We present the case of a 16-year-old girl who suffered from repeated episodes of collapse and loss of consciousness which could be provoked by undertaking a stretching manoeuvre comprising a combined breath hold and neck torsion. A review of the literature is provided on other cases of so-called &quot;stretch syncope&quot; which appears to be a rare form of reflex syncope affecting patients in adolescence

Andrew W Barritt

Bridget K Macdonald

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Case Report
Breakfast Time Blackouts
Andrew W. Barritt1 and Bridget K. MacDonald2
1 Hurstwood Park Neurosciences Centre, Haywards Heath, West Sussex RH16 4EX, UK
2Department of Neurology, St George’s Hospital, Tooting, London SW17 0QT, UK
Correspondence should be addressed to AndrewW. Barritt; awb@doctors.org.uk
Received 12 May 2014; Revised 6 September 2014; Accepted 8 September 2014; Published 18 September 2014
Academic Editor: Peter Berlit
Copyright © 2014 A. W. Barritt and B. K. MacDonald. This is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
We present the case of a 16-year-old girl who suffered from repeated episodes of collapse and loss of consciousness which could be
provoked by undertaking a stretching manoeuvre comprising a combined breath hold and neck torsion. A review of the literature
is provided on other cases of so-called “stretch syncope” which appears to be a rare form of reflex syncope affecting patients in
adolescence.
1. Case History
A 16-year-old female college student presented with episodes
of sudden onset collapse over the previous seven weeks
associatedwith a brief loss of consciousness lasting from three
to eight seconds. The attacks occurred soon after waking in
the morning and always from a standing position. Family
members described her appearance as pale throughout.
However, she was not seen to make additional rhythmic
movements, change her respiratory pattern, sweat noticeably,
bite her tongue or become incontinent. She would be rapidly
orientated afterwards but could not remember the period of
collapse itself. There was no significant past medical history,
including hypermobility syndrome, she was on no regular
medications, and none of her relatives had ever been affected.
General examination of the cardiovascular, respiratory, and
abdominal systems was normal, with a regular pulse at 80
beats perminute, supine blood pressure of 110/70mmHg, and
no postural drop after 3-minute standing. Routine blood tests
were normal including fasting blood glucose of 5mmol/L.
An electrocardiogram demonstrated normal sinus rhythm, a
urine dip was unremarkable, and a routine AP chest radio-
graph showed clear lung fields and a normal cardiac contour.
On closer questioning it became apparent that each episode
was preceded by a yawn-stretchmanoeuvrewhereby yawning
was simultaneously accompanied by flexion, abduction, and
external rotation of both arms, neck extension with lateral
rotation, and arching backwards of her trunk in a hyperlor-
dosis. Loss of consciousness would then ensue within three
to four seconds and the episode would proceed as above.
The phenomenon could thereby be reproduced voluntarily,
although a yawn without stretching was insufficient to elicit
her collapses.
2. Discussion
Syncope induced by stretching is a recognised, but rarely
reported, phenomenon in adolescents. To the authors’ knowl-
edge, there have been only thirteen other cases described in
the literature and, of these, the majority have been adolescent
males [1–5]. However, the precise pathophysiology is unclear
and both direct (vertebral) arterial compression [1, 2, 4] and
reflex mechanisms [3, 5] have been proposed.
A typical “stretch” which encompasses back hyperexten-
sion, shoulder abduction, and neck extension has long been
considered to include a straining phase against a closed glottis
(or Valsalva manoeuvre). Sharpey-Schafer recognised back
in 1965 that such posturing in “young males who leap out of
bed, stand on tiptoe, and stretch yawn” could provoke loss of
consciousness [6]. It is, however, worth noting the suggestion
that a yawn-stretch manoeuvre may not incorporate a typical
Valsalva strain owing to the relative predominance of the
