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Central sleep apnea and arterial compression of the medulla.

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Central Sleep Apnea and
Arterial Comtxession
of the M e d i a
Masahito Miyazaki, MD, Toshiaki Hashimoto, MD,
Noriko Sakurama, MD, Tsutomu Yoshimoto, MD,
Masanobu Tayama, MD, and Yasuhiro Kuroda, MD
We report a 5-year-old with central sleep apnea associated with compression of the medulla oblongata by abnormal looping of the left vertebral artery. T h e magnetic resonance imaging findings raise the possibility
that compression of the respiratory center by an aberrant vertebral artery might cause central sleep apnea
Miyazaki M, Hashimoto T, Sakurama N, Yoshimoto T,
Tayama M, Kuroda Y . Central sleep apnea
and arterial compression of the medulla.
Ann Neurol 1991;29:564-565
Central sleep apnea (CSA) is a phenomenon in which
respiratory movement disappears transiently because
of dysfunction of the respiratory center [l}.The exact
mechanism of occurrence of CSA is disputed [2-4}.
From the Department of Pediatrics, School of Medicine, University
of Tokushima, Tokushima, Jdpan.
Received Oct 4, 1990, and in revised form Nov 26. Accepted for
publicacion Dec 12, 1990.
Address correspondence to Dr Miyazaki, Department of Pediatrics,
University of Tokushima, Kuramoto-cho, Tokushima 770, Japan.
Recently, we observed a 5-year-old boy with CSA and
compression of the medulla oblongata caused by abnormal looping of the left vertebral artery, as evidenced by magnetic resonance imaging (MRI).
Patient Report
The patient was born in 1983 after a full-term uncomplicated
delivery. H e had a febrile convulsion at the age of 3 years.
Otherwise, he was well until July 1989, when he developed
frequent episodes of sleep apnea, each lasting for 10 to 20
seconds. Neurological examination revealed intact cranial
nerve functions, but hyperreflexia in the left extremities, with
no pathological reflexes. Routine laboratory investigations,
blood gas analysis, and a computed tomographic (CT) examination revealed no abnormalities. An MRI examination revealed abnormal looping of the left vertebral artery compressing the ventral side of the medulla oblongata, with a
hypointensity on TI-, T2-, and proton density-weighted images (Fig A, B). Vertebral angiography demonstrated abnormal looping in the fourth segment of the left vertebral artery
(Fig C). The results of electroencephalography and multimodal evoked potential examinations, including auditory
brainstem responses, visual evoked potentials, and shortlatency somatosensory evoked potentials, were essentially
normal. Polysomnographic analysis revealed approximately
20 episodes, overnight, of CSA lasting 10 to 20 seconds in
any of the sleep stages. The C0,-loading test during sleep,
evaluating the response of the central chemoreceptor, was
normal. The patient's parent refused surgical treatment, and
he has been treated with oral and parenteral administration
of acetazolamide with no apparent benefit.
Discussion
CSA is a phenomenon in which respiratory movement
disappears transiently as a result of the dysfunction of
the respiratory center [11. Previous reports indicated
that lesions including medullary disorders, for example, Arnold-Chiari malformation [ S , 6), brainstem infarction [7], and Shy-Drager syndrome [ 8 ] , caused
CSA. The pathological lesions of CSA, however, are
now disputed. For instance, Duffin and H u n g [2} reported that dysfunction of the nucleus tractus solitarii
and the nucleus ambiguus caused CSA. Some reports
have indicated that dysfunction of the central chemoreceptor is o n e of the causes of CSA [ 3 , 41; however,
few systematic studies of MRI in CSA have been performed, except for some case reports 191. In our patient, MRI examination revealed that the left vertebral
artery was pressing o n the ventral side of the medulla
oblongata, the location of the central chemoreceptor
[ IOJ, and angiography confirmed abnormal looping of
the left vertebral artery at that site. CSA in ArnoldChiari malformation has been suggested to be due to
a vascular lesion like that in our patient. Papasozomenos and Roessmann [ 5 } reported that CSA in
Arnold-Chiari malformation resulted from direct
brainstem compression and ischemia produced by vas-
564 Copyright 0 1991 by the American Neurological Association
A
C
(A)Magnetic resonance image;proton density-weighted spin echo
sequence {repetition time {TR}lecho time {TE), 2,000 mseci30
msec), transaxial v i m . (Bj T1-weighted spin echo sequence (TRI
TE, 300 msecil4 msec), coronal v i m showing thud the left vertebral artery, which shows hypointensity (arrow), is pressing on
the ventralsid? of the medulla oblongata. (C) L& vertebralungiography; anteroposterior view showing looping in thefourth segment
of the lejit vertebral artevy (arrow).
References
B
cular stretching including the vertebral artery, on the
basis of autopsy findings. MRI and CT scanning, however, have never shown brainstem compression by the
vertebral artery in patients with Arnold-Chiari malformation {GI.
Our patient is the first to raise the possibility that
compression of the respiratory center by an aberrant
vertebral artery might be a cause of CSA.
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342-346
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Arnold-Chiari malformation. Neurology 1981;31:97-100
6. Dure LS, Percy AK, Cheek WR, Laurent JP. Chairi type I malformation in children. J Pediatr 1989;115:573-576
7. Askenasy IJM, Goldhammer 1. Sleep apnea as a feature of bulbar stroke. Stroke 1988;19:637-639
8. Lockwood AH. Shy-Drager syndrome with abnormal respirations and antidiuretic hormone release. Arch Neurol 197633:
292-295
9. Weese-Mayer DE, Brouillette RT, Naidich TP, et al. Magnetic
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eds. Physiology. St Louis: CV Mosby, 1988:624-635
Brief Communication: Miyazaki et al: MRI in Central Sleep Apnea
565
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