THE FACIAL NERVE (SEVENTH CRANIAL NERVE) Medical Assignment Help

This nerve is largely motor in function, supplying the muscles of facial expression. The nerve carries sensory taste fibres from the anterior two-thirds of the tongue via the chorda tympani. The complex arrangement of the nerves to the face, their nuclei and connections.
The facial nerve arises from the seventh nerve nucleus in the pons and leaves the skull through the stylomastoid foramen.
Part of each facial nucleus supplying the upper face (principally the frontalis muscle) receives some supranuclear fibres from each hemisphere.

Unilateral facial weakness

LOWER MOTOR NEURONE (LMN) LESIONS. A unilateral LMN lesion causes weakness of all the muscles of facial expression on the same side. The face, especially the angle of the mouth, falls, and dribbling occurs from the corner of the mouth. There is weakness of frontalis and of eye closure since the upper facial muscles are weak.

Corneal ulceration may occur if the cornea is exposed during sleep. The platysma muscle is also weak.
UPPER MOTOR NEURONE (UMN) LESIONS. UMN lesions cause weakness of the lower part of the face on the side opposite the lesion. The frontalis muscle is spared; the normal furrowing of the brow is preserved, and eye closure and blinking are not affected. In UMN lesions there is relative preservation of spontaneous ’emotional’ movement (e.g. smiling) compared with voluntary movement.

Causes of facial weakness

he commonest cause of facial weakness is a supranuclear lesion, e.g. cerebral infarction, leading to UMN facial weakness and hemiparesis.
Lesions at four other levels may be recognized by the associated signs .
PONS. The sixth nerve nucleus is encircled by the seventh nerve fibres and is therefore often involved in pontine lesions of the seventh nerve, causing a lateral rectus palsy. If there is accompanying damage to the neighbouring centre for lateral gaze  and corticospinal tract, there is the combination of:
• LMN facial weakness
• Failure of conjugate lateral gaze (towards the lesion)
• Contralateral hemiparesis
Causes include pontine tumours (e.g. glioma), demyelination and vascular lesions.
The facial nucleus is affected in poliomyelitis and in motor neurone disease; the latter usually causes bilateral weakness.
CEREBELLOPONTINE ANGLE. The fifth, sixth and eighth nerves are affected with the seventh nerve in lesions in the cerebellopontine angle. Causes are acoustic neuroma and meningioma.
WITHIN THE PETROUS TEMPORAL BONE. The geniculate ganglion (a sensory ganglion for taste) lies at the genu of the facial nerve. Fibres join the facial nerve in the chorda tympani and carry taste from the anterior two-thirds of the tongue. The (motor) nerve to the stapedius muscle leaves the facial nerve distal to the genu.
Lesions within the petrous temporal bone cause:
• Loss of taste on the anterior two-thirds of the tongue
• Hyperacusis (an unpleasantly loud distortion of noise)

Due to paralysis of the stapedius muscle Causes include:
• Bell’s palsy
• Trauma
• Infection of the middle ear
• Herpes zoster (Ramsay Hunt syndrome)
• Tumours (e.g. glomus tumour)
WITHIN THE FACE. Branches of the facial nerve pierce the parotid gland and supply the muscles of facial expression. The nerve can be damaged here by parotid gland turnours, mumps (epidemic parotitis), sarcoidosis  and trauma.
The nerve is also affected in polyneuritis (e.g. Guillain- Barre syndrome, see p. 946), usually bilaterally. Weakness of the muscles of the face also occurs in primary muscle disease and disease of the neuromuscular junction. Weakness is usually bilateral. Causes include:
• Dystrophia myotonica
• Facio-scapulo-hurneral dystrophy
• Myasthenia gravis

Bell’s palsy

This is a common, acute, isolated facial nerve palsy believed to be due to a viral infection that causes swelling of the nerve within the petro us temporal bone.

SYMPTOMS

The patient notices marked unilateral facial weakness, sometimes with loss of taste on the anterior two-thirds of the tongue. Pain behind the ear is common at onset. The diagnosis is made on clinical grounds. No other cranial nerves are involved.

MANAGEMENT AND COURSE

Spontaneous improvement usually occurs towards the end of the second week. Thereafter, continuing recovery occurs but this may take 12 months to become complete. About 15% of patients are left with a severe, unsightly, residual weakness.
Electrophysiological tests are of some help in predicting the outcome. After the third week, the absence of an evoked potential from muscle (the nerve is stimulated over the parotid gland) indicates that recovery is unlikely. Steroids (e.g. prednisolone 60 mg daily, reducing to nil over 10 days) or adrenocorticotrophic hormone (ACT H) reduce the proportion of patients left with a severe deficit, provided the drugs are given at the onset. A tarsorrhapy (suturing of the upper to the lower lid) may be necessary if there is prolonged corneal exposure. Adhesive tape is a useful temporary measure. Cosmetic surgery and/or reinnervation (e.g. anastomosis of the lingual nerve to the facial nerve) are sometimes indicated after a year has elapsed from the initialattack if there is severe residual paralysis.  The condition occasionally recurs and is very rarely bilateral.

Ramsay Hunt syndrome

This is herpes zoster (shingles) of the geniculate ganglion. There is a facial palsy (identical to Bell’s palsy) with herpetic vesicles in the external auditory meatus (which receives a sensory twig from the facial nerve) and sometimes in the soft palate. Deafness may occur.
Treatment for shingles should be given.

HEMIFACIAL SPASM

This is an irregular clonic spasm of the facial muscles, usually occurring in middle-aged women. It varies in severity from a mild inconvenience to a severe and disabling condition when it affects all the facial musculature of one side.
The causes are:
• Idiopathic
• Acoustic neuroma
• Paget’s disease of the skull
• Following Bell’s palsy
• Pressure from aberrant vessels in the cerebellopontine angle

SIGNS

There are clonic spasms of the facial muscles on one side. A mild LMN facial weakness is common.

MANAGEMENT

Mild cases require no treatment. In severe cases various destructive or decompressive procedures on the facial nerve in the cerebellopontine angle are helpful. Local injection of botulinum toxin reduces the movements for some months. Drugs are of no value.

Myokymia

Facial myokymia is a rare, continuous, fine, sinuous movement of the lower face that is seen in brain stem lesions (e.g. MS, brain stem glioma). The term myokymia is also used to describe the innocent twitching around the eye that commonly occurs in fatigue.

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