Programme
Leader of the MSc Clinical Programme,
Bournemouth University, United
Kingdom
INTRODUCTION
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.
EXPLORING THE
EVIDENCE
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).
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). 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.
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 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?
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-
18.
Thompson, S.B.N., 2006.
Dementia and Memory: A Handbook for
Professionals and Students. Aldershot:
Ashgate.
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.
