Neurological complications of
electroconvulsive therapy (ECT) include amnesia,
delirium, peripheral neuropathy, headaches, and
seizures (American Psychiatrie Association,
1978). We report a case of intractable
yawning that developed after a course of
ECT.
Case Report : Mrs. A., a 68-year-old
Caucasian woman with a 4-year history of
recurrent major depression, was admitted to our
unit when she discontinued her antidepressant
medications and subsequently decompensated. She
initially presented with a 3-week period of
progressive depression characterized by
insomnia, anorexia, a 13-pound weight loss,
anergia, psychomotor agitation, and refusal to
care for herself. The staff of the group home in
which she resided reported that the patient had
been grunting and sereaming loudly and had
expressed the fear that "helicopters were coming
to get her!" The patient also demonstrated
nihilistic delusions, reporting that she could
not swallow food or fluids because she "had lost
her stomach!" and because she was absolutely
"unable to urinate."
The patient had a history of two previous
depressive episodes. The first episode occurred
at the age of 35 years and lasted 18 months, and
the second one occurred at the age of 63 years
and lasted 1 year. Her history also revealed the
onset of an essential tremor at the age of 48
years, which had been treated with
beta-blockers. In the months preceding this
admission she had been maintained on a
combination of propranolol, trazodone, and
diazepam. Our initial diagnostic impressions
ineluded recurrent major depression with
melancholia and depressive delusions, possible
benzodiazepine withdrawal, and essential
tremor.
The patient was placed on a neuroleptic
regimen of thiothixene on her second hospital
day and the dose was subsequently increased to 5
mg orally t.i.d. On her sixth hospital day
trazodone was added at 25 mg b.i.d. with
gradually increasing increments. Within a week
of admission her appetite had improved such that
she was able to eat mûre than half of her
meals without outside assistance. During the
subsequent month, her vegetative signs further
improved but she remained pessimistic about
herself and the future. She continued to express
fears of leaving the hospital and complaining
that her clothes were just not clean enough,
even after they were freshly laundered. She was
afraid to visit with her family or to go for
walksoutside the hospital. By this time the
patient was maintained on a combination of
trazodone, 50 mg t.i.d., achieving a serum level
of 390 ng/mI (reference range, 800 to 1600 ng/
ml). The antidepressant was increased to 50 mg
q.i.d. to raise the subtherapeutic level. At
that dose she developed orthostatic hypotension,
which precluded any further dose increase.
Consultation was sought with colleagues and ECT
was arranged after having obtained the patient's
informed consent.
A month later the patient received a course
of eight modified ECT treatments. The MECTA
equipment was used at the following stimulus
parameters: frequency, 60 Hz; pulse width, 0.75;
stimulus duration, 1.5 seconds. EEG-monitored
seizures were successfully achieved with each
stimulus. When the first stimulus failed to
produce a seizure the second stimulus was
applied 3 minutes later.
After the first two treatments, the patient's
affect improved appreciably and she showed a new
optimism about the future. After the fourth
treatment, howver, progressive anterograde and
retrograde amnesia set in. Her antipsychotic
regimen of haloperidol was tapered and
discontinued at this point; she was clearly
nondelusional. After the eighth session she had
begun to yawn incessantly. In fact, her
mouth remained open for hours at a time. As
opposed to common yawning, the patient's yawning
was not accompanied by pandiculation (stretching
of the arms); instead she appeared like a person
who had lockjaw. The patient was unable to give
us a cogent explanation for this behavior. She
denied feeling tired or bored, but simply stated
that she "felt like yawning." During this period
the patient was often disoriented to time of day
and demonstrated word-finding difficulty. A
21-lead EEG was recorded with intentional
placement, bipolar, and referential recording.
Intermittent generalized delta slowing was
observed, suggesting of diffuse cortical or
subcortical dysfunction. The course of ECT was
interrupted. A week later her sensorium cleared,
her cognitive deficits receded and her yawning
behaviors subsequently subsided. She was
discharged froin the unit to return to her group
home 2 weeks later, much improved.
Discussion : this is a case in which
frequent yawning and global amnesia were caused
by a course of ECT. The onset of yawning
coincided with that of the acute confusional.
state induced by shock treatment and with the
withdrawal of antipsychotic medication. It
subsequently cleared up as the confusional state
resolved.
The act of yawning consists of a tonic
contraction of several muscle groups resulting
in a deep inspiration. It involves dilation of
the pharynx and depression of the tongue and the
lower j aw. The physiological effects of the
deep inspiration include an increase in the
venous return to the heart and the opening of
pulmonary alveoli, which may have closed during
a prolonged period of quiet breathing (Fleming,
1979).
Little is known of the etiology of yawning.
Boredom and drowsiness can provoke yawning. So
does the sight or sound of another yawn. This
remarkable contagiousness of yawning is well
known but has not been satisfactorily explained.
Yawning is a reflex action the pathways of which
reach no higher than the basal ganglia.
Occasionally, frequent yawning may be evidence
of organic brain disease. It may be an
epileptiform phenomenon or could occur as a
sequela of encephalitis in conjunction with
other associated disorders of respiration
(Cheyne Stokes respiration, hyperventilation).
Paroxysms of yawning may also be caused by
cerebral tumors (especially those located in the
posterior fossa), opiate withdrawal, and
hypothalamic disease (DeJong, 1979; Fleming,
1979).
The pathophysiology of the electroconvulsive
therapy amnestie syndrome remains to be defined.
It has been speculated that the electric shock
induces cerebrovascular constriction and hence
alters the permeability of the blood-brain
barrier (Essman, 1982). ECT has been known to
induce seizures, even status epilepticus (Weiner
et al., 1980). Both yawning and amnesia can
be produced by hypothalamic lesions. In this
patient both phenomena apparently developed
during a course of electroshock treatment and
later subsided days after the treatment was
terminated.
Whether yawning occurred as a consequence of
ECT induced brain changes or as a manifestation
of withdrawal emergent tardive dyskinesia is not
clear. Although yawning has not previously been
described as a possible adverse effect of ECT,
neither is it considered to be a manifestation
of neuroleptic induced dyskinesia. Further
exploration of the pathophysiology of ECT
amnestic syndromes may help define the
association if any does exist.
