Chapter 5: Facial sensations & movements
In this chapter, the functions of the trigeminal (CN V) and facial (CN VII) nerves will be discussed. Symptoms of damage to the trigeminal system are mainly loss of sensation in the face, although the mandibular division of the trigeminal nerve also controls jaw motion. Damage to the facial nerve mainly manifests as weakness of the muscles of facial expression, although it may also affect taste sensation in the anterior part of the tongue. It is critical to distinguish damage of the facial nerve from damage to the connections from the cerebral cortex to the brain stem, which selectively weakens muscles of the lower portion of the face, contralateral to the side of damage.
The three divisions of the fifth nerve (I. Ophthalmic, II. Maxillary, and III. Mandibular) are the source for somatic sensation over the entire face (Figs. 5-1 and 5-2), the eye, the nasal passages and the oral cavity.
Facial sensation can be tested simply at the bedside by having the patient close their eyes and respond affirmatively to touch with a light wisp of cotton over the three divisions of the trigeminal nerve. The patient should be asked to compare the perception on the two sides. Pain perception as tested by a pin can be similarly checked, although temperature sensation (which is mediated by the same pathways), can replace the use of a pin. Sensory testing is, by nature, subjective (i.e., the examiner depends on the reliability of the subject). It is important to define the pattern and distribution of sensory alteration since that can go a long way to both localizing the lesion and also validating the sensory findings. The patient with hysterical or feigned sensory loss in the face frequently has bizarre perceptive patterns such as a hairline or perfect midline demarcation of hyposensitivity. Neither pattern can be explained on the basis of the central or peripheral distribution of the trigeminal system (see Fig. 5-1). Additionally, the inability to detect the vibrations of a tuning fork placed on one side of the head (when the other side can detect it) is not physiological since the entire head vibrates. The subjective tests of facial sensation can be objectified by examining certain reflex responses such as the corneal reflex (where the eye briskly closes in response to a wisp of cotton touching the cornea). Asymmetries of this are a good sign of sensory impairment, at least in the distribution of the ophthalmic division of the trigeminal nerve (see below).
The temporalis, masseter, and pterygoid muscles (muscles of mastication) are supplied by the motor division of the mandibular branch of cranial nerve V and subserve jaw movement. Supranuclear innervation of these muscles (hemispheric and brainstem pyramidal and extrapyramidal systems) is essentially symmetrical bilaterally. A unilateral lesion above the level of the fifth-nerve motor nucleus, therefore, does not cause any obvious weakness of jaw motion. Large bilateral lesions of the hemisphere or brain stem (above the fifth-nerve nucleus) can cause bilateral weakness of voluntary jaw movement. If the bilateral involvement lies above the brain stem, very basic brain stem-mediated chewing reflexes may remain and actually become hyperactive. The jaw jerk reflex is a muscle stretch reflex in which both the sensory and motor nerve fibers are contained in the trigeminal nerve. This is elicited by lightly tapping the relaxed open jaw in a downward direction. This would be lost after trigeminal nerve damage and hyperactive with injury above the pons (see Chap. 10).
The paired temporalis and masseter muscles function in jaw closure, and the medial pterygoid muscle closes the jaw and moves it from side-to-side (grinding motion). The lateral pterygoid muscles (along with some of the upper neck muscles) open the jaw in concert with a downward and opposing inward motion (Fig. 5-3). When one lateral pterygoid is weak, the jaw deviates toward the weak side on opening, with the inward vector of the opposite pterygoid being unopposed (Fig. 5-4).
Observation of temporal region for atrophy and palpation of the symmetry of muscle bulk and tension during tight jaw closure test the innervation of the temporalis and masseter muscles.
The corneal reflex is mediated by sensory fibers in the trigeminal nerve and motor fibers in the facial nerve. It consists of a bilateral blink response when the edge of the cornea is touched from the side with a wisp of cotton. The examiner should approach from the extreme corner of the eye in order to avoid a visually evoked blink response. It is a useful and objective test for evaluating simultaneously the ophthalmic division of the fifth-nerve (the afferent limb) and the seventh-nerve motor innervation of the orbicularis oculi (the efferent limb). Both the eye that is touched and the opposite eye are observed since they should both close equally and consensually (a consensual reflex is one in which the motor response is bilateral to a unilateral stimulus). The corneal reflex is a sensitive and objective indicator of fifth- and seventh-nerve dysfunction. A good example of dysfunction occurs with eight-nerve tumors (acoustic neuromas), which comprise approximately 5% of all intracranial tumors in adults (see Fig. 5-2). Patients may present with unilateral hearing loss, and on routine neurologic evaluation the only other indication of involvement may be depression of the ipsilateral direct and contralateral consensual corneal reflex. This results from pressure by the tumor, which lies in the angle between the cerebellum and pons, on the superficially positioned descending tract and nucleus of the trigeminal nerve (which mediates pain and temperature sense from the face). If the depression of the reflex were secondary to seventh-nerve hypofunction, only the direct response would be depressed; the contralateral consensual response would be full because the sensory limb of the reflex, mediated by the trigeminal nerve, would be intact.
