Investigation of cranial nerves. VII pair: facial nerve (n. Facialis)
Last reviewed: 23.11.2021
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Investigation of the functions of the facial nerve begins with the evaluation of the symmetry of the patient's face at rest and with spontaneous facial expressions. Particular attention is paid to the symmetry of nasolabial folds and eye slits.
The motor fibers of the facial nerve innervate the facial muscles, the subcutaneous muscle of the neck (platysma), the tyillo-, the occipital muscles, the posterior abdomen of the digastric muscle, and the stremal muscle. Vegetative parasympathetic fibers innervate the lacrimal gland, the sublingual and submandibular salivary glands, as well as the glands of the nasal mucosa, the hard and soft palate. Sensitive fibers conduct taste impulses from the front two-thirds of the tongue and from the hard and soft palate.
The force of the facial muscles is alternately examined, suggesting that the patient wrinkle his forehead (m. Frontalis), close his eyes (m. Orbicularis oculi), cheet his cheeks (m. Buccinator), smile, show teeth (m. Risorius and m. Zygomaticus major), squeeze lips and not let them be unraveled (m. Orbicularis oris). Ask the patient to put air in his mouth and inflate his cheeks; Normally, under pressure on the cheeks, the patient keeps the air, not releasing it through the mouth. If a weakness of the facial muscles is detected, it is determined whether it touches only the lower part of the face or extends to the entire half (both lower and upper).
Taste is checked on the front third of the tongue. Ask the patient to stick out his tongue and hold it by the tip with a gauze napkin. With the help of a pipette, drops of sweet, saline, neutral solutions are alternately applied to the tongue. The patient should report the taste of the solution, indicating the corresponding inscription on a sheet of paper. It is noted that tears are not released during the application of taste stimuli (this paradoxical reflex is observed in patients with improper germination of secretory fibers after the preceding damage to the branches of the facial nerve).
The facial nerve contains a very small number of fibers that conduct pulses of general sensitivity and innervate small areas of the skin, one of which is located on the inner surface of the auricle near the external auditory canal, and the second - directly behind the ear. Examine the pain sensitivity, applying a pin prick directly to the back of the external auditory canal.
Signs of lesions of the facial nerve
The defeat of the central motor neuron (for example, with hemispheric stroke ) is the cause of central, or "supranuclear", paralysis of the facial musculature. It is characterized by contralateral paresis of facial muscles located only in the lower half of the face (there is a very slight weakness in the circular muscle of the eye and a slight asymmetry in the eye cracks, but the ability to wrinkle the forehead is preserved). This is because that part of the motor nucleus is n. Facialis, which innervates the lower mimic muscles, receives impulses only from the opposite hemisphere, whereas the part innervating the upper mimic muscles is influenced by the cortical-nuclear tracts of both hemispheres. Due to the defeat of the peripheral motor neuron (motor neurons n. Facialis and their axons), peripheral paralysis of the facial musculature (prozoplegia) develops , which is characterized by weakness of the facial muscles of the entire ipsilateral half of the face. Closing of eyelids on the affected side is impossible ( lagophthalmus ) or is incomplete.
In patients with peripheral paralysis of facial muscles, faces often observe Bell's symptom : when the patient tries to close his eyes, the eyelids on the side of the facial nerve do not close, and the eyeball goes up and out. The movement of the eyeball in this case is a physiological synkinesia, consisting in moving the eyeballs upward when closing the eyes. To see her from a healthy person, you must forcibly keep his eyelids in the raised state, asking him to screw up his eyes. Peripheral paralysis of facial muscles may in some cases be accompanied by a taste disorder in the anterior two-thirds of the ipsilateral half of the tongue (with damage to the trunk of the facial nerve beyond the distal part of the chorda tympani fibers ). In the central paralysis of facial muscles, that is, when the cortical-nuclear tracts that go to the motor nucleus of the facial nerve are damaged, there is no taste disturbance.
See also: Paralysis of the facial nerve
If the facial nerve is affected above the departure of the fibers from it to the stumbling muscle, there is a perversion of the timbre of perceived sounds - hyperacusia. When the facial nerve is damaged at the level of its exit from the temporal bone pyramid through the stylophyllar opening, the parasympathetic fibers to the tear gland (n. Petrosus major) and the sensitive fibers coming from the taste receptors (chorda tympani) do not suffer, so the taste and teardrop remain intact. Characterized by tearing on the side of the lagophthalmus, which is explained by excessive irritation of the mucous membrane of the eye due to the absence of a protective blinking reflex and the difficulty of moving the tear into the lower tear duct due to the sagging of the lower eyelid. All this leads to the fact that tears freely flow down the face.
A bilateral acute or subacute lesion of the facial nerve is observed peripherally in Guillain-Barre syndrome (GBS). Acute or subacute unilateral peripheral paralysis of facial muscles most often occurs with compression-ischemic neuropathy of the facial nerve (with compression-ischemic changes in that part of the nerve that passes through the facial canal in the pyramid of the temporal bone.
In the recovery period after peripheral paralysis, pathological regeneration of the fibers of the facial nerve is possible.
At the same time, on the side of paralysis, the contraction of facial muscles develops over time, because of which the optic cleft becomes narrower, and the nasolabial fold is deeper than on the healthy side (the face "tilts" no longer to the healthy but to the sore side). The contraction of facial muscles usually arises against the background of residual phenomena of prozoparesis and is combined with pathological syncopeies of facial facial muscles. For example, when the eyes are screwed up on the patient side, the angle of the mouth (the syncopation of syncopeesis) involuntarily rises at the same time, or the wing of the nose is raised, or platysma is shortened ; when inflating the cheeks, the narrowing of the eye gap occurs, and so on.