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11/17. Respiratory complications in patients with myelodysplasia and arnold-chiari malformation.

    Respiratory complications in four patients with myelodysplasia and the arnold-chiari malformation included abnormal control of breathing, upper-airway dysfunction, aspiration pneumonia, and cor pulmonale. Early and prolonged ventilatory support resulted in a favorable outcome in three of four patients.
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12/17. Multifactorial obstructive sleep apnea in a patient with Chiari malformation.

    We report a patient with severe obstructive sleep apnea (OSA) associated with a unique combination of syringobulbia-myelia, Chiari malformation type I (CM), absent hypoxic ventilatory drive, vocal cord paralysis, post-menopausal status, obesity, and acute respiratory failure necessitating mechanical ventilation. The remote onset of OSA five years after surgery underscores the need for long-term follow-up of patients with syringobulbia-myelia and CM and the importance of addressing multiple interacting neurologic, metabolic, and mechanical predispositions to sleep-disordered breathing.
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13/17. Laryngologic management of infants with the Chiari II syndrome.

    As a part of a prospective multi-disciplinary study, all children born with a Chiari II malformation within the Uppsala region during a 3-year period were evaluated for any difficulties in breathing or swallowing. The evaluation was repeated at regular intervals during their first 18 months. Direct laryngoscopies were performed using flexible fiberscopes. Four out of 22 children were found to have disturbed breathing. Among those, two suffered from central apnoeic spells as well as bilateral vocal fold motion impairment, one from apnoeic spells only and one from bilateral vocal fold motion impairment only. All four also had dysphagia with aspiration. Three of the children developed respiratory symptoms within the first 3 months and the symptoms of the fourth begun within the first 6 months. One infant with severe symptoms expired at the age of 3 months. The vocal fold paralysis, apnoeic spells and swallowing difficulties of another infant resolved following active neurosurgical management. The conclusion that laryngologic issues are prominent in the severe Chiari II syndrome was further supported by a review of four more cases managed in recent years. Laryngologic assessment in the neonatal period can help to raise the issue of early neurosurgical intervention as well as identify some of the infants who will need extensive habilitation. Screening of laryngeal function by means of flexible fiberoptic laryngoscopy is recommended.
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14/17. Respiratory function in infants with arnold-chiari malformation.

    The respiratory pattern of each of eight infants with arnold-chiari malformation was studied, employing an especially constructed nosepiece for the pneumotachograph. The apparatus was developed, using the principle that infants are nose breathers. Respiratory function was normal in seven infants and abnormal in one. The respiratory pattern of infants with ACM should be critically reviewed upon observing any changes in breathing.
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15/17. A case of Arnold-Chiari Type I malformation presenting with dysrhythmic breathing during sleep.

    A 43-year-old woman presented with dull headache, left tinnitus and dizziness. Neurological examination revealed down-beat gaze nystagmus, left tinnitus, positive Romberg sign, poor standing on the left foot, poor tandem gait, left spastic gait and positive pathological reflexes in the bilateral upper and lower extremities. Plain X-ray of the skull and cervical vertebrae demonstrated basilar impression and atlantoaxial fusion. magnetic resonance imaging of the brain and cervical spine showed cerebellar tonsil descent and syringomyelia located in the left side of the spine at the II-III vertebral level which communicated with the fourth ventricle. The patient was diagnosed as having cervical syringomyelia. Arnold-Chiari type I malformation and basilar impression. Preoperative polysomnography showed dysrhythmic breathing and bradypnea during sleep. Abnormal breathing improved after suboccipital decompression craniotomy and upper cervical laminectomy. It was suggested that dysrhythmic breathing was caused by a disorder of the medullary respiratory center. Herniation of the cerebellar tonsil and syringomyelia might have compressed the medulla.
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16/17. Chronic respiratory failure in a patient with type I arnold-chiari malformation (ACM1) and syringomyelia.

    We present the case of a young adult with type I arnold-chiari malformation (AMC1) and syringomyelia who developed central sleep apnoea and chronic respiratory failure, successfully treated with nocturnal noninvasive positive pressure ventilation ventilation (NIPPV). An extensive syringomyelic cavity (from bulbar to L4 segment) with severe impairment of the IX cranial nerve was documented and remains, although reduced, after the neurosurgical treatment. At baseline evaluation, the patient showed a moderate restrictive ventilatory defect, severe hypercapnic respiratory failure, abnormal control of breathing characterized by the absence of response to hypoxia and hypercapnia, and severe nocturnal central apnoeas. Nocturnal NIPPV was then started in the A/C mode with an improvement in blood gas values. Further evaluations were performed 10 and 18 months later. A progressive significant improvement of lung volumes, both in sitting and supine position, associated with a slight improvement of blood-gas values were observed. Nonetheless, the breathing pattern abnormalities persisted. Polysomnographic evaluation during mechanical ventilation showed a normalization of breathing pattern with arterial oxygen saturation (SaO2) > 90% throughout the night.
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17/17. Central sleep apnoea in arnold-chiari malformation: evidence of pathophysiological heterogeneity.

    We report on the case of two young patients with type I arnold-chiari malformation (ACM), as revealed by a central sleep apnoea (CSA) syndrome without any other neurological defect. Case 1 was a 14-yr-old male patient, who developed severe alveolar hypoventilation and needed long-term mechanical ventilation via a tracheostomy. Case 2 was a 39-yr-old male patient, who developed features suggestive of sleep apnoea and responded to nasal continuous positive airway pressure ventilation despite the central type of apnoeas. These two cases illustrate the different pathophysiological mechanisms involved in CSA, namely a blunted chemical drive (in hypercapnic patients) and an increased chemical drive, which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). Central sleep apnoea can be the initial manifestation of arnold-chiari malformation and can lead to a life-threatening condition.
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