The clinical symptoms of progressive
supranuclear palsy (PSP) characteristically
include abnormal gait and posture, axial
rigidity, and supranuclear gaze palsy.
Pathologically, there is widespread neuronal
cell loss in the brainstem and diencephalon that
does not follow the pathways of any single
recognized neurotransmitter (Steele et al.,
1964).
Early diagnosis of PSP may be intriguing, and
of 415 patients with a possible diagnosis of
Parkinson disease, only 3.9% met the criteria
for PSP (Jackson et al., 1983). In contrast to
Parkinson's disease, tremor is an uncommon
feature of PSP, but falling, postural
instability, visual disturbances, an axial
rigidity dominate the early course of the
disease (Jackson et al., 1983). I have recently
encountered 5 patients aged 58-70 yeais with
classical symptoms and signs of PSP (Jackson et
al., 1983) who experienced an unexplained
excessive yawning at the onset of the
disease. In all patients excessive yawning
occurred predominantly during the day at a
frequency of 1-3 yawning attacks/min., which
produced severe social embarassment. In 3
patients, yawning subsided with administration
of Sinemet or bromocriptine, while 2 other
patients noted marked reductions in the
frequency of yawning with the initiation of
anti-Parkinson medication.
The ubiquitous and apparently nonsignificant
nature of the act of yawning might have
contributed to the relative lack of attention
given by physiologists to this behavioral
phenomenon. The physiological significance of
yawning and the central nervous mechanisms
triggering and coordinating its various
components remain unclear (Urba-Holmgren et al.,
1977). Frequent yawning has been mentioned as a
symptom in some diseases of the CNS, including
frontal lobe tumors and encephalitis (Brock
& Krieger, 1963). Excessive yawning was also
reported with administration of sodium valproate
in a patient with postanoxic action myoclonus
(Rollinson et al., 1979).
A stretching and yawning syndrome bas been
observed in cats, dogs, and monkeys after
intracisternal or intraventricular injections of
ACTH and/or MSH (Ferrari et al 1963). Both
cholinergic and dopaminergic antagonists were
reported to inhibit MSH-induced yawning in
animals (Yamada & Furukawa, 1981).
On the other hand, cholineigic agonists have
been reported to induce yawning in infant and
adult rats (Holmgren & Urba-Holmgren,.
1980). In another study, small doses of dopamine
agonists (eg.apomorphine) produced recurrent
episodes of yawning in rats (Mogilnicka &
Klimek. 1977). The latter was blocked by
administration of neuroleptics. Dopamine agonist
used at higher doses failed to produce yawning,
suggestive that only slight dopaminergic
stimulation is necessary. The study by Yamada
and Fukurowa (1980) suggested that both
dopaminergic inhibition and cholinergic
activation are concomitantly involved in the
mechanism of yawning in rats.
In our PSP patients, excessive yawning was
reduced or abolished by administration of
dopaminergic drugs supporting a central role for
dopaminergic dysfunction in triggering excessive
yawning in our patients. Excessive yawning has
not been, to my knowledge previously reported to
occur as an early symptom in PSP. Since,
however, the yawning reflex involves a complex
reflex brainstem arc (Brock & Krieger,
1963), the presence of excessive yawning in PSP
indicate deranged brainstem functions involving
dopaminergic and cholinergic mechanisms.
