mise à jour du
21 mars 2010
Liste des orateurs
Les résumés par thème
Programme et horaires pdf   
FICY dans les médias
Index du site
Recherche par thèmes
Recherche par mot du site :


avec l'aide de


Première conférence internationale sur le bâillement
First International Conference on Yawning
Paris 24 - 25 juin 2010
Galerie des Photos de FICY
The dawn of the yawn: Is yawning a warning ? Linking neurological disorders
Simon B N Thompson
Programme Leader of the MSc Clinical Programme, Bournemouth University, United Kingdom
Simon B N Thompson
Yawning is a primitive and misunderstood mechanism that has attracted new interest in recent years amongst academics and neuroscientists alike. The most common theory of yawning is to replace an oxygen deficiency in the blood. Alternative theories are that stretching the lungs leads to a feeling of being more awake. This is plausible since stretching of these muscles involves special control systems such as the locus coeruleus, paraventricular nucleus of the hypothalamus, and the reticular activating system.
Some researchers believe that our brains are more efficient when they are cooler and therefore a deep breath of fresh air can cool an overheated brain. The contagious yawn may be an innate action that recognises a particular behavioural state as fifty per cent of us yawn within five minutes of seeing another person yawn.
Olivier Walusinski (2007) has been influential in re-writing our knowledge of the "yawn". He coined the term "parakinesia brachialis oscitans" (Walusinski, Neau & Bogousslavsky, 2010) to describe cases of hemiplegia where the onset of yawning coincides with involuntary raising of the paralysed arm. Furthermore, he has proposed that mapping of the neural network for yawning behaviour may be possible from knowledge of stroke localisation. This invites an exciting new area of research potentially linking together several neurological disorders.
In rats, cholinesterase inhibitors such as E2030 can induce yawning. Ogura and colleagues (2001) showed that Scolopolamine, a centrally acting anti-muscarinic drug, completely inhibited E2030-induced yawning as compared with the peripherally acting Methylscopolamine (Ogura, et al., 2001). Yet Scopolamine did not block Donepezil Hydrochloride E2020-induced yawning suggesting that central cholinergic and dopaminergic mechanisms are to some extent involved in E2030-induced yawning.
Cattaneo and colleagues (2006) have proposed that excessive yawning may give rise to brain stem ischaemia. They report two cases of brain stem stroke involving the upper ponto-mesenchephalic junction in which excessive pathological yawning was evidenced. In one patient this was associated with gait ataxia and in the other with upper limb and facial hemiparesis. A causal relation is hypothesised between the brain stem lesion and pathological yawning. This is possibly related to denervation hypersensitivity of a putative brain stem yawn centre.
For some time, researchers have suspected that the brain stem is implicated in yawning. However, in the past, researchers have questioned whether the brain stem is solely implicated in yawning (Wimalaratna & Capildeo, 1988) with others reporting on findings involving brain stem stroke and lesions in cortical and sub-cortical areas.
In particular, Singer and colleagues (2007) hypothesise that excessive yawning is a consequence of lesions in cortical or sub-cortical areas which pathologically control diencephalic yawning centres despite not having diencephalic lesions. Reporting on seven patients with pathological yawning caused by acute middle cerebral artery stroke, they suggest that pathological yawning also occurs in supratentorial stroke.
Yawning despite trismus (the inability to open the mouth which usually involves the trigeminal nerve), has been reported in a patient with locked-in syndrome caused by a thrombosed megadolichobasilar artery (Krasnianski, et al., 2009). A vascular malformation of the basilar artery-megadolichobasilar artery (fusiform aneurysm, vertebrobasilar dolichoectasia 1) was determined to be the underlying cause of this rare combination of symptoms. A thrombus in the megadolichobasilaris as well as an
almost total pontine infarction were demonstrated on CT- and MRI-scans. The authors conclude that trismus may be associated with locked-in syndrome due to megadolichobasilar artery thrombus, although yawning is still possible.
The suggestion that neocortical brain areas have an inhibitory effect on the paraventricular nucleus of the hypothalamus and that repetitive yawning may be elicited because of liberation of this area in some middle cerebral artery strokes has also been hypothesised (Singer, et al., 2007). Walusinski (2007) puts it succinctly when he says that "yawning is an exterior manifestation of the tonic stimulation of the cortex by sub-cortical structures, particularly when the brain stem does not receive appropriate feedback from the cortex." (paragraph 6, Walusinski, 2007).
We do not fully understand the origination of yawning partly because there is a lack of consensus of the specific and necessary or primary neurotransmitters involved in yawning together with precise knowledge of all the neurotransmitter pathways and their implication in neurological disorders. The clinical and neuro-chemical picture is of course fairly sophisticated with considerable knowledge on the subject in a number of sources ranging from neuroscience, neuropsychology to neurology.
A good example of the complex yet revealing nature of linking neurological disorders through their neuro-chemical pathways has already been seen with the initial lack of clarity of the neurotransmitters thought to be involved in Parkinson's disease (PD). Once thought to be the consequence of solely dopamine depletion and irregularity, PD is now commonly associated with an additional irregulation of serotonin. Depression is frequently observed in PD patients and has been associated with serotonin depletion. The intraneuronal monoamine oxidase (MAO-A) is active for dopamine, noradrenaline, and serotonin. These have a paramount influence in the pathogenesis of depression (Jansen Steur, 1997) and are implicated in PD.
