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Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
http://www.baillement.com
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mise à jour du
5 septembre 2010
Medical Hypotheses
2010;75(6):630-633
The dawn of the yawn: is yawning a warning?
linking neurological disorders
Simon B N Thompson
Formerly, Visiting Professor of Clinical Neuropsychology, University of Portsmouth; now at Bournemouth University, UK

Chat-logomini

Simon B N Thompson
 
ABSTRACT
 
 Yawning continues to pose as a scientist's conundrum. Evidence is presented of yawning and contagious yawning in a number of different neurological disorders. Explanations are discussed in the context of disparate neurological disorders together with proposals for how theses findings may be linked. Thus, greater understanding of yawning and of neurological disorders may be achieved by exploring common neurochemical pathways and the involvement of neurotransmitters that are implicated in these different disorders. Finally, contagious yawning is discussed in the context of the susceptibility of persons and the similarity this presents with our understanding of the mechanisms involved in hypnosis.
 
Thompson Cortisol Hypothesis : all the publications
 
INTRODUCTION
 
Yawning is a primitive and misunderstood mechanism that has attracted new interest in recent years amongst academics and neuroscientists alike. Yet it has been a fascination of our early ancestral scientists and philosophers. For example, Hippocrates included it on his lists of useful "natures"; and in the ancient Hindu World, yawning was a religious offence [1].
 
Yawning is a stereotyped response that is seen in humans and animals from fish to mammals [2]; in fact, in all classes of vertebrates [3]. In preterm and near term infants, yawn incidence significantly decreases mainly during the day with a marked decrease in yawn frequency with age probably related to the development of circadian and homeostatic control of sleep and wakefulness [4]. In non-primates it has been related to the rest-activity cycle with incidence higher before than after the sleep episode [5].
 
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 [6]. 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. Even hearing a yawn may induce another person to also yawn. Yet in children with autism it is a very different situation. One study showed that yawning faces triggered more than twice as many yawns in non-autistic children than in their counterparts [7].
 
Platek et al. [8] proposed that contagious yawning is part of a more general phenomenon known as mental state attribution where people use their ability to inferentially model the mental states of others. Therefore, yawning may be associated with empathic aspects of mental state attribution and are negatively affected by increases in schizotypal personality traits. Walusinksi [9] goes one step further in suggesting that yawning shares the neural networks involved in empathy. The corollary of this is that we impart an understanding of others through our observation of their behaviour; more importantly, this observation instils feelings and emotions in us that are similar to those observed.
 
Cooper et al. [10] suggest that minor neurons may be responsible during this event since they not only fire when carrying out an action but also during the observation of that action carried out by another. Some researchers advocate perception mechanisms as an explanation for the yawn. For instance, Sarnecki [11] suggests that higher level representational states engage neurophysiological structures in determining our behaviour such as yawning.
 
Matikainen et al. [8] have suggested that the movements and compressions caused by yawning may affect the carotid body that is strategically situated at the bifurcation of the common carotid artery. Hence, yawning may stimulate the carotid body which is highly vascular and which will receive shunted blood giving rise to an increase in pressure and hormones release. Prasad [12] has commented that the yawn may be a physiological trait emerging from a vestigial reflex, similar to the formation of goose bumps in humans under stress, because at one time in evolutionary history, the yawn served to coordinate the aggressive social behaviour of a group of animals.
 
Olivier Walusinski [13] has been influential in re-writing our knowledge of the "yawn". He coined the term "parakinesia brachialis oscitans" [14] 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 may be possible from knowledge of stroke localisation. This invites an exciting new area of research potentially linking together several neurological disorders.
 
EXPLORING THE EVIDENCE
 
In rats, cholinesterase inhibitors such as E2030 can induce yawning. Ogura and colleagues [15] showed that Scopolamine, a centrally acting anti-muscarinic drug, completely inhibited E2030-induced yawning as compared with the peripherally acting Methylscopolamine [15]. 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.
 
There seems to be plenty of evidence of repetitive yawning in various types of patients; for example, Krantz et al.'s [16] case report of repetitive yawning in a patient with cardiac tamponade. Physiologically, yawning can be divided into three distinctive phases: a long inspiratory phase, a brief acme, and a rapid expiration [17].
 
Gallup et al. [18] describe the case histories of two women who suffer from chronic and debilitating episodes of excessive yawning in the absence of sleep problems. Both women curiously showed signs of thermoregulatory dysftmnction. Each also showed symptom relief through means of behavioural cooling, thus the authors suggest this demonstrates that recurrent episodes of excessive yawning are not necessarily related with a sleep disorder but rather may be indicative of thermoregulatory dysfunction.
 
It is known that brain temperature may rise in patients with depression, and fall in patients with mania [19]. Studies revealed that yawning has many physiological consequences that are consistent with those required for the regulation of brain temperature [20]. Also, the majority of therapeutic strategies against mania are hypothermic, while thermogenic strategies are used to combat depressive disorders [21]. Therefore, Prasad [21] proposes that drug induced yawning serves as a compensatory brain cooling mechanism when regulatory mechanisms fail to operate favourably.
 
Examining the literature describing different neurological disorders, such as Multiple Sclerosis (MS), reveals that frequent yawning may be associated with a number of conditions. MS involves thermoregulatory dysftmnction, with heat making symptoms worse and cooling providing symptom relief [22]. According to Gallup et al. [23], increases in facial blood flow resulting from a yawn operate like a radiator, removing hyperthermic blood from the face and head, while introducing cooler blood from the lungs and extremities.
 
