Applied anatomy and physiology
The facial (seventh cranial, VII) nerve provides motor fibres to the muscles of facial expression. It originates in the seventh nerve nucleus in the brain stem (pons), en- ters the middle ear and mastoid and exits the skull at the stylomastoid foramen just in front of the mastoid process. From here it enters the parotid gland where it divides into its branches (Fig. 15.1). Paralysis can be caused by pathology anywhere along the nerve course or in the cortical nerves which control the nucleus (supranuclear or upper motor neurone fibres) resulting in asymmetric movement of some or all of the muscles of facial expression. Facial nerve palsy causes difficulty with smiling, frowning and expressing emotions. It is a devastating condition for the patient. The causes are numerous and are considered in Table 15.1.
‘Supranuclear’ or upper motor neurone causes will often spare the forehead as these muscles receive fibres from both facial nerve nuclei.
Clinical diagnosis
The patient presents with weakness of the facial muscles, difficulty in clearing food from inside the cheek, or drooling from one side of the mouth. Facial asymmetry is accentuated by asking the
patient to attempt to close the eyes tightly, show the teeth or whistle (Fig. 15.2).
Figure 15.2 Post traumatic right facial palsy. Shown at rest (a) and on attempted eye closure (b).
Involuntary movements (e.g. smiling) may be retained even in the lower face. A careful history and aural and neurological examination are essential. Sparing of the forehead suggests a supranuclear pathology. Impaired taste implies the lesion is above the origin of the chorda tympani; reduction of tear production (lacrimation) suggests the lesion is above the geniculate ganglion where the superficial petrosal nerve arises.
Bell’s palsy (idiopathic facial paralysis)
Bell’s palsy is a lower motor neurone facial palsy of unknown cause, but thought to be viral. Bell’s palsy may be complete or incomplete; the more severe the palsy, the worse the prognosis. In practice, full recovery may be expected in over 90% of cases. The remainder may develop persistent paraylsis and other complications including ectropion (weakness of the muscles of the lower eyelid causing persistent overflow of tears) or an aberrant sequence of movements of the face (synkinesis).
Assessment and investigations
• CT or MRI scanning may be needed if the symptoms persist or a specific cause (i.e. other than Bell’s palsy) is suspected.
• Electrodiagnosis is used in the assessment of the degree of involvement of the nerve and includes nerve conduction tests and electromyography. These tests are done in a specialist centre and be invaluable in predicting prognosis.
Management of Bell’s palsy
• Treatment of Bell’s palsy should be commenced as soon as possible.
• Prednisolone given orally is the treatment of choice, but it must commence in the first 72 hours. In an adult, start with 25 mgs twice daily for up to ten days.
• Be vigilant about eye care. The protective blink reflex may be lost and the cornea exposed, especially at night. An eyepad, a tape over the eyelids at night or in persistent cases a ‘tarsorrhaphy’ (surgical approximation of the eyelids) may be needed.
• Antivirals such as acyclovir seem to offer little benefit.
• Persistent facial palsy warrants referral and thorough investigation, including CT or MRI scanning.
Ramsay Hunt syndrome
This is due to herpes zoster infection of the geniculate ganglion, affecting more rarely the glossopharyngeal (IX) and vagus (X) nerves and, very occasionally, the trigeminal (V), abducens (VI) or hypoglossal (XII) nerves. The patient is usually elderly, and severe pain precedes the facial palsy. The patient often has vertigo, and the hearing is impaired. The characteristic clinical feature is a vesicular eruption in the ear (sometimes on the tongue and palate). Recovery of facial nerve function is much less likely than in Bell’s palsy.
Prompt treatment with acyclovir given orally may improve the prognosis and re- duce post-herpetic neuralgia.
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