-
- Yawning is a scientific conundrum that has
baffled scientists for decades. Whilst the
origin and mechanism of yawning may be
understood, its presence and frequency in a
number of neurological disorders is not clearly
understood. The Thompson Cortisol Hypothesis
(2011) proposes a link between yawning and blood
cortisol levels because of the known association
between cortisol (and its elevation in levels)
and other states such as fatigue, stress, and
importantly, a number of neurological disorders
such as multiple sclerosis and stroke.
Investigation to support this hypothesis is
underway.
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- Thompson
Cortisol Hypothesis : all the
publications
- Introduction
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- Yawning is often attributed to boredom and
fatigue and is described as a simultaneous
inhalation of air often accompanied by
stretching (pandiculation) followed by
exhalation of breath (Thompson, 2010). The act
of yawning is a phylogenetically ancient
behaviour with early onset, recognisable by the
end of the third trimester in prenatal human
development (Provine, 2005). However, it is
become such an important subject of
investigation in recent years because of the
potential contribution it may make to our
understanding of neurological disorders
(Thompson, 2006). This is because of the
commonality between neurological disorders,
fatigue, and more recently with cortisol levels
(Thompson, 2011).
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- The Thompson Cortisol Hypothesis (Thompson,
2011) is potentially important as it may serve
as a diagnostic tool for early signs of
underlying untoward neurological sequelae and
development of disorders. Many conditions have
been associated with frequent yawning including
psychosis (Askenasy, 1989), cardiac tamponade
(Krantz, et al., 2004), and multiple sclerosis
(Postert, et al., 1996). The physiological role
of yawning is still not fully understood and its
functional significance is not clear. Askenasy
(1989) proposed that the yawn is an arousal
reflex to reverse brain hypoxia. Although
hypoxia is related to oxygen levels, the
underlying explanation here is that yawning is a
reflex with the aim to reverse drowsiness and to
maintain a level of alertness that is needed for
wakeful activities.
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- More current research has developed this
idea showing that yawning provides transient
increases in arousal in conditions of low
vigilance (Cattaneo, et al., 2006). This is
possibly due to stretching of the lungs (and the
intercostal muscles) which leads to feelings of
awakeness (Provine, 1986). Stretching of these
muscles requires special control systems such as
the locus coeruleus, paraventricular nucleus of
the hypothalamus, and the reticular activating
system (Walusinski, 2007). Association has been
made to wake and sleep patterns (Giganti, et
al., 2007). Findings of higher yawn frequency at
waking decline with age because of changes in
circadian and homeostatic control over sleep and
wakefulness (Giganti, et al., 2007).
-
- While yawning appears to be universal,
contagious yawning does not happen in all
individuals. Many researchers explain yawning in
terms of social cues that serve to synchronise
group behaviour (Deputte, 1994; Daquin,
Micallef, & Blin, 2001); Prasad (2008)
explained contagious yawning in terms of an
atavistic trait presenting as a vestigial reflex
that previously served to coordinate aggressive
social behaviour. The act of contagious yawning
has initiated research into the mirror-neuron
system (MNS) (Cooper, et al., 2001; Schurmann,
et al., 2005) that is activated when people
observe others. While others (Platek, et al.,
2003) have explained this phenomenon with mental
attribution theory, ie an inferential model that
imparts empathy to others who share similar
mental states.
-
- Interestingly, hemiplegic patients have
displayed movement of their paralysed arm while
yawning, termed parakinesia brachialis oscitans
by Walunsinski (2010). While the aetiology of
this is unclear in stroke patients, this
phenomenon disappears as the patient regains
control over the hemiplegic limb. Topper, Mull,
and Nacimiento, (2003) suggest the possibility
of an emotional motor system to explain these
movements in hemiplegic limbs during yawning
though seems unconvincing.
-
- Research into multiple sclerosis suggests
that yawning is triggered by rises in brain
and/or body temperature and may act as a cooling
mechanism. Accordingly, increases in blood flow
resulting from a yawn removes hyperthermic blood
from the face and head, while introducing cooler
blood from the lungs and extremities (Gallup,
& Gallup, 2008). Abnormal thermoregulation
has been found in both stroke and multiple
sclerosis patients who display excessive yawning
(Postert, et al., 1996; Marino, 2009; Sung, Lee,
& Chu, 2009; Gallup, Gallup, & Gallup,
2010a).
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- Thompson Cortisol Hypothesis
-
- Cortisol levels may be directly or
indirectly, associated with yawn frequency.
Yawning, fatigue, stress, cortisol levels, and
neurological disorders are all linked in some
way. For example, fatigue is often present after
onset of disorders and may give rise to yawning
episodes. The link between fatigue and yawning
is known; the link between thermoregulation and
yawning has been proposed; and the instances of
involuntary arm-raising in the parakinesia
brachialis oscitans in stroke patients has been
evidenced. There is also the known link between
elevated blood cortisol levels and fatigue, and
between cortisol levels and stress. Therefore,
Thompson (2011) has proposed that cortisol
levels may be elevated during yawning because
excessive yawning is implicated in a number of
untoward neurological disorders. Thus, yawning,
as a warning of an underlying neurological
disorder, may give rise to elevated cortisol
levels.
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- Discussion
-
- There are established links between yawning
and various states as well as between cortisol
and fatigue and stress. These will be explored
here.
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- Yawning and fatigue
-
- Extensive evidence links yawning to levels
of arousal and sleepiness, for instance, yawn
frequency was increased by up to 70% in
participants when faced with a television test
pattern for 30 minutes (Provine, 2005) while
children often manifest drowsiness through
excessive yawning (Walusinski, Neau, &
Bogousslavsky, 2010). Askenasy (1989) brings
together boredom, arousal and fatigue in
association with yawning: Boredom occurs when
the main source of stimulation in a persons
environment no longer sustains their attention,
by content or form. At this moment, the mind has
to make an effort to maintain contact with the
environment. Boredom induces drowsiness by
stimulating the sleep generating system and when
associated with fatigue the fatigue potentiates
the drowsiness-inducing effect. Drowsiness has
been suggested as the most common stimulus of
the yawn (Askenasy, 1989, p. 611).
-
- The most common cause of frequent and
repeated yawning has been described as sleep
debt (Walusinski, 2009). In humans, the observed
decrease in yawning frequency during the ages of
31-40 weeks is explained through the development
of homeostatic control of sleep and wakefulness
while in non-primates, yawning frequency is
higher before sleep than after, and has been
linked to the rest-activity cycle. Greco,
Baenninger, and Govern (1993) asked volunteers
to record their yawning activity over a period
of a week and found that yawns occurred most
frequently an hour after arising from sleep and
during the last hour before retiring to bed.
