Lesions of the Trigeminal Nerve

The trigeminal n. is responsible for the somatosensory innervation of the skin of the face and forehead and of many of the mucous membranes of the face and head. It also carries motor fibers innervating the muscles of mastication. Lesions of this nerve thus produce sensory deficits and paralysis of the muscles of mastication.

The anatomical course and distribution of the trigeminal n. are shown in Fig. 3.10, p. 23 and the technique of clinical examination is presented on p. 22.

Clinical manifestations. Trigeminal lesions produce sensory deficits in the face and head. The somatosensory distribution of the three branches of the trigeminal n. are shown in Fig. 11.13. A lesion of the motor portion of the third branch causes paralysis of the muscles of mastication. The examiner can usually easily feel the diminished contraction of the masseter m. on one side. When the mouth is opened, the jaw deviates toward the paralyzed side because of weakness of the pterygoid mm. (Fig. 11.14).

Causes. Nuclear lesions of the trigeminal n. are located in the pons or medulla and are usually due to vascular processes, encephalitis, a focus of multiple sclerosis, or a space-occupying lesion (glioma, syringobulbia). The nerve can also be affected in its peripheral course by mass lesions, toxic influences, or mechanical (iatrogenic) factors. The trigeminal n. can also be affected as a component of cranial polyradiculitis. Occasionally, no clear cause can be found (idiopathic trigeminal neuropathy, which is usually unilateral). Trigeminal neuralgia is discussed below on p. 253.

ophthalmic n. (V1) maxillary n. (V2) mandibular n. (V3) nervus intermedius (VII)

glossopharyngeal n. (IX)

vagus n. (X)

Fig. 11.13 Sensory innervation of the face and the mucous membranes of the head.

Lesions of the facial nerve nucleus or of its nerve fascicle within the brainstem are rarer and are mainly evident as a motor deficit including lagophthalmos and an inability to wrinkle the forehead. Lacrimation, salivation, and taste are normal, because the parasympathetic and gustatory fibers of the facial n. are derived from other cranial nerve nuclei in the brainstem.

Lesions above the facial nerve nucleus (= central facial palsy). The typical predominant finding in such cases is perioral weakness. The eye can still be closed on the affected side and the forehead can be symmetrically wrinkled.

Etiological classification. Cryptogenic facial palsy is the most common type and must be distinguished from other, symptomatic varieties. Its cause is unknown and is currently thought to be either a viral infection (e. g., by a herpesvirus) or a parainfectious process (see below). In symptomatic forms, a concrete cause for the facial palsy can be found: a basilar skull fracture, for example, can damage the facial n. Transverse fractures of the petrous bone cause immediate and often irreversible facial palsy. Longitudinal fractures frequently give rise to facial palsy only after a delay, usually because of a slowly expanding hematoma in the wall of the facial canal; the prognosis in such patients is better than in transverse fractures. Middle ear processes (cholesteatoma) can cause facial nerve palsy, as can skull base tumors and viral infections, particularly herpes zoster oticus. Borreliosis (Lyme disease) can affect the facial n. and produce a facial palsy. Bilateral facial palsy can be seen in (cranial) polyradiculitis. A nuclear facial nerve palsy results from infarction affecting the facial nerve nucleus in the pons, or from a brainstem glioma.

The most common type of peripheral facial palsy—the cryptogenic type—will now be described in detail.

Cryptogenic Peripheral Facial Nerve Palsy

Epidemiology. This condition (“Bell palsy”) accounts for three-quarters of all cases of facial palsy and has an annual incidence of ca. 25 per 100 000 individuals.

Etiology. The cause is unknown, but it is probably a viral infection. Swelling of the facial nerve trunk in the narrow confines of the facial canal leads to local compressive ischemia, which, in turn, leads to further swelling (a vicious circle). The result is a local interruption of the blood supply to the facial n. through the vasa nervorum and thus an extension of the ischemic injury, often leading to total axonotmesis.

Clinical manifestations. The most prominent finding is weakness of the muscles of facial expression, which can be of variable extent but is often complete, as depicted in Fig. 11.16. There is also an impairment of taste on the anterior two-thirds of the tongue on the affected side (for the technique of examination, cf. p. 22). “Bitter” tastes can usually still be perceived, because the receptors for this modality lie in the mucosa of the posterior third of the tongue, which is innervated by the glossopharyngeal n. Lacrimation and salivation are also ipsilaterally impaired. Dysacusis or hyperacusis, due to denervation of the stapedius m., is hardly ever clinically evident.

Prognosis. The prognosis is generally favorable: in 80 % of patients, the facial weakness resolves completely in four to six weeks. The remaining patients are those whose facial musculature has been completely denervated. For them, the recovery can take much longer (up to six months). Residual manifestations often include partial facial weakness or pathological accessory movements due to misdirection of regenerating axons. In cases of the latter type, active contraction of one part of the face is accompanied by simultaneous, involuntary contraction of another: thus, the patient’s ipsilateral eye may close involuntarily when he or she whistles (synkinesia, Fig. 11.17).