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Yawning: its cycle, its role
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Fetal yawning assessed by 3D and 4D sonography
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8 octobre 2005
J Neurol
Neurosurg Psychiatry
2005;76:294
lexique
Ondine's curse during pregnancy
Ochoa-Sepulveda JJ, Ochoa-Amor JJ
Neurology, ''Hospital Universitario Reina Sofia'', Cordoba, Spain

Chat-logomini

We report a case of a 34 year old right handed woman seen at 29 weeks' gestation who suffered from apnoea of unknown aetiology. This pregnancy, as well as her first gestation, was complicated by generalised oedema and high blood pressure. Starting at week 25, her husband noticed she had developed intermittent brief periods of apnoea only while sleeping, which lasted as long as one minute but of variable duration. Her husband awakened her each time she had a protracted episode of apnoea. She was asymptomatic while awake. In the 29th week she suffered a more severe apnoea. She was intubated in the field and taken to the hospital for an emergency caesarean section. There was no spontaneous labour. Inability to breathe spontaneously persisted for two weeks postpartum and a neurological consultation was requested.
 
On initial evaluation blood pressure was 140/90 and the heart rate was 90 beats/min. The neurological examination revealed upbeat nystagmus of small amplitude in the primary position which did not change with upward or downward gaze. She had lack of spontaneous breathing. She was fully awake and cooperative, sitting up in bed with no assistance. While intubated she had an obvious cough reflex but the gag reflex was not formally tested. Tongue examination showed normal movement and power with no evidence of atrophy or fasciculation. Otherwise, cranial nerve and sensorimotor examinations were entirely normal. There was normal tone, with downgoing plantar reflexes and no evidence of other pyramidal findings. There was no record of arrhythmia.
 
No yawning, vomiting, or hiccups were present during the examination and they were not seen by nursing staff. It was of interest that this patient had suffered from apnoea presenting immediately after her first vaginal delivery two years previously. This was treated with intubation and resolved spontaneously with successful extubation approximately four hours later. Magnetic resonance imaging of the brain, brain stem, and cervical spinal cord was carried out, and showed a Chiari malformation with tonsillar herniation at C2 level and a cervical syrinx. After posterior cranial fossa decompression the patient recovered spontaneous breathing and was off any ventilatory support within six hours. She and her child have been followed for two years following this event. She remains in good health with normal polysomnographic testing.
 
COMMENT
Ondine's curse is a rare form of central respiratory failure which includes severe sleep apnoea (1). We describe the case of recurrent sleep apnoea associated with pregnancy and delivery and related to a Chiari malformation that became symptomatic only during pregnancy. We hypothesise that the generalised oedema that occurred during pregnancy, with a potentially mild increase in intracranial pressure, produced dysfunction of central chemoreceptors or the respiratory integrative system of the brain stem. Additionally there may have been compression of the lower cranial nerves, impairing input from peripheral chemoreceptors(2). Related to this, our patient suffered severe sequelae from a central malformation that was previously clinically inapparent.
 
Although Ondine's curse has rarely occasionally described in patients with Chiari malformation(3), the expression of secondary sleep apnoea uniquely during pregnancy has not been reported before. Finally we wish to highlight the complete recovery of this patient after posterior fossa decompression, as we found in another published case (4).
ondine
 
Correspondence to: Dr Juan Ochoa-Sepulveda;
jjos@telefonica.net
 
 
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Botelho RV, Bittencourt LR, Rotta JM, et al. Polysomnographic respiratory findings in patients with Arnold-Chiari type I malformation andbasilar invagination with or without syringomyelia: preliminary report of a series ofcases. Neurosurg Rev 2000;23:151Ð5.
Levitt P, Cohn MA. Sleep apnea and the Chiari Imalformation: case report. Neurosurgery 1988;23:508.
Gupta R, Oh U, Spessot A, et al. Resolution ofOndine's curse after suboccipital decompression in a 72-year-old woman. Neurology 2003;61
 