Over 60% of recorded yawns were found to occur
during lectures and studying, car driving and
television watching. These activities require
minimal interaction and are in line with tasks
that encourage minimal arousal. The opposite was
reported during activities of a faster and more
interactive nature such as cooking, cleaning,
washing, and taking part in conversation. Only
6-8% of yawns occurred during these tasks. These
data support the notion that yawning sub-serves
arousal and implicates higher brain activation
following yawn occurrences (Kasuya, et al.,
2005).
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- Yawning has been used in various accident
prevention campaigns focusing on yawning as a
vital sign of the possibility of falling asleep
involuntarily (Walusinski, et al., 2010).
Abtahi, Hariri, and Shirmohammadi (2011)
considered possible methods for detecting driver
drowsiness based on yawning action to prevent
road accidents.
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- Zilli, Giganti, and Uga (2008) conducted a
study aimed at gaining knowledge related to
sleep/wake transitions and time of day in the
assumption that this relation reflects the time
course of sleepiness. Since aging modifies
sleep-wake and tiredness rhythms, they compared
older individuals with young adults expecting to
see yawn frequency and time course vary with
age. They found both groups yawn most frequently
following sleep and just before sleep although
these peaks were earlier in both the morning and
evening for the older sample which was in line
with their earlier sleeping patterns. Older
adults yawned less frequently in general than
younger adults and morning peaks were shorter,
and early afternoon peaks were displayed which
were not apparent in the younger group. Zilli
and coleagues (2008) attributed their findings
to wake-sleep and sleep-wake transitions as
yawning episodes were in line with when such
transitions were about to take place, including
early afternoon bouts for the aged group due to
the increased tendency to nap. These findings
are also in line with yawning being associated
with arousal levels and feelings of
fatigue.
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- Empirically, it appears that yawning is
associated with transitions between wakefulness
and sleep and different levels of arousal.
Greco, Baenninger, and Govern (1993) explain
increases in yawn frequency during activities
such as driving and lecture attendance due to
the easy way relaxation and keen attention
alternates during these tasks. However,
interestingly, it appears that yawning is not as
strongly correlated in distribution when looking
at tiredness or sleep-deprivation (Greco,
Baenninger, & Govern, 1993), suggesting that
yawning is a stronger indicator of fatigue. Of
note here is that fatigue is different to sleep
deprivation and does not only occur due to lack
of sleep, instead it is a state of being and a
symptom of various disorders including stroke
and multiple sclerosis.
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- Cortisol levels and fatigue
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- Cortisol has been strongly linked to fatigue
with cortisol treatments shown to increase
feelings of vigour in both patients and healthy
subjects (Tops, et al., 2006). Disproportionate
low levels of corticosteroids have been reported
in clinical populations including asthenia,
fatigue, and depression. Corticosteroid
treatment was effective when treating chronic
fatigue syndrome (CFS) as well as increasing
feelings of well-being. Nater and colleagues
(2008) found hypo-cortisolism in a sample of CFS
patients and suggested that increased activation
in the immune system due to a lack of cortisol
leads patients to feel fatigued. Various
cortisol hormones have been found to affect
mood; glucocorticoids can cause sleepiness due
to increased arousal and activation (Fadeev,
Gitel, & Melnichenko, 2001); elevated
endogenous cortisol can also cause insomnia and
arousal, and low cortisol levels have been found
in atypical depression (Fries, et al.,
2005).
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- Various clinical trials have indicated that
a range of syndromes in which fatigue is a
symptom, such as post-traumatic stress disorder,
CFS, and fibromyalgia are linked to low levels
of adrenal corticosteroid cortisol (Fries, et
al., 2005; Van Den Eede, et al., 2007; Nater, et
al., 2008). However, this has not always been
found to be the case (Crofford, et al., 2004; Di
Giorgio et al., 2005). When looking at
non-clinical populations, cortisol also appears
to be linked to fatigue especially in
association with burnout and vital exhaustion
(Melamed, et al., 2006; Ter Wolbeek, et al.,
2007). In contrast, the alexithymia trait,
characterised by fatigue and low vigour, is
associated with low cortisol levels (Tops, et
al., 2006).
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- Findings by Lindeberg and colleagues (2008)
suggest that cortisol is related to fatigue
before disease onset as low waking cortisol and
flattened decline in daytime secretion was
linked to exhaustion in healthy individuals,
suggesting changes prior to disease onset.
However, in contrast, Rubin and colleagues
(2005), examining elective surgery patients,
pre-operation and at 6-months post-surgery,
found that cortisol levels differed after
post-operative fatigue had developed.
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- Whilst the authors found no associations
with low levels of cortisol they found patients
to display higher levels of cortisol
post-operation. Rubin and colleagues (2005)
concluded that studies reporting low cortisol
levels in patients are often conducted with
chronically ill patients suggesting that low
cortisol levels may develop after long-term
illness.
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- Typically, cortisol levels are highest
following waking cortisol awakening response or
CAR. At CAR, cortisol concentration can increase
from between 50-60% and then proceed to decline
throughout the day normally reaching its lowest
concentration around midnight (Kumari, et al.,
2009). Evidence suggests that low levels of
morning cortisol may lead to symptoms of fatigue
in non-clinical populations. Healthy women have
been shown to complain of fatigue and muscular
pain when displaying low morning cortisol levels
(Tops, et al., 2006). A directional link was
suggested as previous day fatigue did not
associate with decreased cortisol secretion the
following morning; however, low levels of
morning cortisol was predictive of fatigue later
in the day (Adam, et al., 2006).
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- Kumari and colleagues (2009) conducted the
first longitudinal epidemiological study
measuring cortisol secretion and fatigue in a
large community based population. Cortisol
levels were taken over a day together with
levels of fatigue over a 2.5 year period.
Results supported Adam and colleagues (2006)
findings that low cortisol is indicative of
new-onset fatigue while previous fatigue did not
coincide with future changes in cortisol levels.
Interestingly, the study took into consideration
a variety of possible confounding variables
including gender, age, medication, and health
conditions and found that low cortisol levels
leading to fatigue were independent of all
covariates. The authors concluded that low
levels of cortisol are associated with future
onset of fatigue. Contradicting Rubin and
colleagues (2005), they advocated cortisol
levels to be aetiological, or occur early in the
genesis of fatigue, increasing the risk of
future onset (Kumari, et al., 2009).