Important work emerging from the Laboratoire de Médicine Expérimentale and Clinique de Neurologie et Neuropsychologie, Pitié-Salpêtriére, France (Agid & Javoy-Agid, 1985) reveals that there are several abnormalities in peptide content in Alzheimer's disease (AD) and Huntington's chorea. The authors suggest that whilst brain peptides fulfil most of the criteria required of putative neurotransmitters, it is not known whether they act directly as rapid transmitters of impulse traffic across the synaptic cleft or more generally as modulators of neuronal activity.
This doubt in neurotransmitter function together with multiple implications in chemical pathways provides us with a complicated picture that is not dissimilar to the perplexing phenomenon of the clinical signature of AD in people with co-morbid Down's syndrome (Thompson, 2006). Possession of AD and Down's syndrome does not categorically signal clinical symptoms in later life (Thompson, 2000). The picture is no less complicated when considering the effect of acetylcholine esterase inhibitors such as Aricept on memory functioning (Thompson, MacDonald & Coates, 2001), though perhaps the development of vascular dementia from stroke may provide us with more insight into the link between neurological disorders through our understanding of neuro-chemical pathways in these conditions (Thompson, 2002).
Yet researchers are generally united in thinking that the yawning experience implicates specific neurotransmitters including dopamine (thought to activate oxytocin production in the hypothalamus and hippocampus), acetylcholine (known to be actively involved in memory functioning), serotonin (considered important in the feeling of well-being and pleasure), gamma amino butyric acid (GABA), adreno-corticotrophic hormone (ACTH), sexual hormones, alpha-melanocyte stimulating hormone (_-MSH), and perhaps many others.
Whilst studies of stroke patients have perhaps yielded the closest explanation and localisation of the yawning experience, there is scope in exploring normal subjects in terms of whether an emotional component can explain better the fact that yawning is so contagious that, on occasions, one person can elicit yawning in another by simply talking about it. The suggestibility of yawning invites the possibility of other neuro-chemical pathways being implicated that may have their association in the field of hypnosis.
Yawning represents an exciting challenge to neuroscientists and neurologists; perhaps it is still only the dawn of this science conundrum?
REFERENCES in Medical Hypotheses
Agid, Y. & Javoy-Agid, F., 1985. Peptides and Parkinson's disease. Trends in Neurosciences, 8: pp.30-35.
Cattaneo, L., Cucurachi, L., Chierici, E. & Pavesi, G., 2006. Pathological yawning as a presenting symptom of brain stem ischaemia in two patients. Journal of Neurology & Neurosurgery, 77: pp.98-100.
Jansen Steur, E.N.H., 1997. Moclobemide and selegeline in the treatment of depression in Parkinson's disease. Journal of Neurology, Neurosurgery & Psychiatry, 63: p.547.
Krasnianski, M., Gaul, C., Neudecker, S., Behrmann, C., Schluter, A. & Winterholler, M., 2009. Yawning despite trismus in a patient with locked-in syndrome caused by thrombosed megadolichobasilar artery. Clinical Neurology & Neurosurgery, 106; 1: pp.44-46.
Ogura, H., Kosasa, T., Kuriya, Y. & Yamanishi, Y., 2001. Central and peripheral activity of cholinesterase inhibitors as revealed by yawning and fasciculation in rats. European Journal of Pharmacology, 415; 2 -3: pp.157-164.
Singer, O.C., Humpich, M.C., Lanfermann, H. & Neumann-Haefelin, T., 2007. Yawning in acute anterior circulation stroke. Journal of Neurology, Neurosurgery & Psychiatry, 78: pp.1253-1254.
Thompson, S.B.N., 2000. The Central Executive System in people with Down's
syndrome and dementia. Clinical Gerontologist, 21; 3: pp.3-32.
Thompson, S.B.N., 2002. Memory decline, Alzheimer's disease and vascular
dementia: The clinical picture. The Journal of Cognitive Rehabilitation, 20; 2: pp.12-
Thompson, S.B.N., 2006. Dementia and Memory: A Handbook for Professionals and Students. Aldershot: Ashgate.
Thompson, S.B.N., MacDonald, J. & Coates, T., 2001. Improving visual memory
with Aricept (Donepezil Hydrochloride, E2020) in mild-to-moderate Alzheimer's
disease. Clinical Gerontologist, 24; 1/2: pp.55-73.
Walusinski, O., 2007. Can stroke localisation be used to map out the neural network for yawning behaviour? Journal of Neurology, Neurosurgery & Psychiatry, 78: pp.1166.
Walusinski, O., Neau, J-P., Bogousslavsky, J., 2010. Hand up! Yawn and raise your arm. International Journal of Stroke, 5: 21-27.
Wimalaratna, H.S.K. & Capildeo, R., 1988. Is yawning a brain stem phenomenon? The Lancet, 331; 8580: pp.300.