Pathological Yawing

Yawning 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,

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

See Editorial Commentary, p 3

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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

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