Oral medicine: 8. orofacial sensation and movement

The olfactory nerve (cranial nerve I)

Bilateral anosmia is common after head injuries involving the anterior cranial fossa, but in practice the patient may complain of loss of taste rather than sense of smell.

An olfactory lesion is confirmed by inability to smell substances such as orange or peppermint oil. Ammoniacal solutions or other substances with a pungent odour must not be used since they stimulate the trigeminal rather than the olfactory nerve thereby giving a false positive result.

The optic nerve (cranial nerve II)

Blindness or defects of visual fields are caused by ocular, optic nerve or cortical damage but the type of defect varies according to the site and extent of the lesion.

If there is a complete lesion of one optic nerve that eye is totally blind, there is no direct reaction of the pupil to light (loss of constriction) and, if a light is shone into the affected eye, the pupil of the unaffected eye also fails to respond (loss of the consensual reflex). However, the nerves to the affected eye that are responsible for pupil constriction run in the IIIrd cranial nerve and should be intact. If, therefore, a light is shone into the unaffected eye, the pupil of the affected eye also constricts, even though it is sightless.

Lesions of the optic tract, chiasma, radiation or optic cortex cause various defects involving both visual fields but without total field loss on either side.

An ophthalmological opinion should always be obtained if there is any suggestion of a visual field defect.

The oculomotor nerve (cranial nerve III)

The oculomotor nerve supplies the muscle that raises the upper eyelid, most of the orbital muscles that move the eye (except the lateral rectus and superior oblique), and the ciliary muscle and pupil constrictor.

Normally, the medial rectus (supplied by the IIIrd nerve) moves the eye medially (adducts). The lateral rectus (VIth nerve) abducts the eye. When the eye is abducted it is elevated by the superior rectus (IIIrd nerve) and depressed by the inferior rectus (IIIrd nerve). The adducted eye is depressed by the superior oblique muscle (IVth nerve) and elevated by the inferior oblique (IIIrd nerve).

Disruption of the oculomotor nerve therefore causes:

The trochlear nerve (cranial nerve IV)

The trochlear nerve supplies only the superior oblique muscle which moves the eye downwards and medially towards the nose.

The lesion is characterized by:

There is often damage to the IIIrd and VIth nerves as well.

Damage to the trochlear nerve causes serious disability, because there is diplopia maximal on looking down and the patient may therefore have difficulty reading, going down stairs or seeing obstructions on the ground.

The trigeminal nerve (cranial nerve V)

The trigeminal nerve supplies sensation over the whole face apart from the angle of the jaw, and the front of the scalp back to a line drawn across the vertex, between the ears. It also supplies sensation to most of the mucosa of the oral cavity, conjunctivae, nose, tympanic membrane and sinuses.

The motor division of the trigeminal nerve supplies the muscles of mastication (masseter, medial and lateral pterygoids, temporalis, mylohyoid and anterior belly of the digastric).

Taste fibres from the anterior two-thirds of the tongue, and secretomotor fibres to the submandibular and sublingual salivary glands and lacrimal glands, are also carried in branches of the trigeminal nerve.

Damage to a sensory branch of the trigeminal nerve causes hypoaesthesia in its area of distribution; infection, such as with herpes zoster (Figure 1), causes pain. Lesions of the sensory part of the trigeminal nerve initially result in a diminishing response to pin-prick to the skin and, later, complete anaesthesia. Lesions involving the ophthalmic division also cause corneal anaesthesia: this is tested by gently touching the cornea with a wisp of cotton wool twisted to a point. Normally this procedure causes a blink, but not if the cornea is anaesthetic and the patient does not see the cotton wool.

It is important, with patients complaining of facial anaesthesia, to test all areas, but particularly the corneal reflex with a wisp of cotton wool, and the reaction to pin-prick over the angle of the mandible. If the patient complains of complete facial or hemifacial anaesthesia, but the corneal reflex is retained or there is anaesthesia over the angle of the mandible, then the symptoms are probably functional rather than organic as the skin overlying the angle of the mandible is not supplied by the trigeminal nerve.

Taste can be tested with sweet, salt, sour or bitter substances (sugar, salt, lemon juice or vinegar) carefully applied to the dorsum of the tongue, or by asking the patient to touch his tongue between the terminals of a pocket torch battery: this normally gives a tingling sensation and a characteristic metallic taste.

Damage to the motor part of the trigeminal nerve can be difficult to detect and is usually asymptomatic if unilateral, but the jaw may deviate towards the affected side on opening. It is easier to detect motor weakness by asking the patient to open the jaw against resistance, rather than by trying to test the strength of closure.

The abducens nerve (cranial nerve VI)

The abducens nerve supplies only one eye muscle, the lateral rectus. Lesions comprise:

Lesions of the abducens can, however, be surprisingly disabling.

The facial nerve (cranial nerve VII)

The facial nerve carries:

The neurones supplying the lower part of the face receive upper motor neurones (UMNs) from the contralateral motor cortex, whereas the neurones to the upper face receive bilateral UMN innervation.

An UMN lesion therefore causes unilateral facial palsy with some sparing of the frontalis and orbicularis oculi muscles because of the bilateral cortical representation. Furthermore, although voluntary facial movements are impaired, the face may still move with emotional responses, for example on laughing. Paresis of the ipsilateral arm (monoparesis) or arm and leg (hemiparesis), or dysphasia may be associated because of more extensive cerebrocortical damage.

