Thursday, May 8, 2014


Source: Olivier Walusinski MD.  2014/05/08

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.

Yawning can be divided into 3 distinct phases: a long inspiratory phase, a brief acme and a rapid expiration, frequently but not always associated with stretching, tears, shivering, obstruction of the eustachian canal (causing a reduction in audiologic acuity), followed with a feeling of comfort. The average duration of the yawn is 5 s, (range, 3 to 45 s). The earliest appearance of yawning was observed in a 15-week-old embryo.

This semi-voluntary event increases vigilance and aims to alert when drowsiness occurs ( In animals it subserves behaviour related to stressful situations). Yawning probably has an important role for social communication as well. Excessive or pathological yawning, "chasm", is defined as a compulsive, repetitive action which is not trigered by "physiological" stimuli such as fatigue or boredom, discribed in cases of frontal lobe tumors, encephalitis, progressive supranuclear palsy, following thalamotomy, after electroconvulsive therapy and as an early manifestation of vasovagal response and many drugs.

Yawning occurs after waking up, before eating, before sleeping, and in passive activities when it is necessary to maintain a certain level of vigilance. 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.

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.

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&endash;C4), and dorsal nerves. Yawning is probably a reflex answer of the brainstem 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 complex neuronal reflex system of yawning appears to be located in a reticular brainstem system closely related through the diencephalo-hypothalamic network with large associative cortical areas.

The neuro-pharmacology of yawning is complex and knowledge of its mechanisms is incomplete. While under the control of several neurotransmitters, yawning is largely affected by dopamine. Dopamine may activate oxytocin production in the paraventricular nucleus of the hypothalamus, oxytocin may then activate cholinergic transmission in the hippocampus, and finally acetylcholine might induce yawning via the muscarinic receptors of the effectors. In fact, this scheme is over simplified. Many other molecules can modulate yawning, such as nitric oxide, glutamate, GABA, serotonine, ACTH, MSH, sexual hormones and opium derivate peptides, hypocretin. Dopamine involvement in yawning could have practical applications in the study of new drugs or the exploration of neurological diseases such as migraine or psychosis.

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, which implicated the precuneus or the posterior cingulate regions, functional regions associated with the identification of selreferent information, a primitive form of empathy.