuromas
- Congenital cholesteatomas
- Hemangiomas
- Acoustic neuromas
- Parotid gland neoplasms
- Metastases of other tumours
Stroke:
Central facial palsy can be caused by a lacunar infarct affecting fibres in the internal capsule going to the nucleus
Disease associations:
Usually result in bilateral facial nerve palsy
- Diabetes mellitus
- Neurosarcoidosis: Sarcoidosis of the nervous system
- Guillain–Barré syndrome: Autoimmune condition of the peripheral nervous system causing bilateral facial nerve paralysis
- Moebius syndrome (rare): Bilateral facial paralysis resulting from underdevelopment of VII cranial nerve (facial nerve)
- CN VI, (controls lateral eye movement) is also affected
- C/F: Cannot form facial expression or move their eyes from side to side
Presentation
- Unilateral facial weakness
- Other symptoms:
- Loss of taste
- Hyperacusis
- Heightened sensitivity to some sounds
- Decreased salivation & tear secretion
Diagnosis
Physical examination:
- Blink test (corneal reflex): When tapping on patient’s glabella, a suspension in blinking will occur on the affected side (ophthalmic division of trigeminal nerve controls afferent limb, the efferent limb is the temporal and zygomatic branch of facial nerve)
- Schirmer test (assessing lacrimation of the lacrimal gland): Lacrimation decreased by 75% compared to normal side using a folded strip of blotting paper in lower conjunctival fornix
- Stapedial test (performed using tympanometry): Involuntary reaction in response to high-intensity sound stimuli causes contraction of stapedius muscle and gets mediated by facial nerve.
- Salivation test: Rate assessed from submandibular duct following stimulation with 6% citric acid solution. If positive, there will be a reduction in salivation by 25% at affected side and indicate lesion at or proximal to the root of the chorda tympani.
- Taste test: Using salt sweet, sour, and bitter tastes along the lateral aspects of the anterior two-thirds of the tongue. A positive result will indicate a lesion at or proximal to the root of the chorda tympani.
House–Brackmann score:
Testing facial movements will help distinguish between an upper (the forehead will be spared) and lower (entire facial movements are compromised) motor neuronal lesion. The degree of facial nerve paralysis is evaluated using the House-Brackman grading system
- I: Normal symmetrical function throughout
- II: Slight weakness on close inspection + slight asymmetry of smile
- III: Obvious non-disfiguring weakness, complete eye closure
- IV: Obvious disfiguring weakness, cannot lift the brow, incomplete eye closure, severe synkinesis
- V: Barely perceptible motion, incomplete eye closure, slight movement of corner of mouth, absent synkinesis
- VI: No movement, atonic
Electrophysiological tests:
Suitable for prognosis; however, they are expensive, time-consuming, and has a short time to be useful (less than three weeks after symptom onset)
- Minimal to maximal stimulation tests: Facial nerve stimulated with low current on affected side and gradually increased until maximal response or patient tolerability. This response then gets compared to the unaffected side with a 4-stage grading system. The test is positive if there is a clinically significant difference between the two sides.
- Electroneurography (ENOG): Establish muscle action potential amplitude and is the most accurate at determining the level of palsy. It involves facial nerve stimulation around the level of the stylomastoid foramen and the detection of a motor response near the nasolabial fold. This response then gets compared with the normal side.
- Electromyography (EMG): Determines activity within the facial muscles through the detection of fibrillation potentials that only manifest after around three weeks of denervation.
- Magnetic stimulation test: Tests intratemporal and brain stem aspects of facial nerve through transcranial stimulation. The test needs to be performed immediately as Wallerian degeneration of the nerve will alter the result findings.
Management
- Treat underlying cause
- Steroids (within 72 hours)