State of the art. Sleep and control of breathing.
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Biomedical subjects
Publications and source records attributed to C Guilleminault.
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Twenty narcoleptic patients and ten age-matched normals were polygraphically monitored for 58 consecutive hours. All subjects were on regimented sleep (hours between 2230 and 0700). Group A (11 patients and 10 normals) had enforced wakefulness during the day whereas Group B (9 patients) were permitted to sleep (mean = 2 1/2 hr.). On day 2, all subjects were permitted to sleep for 15-min periods every 2 hr. In narcoloptics, sleep recordings demonstrated a reduction of sleep latency, an increase of stage 1, and a decrease in stages 3 and 4 compared to normals, but total REM time and percentage of REM sleep were similar. Groups A and B showed no difference in the incidence of nocturnal awakenings. REM cyclic periodicity was larger in narcoleptics who also demonstrated a REM-sleep fragmentation. This fragmentation became more pronounced as time passed, with several shifts from REM to wakefulness and stage 1. Narcoleptics present REM onset sleep period but also show an inability to remain in REM sleep.
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A patient with autonomic insufficiency and extrapyramidal signs (Shy-Drager syndrome) and sleep apnea syndrome (SAS) underwent hemodynamic studies. In comparison to patients with SAS and intact autonomic reflexes, systemic hypertension was absent and marked sinus arrhythmia during sleep was blunted. Cyclical pulmonary hypertension associated with frequent apneic episodes during sleep persisted, reflecting a minor role of autonomic reflexes in the generation of this abnormality. Autopsy confirmed the Shy-Drager syndrome and multiple areas of degeneration were observed in areas of the CNS outside the medullary respiratory centers, suggesting their importance in the origin of the respiratory abnormalities in SAS.
The sleep and respiratory patterns of eight apneic preterm infants were polygraphically recorded for 24 hours. This polygraphic study was designed to test and extend our previous finding that gently oscillating water beds reduce apnea in premature infants. The infants who ranged in gestational age from 27 to 32 weeks and in birth weight from 1,077 to 1,650 gm served as their own controls, off and on the water bed. The 24-hour recordings were divided into four time blocks with the infant being placed on the water bed during alternate six-hour periods. Apnea was significantly reduced while the infants were on the oscillating water beds, with the longest apneic periods and those associated with severe bradycardia being reduced the most. Reduction of apnea was most consistent during indeterminate sleep and most pronounced during quiet sleep. Short respiratory pauses and periodic breathing were not significantly reduced. Reductions of central, obstructive, and mixed apneas were approximately equal.
In 22 children (11 boys and 11 girls), aged 9 to 13 years, respiration was monitored during one night of sleep. No child had a significant history of breathing problems during sleep. Sleep was recorded using standard techniques (electroencephalography, electrooculography, electromyography), and respiration was measured with nasal thermistors and abdominal or thoracic strain gauges. Respiratory pauses (five seconds or longer) were determined for all sleep stages. Respiratory rate was scored only in the first and last sleep cycles and during ten waking minutes before sleep onset. Respiratory rate was significantly affected by wakefulness or stage of sleep: highest in wakefulness and stage 1, lowest in stage 2 of the last sleep cycle. Regularity of respiratory rate showed a similar effect. Variance of respiratory rate was significantly lower in girls than boys. Respiratory pauses during sleep were seen in every child, ranging from 3 to 40 pauses per night (average, 17.2 for boys and 18.0 for girls). Significantly greater numbers of pauses per minute were seen in stage 1 and rapid eye movement (REM) sleep than in stages 2, 3 and 4. The longest respiratory pause was 25 seconds. The conclusion is made that a small number of respiratory pauses during sleep are normal in children of this age.
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Six patients between the ages of 17 and 32 years presented with unusual sleep-walking epidodes characterized by screaming or unintelligible vocalizations; complex, often violent automatisms; and ambulation. Two or more attacks could occur in a single night and were most common in the early morning hours. Family and personal histories did not show epilepsy, psychiatric disorders, or (with 1 exception) previous somnambulism. Electrographic investigation revealed that all patients had normal waking-sleep cycles but that 4 of them had epileptiform abnormalities on their electroencephalograms. All patients were treated with either phenytoin or carbamazepine, with cessation of the abnormal nocturnal behavior during follow-up periods ranging from 9 to 48 months. This syndrome appears to be distinct from more typical non-rapid eye movement dyssomnias and suggests an atypical form of epilepsy.
Cardiac arrhythmias during wakefulness and sleep in 15 patients with sleep-induced obstructive apnea, and the effect of atropine and tracheostomy on these arrhythmias were studied by continuous overnight Holter electrocardiographic, respiratory and electroencephalographic recordings. Sleep was characterized by marked sinus arrhythmia in 14, extreme sinus bradycardia ( less than 30 beats/minute) in six, asystole of 2.5 to 6.3 seconds in five, second degree atrioventricular (A-V) block in two, and ventricular arrhythmias--complex premature ventricular beats in 10 and ventricular tachycardia in two. Arrhythmias during wakefulness were limited to premature ventricular beats in six. Atropine administration was partially and tracheostomy highly effective in preventing the majority of these arrhythmias during sleep. Marked sinus arrhythmia during sleep is characteristic of the syndrome of obstructive sleep apnea and is frequently accompanied by potentially life-threatening tachy- and bradyarrhythmias. Possible mechanism of production of these arrhythmias, the mode of action of tracheostomy and atropine, and the probable role of similar arrhythmias in the sudden infant death syndrome are discussed.
