Bell's palsy Flashcards
What is Bell’s palsy?
Acute unilateral LMN facial (VII) nerve palsy.
What is the aetiology of Bell’s palsy? (x3 points)
- Largely idiopathic
- Most are preceded by an URTI, suggesting a viral or post-viral aetiology.
- Reactivation of HSV-1 within the geniculate ganglion
What is the structural anatomy of the facial nerve (CNVII)?
- INTRACRANIAL: large motor root and small sensory root fuse to form facial nerve and pass through internal acoustic meatus in temporal bone. It then enters the facial canal where three branches are given off.
- (1) It forms the geniculate ganglion (where the greater petrosal nerve arises to parasympathetically innervate the lacrimal gland).
- (2) The nerve then gives rise to the nerve to the stapedius muscle (motor fibres)
- (3) Chorda tympani (special sensory fibres to anterior 2/3 tongue and PSNS to submandibular and sublingual glands).
- Leaves cranium through stylomastoid foramen
- EXTRACRANIAL: runs anterior to the outer ear where it gives off the posterior auricular nerve (motor to muscles around ear), nerves to digastric muscle and to stylohyoid.
- The nerve then continues antero-inferiorly into the parotid gland (though does not contribute to it) where it splits into the temporal, zygomatic, buccal, marginal mandibular and cervical branches. These branches innervate the muscles of facial expression
Recap: What are the 7 functional types of nerve?
- General somatic afferent: general sensation from skin and mucous membranes
- Special somatic afferent: vision, hearing, balance
- General visceral afferent: PSNS stuff e.g., pharynx, lung, heart
- Special visceral afferent: smell and taste
- General somatic efferent: voluntary muscle
- Special visceral efferent: to pharyngeal arch structures
- General visceral efferent: to involuntary muscle/glands
- There is no special somatic efferent
What is the functional anatomy of CNVII? (x4)
- Special visceral efferent (this doesn’t fit the normal functional categorisation, but CNVII is special case): muscles of facial expression, strapedius muscle, posterior belly of digastric muscle and stylohyoid muscle
- General visceral efferent: pre-ganglionic PSNS innervation to salivary and lacrimal glands
- Special visceral afferent: taste to tongue
- General somatic afferent: cutaneous sensation from posterior wall of external auditory canal, concha and postauricular area
What is the pathophysiology of HSV-1-related Bell’s palsy?
Virus destroys ganglion cells and infects Schwann cells leading to demyelination and neural inflammation.
What is the epidemiology of Bell’s palsy: Age?
Peak age: 20-50 years.
! What are the signs and symptoms of Bell’s palsy: GSA? SVE? GSA? GVE? (x1, x3 +1, x1 and x2) Nature of branch involvement?
- All branches are affected equally since the palsy originates proximal to the geniculate ganglion
- GSA: prodrome of pre-auricular pain
- SVE: acute onset unilateral facial weakness and droop, reaching maximum severity within 1-2 days. Hypersensitivity to sound (hyperacusis caused by ipsilateral stapedius paralysis). 50% experience facial, neck or ear pain/numbness
- GSA: Loss of taste sense (uncommon) in ipsilateral anterior two-thirds tongue
- GVE: keratoconjunctivitis sicca (dry eye) occurs due to parasympathetic dysfunction to the lacrimal gland (and inadequate blink function (SVE; motor function to orbicularis oculi by zygomatic nerve)). May also lead to corneal ulcer and subsequent blindness
How can LMN facial nerve palsy be differentiated from UMN facial nerve palsy?
LMN facial nerve palsy does not spare the muscles of the upper part of the face as seen in UMN.
What is Bell’s phenomenon?
Eyeball rolls up and out when an attempt is made to close the eyes. It is a normal reflex in 75% of the population that has nothing to do with the palsy.
What are the investigations for Bell’s palsy? (x4)
- Clinical diagnosis of exclusion – if symptoms do not resolve after 6 months, symptoms progress, or symptoms affect facial zones in an uneven fashion, it is not Bell’s palsy
- EMG: indicated in patients with more than 90% degeneration in compound muscle action potential (CAMP) (in other words, near complete or complete facial paralysis), to confirm the absence of voluntary motor unit potentials in the affected side. Presence of these potentials would indicate a pathology other than Bell’s
- SEROLOGY for Borrelia burgdorferi: indicated in patients with recent travel to Lyme disease-endemic country. Lyme disease can present with the same symptoms.
- EAR EXAMINATION: exclude herpes zoster oticus and otitis media which may present similarly
What is the management for Bell’s palsy? (x4)
- CORTICOSTEROIDS: prednisolone within 72 hours; to shorten time to complete recovery
- EYE PROTECTION of cornea: protective glasses and artificial tears as needed to protect from keratoconjunctivitis sicca
- VALACICLOVIR/ACICLOVIR: in combination with corticosteroids, reduces long-term sequelae of Bell’s palsy in those with complete or near-complete facial palsy
- SURGICAL DECOMPRESSION in severe Bell’s palsy
What are the complications of Bell’s palsy? (x3)
Corneal ulceration, gustatory hyperlacrimation (gustatory hyperlacrimination is also called Bogorad’s syndrome and epiphora while eating and drinking; secondary to aberrant regeneration of pre-ganglionic PSNS fibres), simultaneous contraction of the angle of the mouth and blinking (from simultaneous innervation of orbicularis oculi and orbicularis oris, secondary to aberrant regeneration of motor axons)
What is synkinesis?
General term for voluntary muscle movement causing simultaneous involuntary contraction of other muscles.
What is the prognosis of Bell’s palsy?
Recovery within 6 months of symptom onset in most patients.