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- The lack of effect of previous fatigue on
cortisol levels was explained by the suggestion
that both the biological and psychological
consequences of fatigue may serve to alleviate
fatigue hypo-cortisolism (Kumari, et al., 2009).
As the study failed to find pre-existing fatigue
episodes effecting cortisol levels, it is
possible that fatigue symptomatology may be the
result of the disorder rather than as a direct
result of fatigue. These findings tend to
support those of other studies that found
cortisol levels occurring with fatigue, and
those that found fatigue as a factor in
affecting the onset of certain neurological
disorders such as CFS (Werbel, & Ober, 1993;
Ter Wolbeek, et al., 2007).
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- Observations from Tops and colleagues (2006)
found oral cortisol treatment, when used on a
healthy female sample, to increase levels of
vigour and decrease levels of fatigue. Findings
were based on prior and post-treatment
self-reports and were compared with a placebo
condition. However, the largest effects where
noted in less than optimal conditions, for
instance, when already fatigued. Here
participants were asked to complete a task and
then asked to report on their mood. After the
task, participants reported increased levels of
fatigue and this is when the largest effects of
cortisol treatment were recorded between the
groups. This may indicate that any cortisol
effects may be stronger and more noticeable in
challenging times or during illness.
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- Nater and colleagues (2008) also found
hypo-cortisolism in a sample of CFS patients
suggesting that low cortisol levels result in
increased activation of the immune system
leading patients to feel fatigued. Data shows
that cortisol levels are linked to fatigue onset
(Kumari, et al., 2009; Adam, et al., 2006), and
a history of unexplained fatigue precedes the
development of CFS which implies a continuum
between fatigue in the healthy population and
fatigue-related illnesses (Kumari, et al.,
2009). Not all research has found predicative
ability in cortisol to future fatigue and some
have shown hypo-cortisolism to coincide with
better health (Kumari, et al., 2009). The
research on cortisol levels and fatigue are
vast; however, there is inconsistency in
findings. While most report cortisol alterations
as the initiating factor, a few report
alterations as likely to occur after symptom
onset. The type of alteration is also
controversial; Crofford and colleagues (2004)
found increased activity in fibromyalgia, while
patients with CFS showed low activity. They
suggested that elevated levels of cortisol could
be due to loss of resiliency of the
hypothalamic-pituitary-adrenal (HPA) axis, and
being unable to return to baseline after periods
of pre-longed stress.
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- Cortisol and stress
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- Researchers have used chronic stress to
explain hypo-cortisolism (Fries, et al., 2005),
with such patterns being indicative of pathology
or disease severity, predicting mortality in
clinical populations (Sephton, Kraemer, &
Spiegel, 2000). Out of 9 confounding factors in
a large scale cortisol study, stress, smoking,
early waking, and cardiovascular disease
medications showed a connection to cortisol
levels (Kumari, et al., 2009). Low cortisol
levels have been linked to an array of
disorders, many of which appear to be
stress-related (Clauw & Crofford, 2003).
This led to investigation into a possible common
physiological pathway for hypo-cortisolism
development emphasising alterations and reduced
responsiveness in HPA axis activity.
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- Clauw and Crofford (2003) found that
hypo-cortisolism can be caused by different
types of HPA axis alterations (although
alterations do not appear to be population
specific), with different alterations emerging
in patients within the same clinical population
(Fries, et al., 2005). Such changes can be due
to various dysfunctions: (1) reduced
biosynthesis in releasing hormones, as well as
decreased receptor stimulation; (2)
hyper-secretion of any secretagogue with
down-regulation of the target receptors; and (3)
glucocorticoids increased sensitivity to
negative feedback causing a decrease in free
cortisol and/or in cortisol resistance (Heim,
Ehlert, & Hellhammer, 2000).
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- It is well established that stressors
including infection, trauma and mental stress
result in HPA axis activation which serves to
produce cortisol. In response to stressful
stimuli the HPA axis leads to increases in
peripheral cortisol production. Cortisol helps
to provide energetic resources needed when faced
with stressors while also helping to modulate
and contain other physiological stress response
components; hence, the ability to affect
physiological changes encompassing most of the
main organ systems (Adam, & Kumari, 2009).
Short-term HPA activations are necessary for
efficient everyday functioning; however,
excessive or chronic activation has been
associated with detrimental health outcomes with
research implementing the HPA axis in the
development of a variety of both clinical and
sub-clinical conditions.
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- Hellhammer and Wade (1993) put forward a
developmental model for hypo-cortisolism based
on stress-related disorder patients and their
display of hypo-cortisolism symtomatolgy
including fatigue, pain and stress-sensitivity.
They explain hypo-cortisolism through stress
time course with a change from hyperto
hypo-cortisolism in the HPA axis activity.
Hence, during times of stress, our HPA activity
is hyper-reactive. Once the stress period
ceases, there is over-compensation and the
activity becomes attenuated and lower than
non-stressed individuals.
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- Numerous studies support such
over-adjustment explanations; for instance,
Houshyar and colleagues (2003) found rats
following a period of continued morphine use
displayed elevated levels of corticosterone
during withdrawal which was followed by a
continuous drop in levels. The authors also
found that administration of dexamethasone
suppressed the stress response indicating
increased pituitary glucocorticoid negative
feedback. Fries and colleagues (2005) concluded
that the primary mechanism behind
hypo-cortisolemic stress responses is enhanced
pituitary sensitivity to glucocorticoid negative
feedback as indicated by cortisol
super-suppression. Research indicates that
stress-related hypo-cortisolism is often
displayed alongside increased catecholamine
concentrations; and hypo-cortisolism may be due
to reduced inhibitory cortisol feedback on
catecholamine release resulting in
stress-related disorders (Fries, et al.,
2005).
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- Hormone glucocorticoid acts to regulate
cytokine production from the immune system as a
response to stress. In doing so, low cortisol
levels may result in an over-reactive immune
system in terms of inflammatory responses.
Suggestion is of a preliminarily nature due to
the uncertainty of the literature in this area
with some researchers gaining data that are not
consistent with the suggestion of a co-
relationship (Fries, et al., 2005).