 
 
Respiratory control and behavior in humans: lessons from imaging and experiments of nature
Ravé Moss I.
The Canadian Journal of Neurological Sciences
2005; 32; 3; 287-297
 
Departments of Pediatrics and Physiology, McGill University and McGill University Health Centre Research Institute, Montreal Children's Hospital and, Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
 
Respiratory control
 
Abstract: The purpose of this review is to demonstrate that respiration is a complex behavior comprising both brainstem autonomic control and supramedullary influences, including volition. Whereas some fundamental mechanisms had to be established using animal models, this review focuses on clinical cases and physiological studies in humans to illustrate normal and abnormal respiratory behavior.
 
To summarize, central respiratory drive is generated in the rostroventrolateral medulla, and transmitted to both the upper airway and to the main and accessory respiratory muscles. Afferent feedback is provided from lung and muscle mechnoreceptors, peripheral carotid and aortic chemoreceptors, and multiple central chemoreceptors. Supramedullary regions, including cortex and subcortex, modulate or initiate breathing with volition, emotion and at the onset of exercise. Autonomic breathing control can be perturbed by brainstem pathology including space occupying lesions, compression, congenital central hypoventilation syndrome and sudden infant death syndrome. Sleep-wake states are important in regulating breathing.
 
Thus, respiratory control abnormalities are most often evident during sleep, or during transition from sleep to wakefulness. Previously undiagnosed structural brainstem pathology may be revealed by abnormal breathing during sleep. Ondine's curse and 'the locked-in syndrome' serve to distinguish brainstem from supramedullary regulatory mechanisms in humans: The former comprises loss of autonomic respiratory control and requires volitional breathing for survival, and the latter entails loss of corticospinal or corticobulbar tracts required for volitional breathing, but preserves autonomic respiratory control.
 
Résumé: Contrôle et comportement respiratoire chez l'humain : leçons tirées de l'imagerie et des expériences naturelles. Le but de cette revue est de démontrer que la respiration est un acte complexe impliquant un contrôle neuro-végétatif provenant du tronc cérébral et des influences supramédullaires, entre autres la volonté. Alors que les mécanismes fondamentaux ont dû être établis grâce à des modèles animaux, cette revue est axée sur des cas cliniques et des études physiologiques chez l'humain afin d'illustrer le comportement respiratoire normal et anormal.
 
En résumé, la stimulation respiratoire centrale origine de la moelle rostro-ventro-latérale et elle est transmise aux voies aériennes supérieures et aux muscles respiratoires principaux et accessoires. La rétroaction afférente provient de mécanorécepteurs pulmonaires et musculaires, de chémorécepteurs périphériques à la carotide et à l'aorte et de multiples chémorécepteurs centraux. Des régions supramédullaires corticales et sous-corticales jouent un rôle dans la modulation ou le déclenchement de la respiration par la volonté, l'émotion et en début d'exercice. Le contrôle neuro-végétatif de la respiration peut être perturbé par une pathologie du tronc cérébral, soit par une lésion expansive, une compression, le syndrome congénital d'hypoventilation alvéolaire central et le syndrome de la mort subite du nourrisson. Les états de sommeil et d'éveil sont importants dans la régulation de la respiration. Des anomalies du contrôle respiratoire sont plus souvent évidentes pendant le sommeil ou pendant la période de transition du sommeil à l'éveil. Une respiration anormale pendant le sommeil peut révéler une pathologie structurale du tronc cérébral encore non détectée.
 
Le syndrome d'Ondine et le syndrome de déefférentation motrice (locked-in syndrome) distinguent les mécanismes régulateurs du tronc cérébral des mécanismes supramédullaires chez l'humain: les premiers comportent une perte du contrôle respiratoire neuro-végétatif et la survie dépend alors de la respiration volontaire et les derniers impliquent la perte des voies corticospinales ou corticobulbaires nécessaires à la respiration volontaire, mais préservent le contrôle respiratoire neurovégétatif.
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