The trigeminal nerve is mainly sensory but contains some motor fibres.
from the three divisions-ophthalmic (VI)’ maxillary (V2) and mandibular (V,) – pass to the trigeminal ganglion at the apex of the petro us temporal bone. From here central fibres enter the brain stem. Ascending fibres transmitting the sensation of light touch enter the nucleus in the pons. Descending fibres carrying pain and temperature sensation form the spinal tract of the fifth nerve and end in the spinal nucleus in the medulla and upper cervical cord.
Motor fibres arise in the upper pons and join the mandibular branch to supply the muscles of mastication. Signs of a trigeminal nerve lesion Diminution of the corneal reflex is often the first sign of a fifth nerve lesion.
A complete fifth nerve lesion causes unilateral sensory loss on the face, tongue and buccal mucosa. The jaw deviates to the side of the lesion when the mouth is opened. Central (brain stem) lesions of the lower trigeminal nuclei (e.g. in syringobulbia,) produce a characteristic circumoral sensory loss.
When the spinal tract (or spinal nucleus) alone is involved, the sensory loss is restricted to pain and temperature sensation, i.e. ‘dissociated’.
Causes of trigeminal nerve lesions
BRAIN STEM. Lesions at this site involve the nuclei and central connections, and include:
• Brain stem glioma
CEREBELLOPONTINE ANGLE. Here the nerve is compressed by:
• Acoustic neuroma
• Secondary neoplasm
APEX OF THE PETROUS TEMPORAL BONE. Infection from chronic middle-ear disease involves the nerve at this site. The combination of this with pain and a sixth nerve lesion is called Gradenigo’s syndrome.
CAVERNOUS SINUS. Here the trigeminal ganglion is compressed by:
• Aneurysm of internal carotid artery
• Extension of a pituitary neoplasm
• Cavernous sinus thrombosis
• Secondary neoplasm
The trigeminal ganglion is infected in ophthalmic herpes zoster, the commonest lesion of the ganglion.
PERIPHERAL BRANCHES OF THE TRIGEMINAL
NERVE. These are affected by neoplastic infiltration of the skull base.
Trigeminal neuralgia (‘tic douloureux’) is a condition of unknown cause, seen most commonly in old age. It is almost always unilateral.
Severe paroxysms of knife-like or electric-shock-like pain, lasting seconds, occur in the distribution of the fifth nerve. The pain tends to commence in the mandibular division (V,) and spreads to the maxillary (V2) and (rarely) to the ophthalmic division (VI)’ It occurs many times a day.
Each paroxysm is stereotyped, brought on by stimulation of a specific ‘trigger zone’ in the face. Washing, shaving, a cold wind or eating are examples of the trivial stimuli that may provoke the pain. The face may be screwed up in agony (hence ‘tic’ -an involuntary movement).
The pain characteristically does not occur at night. Spontaneous remissions last for months or years before recurrence.
There are no signs of trigeminal nerve dysfunction. The corneal reflex is preserved. Diagnosis is on clinical grounds alone.
The anticonvulsant carbamazepine 600-1200 mg daily suppresses attacks in the majority of patients. Phenytoin and clonazepam are also used, but are less effective. If drug therapy fails, surgical procedures (radio frequency extirpation of the ganglion, nerve decompression or sectioning of the sensory root) are useful in difficult cases. Alcohol injection into the trigeminal ganglion or peripheral fifth nerve branches can also be carried out.
‘Secondary’ trigeminal neuralgia
Trigeminal neuralgia also occurs in MS, with lesions of the cerebellopontine angle (see below) and with tumours of the fifth nerve (e.g. neuroma). These lesions are usually accompanied by physical signs (e.g. a depressed corneal reflex).
Idiopathic trigeminal neuropathy
A chronic and isolated fifth nerve lesion may sometimes develop without any apparent cause. When sensory loss is severe, trophic changes (facial scarring and corneal ulceration) occur.
This may occur in the distribution of one division of the trigeminal nerve, commonly the first.