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- Beneficial effects of hypo-cortisolism have
also been put forward. Hypo-cortisol conditions
have shown a significantly higher link to
underlying infections indicating increased
activity to prepare the immune system for
possible reoccurrence. Van Hoof, Cluydts, and De
Meirleir (2003) found fatigue symptomatology as
serving to promote subsequent recuperation
through energy conservation. Elderly
participants with hypo-cortisolaemia displayed a
lower allostatic load comparable to younger
participants despite reporting higher stress
levels (McEwen, 2000). The term allostatic load
was coined by McEwen and Stellar (McEwen, 2000)
and is defined as the physiological consequences
of chronic exposure to fluctuating or heightened
neural or neuroendocrine response that results
from repeated or chronic stress. As allostatic
load is indicative of increased mortality rates,
hypo-cortisolism acts as a protective mechanism
against high allostatic load. Such beneficial
effects serve as a possible reason as to why
cortisol alterations are common in an array of
disorders.
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- Many cortisol studies tend to be conducted
over short periods and some studies analyse
cortisol samples that have been gathered over a
single day, meaning that significant findings
may be situational rather than trait founded
(Hellhammer, et al., 2007); although with large
samples, large bias seems doubtful. Many studies
also regularly use self-report methodology and
as with any self-report measures, compliance
should be considered as a possible bias.
Participants may not always comply with research
instruction, such as at times to gather saliva
samples. The time that samples are taken is
crucial, as waking time rather than clock time,
has been found to make a difference between a
significant effect being obtained (Adam, &
Kumari, 2009). If taken incorrectly, it may
significantly skew data analyses and
interpretation. Self-report measures require
self-perception of individual health and
healthcare interventions meaning that fatigue,
as perceived by subjects, may not correspond to
fatigue as it exists in stress-related
illnesses.
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- Cortisol measures, such as those based on
average urinary measures have also come under
scrutiny (Seeman, et al., 2002), as opposed to
preferred methods based on the diurnal cortisol
rhythm. This view sees deviations from typical
diurnal cortisol rhythm as indicative of
environmental influences on the HPA axis and the
role of the HPA axis in disease processes (Adam,
& Kumari, 2009). In addition, cortisol
studies are often offered in the form of
epidemiological research. While typically
consisting of large sample sizes and benefiting
from covariate control and ascertaining
associations, even larger samples may be needed
to be sufficient for looking at naturally
occurring disease states within the population
(Adam, & Kumari, 2009).
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- Salivary cortisol recordings have been found
to produce more pronounced cortisol responses
than serum samples (Aardal-Eeiksson, Karlberg,
& HoIm, 1998). In addition, Jerjes and
colleagues (2006) suggest that 24-hour urinary
total cortisol metabolite (TCM) excretion may
provide a more reliable reading of cortisol
detection than urinary free cortisol (UFC) in 24
hour samples. However, in spite of this, a study
using UFC (Di Giorgio, et al., 2005) found
differences in cortisol activity between CFS
patients and controls whereas a study using TCM
found no differences (Jerjes, et al., 2006).
Such discrepancies highlight the importance of
different sampling measures and measures need to
be considered in relation to their sensitivity
in detecting cortisol alterations.
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- Stroke
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- The link between yawning and stroke patients
is becoming increasingly documented in case
reports of parakinesia brachialis oscitans, and
neurological pathways associated with yawning.
The possibility of a yawning centre located at
the lower brainstem being involved in the neural
substrate of yawning was hypothesised in a study
evaluating 5 brainstem stroke patients who
presented with frequent pathological yawning
(Cattaneo, et al., 2007). Excessive yawning was
found to be the first symptom displayed
following stroke which would persist for
anything from a few hours to a few days after
initial onset. All patients involved in this
study displayed gait ataxia which continued for
weeks. Some of the patients also displayed
symptoms such as hemiparesis, vertigo, nystagmus
and dysmetria. All patients displayed acute or
sub-acute ischemic lesions involving invariably
a paramedian region in the upper pons and
ponto-mesencephalic junction. This led to the
conclusion that patients displaying excessive
yawning and gait ataxia are associated with
lesions of the paramedian upper pons and
ponto-mesencephalic junction (Cataneo, et al.,
2007). While this suggests that excessive
yawning following brainstem lesions may be the
result of activation of a putative yawning
centre resulting from supra-nuclear control, the
exact mechanism of the yawning is unclear.
Importantly, this study suggests that
pathological yawning can be an early sign of
brain stem infarction (Thompson, 2010).
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- A further study (Singer, et al., 2007)
evidenced the hypothalamus, especially the
paraventricular nucleus (PVN), as playing a
pivotal role in yawning elicitation (Goessler,
et al., 2005; Argiolas, & Melis, 1998). This
may explain why lower brainstem ischemia can
lead to pathological yawning (Cattaneo, et al.,
2006; 2007) as neurons are sent from the PVN to
brainstem structures. Singer and colleagues
(2007) reported on seven patients who
experienced pathological yawning following acute
middle cerebral artery stroke. They determined
that excessive yawning can also be a result of
lesions in cortical or subcortical areas which
physiologically control diencephalic yawning
centres.
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- Findings suggest that the middle cerebral
artery (MCA) plays a part in the anatomical
structure of yawning which proves interesting as
the hypothalamus and brainstem are not supplied
by the MCA. Singer and colleagues (2007) suggest
that such findings could be due to MCA lesions
releasing the PVN from neocortical control
mechanisms, leading to PVN increased activity.
This possible explanation presumes existing
neocortical control mechanisms connected to the
PVN as well as making no suggestion as to
whether this phenomenon is a result of reduction
in the cortical structures inhibitory input or
due to an increase in excitatory input (Singer,
et al., 2007).
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- Temporal lobe epileptic seizures have also
led to excessive yawning (Muchnik, et al., 2003;
Yankovsky, Andermann, & Dubeau, 2006) and
attention is drawn to the vast amounts of
research that has linked neocortical areas to
the phenomenon of contagious yawning (Platek,
Mohamed, & Gallup, 2005; Schurmann, et al.,
2005). Cases of parakinesia brachialis oscitans
(PBO) have been documented for many years but
the term was created in 2005 by Walusinski
(2007). In a clinical case publication by
Walusinski and colleagues (2010), 6 case reports
of patients who had displayed PBO post-stroke
were reported. From their observations, they
attempt to delineate a pathophysiological
explanation for the occurrence of PBO
implicating two main locations: middle cerebral
artery (MCA) territory (lending support to the
the findings of Bladin and Berkovic, 1984), and
the pontomedullary region (supporting the
findings of (Louwerse, 1998, and also Topper,
Mull, and Nacimiento, 2003).
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- Following extensive brain imaging
evaluation, Walusinski and colleagues (2010)
concluded that PBO requires a lesion in the
internal capsule, in turn affecting an
inhibitory pathway which liberates certain
subcortical structures responsible for
coordinating yawn inspiration and quadrupedal
locomotion motor control (Walusinski, 2007).
