Cases reported "Sleep Apnea Syndromes"

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1/23. Nonlinear multivariable modeling and analysis of sleep apnea time series.

    This paper investigates the modeling and analysis of physiological data recorded from a 49-year-old male and are composed of three time series: blood oxygen saturation, heart rate and respiration. In particular, it is desired to verify if the models estimated from data can distinguish between the dynamics underlying two different breathing patterns (normal breathing and apnea). The estimated models are nonlinear autoregressive, moving average with exogenous inputs (NARMAX) and the regressors used to compose such models are carefully chosen, among hundreds of candidates, by an automatic procedure. The results discussed in this paper suggest that the dynamics underlying the data are nonlinear and basically deterministic. Using estimated models it seems to be possible to quantify the stability of the fixed point in phase space reconstructed using the blood oxygen time series. This, as discussed, could be the basis of an algorithmic monitoring system.
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2/23. Unexpectedly severe sleep and respiratory pathology in patients with amyotrophic lateral sclerosis.

    Daytime fatigue and sleep disturbance are frequent complaints in patients with amyotrophic lateral sclerosis (ALS). However, polysomnographic data are sparse. Nocturnal respiratory insufficiency may occur despite nearly normal daytime pulmonary function. We describe the clinical presentation and polysomnographic findings in two patients with clinically and electrophysiologically confirmed ALS with minimal weakness but excessive daytime sleepiness. polysomnography in the first patient showed a respiratory disturbance index of 43.5, and profound oxygen desaturations to 62%. The second patient had prolonged periods of hypoventilation, with oxygen saturations oscillating between 86 and 83%. Both patients showed severe sleep maintenance insomnia with a sleep efficiency < 40% and frequent arousals while asleep. Application of continuous positive airway pressure (CPAP) restored normal nocturnal ventilation, blood oxygenation and sleep parameters in the first patient; compliance, however, was poor. The second patient was unable to tolerate CPAP. We conclude that ALS patients with excessive daytime sleepiness or insomnia should undergo polysomnography to adequately diagnose nocturnal respiratory insufficiency and sleep disturbance. compliance with treatment, however, may be poor.
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3/23. narcolepsy in the older adult: epidemiology, diagnosis and management.

    narcolepsy is a disorder of impaired expression of wakefulness and rapid-eye-movement (REM) sleep. This manifests as excessive daytime sleepiness and expression of individual physiological correlates of REM sleep that include cataplexy and sleep paralysis (REM sleep atonia intruding into wakefulness), impaired maintenance of REM sleep atonia (e.g. REM sleep behaviour disorder [RBD]), and dream imagery intruding into wakefulness (e.g. hypnagogic and hypnopompic hallucinations). Excessive sleepiness typically begins in the second or third decade followed by expression of auxiliary symptoms. Only cataplexy exhibits a high specificity for diagnosis of narcolepsy. While the natural history is poorly defined, narcolepsy appears to be lifelong but not progressive. Mild disease severity, misdiagnoses or long delays in cataplexy expression often cause long intervals between symptom onset, presentation and diagnosis. Only 15-30% of narcoleptic individuals are ever diagnosed or treated, and nearly half first present for diagnosis after the age of 40 years. attention to periodic leg movements (PLM), sleep apnoea and RBD is particularly important in the management of the older narcoleptic patient, in whom these conditions are more likely to occur. diagnosis requires nocturnal polysomnography (NPSG) followed by multiple sleep latency testing (MSLT). The NPSG of a narcoleptic patient may be totally normal, or demonstrate the patient has a short nocturnal REM sleep latency, exhibits unexplained arousals or PLM. The MSLT diagnostic criteria for narcolepsy include short sleep latencies (<8 minutes) and at least two naps with sleep-onset REM sleep. Treatment includes counselling as to the chronic nature of narcolepsy, the potential for developing further symptoms reflective of REM sleep dyscontrol, and the hazards associated with driving and operating machinery. Elderly narcoleptic patients, despite age-related decrements in sleep quality, are generally less sleepy and less likely to evidence REM sleep dyscontrol. Nonpharmacological management also includes maintenance of a strict wake-sleep schedule, good sleep hygiene, the benefits of afternoon naps and a programme of regular exercise. Thereafter, treatment is highly individualised, depending on the severity of daytime sleepiness, cataplexy and sleep disruption. Wake-promoting agents include the traditional psychostimulants. More recently, treatment with the 'activating' antidepressants and the novel wake-promoting agent modafinil has been advocated. cataplexy is especially responsive to antidepressants which enhance synaptic levels of noradrenaline (norepinephrine) and/or serotonin. Obstructive sleep apnoea and PLMs are more common in narcolepsy and should be suspected when previously well controlled older narcolepsy patients exhibit a worsening of symptoms. The discovery that narcolepsy/cataplexy results from the absence of neuroexcitatory properties of the hypothalamic hypocretin-peptidergic system will significantly advance understanding and treatment of the symptom complex in the future.
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4/23. Obstructive sleep apnea in arnold-chiari malformation treated with acetazolamide.