Provine et al. [24] found that yawning tends to follow a circadian pattern occurring most often before and after sleep. People with MS very often experience problems with sleep pattern [25]. Gallup et al. [23] found that their MS patients indeed experienced symptom relief when they were able to nap during the day, which provided some restoration and nourishment to their sleep quotient.
 
Cattaneo et al. [26] have proposed that excessive yawning may give rise to brain stem ischaemia. They report two cases of brain stem stroke involving the upper pontomesencephalic 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. Cattaneo et al. [27] suggest that pathological yawning can be an early sign of brain stem infarction.
 
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 [28] with others reporting on findings involving brain stem stroke and lesions in cortical and sub-cortical areas. In particular, Singer et al. [29] hypothesise that excessive yawning is a consequence of lesions in cortical or subcortical areas which pathologically control diencephalic yawning centres despite not having diencephalic lesions. Reporting on seven patients with pathological yawning hyperthermic blood from the face and head, while introducing cooler blood from the lungs and extremities.
 
Provine et al. [24] found that yawning tends to follow a circadian pattern occurring most often before and after sleep. People with MS very often experience problems with sleep pattern [25]. Gallup et al. [23] found that their MS patients indeed experienced symptom relief when they were able to nap during the day, which provided some restoration and nourishment to their sleep quotient.
 
Cattaneo et al. [26] have proposed that excessive yawning may give rise to brain stem ischaemia. They report two cases of brain stem stroke involving the upper pontomesencephalic 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. Cattaneo et al. [27] suggest that pathological yawning can be an early sign of brain stem infarction.
 
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 [28] with others reporting on findings involving brain stem stroke and lesions in cortical and sub-cortical areas. In particular, Singer et al. [29] hypothesise that excessive yawning is a consequence of lesions in cortical or subcortical areas which pathologically control diencephalic yawning centres despite not having diencephalic lesions. Reporting on seven patients with pathological yawning caused by acute middle 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 [30]. A vascular malformation of the basilar artery-megadolichobasilar artery (fusiform aneurysm, vertebrobasilar dolichoectasia t) 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 MRT-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 [30]. Walusinski [13] puts this succinctly when he says that "yawning is an exterior manifestation of the tonic stimulation of the cortex by subcortical structures, particularly when the brain stem does not receive appropriate feedback from the cortex." (paragraph 6) [30].
 
Gutiénez-Alvarez [31] described two patients treated with Escitalopram for more than 8 weeks for major depressive disorder/generalised anxiety disorder. Ruling out the possibilities of needing sleep or effects related to sedation, the author found that each patient developed excessive daytime yawning. Curiously, their symptoms of yawning disappeared on reduction of dosage rather than on interruption and discontinuation. Therefore, it is worth considering further the individual effects of specific selective serotonin reuptake inhibitors since their effects on excessive yawning may be dose related.
 
Similarly, Propofol-induced yawning has also been investigated with fluctuations in autonomic function being noted [32]. However, pre-treatment with Fentanyl may inhibit Propofol-induced yawning.
 
DISCUSSION
 
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). Although the addition of a dopamine receptor agonist such as pergolide, ropinirole, pramipexole or cabergoline to levo-dopa in patients with motor complications reduces "off' time by about 1.1 to 1.5 hours per day [33], PD is now commonly thought not to be the consequence of solely dopamine depletion and irregularity.
 
PD is also associated with the additional inegulation of serotonin. Depression is frequently observed in PD 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 [34] and are implicated in PD.
 
Important work emerging from the Laboratoire de Médicine Expérimentale and Clinique de Neurologie, Pitié-Salpêtrière, France [35] reveals that there are several abnomialities 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 frmnction 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 [36]. Possession of AD and Down's syndrome does not categorically signal clinical symptoms in later life [37].
 
The picture is no less complicated when considering the effect of acetylcholine esterase inhibitors such as Aricept (Donepezil Hydrochoride, E2020) on memory functioning [38], 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 [39].
 
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), adrenocorticotrophic hormone (ACTH), sexual hormones, alpha-melanocyte stimulating homione (a-MSH), and perhaps many others.
 
Schürmann et al.'s [40] subjects' self-reported tendency to yawn covaried negatively with activation of the left periamygdalar region, suggesting a connection between yawn contagiousness and amygdalar activation. However, compelling evidence remains from a variety of sources that implicate the brain stem. Walusinski's "parakinesia brachialis oscitans" [14] has been further evidenced in two patients following brain stem stroke [41].
 
The rare movement disorder described in some cases of hemiplegia, was seen in a 39year-old man and a 55-year-old man. Munhoz et al. [41] described one of his patients as having systemic arterial hypertension, sudden dysarthria , dysphagia, dysesthesia and incoordination in the left lower limb. When yawning, his left upper and lower limbs had spasm associated to the involuntary elevation of the limb. Brain MRI showed an infarct in the right pontine area.
 
Munhoz et al.'s [41] second case presented with sudden vertigo when he turned his head left, or when riding a bicycle, and was followed by weakness and paresthesias of the left lower limb. Brain MRI showed a small infarct in the right side of the medulla oblongata.
 
CONCLUSIONS
 
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 and that, on occasions, one person can elicit yawning in another by simply talking about it.
 
Walusinski [42] proposes that yawning is a part of interoceptiveness by its capacity to increase arousal and self-awareness. If yawning connects consciousness as well as unconscious interoception to higher mental functions [43], then the suggestibility involved in the act 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. Although there is a growing amount of literature on the topic together with explanations that are not always concordant, there remains a feeling amongst the scientist fraternity that perhaps this is still only the dawn of this science conundrum?
 
 
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