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Facial nerve palsy in children

Thomas J Geller, MD
Section Editor
Douglas R Nordli, Jr, MD
Deputy Editor
John F Dashe, MD, PhD


Facial nerve palsy is a common malady in children that may be congenital or acquired. The underlying etiology often remains unclear despite extensive investigation.

In 1830, Sir Charles Bell first described unilateral facial weakness secondary to facial nerve dysfunction. His description of acquired, idiopathic facial paralysis is often termed Bell's palsy [1]. This topic will review clinical aspects of facial nerve palsy in children.


The facial nerve has a complex anatomy and function that render it susceptible to multiple neurologic disorders based upon the location of the lesion (figure 1). Cranial nerve VII originates from multiple brainstem nuclei that are functionally specialized [2,3].

The motor component of VII, which accounts for movement of the facial musculature, arises from the motor nucleus of VII in the pontine tegmentum. Fibers innervating the forehead receive bilateral input via the corticobulbar tract, whereas the contralateral corticobulbar tract innervates the remaining facial muscles.

The superior salivatory nucleus is the origin of preganglionic parasympathetic fibers that innervate the lacrimal, sublingual, and submandibular glands. Innervating fibers of the submandibular and sublingual gland travel via the chorda tympani nerve, whereas the lacrimal gland fibers travel through the greater petrosal nerve.

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Literature review current through: Nov 2017. | This topic last updated: Apr 18, 2016.
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