An instructive example of trigeminal nerve dysfunction is trigeminal neuralgia (tic douloureux), an irritation of the nerve that probably occurs due to contact with anomalous intracranial blood vessels. This process causes severe paroxysms of pain in one or more divisions of the trigeminal nerve, with the maxillary division being most often affected and the ophthalmic least. In the past, surgeons attempted to cut the various peripheral branches of the trigeminal root. However, this would result in "numbness" and pain would usually return some months later. At one time, complete damage to the root became a popular form of permanent cure. A great difficulty with both of these procedures is that the area of anesthesia can become spontaneously painful (denervation hypersensitivity, a form of neuropathic pain). Also, the eye and face can be damaged because of the loss of sensitivity. These destructive surgical procedures have fallen out of favor.
Fortunately, various medications (mostly in the family of anticonvulsants) suppress the excess excitability in the trigeminal neurons and are successful in relieving tic in many persons for long periods of time. Nonetheless, there are patients who do not get adequate response to medications and several other interventions can be successful in relieving these medically refractory patients. Glycerol, injected into the region around the trigeminal ganglion, often produces relief that extends for years after the procedure (it is thought to produce some selective nerve damage). A radiofrequency probe can be placed into the trigeminal ganglion (percutaneously, through the foramen ovale) and selective lesions can be made to the nerve fibers from the painful region of the face. The most elegant surgical treatment (but most invasive) involves approaching the trigeminal nerve from an occipital craniotomy and placing some Teflon between any irritating arteries and the trigeminal nerve root. This often results in permanent relief of the symptoms.
Most of the facial nerve is comprised of motor innervation of the muscles of facial expression. In addition, it subserves several other functions including: taste perception from the anterior two-thirds of the tongue; perception of cutaneous stimuli in the external auditory canal and over part of the pinna and mastoid region; innervation of the stapedius muscle in the middle ear; and innervation of the lacrimal gland and two of the salivary glands (the submaxillary and submandibular).
Many of these functions are difficult to test and more difficult to quantify (such as salivation and lacrimation; Fig. 5-5). However, some of these functions can be tested and give clues as to the location of facial nerve damage.
The facial nerve begins at the facial motor nucleus of the caudal pons. It is not common to damage this nucleus and due to the proximity of many sensory and motor pathways running through the brain stem, there are almost always other signs of neurologic damage (hemiparesis, hemihypesthesia, gaze palsy, etc) when the facial nerve is affected here.
The most prominent deficit noted by patients with facial nerve damage is weakness of muscles of facial expression. Careful observation of the patient's face during conversation and at rest almost always reveals facial weakness. Additionally, the face may "droop" on the side of damage due to the effects of gravity. The nerve can be further tested by: having the patient close their eyes and lips tightly (the force of closure can be felt by manually trying to open them); having the patient grimace (show their teeth); having the patient look up (elevating the eyebrows and creasing the forehead); and also having the patient fill their cheeks with air with their lips tightly pursed. If one or both sides of the face are weak, s/he will have difficulty holding the air in. Tapping each cheek accentuates the difficulty on the appropriate side.
The most common cause of facial weakness is Bell's palsy, an idiopathic condition that may result from viral infection-induced inflammatory swelling of the facial nerve in its canal. Since the canal is very long and tight, swelling can put pressure on the nerve, resulting in damage either by direct effects or by impairing blood flow in the nerve. In some cases, facial palsy is produced by a very clear viral infection with Herpes Zoster, often associated with ear pain and vesicles on the tympanic membrane. Lyme disease also has a proclivity to produce facial palsy, sometimes bilateral. The hallmark of peripheral facial palsy is that it involves the entire side of the face, including weakness of the forehead muscles as well as those around the eye and mouth. This is because fibers to all of these regions of the face are packed together in the facial canal. Most cases of uncomplicated Bell's palsy recover quite well. In its most severe form, infarction of the nerve may occur with a prolonged and not infrequently incomplete process of regeneration. This is more common when a longer course of the nerve is affected, accompanied by ageusia (loss of taste) and hyperacusis.
