mise à jour du
23 septembre 2001
International Journal of Neuroscience
 Excessive yawning and progressive supranuclear palsy
Dr Reuven Sandyk
University of Arizona


The clinical symptoms of progressive supranuclear palsy (PSP) characteristically include abnormal gait and posture, axial rigidity, and supranuclear gaze palsy. Pathologically, there is widespread neuronal cell loss in the brainstem and diencephalon that does not follow the pathways of any single recognized neurotransmitter (Steele et al., 1964).

Early diagnosis of PSP may be intriguing, and of 415 patients with a possible diagnosis of Parkinson disease, only 3.9% met the criteria for PSP (Jackson et al., 1983). In contrast to Parkinson's disease, tremor is an uncommon feature of PSP, but falling, postural instability, visual disturbances, an axial rigidity dominate the early course of the disease (Jackson et al., 1983). I have recently encountered 5 patients aged 58-70 yeais with classical symptoms and signs of PSP (Jackson et al., 1983) who experienced an unexplained excessive yawning at the onset of the disease. In all patients excessive yawning occurred predominantly during the day at a frequency of 1-3 yawning attacks/min., which produced severe social embarassment. In 3 patients, yawning subsided with administration of Sinemet or bromocriptine, while 2 other patients noted marked reductions in the frequency of yawning with the initiation of anti-Parkinson medication.

The ubiquitous and apparently nonsignificant nature of the act of yawning might have contributed to the relative lack of attention given by physiologists to this behavioral phenomenon. The physiological significance of yawning and the central nervous mechanisms triggering and coordinating its various components remain unclear (Urba-Holmgren et al., 1977). Frequent yawning has been mentioned as a symptom in some diseases of the CNS, including frontal lobe tumors and encephalitis (Brock & Krieger, 1963). Excessive yawning was also reported with administration of sodium valproate in a patient with postanoxic action myoclonus (Rollinson et al., 1979).

A stretching and yawning syndrome bas been observed in cats, dogs, and monkeys after intracisternal or intraventricular injections of ACTH and/or MSH (Ferrari et al 1963). Both cholinergic and dopaminergic antagonists were reported to inhibit MSH-induced yawning in animals (Yamada & Furukawa, 1981).

On the other hand, cholineigic agonists have been reported to induce yawning in infant and adult rats (Holmgren & Urba-Holmgren,. 1980). In another study, small doses of dopamine agonists (eg.apomorphine) produced recurrent episodes of yawning in rats (Mogilnicka & Klimek. 1977). The latter was blocked by administration of neuroleptics. Dopamine agonist used at higher doses failed to produce yawning, suggestive that only slight dopaminergic stimulation is necessary. The study by Yamada and Fukurowa (1980) suggested that both dopaminergic inhibition and cholinergic activation are concomitantly involved in the mechanism of yawning in rats.

In our PSP patients, excessive yawning was reduced or abolished by administration of dopaminergic drugs supporting a central role for dopaminergic dysfunction in triggering excessive yawning in our patients. Excessive yawning has not been, to my knowledge previously reported to occur as an early symptom in PSP. Since, however, the yawning reflex involves a complex reflex brainstem arc (Brock & Krieger, 1963), the presence of excessive yawning in PSP indicate deranged brainstem functions involving dopaminergic and cholinergic mechanisms.