mise à jour du
21 mars 2002
cas cliniques
The yawning reflex : an upper motor neuron sign in amyoytrophic lateral sclerosis
David R Williams
the Alfred Hospital, Melbourne, Australia


Yawning has been observed in most vertebrates. Its physiologic signifiance and the central nervous mechanisms triggering and coordinating its various components are unclear. In man, yawning has been discribed in cases of frontal lobe tumors, encephalitis, progressive supranuclear palsy, following thalamotomy, after electroconvulsive therapy and as an early manifestation of vasovagal response.
Case report : a 64 yaer old woman with hypertension, ischemic heart disease, and type II diabetes mellitus was admitted to stroke unit with a 2 day history of occipital haedache, dysarthria, and dysphagia. She had a 6-month history of increasingly frequent paroxysms of yawning. At the time of presentation, her paroxysms were occurring nightly. Each paroxysm consisted of 20 to 30 yawns in succession, which she described as uncontrollable and socially embarrassing. Tlhese paroxysms were followed by a period of painful cramping sensations in the pharynx and neck. The patient's dysarthria and dysphagia had resolved by the time of her admission and the neurologie examination was normal; in particular there were no signs of a pseudobulbar or bulbar palsy. A noncontrast CT scan was normal. Serum electrolytes and oxygen saturation were normal. The patient was assumed to have had a brainstem ischemie stroke and she was discharged on aspirin.
The frequency of her paroxysms of yawning increased over the next 3 months, occurring up to 7 te, 10 times each evening. Each bout consisted of 20 to 30 yawns in succession followed by painful cramping and a sensation of choking. She began to gag as sbe tried to swallow solids. Her paroxysms were suppressed by thioridazine 10 mg twice daily.
Two months later the patient remained free of paroxysms of yawning although she continued to complain of dysphagia. Her troublesome yawning recommenced when her thioridazine was discontinued. She had evidence of a mixed bulbar and pseudobulbar palsy clinically, although the clinical examination was otherwise normal. Nerve conduction studies and an electromyogram revealed evidence of denervation in all extremities and was thought to be consistent with motor neuron disease. An MRI showed no ischemic or other abnormality in the brainstem or elsewhere. Her yawning became less evident as her bulbar palsy progressed. She died of pneumonia, presumably due to aspiration, 24 months after the onset of her yawning. A postmortem was not obtained.
Discussion : Although yawning bas been widely reported in vertebrates, its physiologie role is unclear. It is usually perceived as an act of inspiration often associated with stretching. In fact, there is no evidence that yawning is a response to oxygen or carbon dioxide levels. It chiefly occurs during transitions from wakefulness to sleep or sleep to wakefulness. It increases arousal, as assessed by skin conductance, and has a greater cumulative effect than mouth opening or deep breathing alone.
The pathways involved in yawning have not been fully defined, although the diencephalon, reticular formation, and midbrain are involved in the characteristic slow involuntary gaping movements of the mouth. In rodents, yawning is initiated in the hypothalamus. Yawning may be influenced by a number of neurotransmitters and neuropeptides. It is facilitated by neurons in the paraventricular nucleus of the hypothalamus by oxytocin, excitatory amino acids, dopamine, and dopaminergic agonists such as apomorphine, and appears to require the action of both DI and D2 receptors. Dopaminergic antagonists may inhibit yawning as seen in the patient reported here. The hypothalamus projects to bulbar and spinal cord nuclei where the complex activity associated with yawning is generated.
Yawning may be inhibited by mature humans. The brainstem and spinal neurons involved must be subject to cortical influences that can only be expressed if the upper motor neuron pathways are intact. Thus, inhibition may be lost in pseudobulbar palsy. The ability to yawn will disappear when there is significant disturbance of the bulbar nuclei. That appeared to be the sequence in the case described here. The current case is interesting because of the unusual prominence of yawning and the apparent lack of any theoretical framework within which to account for it. Yawning may be a frequently overlooked clinical sign. Its occurrence may be useful as a subtle sign of a pseudobulbar palsy.
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