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SHORT REPORT

Pathological yawning as a presenting symptom of
brain stem ischaemia in two patients
L Cattaneo, L Cucurachi, E Chierici, G Pavesi
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See Editorial Commentary, p 3

J Neurol Neurosurg Psychiatry 2006;77:98–100. doi: 10.1136/jnnp.2005.075267

Two cases of brain stem stroke involving the upper pons and
the ponto-mesencephalic junction presented with transient
excessive pathological yawning, associated with gait ataxia
and in one subject with upper limb and facial hemiparesis. A
causal relation is hypothesised between the brain stem lesion
and pathological yawning, possibly related to denervation
hypersensitivity of a putative brain stem yawn centre.
Excessive yawning may herald brain stem ischaemia.

Y

awning is a very common and phylogenetically ancient
behavioural event that occurs in vertebrates under
different conditions. A yawn consists of a stereotyped
behavioural pattern that begins with an inspiration associated with marked dilatation of the pharynx. At the peak of
inspiration there are associated facial movements and the
final part of yawning is passive rapid expiration. During
yawning a coordinated sequence of events takes place
involving facial, oropharyngeal, tongue, and respiratory
muscles, associated with activity in the axial extensor and
limb extensor muscles and with autonomic changes characterised by an increased parasympathetic outflow.1 The
physiological stimuli that give rise to the yawning response
and its functional significance are not clear. It has been
shown that yawning frequency is not modified by hypercapnia or by pure oxygen breathing; it does not seem, therefore,
to have a straightforward respiratory function.2 Yawning
occurs preferentially in conditions of low vigilance and causes
transient increases in arousal as indicated by EEG desynchronisation, though an active role in the maintenance of
arousal has not been demonstrated. The social importance of
yawning is particularly evident in mammals, where it seems
to have a communicative role in conditions of decreased
vigilance.2 The neural structures that control yawning are
presumably located in the brain stem near to or within other
respiratory and vasomotor centres, especially those that
control facial mimicry, mastication, throat movements,
respiration, and possibly stretching.3 Excessive or pathological yawning is defined as a compulsive, repetitive action that
is not triggered by appropriate stimuli such as fatigue or
boredom. We describe here two cases of excessive yawning
behaviour associated with ischaemic lesions in the brain
stem.

CASE REPORTS
Patient 1
A 74 year old man was admitted to our clinic complaining of
unsteadiness of stance and gait, lasting for 12 hours. The
patient described an acute onset of excessive, repetitive,
compulsive yawning that he was unable to control; the
yawns were repeated at a frequency of about 3/minute. Forty
minutes later the patient also noticed gait ataxia and inability
to stand without assistance. When admitted to the hospital,

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neurological examination showed a slight intention tremor of
the left arm and slight dysmetria in the finger–nose
manoeuvre; no limb weakness was present and tendon
reflexes were normal. The patient was able to stand and walk
but gait was possible only with broad based, irregular steps
and leftward veering. The cranial nerves were unaffected and
nystagmus was not present. His state of vigilance remained
normal. He reported abnormally frequent yawning for three
days following the acute onset, with progressively longer
intervals between one yawning act and the next. Three days
later, neurological examination was normal and all symptoms had disappeared.
Magnetic resonance imaging (MRI), done three days after
the onset of the neurological deficit, showed a small
hyperintense lesion in the left paramedian region of the
middle pons on fluid attenuated inversion recovery (FLAIR)
images (fig 1, left panel). The lesion was also evident as an
area of hyperintense signal in T2 weighted images. At a three
months follow up the patient was free of all symptoms.
Patient 2
A 66 year old woman presented with the acute onset of
imbalance of stance and gait, followed two hours later by a
single episode of vomiting and by weakness of the left upper
limb. She reported an episode of unjustified excessive
yawning, at a frequency of approximately one event every
two minutes, which began 20 to 30 minutes before the
neurological symptoms. On admission to hospital, clinical
examination showed a slight left lower facial paresis,
horizontal nystagmus beating leftwards, and a right sided
internuclear ophthalmoplegia. A pronator drift in antigravity
posture and clumsiness in distal finger movements were
observed in the left upper limb. Slight proximal weakness was
present in the left lower limb as well. Tendon reflexes were
normally elicitable in the four limbs. An extensor plantar
response was present on the left side. Finger–nose and
reaching manoeuvres showed slight dysmetria on the right
and could not be evaluated on the left because of the motor
deficit. No sensory deficit could be observed in the trigeminal
or the somatic territory. The patient had a broad based gait and
a marked left lateropulsion on standing. Vigilance was normal.
MRI done five days after the onset of symptoms showed right
pontine ischaemia (fig 1, right panel) and MRI-angiography
showed a pseudo-occlusive stenosis of the basilar artery. The
frequency of yawning gradually decreased and returned to
normal within 36 hours. The motor deficit on the left side and
the gait ataxia was still present, though moderately improved,
at three weeks after symptom onset.

