Muscular tension dysphonia, episodic laryngospasm, globus, and cough may be
considered to be hyperfunctional laryngeal symptoms. Suggested etiological
factors for these symptoms include gastroesophageal reflux, psychological
problems, and/or dystonia. We propose a unifying hypothesis that involves n
eural plastic change to brainstem laryngeal control networks through which
each of the above etiologies, plus central nervous system viral illness, ca
n play a role. We suggest that controlling neurons are held in a "spasm-rea
dy" state and that symptoms may be triggered by various stimuli. Inclusion
criteria for the irritable larynx syndrome are episodic laryngospasm and/or
dysphonia with or without,globus or chronic cough; Visible or palpable evi
dence of tension or tenderness in laryngeal muscles; and a definite symptom
-triggering stimulus. thirty nine patients with irritable larynx syndrome w
ere studied. Gastroesophageal reflux was felt or proven to play a major rol
e in a large number of the group (>90%), and about one third were deemed to
have psychological causative factors. Viral illness seemed quite prevalent
, with one third of patients able to relate the onset of symptoms to a vira
l illness that we feel might lead to central nervous system changes. Our pr
oposed hypothesis includes a mechanism whereby acquired plastic change to c
entral brainstem nuclei may lead to this form of hyperkinetic laryngeal dys
function. It gives structure and reason to an array of therapy measures and
suggests direction for basic research.