Case report : a 64 yaer old woman
with hypertension, ischemic heart disease, and
type II diabetes mellitus was admitted to stroke
unit with a 2 day history of occipital haedache,
dysarthria, and dysphagia. She had a 6-month
history of increasingly frequent paroxysms of
yawning. At the time of presentation, her
paroxysms were occurring nightly. Each paroxysm
consisted of 20 to 30 yawns in succession, which
she described as uncontrollable and socially
embarrassing. Tlhese paroxysms were followed by
a period of painful cramping sensations in the
pharynx and neck. The patient's dysarthria and
dysphagia had resolved by the time of her
admission and the neurologie examination was
normal; in particular there were no signs of a
pseudobulbar or bulbar palsy. A noncontrast CT
scan was normal. Serum electrolytes and oxygen
saturation were normal. The patient was assumed
to have had a brainstem ischemie stroke and she
was discharged on aspirin.
The frequency of her paroxysms of yawning
increased over the next 3 months, occurring up
to 7 te, 10 times each evening. Each bout
consisted of 20 to 30 yawns in succession
followed by painful cramping and a sensation of
choking. She began to gag as sbe tried to
swallow solids. Her paroxysms were suppressed by
thioridazine 10 mg twice daily.
Two months later the patient remained free
of paroxysms of yawning although she continued
to complain of dysphagia. Her troublesome
yawning recommenced when her thioridazine was
discontinued. She had evidence of a mixed bulbar
and pseudobulbar palsy clinically, although the
clinical examination was otherwise normal. Nerve
conduction studies and an electromyogram
revealed evidence of denervation in all
extremities and was thought to be consistent
with motor neuron disease. An MRI showed no
ischemic or other abnormality in the brainstem
or elsewhere. Her yawning became less evident as
her bulbar palsy progressed. She died of
pneumonia, presumably due to aspiration, 24
months after the onset of her yawning. A
postmortem was not obtained.
Discussion : Although yawning bas
been widely reported in vertebrates, its
physiologie role is unclear. It is usually
perceived as an act of inspiration often
associated with stretching. In fact, there is no
evidence that yawning is a response to oxygen or
carbon dioxide levels. It chiefly occurs during
transitions from wakefulness to sleep or sleep
to wakefulness. It increases arousal, as
assessed by skin conductance, and has a greater
cumulative effect than mouth opening or deep
breathing alone.
The pathways involved in yawning have not
been fully defined, although the diencephalon,
reticular formation, and midbrain are involved
in the characteristic slow involuntary gaping
movements of the mouth. In rodents, yawning is
initiated in the hypothalamus. Yawning may be
influenced by a number of neurotransmitters and
neuropeptides. It is facilitated by neurons in
the paraventricular nucleus of the hypothalamus
by oxytocin, excitatory amino acids, dopamine,
and dopaminergic agonists such as apomorphine,
and appears to require the action of both DI and
D2 receptors. Dopaminergic antagonists may
inhibit yawning as seen in the patient reported
here. The hypothalamus projects to bulbar and
spinal cord nuclei where the complex activity
associated with yawning is generated.
Yawning may be inhibited by mature humans.
The brainstem and spinal neurons involved must
be subject to cortical influences that can only
be expressed if the upper motor neuron pathways
are intact. Thus, inhibition may be lost in
pseudobulbar palsy. The ability to yawn will
disappear when there is significant disturbance
of the bulbar nuclei. That appeared to be the
sequence in the case described here. The current
case is interesting because of the unusual
prominence of yawning and the apparent lack of
any theoretical framework within which to
account for it. Yawning may be a frequently
overlooked clinical sign. Its occurrence may be
useful as a subtle sign of a pseudobulbar
palsy.