Believing that the brain follows an
organisational structure (MacLean, 1985), with
each functional level gaining in complexity and
functionality, means that if any of these
structures are disrupted, as is the case in
certain stroke localisations, phylogenetically
primitive functions may become liberated that
are normally inhibited by a more sophisticated
structure (Lapresle, 1986). Topper, Mull, and
Nacimiento (2003) reported on 3 patients
following stroke and concluded that the raising
of the paralysed arm is the display of an
automatic motor pattern that is usually
inhibited in the presence of intact
corticobulbar fibres that when damaged, this
automatic motor pattern appears in a stereotyped
fashion. Displayed motions of this sort are only
present until voluntary limb movements are
restored.
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- Explanation for repetitive yawning often
witnessed in stroke patients supposes that
through yawning arousal, mechanisms are
stimulated that allows recovery movement in the
arm. Arousal stimulation occurs via activation
of the PVN of the hypothalamus, locus coeruleus
and reticular activating system (Walusinski,
2007). It is suggested that yawning is an
outward homeostatic mechanism triggered by
similar subcortical structures and regulated by
the same neurotransmitters that relate to body
temperature, breathing, locomotion and vigilance
(Walusinksi, 2007). Through the study of stroke
as well as bilateral anterior opercular syndrome
patients, a distinction between automatic and
voluntary pathways seem to be demonstrated.
While the patients suffer from facial/arm
paralysis and are unable to conduct any
voluntary acts of these parts, emotional
expression such as blinking, laughing and
physiological yawning remain possible as does
the movement of the extremities while yawning
(Walusinski, 2009).
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- Meenakshisundaram and colleagues (2010)
conducted an observational study of 75 stroke
patients to describe the associated movements of
hemiplegic limbs during yawning. They found that
80% of the patients displayed such movements. A
similar figure was found by Mulley (1982). The
authors explained limb movements as a result of
the movement of the diaphragm while yawning,
enabling the paralyzed arm to receive motor
stimulation from the lateral reticular nucleus
of the medulla which is involved in ventilation
and locomotion in animals (Meenakshisundaram, et
al., 2010). Important data is available showing
cases of pathological yawning prior to injury
which suggests that yawning may be an indicator
of underlying problems. A case report speculated
that a woman experiencing excessive spontaneous
yawning months prior to the development of a
bulbar/pseudobulbar palsy due to amyotrophic
lateral sclerosis, was caused by dysfunction of
the upper motor neurons losing their inhibitory
influence on the brainstem and lower motor
neurons (Williams, 2000). Cattaneo and
colleagues (2006) also reported on two case
studies of patients who suffered from brainstem
ischemia, both reporting cases of excessive
yawning prior to neurological symptoms becoming
apparent.
-
- An hypothesis has linked thermoregulation to
yawning, explaining the functionality of yawning
is to act as a cooling mechanism (Gallup, &
Gallup, 2008). If this is to be the case,
patients with central nervous system injury
(Dietrich, & Bramlett, 2007) and
brain-injured patients (Soukup, et al., 2002)
both display excessive brain temperature. Also
lesions within the central nervous system may
also develop in areas which affect
thermoregulatory control such as the
hypothalamus (Marino, 2009). Temperature
fluctuation is normally due to infection fever
and is a common finding in stroke patients;
20-40% will suffer from fever (Sung, Lee, &
Chu, 2009). Furthermore, it has been reported
that stroke can induce mild elevations in body
temperatures as well as animals showing
spontaneous increases in body temperature
following stroke. Sung, Lee, and Chu (2009)
found that stroke resulting in destruction of
the brainstem, directly and significantly
influences body temperature. This could be a
possibility as to why excessive yawning is
implicated as a symptom in stroke patients.
-
- During an ischaemic or haemorrhagic stroke,
deficits in vigilance occur that are accompanied
yawning episodes regardless of whether the
patient is conscious or not; although, in coma
states, yawning can be a serious prognostic sign
(Walusinski, 2009). The evidence suggests that
the occurrence of yawning during stroke
signifies cortical, subcortical circuitry and
brainstem damage. In ischaemic cases this
usually occurs with hemiplegia and normally
indicates pyramidal tract lesions while the
extrapyramidal pathways remain intact. Cases of
parakinesia brachialis oscitans are suggested to
be the course of cortical control disruption
resulting in connected neurological structures
retrieving their ancestral functions that would
otherwise have been inhibited by the cerebral
structures (Walusinski, 2009). Stroke studies
have possibly been the most useful in providing
both an explanation and the neurological
pathways of yawning; however, there still exists
ambiguity within the literature (Thompson,
2010).
-
- Multiple sclerosis
-
- it has been well documented that temperature
changes can have significant affects on multiple
sclerosis (MS) symptoms (Smith & McDonald,
1999; Redford, Kapoor, & Smith, 1997). An
estimated 60-80% of MS patients experience
temporary worsening of clinical signs and
neurological symptoms with heat exposure (Davis,
et al. 2010). While heat worsens, cooling can
improve negative symptoms. Sensitivity to
temperature can be extreme and very small
changes can have profound effects (Baker, 2011),
as little as 0.5?C can make a difference (Davis,
et al., 2010). Such effects are due to
temperature influences over sodium channels on
current necessary for depolarisation of the
axon; increases in temperature diminish the
depolarising current, decreases have the
opposite effect (Smith, & McDonald, 1999).
The hypothalamus has been linked to the neural
network of yawning and lesions particularly in
this area have been suggested as impairing the
homeostatic control of body temperature in
individuals with MS and may increase atypical
fluctuations in body temperature (Davis, et al.,
2010).
-
- Ample evidence exists relating yawning to
temperature change, with yawns occurring before,
after and during instances of abnormal
thermoregulation, heat stress, and hyperthermia
(Gallup, & Gallup, 2008). Also
pharmacological treatments are hypothermic for
mania, where brain temperature falls, and
thermogenic in depression, where brain
temperature rises. Such pharmacological
treatment has been found to suppress or induce
yawning respectively (Prasad, 2008). It is
suggested that yawning may serve as a
compensatory brain cooling mechanism when
regulatory mechanisms fail to operate favourably
helping to maintain optimal levels of mental
efficiency (Thompson, 2010). Likewise nasal
breathing, which pre-cools arterial blood to the
brain, and forehead cooling, has been shown to
block yawning (Gallup & Gallup, 2007).
Studies on animals have also shown yawning
incidences to rise as ambient temperature
rises.
