Central voice production and pathophysiology of spasmodic dysphonia

Abstract

Objective: Our ability to speak is complex, and the role of the central nervous system in controlling speech production is often overlooked in the field of otolaryngology. In this brief review, we present an integrated overview of speech production with a focus on the role of central nervous system. The role of central control of voice production is then further discussed in relation to the potential pathophysiology of spasmodic dysphonia (SD).

Data sources: Peer-review articles on central laryngeal control and SD were identified from PUBMED search. Selected articles were augmented with designated relevant publications.

Review methods: Publications that discussed central and peripheral nervous system control of voice production and the central pathophysiology of laryngeal dystonia were chosen.

Results: Our ability to speak is regulated by specialized complex mechanisms coordinated by high-level cortical signaling, brainstem reflexes, peripheral nerves, muscles, and mucosal actions. Recent studies suggest that SD results from a primary central disturbance associated with dysfunction at our highest levels of central voice control. The efficacy of botulinum toxin in treating SD may not be limited solely to its local effect on laryngeal muscles and also may modulate the disorder at the level of the central nervous system.

Conclusion: Future therapeutic options that target the central nervous system may help modulate the underlying disorder in SD and allow clinicians to better understand the principal pathophysiology.

Level of evidence: NA.Laryngoscope, 128:177-183, 2018.

Keywords: Laryngeal motor cortex; botulinum toxin; laryngeal dystonia; phonation; spasmodic dysphonia; voice.

Figure 1

Hierarchical organization of central voice control depicting different interconnected levels of the voice control. The lowest level represented by the brain stem and spinal cord. Higher level of voice control is represented by the periaqueductal gray (PAG) and cingulate cortex (CC). The highest level is represented by the laryngeal/orofacial motor cortex (LMC). The dotted lines represent interconnections between regions.

Figure 2

A) Motor sequence within the primary motor cortex with the vocalization region in the inferior portion of the precentral gyrus. B) Functional Magnetic Resonance Imaging studies of 19 patients during voice production. Bilateral peaks of laryngeal/orofacial motor cortex (LMC) activation were found in the area 4 with an additional peak of activation in the left area 6. TR. PYR. = tractus pyramidalis [With permission from Simonyan K. The laryngeal motor cortex: its organization and connectivity. Current Opinion in Neurobiology 2013; 28:15–2]

Figure 3

Interplay between structural, functional and neurochemical alterations. Microstructural changes of the basal ganglia and sensorimotor cortex noted by Functional Magnetic Resonance Imaging have a global effect on brain sensorimotor network, organization and function.

Figure 4

Anastomoses between the laryngeal nerves. SLN = superior laryngeal nerve; ILN = internal laryngeal nerve; ELN = external laryngeal nerve; RN = recurrent nerve; 1 = Galen’s anastomosis; 2 = deep arytenoid plexus; 2’ = superficial arytenoid plexus; 3 = cricoid anastomosis; 4 = thyroarytenoid anastomosis; 5 = foramen thyroideum anastomosis; 6 = cricothyroid anastomosis. [With permission from Sanudo, JR, Maranillo E, Leon, X, Mirapeix RM, Orus C, Quer M. An Anatomical Study of Anastomoses Between the Laryngeal Nerves. The Laryngoscope. 1999; 109(6): 983-987]