Introduction
Facial weakness
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facial weakness can be due to disease of the:
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facial muscles
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neuromuscular junction
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seventh nerve
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brain
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patients with facial weakness frequently present to ophthalmologists with symptoms of corneal exposure. The role of the ophthalmologist is twofold:
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ensure that the cause of the weakness has been established and, if possible, treated
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protect the eye from complications such as corneal ulceration, while maintaining good vision and cosmesis
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all patients with facial weakness must have their corneal sensation assessed. The combination of loss of sensation and loss of eyelid closure places the affected eye at great risk of potentially blinding complications. In addition, the finding of reduced corneal or facial sensation is of diagnostic importance (see Fig. 11.2 , p. 310)
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the most common cause of facial weakness is a unilateral lesion of the facial (seventh cranial) nerve. Rarer causes include myotonic dystrophy and other myopathies, myasthenia gravis and brainstem or cortical disease
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it is essential to resist the temptation to call all facial palsies “Bell’s palsy”. Although this is the most common diagnosis, it should be considered a diagnosis of exclusion. In view of the other possible diagnoses, all patients with new-onset facial nerve weakness should also be assessed by an otolaryngologist or neurologist
Involuntary facial movements
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involuntary spasm of the orbicularis or other facial muscles can be due to disease of the:
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seventh nerve
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brain
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patients with involuntary facial movements frequently present to ophthalmologists, particularly if the movements are centered on, or include, the orbicularis oculi muscles. The three most common patterns of abnormal movement are:
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fine contractions of the eyelid muscle: orbicularis oculi myokymia
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bilateral, usually forceful closure of eyes: blepharospasm
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unilateral contractions of facial muscles: hemifacial spasm
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many patients are concerned that their movement disorder is a marker of either serious neurologic disease or psychiatric illness. Part of the ophthalmologist’s role is to reassure such patients that this is not usually the case. Once the disorder has been characterized, and investigations organized for the few patients who may have an underlying neurologic disorder, the main aims of the ophthalmologist are to identify any ocular disease that might be exacerbating the condition and (if necessary) to provide or organize appropriate treatment
Examination checklist
Facial weakness or spasm
Have you asked about, and looked for, all the following key features?
History
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the weakness or spasm
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when did it start?
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speed of onset?
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development over time?
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variation through the day or from day to day?
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getting better or worse or staying the same?
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other ophthalmic symptoms: diplopia, blurred vision?
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other neurologic symptoms?
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deafness, tinnitus or vertigo? (eighth plus seventh nerve palsy: high risk of cerebello pontine angle [CPA] tumor, e.g. vestibular schwannoma)
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in patients with facial spasm: is there spasm elsewhere in the body?
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numbness (particularly of same side of face), weakness, loss of balance?
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previous medical and surgical history: cancer?
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if patient over 50: symptoms of giant cell arteritis (GCA)?
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system review questions
Examination
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visual acuity
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visual field defect to confrontation?
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limitation of eye movements: sixth plus seventh nerve palsy: high risk of CPA tumor, e.g. vestibular schwannoma
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pupils: is there anisocoria?
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eyelids: ptosis?
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corneal and facial sensation to light touch: fifth plus seventh nerve palsy: high risk of CPA tumor, e.g. vestibular schwannoma
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orbicularis and facial muscle power: in the case of spasm, is there weakness as well as spasm?
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hearing (to finger rub)
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if patient over 50: palpate temporal arteries
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perimetry if: field defect to confrontation, decreased vision, relative afferent pupillary defect (RAPD), diplopia or motility defect
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full neurologic examination if:
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the patient has a seventh nerve palsy that has not yet been fully investigated
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the patient has unilateral facial spasm that has not yet been fully investigated
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Facial weakness
Facial nerve palsy
Causes
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damage to the facial nucleus or fascicle
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pontine infarction
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demyelination
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infiltration by tumor
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compression of the peripheral nerve
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acoustic neuroma (schwannoma of the eighth cranial nerve)
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other CPA or skull base tumors
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parotid tumor
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inflammation of the peripheral nerve
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viral infection (e.g. varicella zoster infection: Ramsay–Hunt syndrome)
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infectious mastoiditis
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sarcoidosis
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trauma (including surgical)
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idiopathic: “Bell’s palsy”
Symptoms and signs ( Figs. 11.1 and 11.2 , )
Ophthalmic
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sore and/or watering eye
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blurred vision (corneal exposure)
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incomplete eyelid closure
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lower lid paralytic ectropion
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punctate epithelial loss of cornea
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reduced tear film (if nerve supply to lacrimal gland affected) or epiphora (failure of the lacrimal pump)