-
- Repetitive yawning is associated with a
number of diseases linked with heat stress and
abnormal thermoregulation (Gallup & Gallup,
2008), including MS (Postert et al., 1996). As
well as thermoregulation dysfunction it is not
uncommon for MS patients to have impaired sweat
gland function (Davis et al., 2005) contributing
to increases in body temperature. Another
striking point is that MS patients report
worsening of symptoms during daytime heat whilst
experiencing symptom relief following external
cooling such as cold baths, head, neck and body
cooling through cold packs (Gallup, &
Gallup, 2007).
-
- Excessive yawning witnessed in MS patients
has also been explained in anatomical terms.
Postert and colleagues (1996) reported on a
multiple sclerosis patient who displayed
excessive yawning during an MS episode.
Following various testing it was concluded that
yawning has anatomical aspects putting forward
the suggestion that inflammatory affection of
the brain stem in MS patients may cause the
phenomenon of excessive yawning. They described
excessive yawning as a symptom of brain stem
localisation in multiple sclerosis. These
thermoregulation associations alongside frequent
yawning witnessed in MS patients support the
hypothesis of yawning as a cooling mechanism
(Gallup, & Gallup, 2008).
-
- As thermoregulatory dysfunction affects
sleep it is not surprising that sleep problems
are also a common symptom experienced by
multiple sclerosis patients (Gallup et al.,
2010b). A following suggestion is that yawning,
sleep and thermoregulation are connected and
indeed yawning and thermoregulation follow a
circadian pattern with particular regard to
prior and post sleep (Provine et al., 1987).
Findings suggest that excessive yawning may not
necessarily be related to sleep disorders but
rather may be indicative of thermoregulatory
dysfunction (Thompson, 2010).
-
- Fatigue is a symptom commonly seen in MS
patients and it can often be disabling (Bamer,
et al., 2008; Merlino, et al., 2009). According
to reports up to 90% of MS patients experience
fatigue (Brass, et al., 2010). Fatigue is
different to sleepiness in that there can be no
desire to sleep when laying down to rest and is
aggravated by thermal stress and humidity. It
normally occurs early in the morning and is
progressive through the day, often reported as
one of their worst symptoms (Brass, et al.,
2010).
-
- Excessive daytime sleepiness and fatigue can
easily be confused. Daytime sleepiness may be
the result of insufficient sleep or an
underlying sleep disorder. Chervin (2000) found
that 57% of obstructive sleep apnoea patients
reported problems of fatigue in spite of
objective evidence of sleepiness. Likewise, MS
patients with sleepiness would often complain of
fatigue (Kaynak, et al., 2006). This indicates
the importance of appropriate evaluation of MS
patients complaining of fatigue to ensure that
any possible sleep disorders are ruled out first
(Brass, et al., 2010).
-
- Due to such discrepancies, Mills and Young
(2007) attempted to define the term of fatigue
in MS patients. They found that all MS patients
reported fatigue which was associated with motor
paresis, inability to maintain mental function
in task completion and lack of
-
- desire to complete or partake in tasks, a
strong desire to rest (72% reported the need for
rest without sleep compared to 49% with sleep),
and daily occurrence normally following a
circadian rhythm. Also, the data gathered also
found 47.8% of patients reported excessive
yawning which did not just occur during episodes
of fatigue. Appearing to support the
thermoregulation hypothesis, patients reported
sweating when fatigued and heat was found to be
the most dominant contributing factor to fatigue
onset. However patients made a clear distinction
between humid heat which worsened fatigue as
opposed to dry heat encountered abroad which
could sometimes improve severity of symptoms
(Mill, & Young, 2007).
-
- Evidence for cortisol and
yawning
-
- While research on a direct link between
cortisol and yawning is scarce, some older
studies have examined the effects of
drug-induced or drug-inhibited yawning and
hormonal activation. Current studies acknowledge
and refer to such relationships but most of the
research found is based on animal samples and
dated predominately between the 50s and 90s. In
1964, a link between ACTH and the induction of
stretching-yawning behaviour was published
(Anias-Calderon, Verdugo-Diaz, &
Drucker-Colin, 2004), while a link between
dexamethasone and yawning behaviour in animals
has been suggested, concluding that dopaminergic
and cholinergic are distinctly altered by
dexamethasone in yawning behaviour (Hipolide, et
al., 1999).
-
- A study published in 2004 provides
compelling support for the Thompson (2011)
Cortisol Hypothesis. The authors found that
following adrenalectomy in rats both spontaneous
and apomorphine-induced yawning stopped while
treatment of dexamethasone reverted this effect
(Anias-Calderon, Verdugo-Diaz, &
Drucker-Colin, 2004). This was explained by the
fall in blood corticosterone levels that follow
adrenalectomy as well as the changes in
function, structure and glucocorticoid receptor
levels which in turn can affect activity of the
paraventricular nucleus, an important structure
involved in yawning behaviour (Anias-Calderon et
al, 2004).
-
- Furthermore, the paper provides support for
the reduction of corticosterone levels as a yawn
suppressor as dexamethasone treatment restored
yawning behaviour. Although this effect was dose
dependant with no effect gained for 1mg/kg
administration, all other doses of 5, 10 and
20mg/kg showed significant restoration in
yawning behaviour. The authors concluded that
the adrenal glands have an important role in
yawning frequency; while there are probably
several altering factors which may impact on
yawning, results still point to the important
role of adrenal glands and glucocorticoids in
the control of yawning (Anias-Calderon
Verdugo-Diaz, & Drucker-Colin, 2004).
-
-
- Conclusions
-
- Stress, fatigue and disorders
-
- Considerable evidence has been provided from
epidemiologic studies for a link between
traumatic events and fatigue symptomatology
(Asmundson, Wright, & Stein, 2004; Raphael,
Janal, & Nayak, 2004). The trauma of stroke
and MS in relation to diagnosis, the illness,
and change of lifestyle often lead to worsening
of symptoms and stress (Brown, et al., 2006;
Capes, et al., 2001). As an individuals response
to stress includes F-IPA axis activation in
seems reasonable to suggest that differing
cortisol levels may elicit propensity to yawn in
these patients which is particularly noticeable
in episodes of disease aggravation. Excessive
yawning is more common in episodes of MS and in
the acute stage of stroke, with yawning becoming
attenuated with remission possibly because of
diminishing cortisol levels as stress periods
weaken.
