“One person yawning sets off everyone else”

Short abstract

The precise role of yawning in human physiology remains unclear

Yawning is a stereotyped behaviour present in most mammals from rodents to humans and has been described since antiquity. Hippocrates considered yawning to be an exhaustion of the fumes preceding fever. Modern medicine did not pay much attention to it until the 1980s, when, with advances in neuropharmacology, yawning proved to be a valuable tool for the assessing dopaminergic activity and the pharmacological properties of new drugs. However, its precise role in human physiology is still unknown and its mechanisms remain unclear. The paper by Cattaneo et al (see pages 98–100) reports two cases of pathological yawning as the earliest symptom of brain stem infarction which introduces new arguments for locating this neuronal network in the lower brain stem.

Yawning occurs after waking up, before eating, before sleeping, and in passive activities when it is necessary to maintain a certain level of vigilance.¹ It is then followed by an acceleration of the electroencephalographic rhythms. It does not serve a primary respiratory function and it clearly has a non‐verbal communicative status. Nevertheless, it is also a clinical sign in intracranial hypertension, migraine, or iatrogenic side effects of dopaminergic drugs and serotonin reuptake inhibitors.² In basal ganglia disorders, yawning is reduced in patients with Parkinson's disease, and occurs more often in patients with Huntington's disease and supranuclear palsy than in controls. In healthy volunteers, apomorphine induces yawning which is also observed at the beginning of the “on” periods in Parkinson's disease.²

The anatomical structures known to be implicated in the occurrence and control of yawning are the paraventricular nucleus of the hypothalamus (PVN), the hippocampus, the reticular formation, the neostriatum, and the cranial (V, VII, IX, X, XI, XII), cervical (C1–C4), and dorsal nerves. Yawning is probably a reflex answer of the brain stem reticular formation aimed to increase the cortical level of vigilance. Dopamine and oxytocin are the main neurotransmitters implicated in its modulation. Indeed yawning induces sensory efferents from the terminals of the fifth facial nerve to the reticular formation or the PVN through the spinothalamic and hypothalamic tracts. Stimulation of the dopamine D2 receptors of the PVN activates the oxytocin neurones that project either to the pons (reticular formation, locus coeruleus), to the hippocampus, to the insula, or to the orbitofrontal cortex, leading to the transient feeling of wellbeing that follows yawning. This pathway is modulated by acetylcholine, serotonin, opioid peptides, sexual hormones, and orexin. The paper by Cattaneo et al provides important data on the crucial role of the lower brain stem.

Contagious yawning is an even more intriguing phenomenon. It is triggered by seeing, hearing, or even thinking about someone else yawning. Contagious yawning does not occur in species that do not recognise themselves in mirrors or in infants younger than two years old. The phenomenon has been investigated with functional magnetic resonance imaging,³ which implicated the precuneus or the posterior cingulate regions, functional regions associated with the identification of self referent information, a primitive form of empathy. Further studies are needed before conclusions can be drawn.