![]() ![]() From there these projections reach the tractus solitarius to synapse in the caudal nucleus solitarius. The visceral sensory component carries impulses from the baroreceptors of the carotid sinus and the chemoreceptors of the carotid body via the sinus nerve to join the 9 th cranial nerve at the inferior glossopharyngeal ganglion. Postganglionic fibers travel with the auriculo-temporal branch of the mandibular nerve to enter the parotid gland. Parasympathetic fibers leave the plexus as the lesser petrosal nerve, re-enter the middle cranial fossa to exit the skull via the foramen ovale along with the mandibular nerve and synapses in the otic ganglion. The tympanic nerve ascends into the tympanic cavity to form a plexus, which provides the general sensation of the middle ear. Together with other components of the nerve, parasympathetic fibers cross the two glossopharyngeal ganglia in the jugular foramen to form the tympanic nerve. Preganglionic fibers originate from the inferior salivatory nucleus (receives afferents from the hypothalamus and the olfactory system) to exit the medulla between olive and inferior cerebellar peduncle. The visceral (parasympathetic) motor branch of the nerve innervates the ipsilateral parotid gland. The branchial motor branch originates from the nucleus ambiguus in the reticular formation of the medulla, emerges from the lateral aspect of the medulla, exits the skull via the jugular foramen, and descends to the styloid process to innervate the target muscles. There is also a communicating branch to the vagal nerve. Branches of the nerve include the tympanic, the pharyngeal, the lingual, the sinus caroticus, the tonsillar, and the stylopharyngeal branch. The nerve mediates five distinct functions: A branchial motor function providing voluntary control of the stylopharyngeal muscle (dilates and elevates pharynx during swallowing and speech) visceral motor functions to innervate the parotid gland via preganglionic fibers to the otic ganglion and postganglionic fibers to the parotid gland visceral sensory functions providing visceral sensory input from the carotid sinus and carotid bodies, general somatic afferent functions providing sensory information for the skin of the external ear, the internal surface of the tympanic membrane, the upper pharynx, the soft palate, the tonsils, and the posterior third of the tongue and a special sensory function providing taste sensation from the posterior third of the tongue. The ninth cranial nerve is a mixed nerve carrying motor efferents and sensory afferents. To correctly assess manifestations of LCN lesions, precise knowledge of the anatomy and physiology of the area is required. LCN lesions need to be considered in case of disturbed speech, swallowing, coughing, deglutition, sensory functions, taste, or autonomic functions, neuralgic pain, dysphagia, head, pharyngeal, or neck pain, cardiac or gastrointestinal compromise, or weakness of the trapezius, sternocleidomastoid, or the tongue muscles. An effective treatment is available in the majority of the cases, but a prerequisite for complete recovery is the prompt and correct diagnosis. ![]() Treatment of LCN lesions depends on the underlying cause. Causes of LCN lesions can be classified as genetic, vascular, traumatic, iatrogenic, infectious, immunologic, metabolic, nutritional, degenerative, or neoplastic. LCN lesions have to be suspected if there are typical symptoms or signs attributable to a LCN. LCN may be affected solely or together with more proximal cranial nerves, with central nervous system disease, or with nonneurological disorders. Affection of multiple LCN is much more frequent than the affection of a single LCN. Review of publications dealing with disorders of the LCN in humans. ![]() This review aims at summarizing and discussing diseases affecting LCN. Lesions of the lower cranial nerves (LCN) are due to numerous causes, which need to be differentiated to optimize management and outcome.
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