Anatomical or physiological airway obstructions during sleep, of which the patient is unaware, cause daytime sleepiness at first, then signs of decreasing mental function, and eventually in some individuals, pulmonary and systemic hypertension. A few of these patients had been recognized before, the Pickwickian syndrome and in children with cardiac problems and large tonsils. The majority, however, present as sleep disorders. This paper describes our surgical experience with improving the airways of 19 children and adults with daytime somnolence.
A sleep apnea syndrome due to upper airway obstruction was diagnosed in 25 adult men (25 to 65 years of age) using nocturnal polygraphic monitoring. Excessive daytime somnolence, hypnagogic hallucinations, and automatic behavior, personality changes with abnormal behavioral outbursts, impotence, morning headaches, abnormal motor activity during sleep, nocturnal enuresis, and high blood pressure should suggest this diagnosis when any of the symptoms are associated with loud snoring. Respiratory monitoring during sleep and nocturnal cardiovascular evaluation bring prognostic information and indications for therapy. Three types of therapeutic trials, namely, diet, medications with or without diet, and surgery have been performed. Only surgery has been beneficial in these cases.
Sleep, respiratory, and cardiac data obtained during sleep and wakefulness by continuous 24-hour polygraphic monitoring from twelve infants who were "near misses" for the sudden-infant-death syndrome were compared with similar information obtained from seven low-risk infants. Although the sleep variables studied were of limited value in differentiating between the low and high risk patients, respiratory and cardiac abnormalities were strikingly more common in near-miss infants. High-risk infants demonstrated both obstructive and mixed stopped-breathing episodes (S.B.E.). Bradycardia was seen secondary to S.B.E. but also simultaneously with or independent of S.B.E. Sudden asystole associated with S.B.E. was seen in one case. These results suggest an autonomic-nervous-system dysfunction in high-risk infants.
Insomnia may be associated with a sleep-induced apnea syndrome in nonobese patients who snore. The "central" type of apnea appears to be predominant in this population, in opposition to Pickwickian and nonobese hypersomniacs. An abnormal "swallowing reflex syndrome," also induced by sleep, may be a differential diagnosis. Sleeping pills that are central nervous system depressants should be cautiously prescribed for patients with such syndromes.
A sleep apnea syndrome has been diagnosed in eight children (age range 5-14). Before undertaking therapeutic trials, sleep and respiration were extensively studied. Sleep and respiration were again analyzed 3 months after tonsillectomy and adenoidectomy (6 cases) or tracheostomy with insertion of valve (2 cases). Sleep induced apneic apisodes in these children who had normal respiration during wakefulness. Three types of apnea (central, upper airway, and mixed) were recorded in each case. The minimum number of apneas recorded during a single night was 75; the maximum was 816. Polygraphic monitoring demonstrated greatly disturbed sleep. Sleep changes were quantitative as well as qualitative. REM sleep percent was decreased, but stages 3 and 4 NREM sleep were also impaired. A relationship between stages 3-4 NREM sleep and respiration was noted: stages 3-4 sleep disappeared when apneic episodes were numerous; no apnea was recorded during stage 4 sleep. Follow-up nocturnal recordings of two tracheostomized children with valve open, then closed, confirmed this "stage 4/no apnea" relationship. Apneas were also noted to induce marked sinus arrhythmia during sleep.
Clinical examinations, questionnaires, and 24- or 36-hour polygraphic recordings were performed on 21 adult patients with the narcolepsy syndrome to investigate the short- and long-term effects of clomipramine HCL. Cataplexy was improved by the medication, but tolerance was observed 4 1/2 months of treatment. Clomipramine HCL induced significant changes in the sleep EEG, chin EMG, and EOG. In two patients, clomipramine HCL caused a nocturnal myoclonia that produced insomnia. Sexual side effects were seen with clomipramine HCL, particularly in males. A combination of clomipramine HCL and L-Dopa apparently prevented this difficulty in one patient. A rebound of cataplexy was seen during the 15 days following withdrawal of the drug. Methysergide maleate was found to be ineffective on cataplexy in four patients.
The authors compared the sleep laboratory recordings of 122 drug-free subjects who complained of chronic insomnia with the subjects' estimates of their habitual sleep characteristics and their estimated sleep time on the morning after sleeping in the laboratory. Most subjects consistently underestimated the amount of time they slept and overestimated the amount of time it took them to get to sleep in comparison with laboratory data. All subjects consistently underestimated the number of arousals they experienced. The authors discuss the implications of these findings for the treatment and definition of insomnia and for further research.
Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.