CN7 (a hook — Fig. 30) pulls down, closing the eye, whereas CN3 (3 pillars — Fig. 30) opens the eye. This is a vital clinical point.
Figure 31 illustrates the clinical difference between upper motor neuron and lower motor neuron damage to CN7. If one severs CN7, which innervates one entire side of the face, including the eyelids and eyebrows, that entire side of the face becomes paralyzed. The forehead on the affected side appears
ironed out. The eye will not close and there is flattening of the nasolabial fold. If the lesion is above the level of the nucleus of 7, i.e., an upper motor neuronal lesion, only the area of the face below the eyes is paralyzed because of the bilateral innervation of the upper face by the two cerebral hemispheres. Hence, the typical stroke patient with an upper MN lesion rarely needs a tarsorrhaphy (an operation to keep the eyelids closed) whereas the patient with Bell's palsy (a spontaneous peripheral nerve 7 palsy of unknown etiology) may, because of marked difficulty in closing the eye. In severe cases, this results in drying of the eye unless the lids are sutured together or medication applied topically. The usual site of injury in Bell's palsy is somewhere in the facial canal (which lies between the internal acoustic meatus and the stylomastoid foramen—Fig. 32), and may involve other branches of CN7 (to the stapedius muscle, lacrimal and salivary glands—Fig. 32). Since the stapedius dampens sound waves, its nonfunctioning leads to hyperacusis, wherein sounds appear excessively loud. Usually, function returns after Bell's palsy. The patient may then experience "crocodile tears," in which the patient tears on eating, instead of salivating, owing to misguided growth of the regenerating salivary and lacrimal fibers.
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