DISCUSSION
We describe here, for the first time, patients with brain stem
ischaemic stroke presenting with excessive yawning. The
possible causal relation between the brain stem lesion and
Abbreviation: FLAIR, fluid attenuated inversion recovery

Yawning in brain stem stroke

99

Figure 1 Fluid attenuated inversion recovery (FLAIR) brain images of the two patients. (A) Patient 1: axial section showing a small hyperintense left
paramedian area at the ponto-mesencephalic border. The scan was acquired at three days after the onset of symptoms. (B) Patient 2: coronal section,
showing the ischaemic area in the right paramedian pons and ponto-mesencephalic border. The scan was acquired five days after the onset of
symptoms.

the excessive yawning behaviour could provide useful
information on the anatomical location of the neural systems
controlling yawning in humans.
The central anatomical pathways subserving yawning have
not been clearly defined.4 The published evidence indicates
the presence in mammals of a subcortical circuit mediating
the yawning phenomenon, involving the hypothalamus, the
midbrain, and the reticular formation of the pons and
medulla.2–4 In the rat experimentally induced excessive
yawning behaviour can be produced by direct or indirect
activation of the oxytocinergic neurones in the paraventricular hypothalamic nucleus, which is thought to play a
primary role in initiating the yawning phenomenon. The
activity of hypothalamic yawning related neurones is subject
to a complex pharmacological control, being enhanced by
dopamine D2 and possibly D3 agonists, nitric oxide,
acetylcholine, and ACTH–MSH peptides, orexins, and serotonin and downregulated by opioids.5 Similar pharmacological mechanisms may act in humans, where D2 agonists,
SSRI agents, and withdrawal from morphine exert a
facilitatory effect on the yawning behaviour. Valproate
overdose, imipramine, and oestrogen substitution may also
cause pathological excessive yawning.5
The existence in humans of a similar putative yawning
centre in the lower brain stem is suggested by lesional data.
Three reports6–8 have described patients with locked-in
syndrome, with preserved yawning movements and complete
volitional paralysis of the bulbar musculature. It has also
been observed that yawning movements persist in anencephalic infants.2 Up to now the existence of a cortical
representation of yawning has not been clearly demonstrated, though a recent brain imaging study showed the
presence of an area in the posterior cingulated cortex that is
activated by observation of yawning and is supposed to be
involved in the well known phenomenon of contagious
yawning.9
In both of our cases there was excessive yawning behaviour
associated with a brain stem infarct. The lesion was located in

the paramedian region in the ponto-mesencephalic junction
in both cases, though the lesion in patient 2 extended much
more caudally, involving also the upper half of the pons (fig 1,
right panel). The clinical picture was characterised by gait
ataxia in both patients, which is known to occur frequently in
paramedian mesencephalic and pontine infarction.10 11 A
motor deficit was present only in patient 2, because of the
anterior extension of the lesion. Focal brain stem lesions have
already been found to cause pathological yawning. Jurko and
Andy12 reported excessive yawning during hyperventilation in
patients who had previously undergone thalamotomy or with
recent head trauma, and concluded that it can be a sign of
brain stem damage. In neither of our patients did there
appear to be a facilitatory effect of hyperventilation. Arai et
al13 reported excessive yawning in a patient with a tumour of
the floor of the fourth ventricle, and Postert et al described
excessive yawning as a symptom of brain stem localisation of
multiple sclerosis.14 Additionally, excessive yawning has been
observed in progressive supranuclear palsy, intracranial
hypertension, and temporal lobe epilepsy, though in the
latter it was not assigned specific value in the localisation of
the epileptic focus.15 16
The exact mechanism of excessive yawning following focal
brain lesions is not fully understood. Possibly the pathological behaviour is an expression of liberation from the control
of more cranial structures of a putative yawning centre,
caudal to the lesion, analogously to the hypothesis postulated
for hiccups caused by medullary lesions,17 or for the symptom
of excessive yawning behaviour in patients with amyotrophic
lateral sclerosis.18 In our two patients we hypothesise also
that the pathogenesis of the excessive yawning could be
related to a denervation hypersensitivity mechanism. To our
knowledge, this is the first report of excessive yawning after
brain stem stroke and, more importantly, in both patients
yawning appeared to be the first symptom of the ischaemic
insult. We conclude that excessive yawning can be a
presenting symptom of an acute brain stem lesion and
should not be overlooked.

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Authors’ affiliations

L Cattaneo, L Cucurachi, E Chierici, G Pavesi, Sezione di Neurologia,
Dipartimento di Neuroscienze, Università degli Studi di Parma, Parma,
Italy
Competing interests: none declared
Correspondence to: Dr Luigi Cattaneo, Sezione di Neurologia,
Dipartimento di Neuroscienze, Università di Parma, Via Gramsci 14,
43100 Parma, Italy; luigi.cattaneo@nemo.unipr.it
Received 1 July 2005
In revised form 11 August 2005
Accepted 11 August 2005
Published Online First 20 September 2005

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