|THE FACIAL NERVE CN VII|
| The Origin(s)
Facial nucleus - pons
Superior salivary nucleus- pons
Gustatory nucleus - medulla oblongata
Spinal nucleus of the trigeminal nerve - medulla oblongata
The Course and distribution
Branchiomotor (SVE) to muscles of facial expression; and also to digastric and stylohyoid. These fibres are in the facial nerve proper.
General visceral efferent, GVE ( parasympathetic) to the submandibular and sublingual and lingual gland; to the lacrimal, palatine, pharyngeal, nasal and oral glands.
General visceral afferent (GVA) from the nasal cavity; the sinus cavities, and part of soft palate.
Special visceral afferent, SVA (taste) from the anterior 2/3 of the tongue
General somatic afferent (GSA) from the pinna of the ear and the external auditory meatus.
Probable cause and sites of injury
Brain stem vascular lesions
CP angle lesions e.g. acoustic neuroma
Facial canal oedema
Geniculate ganglion herpes zoster
Otitis media/mastoiditisBirth trauma e.g. during forceps delivery
Clinical disorders of the facial nerve
(+) Normal facial folds, wrinkles and creases due to the insertion of the muscles into the skin disappear, giving
(+) The corner of the mouth tends to droop, and there is a tendency for the patient to drool out of that of the
(+) The patient is unable to close the affected eye. If there is a lack of tearing the cornea tends to dry out.
(+) With time, the muscles on the affected side tend to atrophy
(+) Food accumulates in the vestibule of the affected side
Supranuclear facial palsy, has a very characteristic feature, sparing of the upper muscles of facial expression (above the level of the palpebral fissure). Corticobulbar projections of facial neurons innervating the upper muscles of facial expression are both crossed and uncrossed, whereas those to neurons innervating the lower muscles of facial expression are all crossed. Hence, lesions affecting the corticobulbar projections produce contralateral paralysis of the lower muscles of facial expression, and spare the upper muscles. Patients are able to close both eyes and wrinkle both brows. In addition, because it is an upper motor neuron lesion, there is no accompanying atrophy of the muscles and there is a retention of facial reflexes i.e. the patient's ability to smile reflexly or show other emotional expressions.
Loss of taste in the anterior 2/3 of the tongue in combination with a facial palsy indicates damage to the facial nerve central to the exit of chorda tympani nerve. Also, the loss of the pre-ganglionic parasympathetic fibres to the submandibular ganglion causes diminished salivation (However, this sign may be difficult to detect, because the parotid gland is functional). The loss of taste over anterior 2/3 of the tongue and diminished salivation, without motor palsy suggest involvement only of the chorda tympani nerve. When anaesthesia of the anterior 2/3 of the tongue accompanies the loss of taste and diminished salivation, an involvement of the lingual nerve is likely.
An accompanied loss of tearing (lacrimal gland innervation) occurs only if the facial nerve lesion is central to the geniculate ganglion. Lacrimal gland innervation is via the greater petrosal nerve.
Hyperacusis, an increase in auditory sensitivity on the affected side, often occurs if there is paralysis of the stapedial muscle. This indicates injury to the facial nerve central to nerve to stapedius.
Herpes zoster infection of the geniculate ganglion primarily affects the regions with sensory supply from the facial nerve. The motor components are affected by the oedema. The collection of the effects comprises Ramsay-Hunt syndrome.