It should be obvious that face movement is under voluntary control. However, it is also under control of the limbic system, where strong emotions can be seen in the face involuntarily. Accordingly, there is more than one pathway for "supranuclear" control of the face and these pathways can be damaged independently. Corticobulbar (pyramidal) projections from the motor cortex (precentral gyrus) through the genu of the internal capsule are the major pathway for voluntary facial movement (Fig. 5-6). The cerebral cortical projections to the facial motor neurons innervating the upper face are essentially bilateral (i.e., each cortical hemisphere provides innervation to both sides). Therefore, unilateral lesions (such as a stroke affecting one hemisphere or the internal capsule) will not produce weakness of the upper face muscles. On the other hand, facial motor neurons that innervate the muscles of the lower face receive input largely from the contralateral hemisphere (i.e., the right hemisphere activates motor neurons of the left facial nucleus, and vice-versa). Therefore, a lesion involving the right motor cortex (e.g., carotid-middle cerebral arterial system occlusion and hemispheric infarction) causes a weakness of voluntary left lower facial movement that is especially noticeable while the patient is talking, grimacing (usually elicited by asking the patient to bare their teeth or gums), or resting. In the latter instance, the corner of the mouth droops and there may be some widening of the palpebral fissure (eye) (Fig. 5-7). On the other hand, the forehead is normally creased when a person raises their eyebrows or looks toward the ceiling. This distinguishes the "supranuclear" weakness of the face from the weakness of the whole side of the face due to damage of the peripheral facial nerve, as seen with Bell's palsy.
Interestingly, despite severe weakness around the mouth with "supranuclear facial palsy", the mouth may actually move more than normal with emotional triggers (hypermimia, Fig. 5-7). This illustrates that limbic motor pathways (governing postures and movements in response to strong emotion) are distinct from the more usual motor pathways that we employ for normal voluntary movements. When there is bilateral damage to voluntary motor pathways, the face may be markedly over-expressive and may not actually reflect the patient's consciously perceived emotions. This is termed a "pseudobulbar affect".
Taste in the anterior tongue is tested with application of a thick sugar solution on a Q-tip to the protruded tongue. Care must be taken to prevent this from spreading to the other side and the mouth must be rinsed out thoroughly between trials. The chorda tympani (the branch mediating this sensation) leaves the parent nerve, crossing through the middle ear, where it can also be damaged by severe infections, etc.
Loss of function of the stapedius muscle may reflect as "hyperacusis," i.e., perception of sound as excessively loud and irritating on the side of damage. This branch also arises at the level of the middle ear.
The facial nerve has only a very small cutaneous distribution to the skin of the external auditory canal and over the tympanic membrane, where it overlaps with the small somatic branches of cranial nerves IX, X, and possibly V. Additionally, nerve VII variably supplies small branches to the ear lobe and the mastoid, which overlap with the distributions of the trigeminal nerve and cervical nerves 2 and 3. It is not surprising with the considerable overlap of dermatomes that sensory testing seldom reveals hypoesthesia when the facial nerve is damaged. However, patients with Bell's palsy may complain of pain in the external canal and over the mastoid region due to irritation of these nerve fibers. Herpes zoster infection may afflict the geniculate ganglion (the sensory ganglion of the facial nerve) and manifests itself as pain and vesicular eruption over the preceding distribution. Facial weakness or paralysis is common with geniculate zoster, due to swelling.
- Brodal, A.: Neurological Anatomy in Relation to Clinical Medicine, ed. 2. New York, Oxford University Press, 1969.
- Cogan, D.G.: Neurology of the Ocular Muscles, ed. 2. Springfield, IL, Charles C. Thomas, Publisher, 1956.
- Monrad-Krohn, G.H., Refsum, S.: The Clinical Examination of the Nervous System, ed. 12. London, H.K. Lewis & Co., 1964.
- Spillane, J.D.: The Atlas of Clinical Neurology, ed. 2. New York, Oxford University Press, 1975.
- Walsh, F.B, Hoyt, W.F.: Clinical Neuro-ophthalmology, ed. 3. Baltimore, Williams & Wilkins Co., 1969.
Define the following terms:hyperacusis, ageusia.
5-1. Which division of the trigeminal nerve has motor fibers?
5-2. What are some good ways to distinguish hysterical sensory loss on the face?
5-3. Where is the trigeminal ganglion located?
5-4. Where does the trigeminal nerve root enter the brain?
5-5. Which modalities would test the integrity of the spinal tract of the trigeminal nerve?
5-6. Where do pain and temperature nerve fibers in the trigeminal nerve run after entering the pons?
5-7. What is the pathway of the corneal reflex?
5-8. What are the symptoms of Bell's palsy?
5-9. How can you distinguish weakness of the face that is due to damage to the brain (such as with a stroke) from weakness due to damage of the facial nerve?
5-10. Describe the reflex arc of the jaw-jerk reflex.