mise à jour du
15 décembre 2001
Journal of neurology
1999; 243; 3; 300-301
cas cliniques
Pathological yawning
as a symptom of multiple sclerosis
T. Postert D, Pëhlau S, Meves Nastos H, Przuntek
Ruhr University Bochum, Department of neurology in St Joseph Hospital D44791 Bochum, Germany
The biological significance of Yawning elicited by application of electromagnetic fields in multiple sclerosis.Sandyk R


Yawning is an arousal reflex to reverse brain hypoxia [?]. Physiologically boredom and tiredness induce the involuntary wide opening of the mouth with massive air inhalation through mouth and nose followed by slow expiration. Ancyloglossia, epilepsy, psychosi, encephalitis and brain tumours are known causes of yawning as a repetitive phenomenon. Pharmacologically it can be provoked by drug overdose with valproate, dopamine agonists, tricyclic antidepressants or by of morphine. Owing to the unclear mechanisrn and borderline position between psychology and neurology, there has been little medical research on the phenornenon. We report the case of a patient with excessive pathological yawning, hemiparesis and facial paresis as symptoms of multiple sclerosis (MS). A 28-year-old man had clinically definite MS for 2 years. The patient was admitted to hospital because of a relapse with mild weakness of the left extremities. At the same time, yawning occurred 4 times/min despite regular and long sleep. Neurological examination showed central left facial paresis and mild left spastic hemiparesis. Abdominal reflexes were not present. Cerebellar function, cranial nerves and sensory pathways were normal. On T2-weighted images MRI disclosed multiple lesions of the brain stem. Visual evoked potentials and brain stem auditory evoked potentials showed a marked delay bilaterally. Cerebrospinal fluid revealed a normal cell count and protein concentration; oligoclonal bands were positive. A restrictive or obstructive respiratory tract disease was excluded using a pulmonary function test. Arterial blood gas analysis was normal. Ancyloglossia or deviation of the epiglottis were not found.

The patient received high-dose intravenous steroid therapy (methylprednisolone 500 mg for 5 days). On the 3rd day, there was complete remission of pathological yawning; mild hemiparesis and facial paresis remitted after 5 days. Although the exact mechanism of yawning is poorly understood, some trials support the hypothesis that the ascending activating reticular system (AARS) and adjoining reticular neuron complexes can be considered as the yawning centre. Patients with pons tumours were able to yawn despite paralysis of the masticatory muscles. Probably reflex yawning was possible because of the undisturbed short interconnections between the reticular neurons and the motor axons of the fifth and seventh cranial nerve.

These reports on anatomical aspects of yawning suggest that an inflammatory affection of the brain stem in MS patients may also cause the phenomenon by irritating the AARS. The discrepancy of the frequently existing brain stem lesions in MS and the rare incidence of pathological yawning remains unclear. High-dose intravenous steroid therapy reverses breakdown of the blood-brain barrier that is associated with a loss of gadolinium-enhancing lesions on MRI. Another cause of favourable short-terin recovery is the resolution of perifécal oedema. The rapid clinical response of our patient with complete remission of the repetitive phenomenon and hemiparesis may be explained by these effects, although spontaneous remission cannot be excluded. Unlike pathological laughter and weeping, yawning has not been known to be a pathological phenomenon in MS. Because of the subjective impairment, high-dose steroid therapy should be carried out, even if the phenomenon occurs as a single symptom.