Examination of facial nerve motor functions centers on assessment of the actions of the muscles of facial expression. A great deal can be learned from simple inspection. At rest the face is generally symmetric, at least in young individuals. With aging, the development of character lines may cause asymmetry that does not indicate disease. Note the tone of the muscles of facial expression, and look for atrophy and fasciculations. Note the resting position of the face and whether there are any abnormal muscle contractions. Note the pattern of spontaneous blinking for frequency and symmetry. A patient with parkinsonism may have infrequent blinking and an immobile, expressionless, “masked” face. Facial dystonia causes an abnormal fixed contraction of a part of the face, often imparting a curious facial expression. Progressive supranuclear palsy may cause a characteristic facial dystonia with knitting of the brows and widening of the palpebral fissures (omega sign). Synkinesias are abnormal contractions of the face, often subtle, synchronous with blinking or mouth movements; they suggest remote facial nerve palsy with aberrant regeneration. Spontaneous contraction of the face may be due to hemifacial spasm (HFS). Other types of abnormal involuntary movements that may affect the facial muscles include tremors, tics, myoclonic jerks, chorea, and athetosis.

Observe the nasolabial folds for depth and symmetry and note whether there is any asymmetry in forehead wrinkling or in the width of the palpebral fissures with the face at rest. A flattened nasolabial fold with symmetric forehead wrinkles suggests a central (upper motor neuron) facial
palsy; a flattened nasolabial fold with smoothing of the forehead wrinkles on the same side suggests a peripheral (lower motor neuron) facial nerve palsy. Eyelid position and the width of the palpebral fissures often provide subtle but important clinical clues. A unilaterally widened palpebral fissure suggests a facial nerve lesion causing loss of tone in the orbicularis oculi muscle, the eye closing sphincter; this is sometimes confused with ptosis of the opposite eye. It is a common misconception that facial nerve palsy causes ptosis.

Observe the movements during spontaneous facial expression as the patient talks, smiles, or frowns. Have the patient grin, vigorously drawing back the angles of the mouth and baring the teeth. Note the symmetry of the expression, how many teeth are seen on each side and the relative amplitude and velocity of the lower facial contraction. Have the patient close her eyes tightly and note the symmetry of the upper facial contraction. How completely the patient buries the eyelashes on the two sides is a sensitive indicator of comparative orbicularis oculi strength.

Other useful movements include having the patient raise the eyebrows, singly or in unison, and noting the excursion of the brow and the degree of forehead wrinkling; close each eye in turn; corrugate the brow; puff out the cheeks; frown; pucker; whistle; alternately smile and pucker; contract the chin muscles; and pull the corners of the mouth down in an exaggerated frown to activate the platysma. The platysma can also be activated by having the patient open the mouth against resistance or clinch the teeth. The patient may smile spontaneously after attempting to whistle, or the examiner may make an amusing comment to assess emotional facial movement. Because of their paucity of facial expression, patients with Parkinson disease may fail to smile after being asked to whistle: the whistle-smile (Hanes) sign.

Trying to gently push down the uplifted eyebrow may detect mild weakness. It is difficult to pry open the tightly shut orbicularis oculi in the absence of weakness. Vigorously pulling with the thumbs may sometimes crack open a normal eye. If the examiner can force the eye open with her small fingers, then the orbicularis oculi is definitely weak. Likewise, it is difficult to force open the tightly pursed lips in a normal individual. When the orbicularis oris sphincter is impaired, the examiner may be able to force air out of the puffed cheek through the weakened lips. With stapedius weakness, the patient may complain of hyperacusis, especially for low tones.

Testing of CN VII sensory functions is limited to taste. The peripheral receptors are the taste buds embedded in the tongue epithelium, and to a lesser extent in the soft palate and epiglottis. Taste is also carried through CN IX and probably CN X. There are four primary tastes, in order of decreasing sensitivity in humans: bitter, sour, sweet, and salty. A fifth modality, umami (delicious or savory), may exist in response to compounds of some amino acids. The many flavors encountered in life are a combination of the four primary tastes plus olfaction and oral sensory information (“mouth feel”). Sweet and salty substances are most commonly employed for clinical bedside testing due to their ready availability. Cranial nerve VII only subserves taste on the anterior two-thirds of the tongue. When the tongue is retracted into the mouth, there is rapid dispersion of the test substance outside the area of interest. The tongue must therefore remain protruded throughout testing of an individual substance, and the mouth must be rinsed between tests.

Since the patient will be unable to speak with the tongue protruded, instructions must be clear in advance. A damp applicator stick may be dipped into a packet of sugar, artificial sweetener or salt and coated with the test substance, then placed on one side of the patient’s tongue and rubbed around. The patient signals whether she can identify the substance. Most patients will identify the test substance in less than 10 seconds. Taste sensation is less on the tip of the tongue, and the substance is best applied to the dorsal surface at about the junction of the anterior and middle third of the tongue. The sweetness of artificial sweeteners such as saccharine and aspartame is more intense, and they may make better test substances than ordinary sugar.