slow maximal inspiration and expiration of the yawn [7].
Hindawi Publishing Corporation
Case Reports in Neurological Medicine
Volume 2014, Article ID 568983, 3 pages
http://dx.doi.org/10.1155/2014/568983
2 Case Reports in Neurological Medicine
Nevertheless, patients affected by syncope induced purely by
stretching, so-called stretch syncope in adolescence (SSA),
have described feelings of light-headedness, visual blur-
ring, occipital headache, depersonalization, and even déjà
vu precipitated within seconds by a stretch even without
yawning and preceding a frank loss of consciousness [1–4].
In some instances, these “presyncopal” symptoms have been
terminated and a collapse averted, by reassuming a forward
neck flexion [1, 4]. In addition, several patients have been seen
to have occasional muscle twitches affecting the head and
upper limbs either prior to or during the fall to the ground,
and one patient only ever suffered brief periods of altered
awareness rather than a frank loss of consciousness prompt-
ing prolonged, yet unsuccessful, treatment with antiepileptic
medication [3]. The case series by Pelekanos and colleagues
recognised that a Valsalva manoeuvre alone was insufficient
to induce the patients’ syncope, which has been corrobo-
rated in subsequent cases [1, 4, 5], and that simultaneous
hyperextended head posturing was required [2]. Indeed, it
was first hypothesised that this posturing caused warping
of the posterior cervical tissues and subsequent obstruction
to blood flow within the vertebral arteries, thereby causing
vertebrobasilar ischaemia.
Sturzenegger and colleagues reported two male cases
of SSA and used Doppler ultrasound over the temporal
bone “window” to monitor blood flow within their pos-
terior cerebral arteries (PCAs) during a selection of head
manoeuvres along with concurrent arm flexion and shoulder
hyperabduction.Only the combination of neck extension and
the outstretched arm posturing was seen to precipitate a sig-
nificant decreased flow of blood with presyncopal symptoms
being reported about 4 seconds later [4]. A transient reactive
hyperaemia was then seen roughly 15 seconds after returning
the head to a neutral forward position. Baseline imaging tests
on these patients, including brain and cervical spine MRI,
cervical radiographs, extracranial Doppler ultrasound, and
four vessel catheter angiogram, were normal. Attempts to
reproduce the stretching steps during the angiogram were
technically difficult and abandoned. Mazzuca and Thomas
[1] subsequently described a male case who complained of
either visual flashes or collapses preceded by stretching and
to whom they subjected the same combinations of head
and arm posturing mentioned above. He reported his visual
flashes within five seconds of neck hyperextension and arm
abduction/extension. Decreased blood flow within the PCAs
on transcranial Doppler was, similarly, demonstrated along
with the reactive hyperaemia and tachycardia 15 seconds after
reassuming a neutral head position. Electroencephalography
and electrocardiography were also performed during these
episodes: low amplitudeQRS complexes were seen during the
stretch, consistent with a Valsalva manoeuvre, and slowing
of the EEG rhythms into the theta range coincided with his
symptoms 5 seconds later. If loss of consciousness ensued,
then earlier and more marked slowing of the EEG into the
delta range was seen just two seconds after stretching, and
these patterns are consistent with the nonspecific delta/theta
slowing recorded elsewhere during tilt table-induced syn-
copal episodes [8] which likely reflect widespread cerebral
dysfunction.No comment ismade about the heart rate during
this time and intra-arterial blood pressure analysis was
not done. Again, baseline brain MRI, extracranial Doppler
ultrasound, ECG, EEG (waking and sleep), and tilt table
tests were all normal. Also normal was their response to a
carotid sinus massage which would suggest that the head
turning manoeuvre itself was not mechanically stimulating
a hypersensitive carotid baroreceptor. In any case, reduced
blood flow within the vertebrobasilar circulation alone in
young patients with normal intracranial vessels, otherwise,
