Review Article
The superior laryngeal nerve: function and dysfunction

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Anatomy

The SLN arises from the bottom half of the nodose ganglion, some 36 mm below the jugular foramen [4]. It travels medial to the internal and external carotid arteries; typically, after some 15 to 21 mm, it divides into an external branch (exSLN) and a larger internal branch (inSLN) [4], [5], [6], [7]. In rare cases, these branches may leave the nodose ganglion separately. En route to the larynx, the SLN receives fibers from the cervical sympathetic chain, generally to the exSLN [8]. The greater

Motor function

As described previously, the exSLN supplies motor innervation to both bellies of the cricothyroid muscle. The cricothyroid muscle originates from the ala of the thyroid cartilage and inserts onto the outer surface of the cricoid cartilage [4], [21], [22], [23]. Attribution of insertion and origin are reversed in some descriptions, based on a different understanding of which cartilage moves on cricothyroid contraction. Because the thyroid cartilage is anchored to other neck structures by strap

Superior laryngeal nerve paralysis

In the absence of an objective means of diagnosis, early authors deduced signs and symptoms from their understanding of the function of the SLN, which was sometimes inaccurate and often incomplete. For example, a wavy or serpentine vocal fold margin was considered a hallmark of SLN paralysis for many years [1], [2], [71]—a reasonable supposition of how a vocal fold might respond to a loss of longitudinal tension if one had an imperfect understanding of its elastic properties. Time and further

Summary

Despite long-standing clinical interest in SLN dysfunction, most aspects of this entity continue to require clarification. The replacement of the laryngeal mirror by flexible fiberoptic and rigid rod-lens laryngoscopy (including stroboscopy) and the resulting improvement in laryngeal visualization and documentation of examination has not resulted in a better definition of characteristic signs. Symptoms are often vague, and most are shared with other voice disorders. Under the circumstances,

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      SLN paresis or paralysis may lead to a decrease in pitch and impaired vocal performance, especially for high-pitched sounds.1 The diagnosis is “difficult”1 and “challenging”3,4; consequently, this condition is often neglected5 or misdiagnosed as functional dysphonia.6 The resulting voice changes may be severe in voice professionals, particularly singers.4,6

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      Superior laryngeal nerve paresis (SLNP) is difficult to diagnose because of a lack of consistent laryngeal findings, and its effects on voice likely extend beyond simple pitch elevation control.4 The prevalence of SLN injury and dysfunction is unknown as many cases go undiagnosed, and little has been written about SLNP in regard to its specific effects on voice.5 This is particularly important as alterations in singing voice by SLNP can be a serious detriment to professional singers.2

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