-
- A link between dysfunctional cortisol levels
and MS has been suggested due to
pro-inflammatory cytokines, which are increased
in MS patients, acting on the HPA axis leading
in turn to increased levels of cortisol (Mohr,
& Pelletier, 2006). A link between stressful
life events and worsening of MS symptoms has
been consistent with the degeneration of MS
evolving over time as does the development of
stress. Mohr and Pelletier (2006) suggest that
this intermittent progression over time for both
MS disease development and stress shows how the
two may be associated as they both have an
onset, a period of continual presence and a
resolution stage. Individuals with MS have
reported periods of stress that provoke attacks
or worsen their clinical state. Elevated
dopamine levels found in MS patients
(Barkhatova, et al., 1998) further illuminates
the involvement of stress mechanisms in MS
disease development. In accordance with these
findings, evidence showed psychological distress
to worsen MS fatigue (Mills, & Young, 2007).
Likewise, Wei & Lightman (1997) noted that
there was increased activation of the F-IPA axis
in inflammatory diseases perhaps acting as a
protective mechanism against an excessive immune
response. This shows how fatigue and stress
worsen MS symptoms as well as showing increased
levels of cortisol during such times; excessive
yawning is at its most apparent in these
patients during onset of
-
- symptoms. Hypoglycaemia in diabetics can
often display repeated yawning (Walusinski, et
al., 2010). The adrenal stress hormones,
adrenalin, and cortisol, are critically involved
(Plonk, Bivens, & Feldman, 1974). In fact,
most hypoglycaemic symptoms are caused not by
low blood sugar per se, but by an over-reaction
of adrenalin and cortisol discharge which make
up part of the body's defence system against
falling blood sugar levels (Plonk, et al.,
1974). ONeilI and colleagues (1991) found blood
glucose and cortisol levels to be linked
suggesting that hyperglycaemia in stroke
patients reflects changes in circulating levels
of stress hormones, particularly cortisol,
glucagon, and insulin (ONeilI et al., 1991).
However, not all researchers have found
differences in cortisol levels between clinical
and non-clinical populations (Jerjes, et al.,
2006). Stroke investigations have lead to
establishing increased cortisol levels and
failure of dexamethasone control over cortisol
suppression following acute stroke (Fassbender,
et al., 1994). Of high importance is the
damaging effects that increased cortisol
concentrations have been known to have on
functional outcome (Olsson, 1990). Research
looking at links between cortisol and fatigue
uncovered strong associations between cortisol,
smoking and alcohol intake, these factors were
found to be more powerful than the association
between fatigue and cortisol (Badrick,
Kirschbaum, & Kumari, 2007; Badrick, et al.,
2008). Smoking and drinking are well known risk
factors in stroke. This suggests that life-style
factors prior to stroke may affect cortisol
levels and increase the likelihood of future
strokes. Some stroke patients may already have
pre-existing higher levels of cortisol before
injury.
-
- Confusion and disorientation are commonly
experienced states in stroke patients and
hypercortisolism is commonly reported in
patients suffering from such states. These
states may be linked to influencing levels of
arousal which also serve to influence the
display of excessive yawning in patients. The
observed dissociation in rhythmicity between
ACTH and cortisol levels has been examined in
relation to the possible effect of cytokines on
HPA axis functions. Interleukin, a form of
cytokine, is of a higher plasma concentration
following stroke and is also responsible for
increases in cortisol release (Johansson, et
al., 1997; 2000).
-
- Cortisol levels have been associated with
stroke severity and short-term mortality
following stroke. The activity of the
natriuretic peptide (NP) system has also been
associated with poor outcome. Makikallio and
colleagues (2007) investigated the
interrelations of these two systems on the
effects of hormonal activation in the acute
phase following ischaemic stroke. They found
cortisol levels to be increased showing a
relationship with prognosis; the higher the
levels of cortisol recorded the poorer the
patient outcome. They concluded that the synergy
of increased levels of cortisol and NP system
activity were prognostically unfavourable
(Makikallio, et al., 2007). Furthermore yawning
has been evidenced as both a poor (Lehmann,
1979; Mulley 1982) and good prognostic indicator
(Braunwald, et al, 1987). Perhaps increased
cortisol levels indicate poor prognostic outcome
and these high levels may serve to elicit
yawning and following yawns, cortisol levels may
drop which may help improve prognostic
outcome.
-
- By interfering with neuroendocrine
disturbances we may be able to lessen both brain
damage and neuropsychiatric disturbance
(Johansson, et al., 1997) as hypercortisolism is
associated with cognitive impairment and later
depression in patients. It has been shown that
hypercortisolism impairs immune system function
and this may explain why it is often able to
predict functional outcome following stroke
(Johansson, et al., 1997). Cytokine antagonists
can directly or indirectly reduce cortisol
levels and therefore, perhaps reduce the extent
of brain damage (Johansson et al., 1997). If
cortisol is linked to yawning, yawning may serve
as a warning of underlying neurological problems
(Thompson, 2010). Through persisting release of
hormones, the disease course may be modulated
and disease development prevented or at least
delayed.
-
- Multiple sclerosis
-
- HPA axis hypo- and hyper-activity
alterations have also been displayed in people
suffering from fatigue and MS (Grasser, et al.,
1996). However, more consistent findings have
displayed a stronger trend towards
hyper-activity (Fassbender, et al., 1998;
Heesen, et al., 2002). These findings tend to
support those of animal studies in which higher
cortisol levels were present in animals exposed
to chronic inflammatory stress. Michelson and
colleagues (1994) also found significantly
higher levels of cortisol in MS patients when
compared to matched controls. Many studies have
found a link between MS and depression
(Ferini-Strambi, 2011); and depression and
anxiety were found to have a high positive
predictive value regarding fatigue
symptomatology in MS patients (Iriarte, Subira,
& De Castro, 2000). Both of these conditions
are established in their links with cortisol.
Such high fatigue prevalence in MS alongside
evidence of atypical cortisol levels provides
strong support for a possible link with
pathological yawning.
-
- Barkhatova and colleagues (1998) found
disturbances in neurotransmitter metabolism in
MS patients which they suggested may be directly
associated to the pathogenetic mechanisms of the
disease. Many investigators agree that the
neurotransmitters dopamine, acetylcholine,
serotoni n, gamma-aminobutyric acid and the
hormones oxytocin, adreno-corticotrophic hormone
(and others), as well as nitric oxide, may
modulate yawning (Singer, et al., 2007). Hence,
a multiform pathogenesis is suggested by some,
which may also influence and alter altered
cortisol activity (Michelson, et al., 1994; Wei,
& Lightman, 1997; Barkhatova, et al., 1998)
and excessive yawning (Singer, et al.,
2007).
