http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00300/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w41-2014
Andrew C. Gallup*
- Psychology Department, State University of New York at Oneonta, Oneonta, NY, USA
A commentary on
Insular and caudate lesions release abnormal yawning in stroke patients
Insular and caudate lesions release abnormal yawning in stroke patients
by Krestel, H., Weisstanner, C., Hess, C.
W., Bassetti, C. L., Nirkko, A., and Wiest, R. (2013). Brain Struct.
Funct. doi: 10.1007/s00429-013-0684-6. [Epub ahead of print].
Krestel et al. (2013)
recently investigated the potential contributing factors associated
with abnormal yawning (defined as ≥3 yawns/15 min) in 10 patients with
acute anterior circulation stroke. Though frequent yawning had
previously been observed in stroke patients (Cattaneo et al., 2006; Singer et al., 2007),
this study attempted to assess the influence of specific physiologic
and lesion topographic variables contributing to this association. All
patient parameters were taken within 1 h after admission and emergency
nurses recorded a single axillary body temperature with a digital
thermometer (Krestel, personal communication). Using MRI lesion maps,
and reportedly finding no associations between various physiologic
measures, including blood oxygen saturation, glucose, body temperature,
blood pressure, and heart rate, the authors concluded that ischemic
lesions in the posterior insula and caudate nucleus might facilitate
high frequency yawning in stroke patients. While this report improves
our neurological understanding regarding the association between
frequent yawning in stroke patients, limitations in the analysis and
interplay of temperature need to be addressed.
Yawning is characterized by a powerful gaping of the jaw
with inspiration, a brief period of peak muscle contraction, and a
passive closure of the jaw with shorter expiration (Barbizet, 1958).
The localized circulatory changes resulting from this action pattern
have led researchers to hypothesize that yawns may function to cool the
brain (Gallup and Gallup, 2007). For example, yawns produce increases in blood flow to the skull and enhanced venous return (Bhangoo, 1974),
while the deep inhalation during yawning can modify the temperature of
venous blood draining from the nasal and oral orifices into the
cavernous sinus, which surrounds the internal carotid artery (Zenker and Kubik, 1996).
Together, these processes act like a radiator removing hyperthermic
blood from brain while introducing cooler arterial blood to the brain.
Moreover, the flexing of the musculature during yawning may encourage
the evaporation of the sinus mucosa (see Gallup and Hack, 2011).
Research supporting the brain cooling hypothesis has accumulated over
the past 5 years, including evidence for predicted brain and body
temperature fluctuations surrounding yawning events, indirect
manipulations of brain temperature causing a reduction in yawn
frequency, and an altered expression of yawning which appears to be
driven by ambient temperature manipulation/variation (reviewed by Gallup and Eldakar, 2013).
For example, by directly monitoring continuous changes in prelimbic
cortex temperature of rats it was shown that yawning is preceded by
intermittent and rapid increases in brain temperature (i.e.,
~0.1°C/min), and that following the completion of a yawn the slope of
the temperature change reverses and quickly returns to baseline (Shoup-Knox et al., 2010).
While the breadth of physiologic measures taken by Krestel et al. (2013)
is laudable, a single measure of axillary temperature taken long after
the onset of the yawning episode is inadequate for assessing this
relationship. Since distinct brain temperature changes in rats occur
before and after single yawns on a rather short temporal scale; i.e.,
60–90 s (Shoup-Knox et al., 2010), and isolated bouts of excessive yawning in humans have been shown to reduce skull temperature by as much as 0.4°C (Gallup and Gallup, 2010),
it remains possible that the pathological yawning experienced by these
patients was accompanied by recurrent changes in temperature that were
never recorded. Furthermore, temperature measures taken from the skull
(e.g., oral, tympanic, forehead) would be more informative since the
motor pattern of yawning and the associated circulatory changes are
localized to this area. That said, even these measurements could miss
important temperature fluctuations confined to particular brain regions.
The use of MRI lesion maps to establish a relationship
between ischemic lesions in the posterior insula and caudate nucleus and
the duration of abnormal yawning is certainly of great importance (Krestel et al., 2013).
At this point, however, it is premature to declare that there was “no
evidence of other potential causes” related to abnormal yawning in these
patients. To the contrary, frequent or abnormal yawning in stroke
patients may be a consequence of thermoregulatory dysfunction associated
with the brain injury (Gallup and Gallup, 2008).
Given the close temporal association between yawning and changes in
brain/skull temperature, future research monitoring patients with
abnormal or excessive yawning bouts should take continuous temperature
measures from areas proximate to the cranium in order to properly assess
this relationship.
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