PMC

Anatomical pathways between the cortex, basal ganglia, brainstem and vagus nerves innervating the vocal folds. Pathway injury indicated by solid bars; (A) unilateral lesions do not present with vocal fold paralysis, while (B) bilateral lesions present with aphonia. GPe, globus pallidus external; GPi, globus pallidus interna.

Waveform (left), spectrum (center), and cepstrum (right) from speakers with aphonia (top row), nonaphonic but disordered voice quality (center row), and no voice disorder (bottom row).

Patient selection
Exclusion criteria: *psychogenic aphonia. nt-IONM – surgeons not trained in intraoperative neuromonitoring, t-IONM – surgeons trained in intraoperative neuromonitoring, RLNP(+) – recurrent laryngeal nerve palsy present, RLNP(–) – recurrent laryngeal nerve palsy absent.

Computed tomography scan of the head on day 1, laryngeal fiberscopy on day 10, and brain magnetic resonance imaging on days 11 and 45 in a 22‐year‐old woman with aphonia after carbon monoxide exposure. The scan of the head shows a low density area in the bilateral globus pallidus (GP) (A, arrows). Laryngeal fiberscopy reveals bilateral immobilization of the vocal cords in median position during phonation (B). Diffusion‐weighted images obtained 11 days after carbon monoxide exposure show symmetrical high signal intensity lesions in the bilateral substantia nigra (C, arrows) and in the GP (D, arrows). T2‐weighted images also reveal symmetrical high signal intensity lesions in the bilateral substantia nigra (E) and in the GP (F). There is no alteration in the medulla oblongata and corticobulbar tracts on T2‐weighted image (G, arrow). T2‐weighted images on day 45 show atrophied slightly high signal intensity lesions in the GP (H).