    We studied respiratory patterns and transcutaneous gas pressures in two infants with Arnold-Chiari type II malformation referred to us due to repeated episodes of stridor and cyanosis. During both active and quiet sleep, respiration was irregular and absent or inverse thoracic breathing movements and frequent decreases in oxygen saturation to below 80% were observed. When breathing air with 2% CO2 or when given acetazolamide 10 mg/kg, chest wall movements normalized and oxygenation increased to near normal levels. After three months of treatment with acetazolamide 20 mg/kg/24 h no further episodes of hypoventilation or hypoxemia were observed and further treatment could be discontinued. We conclude that stimulation of respiration by CO2 or by acetazolamide appears to recruit chest wall muscles and promote upper airway patency in arnold-chiari malformation. A treatment trial with acetazolamide seems justifiable in these infants when respiratory problems are present.
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5/23. "Near miss" death in obstructive sleep apnea: a critical care syndrome.

    OBJECTIVE: The objective of this study was to alert critical care physicians to the syndrome of obstructive sleep apnea with respiratory failure ("near miss" death) and to elucidate characteristics that might allow earlier recognition and treatment of such patients. DESIGN: We examined clinical and laboratory characteristics of eight patients with obstructive sleep apnea presenting to the ICU with respiratory failure. These characteristics were compared with those of eight stable apnea patients of similar severity but without a history of presentation with respiratory failure. SETTING: Medical ICU and pulmonary outpatient clinic at the Houston veterans Administration Medical Center, a teaching hospital affiliated with Baylor College of medicine. PATIENTS: Eight patients with obstructive sleep apnea who presented in, or developed, acute respiratory failure requiring tracheal intubation and mechanical ventilation were matched to eight stable obstructive sleep apnea outpatients from the chest clinic. MEASUREMENTS AND MAIN RESULTS: The records of these 16 patients were reviewed and multiple characteristics that might predict these obstructive sleep apnea patients prone to respiratory failure and death (called the "near miss" death group; n = 8) were examined. The mean age of the near miss group was 57 yrs. All eight patients presented with respiratory acidosis (mean pH 7.22), hypercarbia (mean PaCO2 82 torr [10.9 kPa]), and hypoxemia (mean PaO2 45 torr [6.0 kPa]). Six of the eight patients had concomitant chronic obstructive pulmonary disease as determined by clinical characteristics and spirometry. Predisposing factors included facial trauma, lower respiratory tract infections or bronchospasm, and use of pain medication. All but one of the near miss subjects had awake hypercarbia (mean PaCO2 49 torr [6.5 kPa]) and hypoxemia (mean PaO2 58 torr [7.7 kPa]) during periods of clinical stability while only two controls had concomitant chronic obstructive pulmonary disease and none had hypercarbia. The prevalence of a history of wheezing and prior hospitalization for "respiratory problems" were greater in the near miss group. Once cured of apnea, no patient presented with recurrence of respiratory failure in follow-up ranging from 6 to 80 months, and cor pulmonale recurred in only one patient during subsequent onset of central apneas. CONCLUSION: Patients with obstructive sleep apnea who have concomitant chronic obstructive pulmonary disease or hypercarbia and hypoxemia are more prone to develop severe respiratory failure and probable death than those patients with apnea alone. The current study shows that recurrent respiratory failure and presumably mortality from this acute complication can be reversed with effective treatment of the obstructive apnea.
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6/23. Obstructive sleep apnea presenting with nocturnal angina, heart failure, and near-miss sudden death.