should not necessarily precipitate a loss of consciousness and
implies a more global cerebral hypoperfusion.
The suggestion that SSA arose solely through a dysfunc-
tion of the posterior circulation was, therefore, challenged
following the publication of further cases in which EEG video
telemetry, intra-arterial blood pressure measurement, and
transcranial Doppler of middle cerebral artery (MCA) flow
were recorded in three patients [3]. Towards the end of a
stretch, but not an isolated Valsalva, sinus tachycardia was
repeatedly seen accompanied by a systemic hypotension and
MCA diastolic flow arrest. Two of the patients experienced
a complete loss of consciousness and the third a decreased
awareness, with the EEG simultaneously demonstrating gen-
eralised slow waves in each. Thus, it was proposed that
SSA is a unique form of reflex syncope with tachycardia
and systemic hypotension, as opposed to vasovagal syncope
and carotid sinus hypersensitivity where hypotension is
accompanied by bradycardia.
In summary, the true prevalence of stretch syncope is
unknown, but the adolescent preponderance of reported
cases might suggest that it is a phenomenon restricted
to the young. Patients may, therefore, present to general
practitioners, emergency departments, and both paediatric
and adult neurology services with their episodes of collapse.
Apart from one case where the blood pressure responses were
abnormal during a Valsalva manoeuvre (although remaining
insufficient to induce syncope on its own) [5], the battery
of neurological and cardiac investigations between attacks
are largely unremarkable [1, 3–5]. Distinction from temporal
seizures may be tricky if altered consciousness states arise,
as noted in one case above, but the “ictal” EEG showed no
epileptiform activity [3]. The key, as ever, is in the history
with each episode preceded, sometimes willfully, by an act
of stretching. Once our patient was advised to avoid the
provoking manoeuvre, her blackouts ceased.
Conflict of Interests
The authors declare that there is no conflict of interests
regarding the publication of this paper.
Authors’ Contribution
AndrewW. Barritt performed the literature search and review
of the literature and drafted the paper. Bridget MacDonald
directed the management of the clinical case and provided
critical appraisal of the paper for submission.
Case Reports in Neurological Medicine 3
References
[1] M. Mazzuca and P. Thomas, “Self-induced stretch syncope of
adolescence: a video-EEG documentation,” Epileptic Disorders,
vol. 9, no. 4, pp. 413–417, 2007.
[2] J. T. Pelekanos, J. M. Dooley, P. R. Camfield, and J. Finley,
“Stretch syncope in adolescence,” Neurology, vol. 40, no. 4, pp.
705–707, 1990.
[3] P. G. Sarrigiannis, M. Randall, R. H. Kandler, R. A. Grunewald,
K. Harkness, and M. Reuber, “Stretch syncope: reflex vasode-
pressor faints easily mistaken for epilepsy,” Epilepsy & Behavior,
vol. 20, no. 3, pp. 450–453, 2011.
[4] M. Sturzenegger, D. W. Newell, C. M. Douville, S. Byrd, K.
D. Schoonover, and S. C. Nicholls, “Transcranial Doppler and
angiographic findings in adolescent stretch syncope,” Journal of
Neurology Neurosurgery and Psychiatry, vol. 58, no. 3, pp. 367–
370, 1995.
[5] J. S. Yeom, Y. Kim, J. Y. Lim, H. O. Woo, and H.-S. Youn,
“Exaggerated valsalvamaneuvermay explain stretch syncope in
an adolescent,” Pediatric Neurology, vol. 45, no. 5, pp. 338–340,
2011.
[6] E. P. Sharpey-Schafer, “Effect of respiratory acts on the cir-
culation,” in Handbook of Physiology Section 2: Circulation,
W. F. Hamilton and P. Dow, Eds., pp. 1875–1886, American
Physiological Society, Washington, DC, USA, 1965.
[7] R. D. Thijs, J. G. Van Dijk, J. B. P. Stephenson, and W. Wieling,
“Mind-stretching faints,” Epileptic Disorders, vol. 9, no. 4, pp.
418–423, 2007.
[8] J. G. van Dijk, R. D. Thijs, E. van Zwet et al., “The semiology
of tilt-induced reflex syncope in relation to electroencephalo-
graphic changes,” Brain, vol. 137, no. 2, pp. 576–585, 2014.
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Case Report Breakfast Time Blackouts

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Case Report Breakfast Time Blackouts

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