-
- Studies have also looked at cytokine levels
which have been found to decrease cortisol
levels in healthy individuals (Lee, et al.,
2010). There is the possibility of
pro-inflammatory cytokines that have a strong
influence on the cortisol releasing hormone
(Fassbender, et al., 1994). These cytokines are
released in relapses of MS; increased cortisol
levels are also apparent during relapse which is
when yawn frequency is at its highest.
-
- Interestingly, the use of interferons (IFN)
to treat MS patients has been seen alongside
elevations in serum cortisol levels (Pende, et
al., 1990) which might suggest that the
therapeutic responses following treatment may
actually be a secondary effect due to elevation
of serum cortisol. However, some studies have
reported no significant increases in cortisol
levels following treatment (Reder, & Lowy,
1992).
-
- ACTH stimulates secretion of cortisol and
ACTH has been known to elicit yawning (together
with stretching behaviour) in animals (Lobo, et
al., 1990). Likewise, surges in ACTH and
cortisol levels before waking and at night are
in line with increases of human yawning
behaviour displayed at such times. Appealing
data is reported by Sandyk (1998) who found MS
patients to respond to pulsed electromagnetic
(alternating electrical current) treatment,
creating a surge of ACTH activity, with
uncontrollable bouts of yawning and
pandiculation which ceased after magnetic field
exposure was stopped. This is supported by
Gallup and Gallup (2008) who state that yawning
may actually help relieve MS symptoms, Sandyk
(1998) found that those patients displaying
yawning and pendiculation behaviour also
reported the most significant degree of symptom
improvement following treatment. These effects
noted by Sandyk (1998) of ACTH on yawning were
only found in female subjects. Altered ACTH
activity resulting in aberrant regulation of
cortisol further supports the possibility that
cortisol levels influences yawning.
-
- Neurotransmitters and neurology
-
- Dopaminergic receptors may be involved in
yawning as they are in Parkinson's disease and
schizophrenia (Corio, 1990; Armbruster, 2009).
It has been suggested that elevated levels of
cortisol may decrease serotonin levels leading
to depressive states (Dinan, 1994); and
treatment of selective serotonin reuptake
inhibitors (SSRI) have been well documented in
conjunction with the side-effects of excessive
yawning (Gutierrez-Alvarez, 2007). The effects
of acute SSRI administration has been seen in
healthy subjects through resulting HPA axis
stimulation and increases in salivary cortisol
levels (1-larmer, et al., 2003). Additional
links have been made between cortisol secretion
and SSRIs (Tucker, et al., 2004); and between
serotonin and excessive yawning (Sommet, et al.,
2007). Holmgren and colleagues (1992) considered
serotonin as a positive modulator that possibly
triggers the yawning response. Serotonin has
been reported in diminished states in MS
patients (Davidson, et al., 1977), and in stroke
patients (Gao, et al., 2008).
-
- Thermoregulation
-
- Heat stress has been accepted as causing
premature fatigue not only in MS patients but
also in healthy populations (Gilbert, et al.,
2004), while thermoregulatory dysfunction and
fatigue have been linked to excessive yawning
(Gallup, & Gallup, 2010a). Research on two
healthy individuals with excessive yawning found
that both reported their yawning episodes to
coincide with thermoregulatory factors (Gallup,
et al., 2010a). One noted a significant drop in
body temperature following the episodes while
both found that attacks were relieved and/or
postponed through cooling.
-
- Perhaps unsurprisingly, the endocrine system
has been found to be involved in many aspects of
thermoregulation (Gale, 1973). Hypothermic lambs
display low plasma cortisol while dexamethasone
treatment is shown to prevent hypothermic body
temperatures (Clarke, Heasman, & Symonds,
1998). The combined action of corticosteroids
and catecholamines appear to be involved in the
control of regulatory heat production in animal
studies (Werner, & Vens-Cappell, 1985).
However, it has also been found that cortisol
levels did not significantly alter during the
course of a 30 minute run in human subjects
despite body temperature rises (Kraemer, et al.,
1989).
-
- There is increasing evidence of yawning as
an indicator of thermoregulatory dysfunction;
and if thermoregulation is related to cortisol
levels, since yawn frequency increases during
times of heat stress, then cortisol levels and
yawning may indeed be linked. Circadian
rhythms
-
- Yawning occurs most frequently during the
first hour after waking and the last hour before
sleep. This is in line with body temperature
peaks, occurring in the evenings before sleep,
then cooling during sleep, curving again to a
rise just before waking. Both such rhythms are
in synergy showing increased yawning when body
temperature is highest in the morning and
evening (Gallup, et al., 2010b). However,
cortisol circadian rhythms peak after waking and
reach a lower point at night. Hence, there is a
discrepancy between increased and decreased
cortisol levels. Perhaps yawning is able to
influence cortisol levels in terms of regulating
cortisol in these circumstances. This would
support the suggestion that yawning may be an
indicator of underlying disease pathology as
research shows hyperactivity (Crofford, et al.,
2004; Di Giorgio, et al., 2005) and hypoactivity
(Tops, et al., 2006; Nater, et al., 2008) can be
linked to disease symptomatology. Suggestion
here is that yawning increases in frequency
during both these instances to attempt to
stabilise cortisol levels.
-
- New research
-
- it is clear that diurnal changes, yawning
and cortisol can be key elements in disease
onset and prognosis and are in need of further
investigation. The meaning and relevance of the
major elements of the diurnal cortisol rhythm
are still unclear (Adam, & Kumari, 2009).
Research regarding circadian patterns could also
aim to determine if cortisol and yawning rhythms
are still evident in the clinical population,
for example, in FMS and CFS patients. Assessment
involving more continuous measures of cortisol
levels may provide information that is of a more
broad relevance to health in the general
population.
-
- Findings from studies suggest that cortisol
treatment may convey protective and therapeutic
effects in some patient groups (Schuder, 2005)
and even provide symptom relief in other
clinical groups following yawning. Data may even
show that cortisol and yawning can serve as
useful diagnostic tool for identifying
thermoregulatory problems or underlying
disorders.
-
- New work is underway by Author 1 at the
Psychology Research Centre, Bournemouth
University, to determine if cortisol levels are
intimately linked with yawning episodes. It is
hoped that findings will support Thompsons
(2011) Cortisol Hypothesis both in healthy
groups as well as in diagnosed clinical
populations. Potentially, this link may provide
a useful indicator of underlying pathology and
the link between neurological disorders that
presently remains rather unclear.
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-
- Oxytocin
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