    An obese woman with a one-year history of episodic nocturnal chest pain was admitted because of shock and pulmonary edema. A clinical diagnosis of acute myocardial infarction and cardiogenic shock was made. She was ventilated and successfully resuscitated. Subsequent investigations showed no evidence of cardiac dysfunction or coronary disease, but sleep study confirmed the diagnosis of obstructive sleep apnea syndrome (OSAS). We suggest that the nocturnal angina and heart failure in this patient might have resulted from extreme hypoxemia produced by OSAS. This case raised the possibility that the high cardiovascular mortality rate reported in OSAS might not necessarily relate to underlying coronary artery disease. Further investigations are required to delineate the true incidence of coronary disease in patients with OSAS.
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7/23. Drivers with untreated sleep apnea. A cause of death and serious injury.

    Three patients with untreated sleep apnea fell asleep while driving and caused serious automobile accidents. One person died, another became permanently paraplegic, and the three patients with sleep apnea were seriously injured in these crashes. This sequela of sleep apnea is not surprising, since subjects with sleep apnea may be poor drivers with a high accident rate and a high incidence of "near-miss" vehicular incidents. Because drivers with untreated sleep apnea may cause a large number of preventable automobile accidents, physicians have specific duties involving these drivers. First, physicians must try to identify impaired drivers with sleep apnea before they have an accident; routinely asking patients about loud snoring and hypersomnolence may help identify these impaired drivers. Second, physicians must consider the diagnosis of sleep apnea when examining patients who fall asleep while driving. Next, physicians must warn their patients with sleep apnea about the risks of driving with untreated sleep apnea. Finally, physicians must treat any seriously impaired driver with sleep apnea and keep these patients from driving until they can receive successful treatment.
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8/23. Ondine's curse in listeria monocytogenes brain stem encephalitis.

    A case of necrotizing brain stem encephalitis due to listeria monocytogenes is described in a 48-year-old man who had brain stem encephalitis of complicated course and with selective destruction of the vasomotoric and respiratory centers. He developed that very rare Ondine's curse syndrome, being only able to breathe when awake. The literature on Ondine's curse and brain stem encephalitis due to LM is reviewed. brain stem encephalitis has a mortality near 100%. The only treatment for Ondine's curse is lifelong artificial ventilation.
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9/23. 'Near miss' sudden infant death and obstructive apnoea.

    A 4 month old girl presented with a 'near miss' sudden infant death episode for which no cause was found. Obstructive sleep apnoea syndrome subsequently developed. All symptoms ceased after adenoidectomy at age 9 months.
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10/23. Five cases of near-miss sudden infant death syndrome and development of obstructive sleep apnea syndrome.

    Five full-term infants were referred for "near miss" sudden infant death syndrome events, which occurred between 3 and 12 weeks of age. After a complete pediatric evaluation and 24-hour polygraphic monitoring, each infant was monitored at home with a cardiorespiratory monitor. Each was followed regularly (with repeat polygraphic recordings) up to 4 years of age. All five infants developed heavy snoring at night and symptoms of obstructive sleep apnea syndrome. The diagnosis of obstructive sleep apnea syndrome was confirmed by polygraphic recordings; surgery was recommended. Four of the five children underwent adenoidectomies between 3 and 4 years of age, and this significantly improved their condition. These five cases are the first polygraphically documented histories of the development of obstructive sleep apnea syndrome.
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