Lower motor neurone (LMN) facial palsy is characterized by unilateral paralysis of all muscles of facial expression (Figure 2) for both voluntary and emotional responses. The forehead is unfurrowed and the patient unable to close the eye on that side. Attempted closure causes the eye to roll upwards (Bell's sign). Tears tend to overflow on to the cheek (epiphora), the corner of the mouth droops and the nasolabial fold is obliterated. Saliva may dribble from the commissure and may cause angular stomatitis. Food collects in the vestibule and plaque accumulates on the teeth on the affected side. Depending on the site of the lesion, other defects, such as loss of taste or hyperacusis, may be associated.

In facial palsy, facial weakness is demonstrated by asking the patient to:

The following investigations may be indicated:

The vestibulocochlear nerve (cranial nerve VIII)

The vestibulocochlear nerve has two components:

Lesions of this nerve may cause loss of hearing, vertigo or ringing in the ears (tinnitus).

An ENT opinion should be obtained if a lesion of the vestibulocochlear nerve is suspected, as special tests are needed for diagnosis.

The glossopharyngeal nerve (cranial nerve IX)

The glossopharyngeal nerve carries:

Symptoms resulting from a IXth nerve lesion include impaired pharyngeal sensation so that the gag reflex may be weakened; the two sides should always be compared. Lesions of the glossopharyngeal are usually associated with lesions of the vagus, accessory and hypoglossal nerves (bulbar palsy).

The vagus nerve (cranial nerve X)

The vagus has a wide parasympathetic distribution to the viscera of the thorax and upper abdomen but is also the motor supply to some soft palate, pharyngeal and laryngeal muscles.

Lesions of the vagus are rare in isolation but have the following effects:

The accessory nerve (cranial nerve XI)

The accessory nerve is the motor supply to the sternomastoid and trapezius muscles. Lesions are often associated with damage to the IXth and Xth nerves and cause:

Testing this nerve is useful in differentiating patients with genuine palsies from those with functional complaints. In an accessory nerve lesion there is weakness on turning the head away from the affected side. Those shamming paralysis often simulate weakness when turning the head towards the ‘affected’ side.

The hypoglossal nerve (cranial nerve XII)

The hypoglossal nerve is the motor supply to the muscles of the tongue. Lesions cause:

The hypoglossal nerve may be affected in its intra- or extracranial course. Intracranial lesions typically cause bulbar palsy. In an upper motor neurone lesion the tongue is spastic but not wasted; in a lower motor neurone lesion there is wasting and fibrillation of the affected side of the tongue.

Intracranial causes of facial sensory loss

Intracranial causes of sensory loss are uncommon but serious and include:

Since other cranial nerves are anatomically close, there may be associated neurological deficits. In posterior fossa lesions, for example, there may be cerebellar features such as ataxia. In middle cranial fossa lesions, there may be associated neurological deficits affecting cranial nerve VI (abducens nerve), resulting in impaired lateral movement of the eye.

Benign trigeminal neuropathy

This is a transient sensory loss in one or more divisions of the trigeminal nerve which seldom occurs until the second decade. The corneal reflex is not affected. The aetiology is unknown, though some patients prove to have connective tissue disorder.

Psychogenic causes of facial sensory loss

Hysteria, and particularly hyperventilation syndrome, may underlie some causes of facial anaesthesia.

Organic causes of facial sensory loss

Include diabetes or connective tissue disorders.

Diagnosis in facial sensory loss

In view of the potential seriousness of facial sensory loss, care should be taken to exclude local causes and a full neurological assessment must be undertaken. Since, in the case of posterior or middle cranial fossa lesions, other cranial nerves are anatomically close, there may be associated neurological deficits. Thus, in the absence of any obvious local cause, or if there are additional neurological deficits, patients should be referred for a specialist opinion.

Management of patients with facial sensory loss

If the cornea is anaesthetic, a protective eye pad should be worn and a tarsorrhaphy (an operation to unite the upper and lower eyelids) may be indicated since the protective corneal reflex is lost and the cornea may be traumatized.

Bell's palsy

Bell's palsy is the most common acute LMN paralysis (palsy) of the face. There is inflammation of the facial nerve which may be immunologically mediated and associated with infection, commonly herpes simplex virus (HSV), leading to demyelination and oedema, usually in the stylomastoid canal.

The condition is usually seen in young adults; predisposing factors, found in a minority of cases, include:

Aetiopathogenesis

LMN facial palsy is usually associated with infections:

Clinical features

Damage to the facial nerve may result in twitching, weakness, or paralysis of the face, in dryness of the eye or the mouth, or in disturbance of taste.

There is:

Up to 10% of patients have a positive family history and a similar percentage suffer recurrent episodes.

Diagnosis of Bell's palsy

The history should be directed to exclude facial palsy caused by other factors, such as:

The examination and investigations are discussed above.

Management of Bell's palsy

Treatment with systemic corticosteroids results in 80–90% complete recovery. There is thus a strong argument for treating all patients with prednisolone 20 mg four times a day for 5 days, then tailing off over the succeeding 4 days.

Since HSV is frequently implicated, antivirals may be used. However, despite the fact that HSV is frequently implicated, there is no evidence of a benefit of adding aciclovir.

Patients to refer:

Any patient with a cranial nerve defect requiring further investigation is outwith the scope of primary dental care.