Showing papers on "Polysomnography published in 1987"

Ambulatory Evaluation of Sleep Disturbance and Therapeutic Effects in Sleep Apnea Syndrome by Wrist Activity Monitoring

Abstract: A new wrist actometer was used to obtain ambulatory activity-rest recordings in 18 patients with sleep apnea syndrome (SAS) and in 22 control subjects A movement index (MI) and a fragmentation index (FI) during sleep time were computed, giving an estimate of the stability of sleep in control subjects, we observed a clear differentiation between night and day activity levels The distribution of MI and FI was very narrow, with a mean ± SD of 139 ± 54 and 181 ± 58% No correlation of MI and FI with body mass index, even in heavily obese subjects, was found; MI and FI decrease significantly with age A diagnosis of SAS was made by standard all-night polysomnography Patients with SAS had a significantly higher MI and FI than did control subjects (p < 0001) With respect to polysomnographlc diagnosis of SAS, the sensitivity of activity recordings was 89%, whereas the specificity was 95% Five patients were studied after treatment, and decrease in MI and FI at home were in good agreement with the improv

Periodic breathing and hypoxia in snorers and controls: validation of snoring history and association with blood pressure and obesity

Abstract: Fifty-two men (aged 41-50 years) of whom 25 reported habitual and 27 of occasional or never snoring were examined clinically. Whole-night sleep recordings of body and breathing movements, snoring and blood oxygen saturation were made. Hypoxic events exceeding 4% from the baseline were counted. Ninety-three percent of those classified snorers by the recordings were habitual or occasional snorers, but 50% of those similarly classified non-snorers had reported habitual or occasional snoring. Four habitual snorers had abnormal breathing indices and polysomnography established obstructive sleep apnea syndrome (OSAS) in one. Thus, self-reported habitual snoring is a reliable OSAS-screening method. Estimated prevalence of OSAS based on this study is 0.4-1.4%. In multivariate regression analysis, the hypoxic events were explained by obesity and apneic events. The diastolic blood pressure level was best explained by obesity, but not hypoxic or apneic events or snoring history.

Risk factors for sleep disordered breathing in heterogeneous geriatric populations.

Abstract: This cross-sectional, multivariate study investigated associations between sleep disordered breathing (SDB) and putative risk factors in a heterogeneous group of 720 individuals over the age of 50 years studied during all-night in-lab polysomnography. Results indicated that: aged men were more likely to show impaired respiration during sleep than aged women; excessive daytime somnolence and parasomniac symptoms (snoring, gasping during sleep) were associated with SDB but insomnia was not; obesity accounted for more variance in SDB than age per se, implying that the prevalence of SDB in some elderly persons could be related to the deposition of body fat seen as individuals grow older. All four risk factors (age, sex, obesity, and symptomatic status) were statistically significant and independent predictors of impaired respiration in sleep in the elderly.

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea.

Abstract: Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (greater than 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

Human Sleep: Research and Clinical Care

Abstract: I Physiology and Pharmacology of Sleep.- 1 An Introduction to Sleep Studies.- Techniques of Human Sleep Studies.- Polysomnography.- Stages of Sleep.- Waking.- Non-REM Sleep.- REM Sleep.- The REM-Non-REM Cycle.- Sleep Stages and Age.- Effects of Temporal Variables on Sleep.- Physiological Variables in Sleep Stages.- Sleep Deprivation.- Total Sleep Deprivation.- Selective Sleep Stage Deprivation.- Natural Long, Short, and Variable Sleepers.- Regulation of Sleep.- Passive versus Active Regulation.- Neurotransmitters.- Models of Sleep Regulation.- Circulating Humors and Sleep.- Hypnotics.- Summary.- 2 Pharmacology and Neurotransmitters in Sleep.- Serotonin and Sleep.- L-Tryptophan.- 5-Hydroxytryptophan.- Parachlorophenylalanine.- Methysergide.- Lysergic Acid Diethylamide.- Fluoxetine.- Quipazine and Fenfluramine.- Ritanserin.- Ventricular Fluid 5-HIAA.- Dopamine.- L-Dihydroxyphenylalanine (L-DOPA).- Dopamine Receptor Agonists and Antagonists.- Pimozide.- Other Studies of Dopamine and Sleep.- Norepinephrine.- Alpha-Methyl-Paratyrosine (AMPT).- Alpha-Methyldopa.- Adrenergic Receptor Blockers.- Other Drugs Influencing Amines.- Reserpine.- Amphetamines.- Chlorpromazine.- Tricyclic Antidepressants.- Monoamine Oxidase Inhibitors.- Endogenous MAO and Biogenic Amines.- The Cholinergic System.- Muscarinic.- Nicotinic Agonists.- Gamma-Aminobutyric Acid.- Adenosine.- Circulating Sleep Factors.- Arginine Vasotocin (AVT).- Delta Sleep-Inducing Peptide (DSIP).- Muramyl Dipeptide (MDP).- Steroids.- Cholecystokinin (CCK).- Discussion.- Serotonin.- Dopamine.- Norepinephrine.- Acetylcholine.- Circulating Sleep Factors.- Gamma-Aminobutyric Acid.- Interaction between Transmitters.- 3 Pharmacological Treatment of Insomnia.- Aspects of Insomnia.- Pharmacology of Hypnotics.- Barbiturates.- Benzodiazepines.- Nonbarbiturate, Nonbenzodiazepine Hypnotics.- Efficacy Studies of Hypnotics.- Flurazepam.- Temazepam.- Triazolam.- Residual Daytime Effects.- General Issues.- Data on Performance and Wakefulness.- The Elderly.- Benzodiazepines and Respiration.- Reliance and Dependence.- Hypnotics and Alcohol.- Hypnotics and Acute Time Shifts.- Clinical Recommendations.- Conclusions.- 4 The Benzodiazepine Receptor and Sleep.- Pharmacological Probes of the BZ Recognition Site.- Studies with Beta-Carbolines.- The B10 Enantiomers.- Do Alterations in Calcium Flux Mediate Some Pharmacological Effects of BZs?.- Dihydropyridines and Diazepam-Stimulated Calcium Uptake into Synaptosomes.- Nifedipine Blocks Sleep Induction by Flurazepam.- BAY K 8644 Enhances Hypnotic Effect of Flurazepam.- The Relation of Barbiturates and Ethanol to the BZ Receptor Complex.- Effects of PB and Ethanol on Ion Channels.- Chloride Channel Function: Ethanol and PB Toxicity.- Relation of PB to BZ Recognition Site Function: Hypnotic, Anticonvulsant, and Anxiolytic Properties.- Heterogeneity of BZ Receptors.- Issues for the Future.- Endogenous Compounds.- Separation of Pharmacological Properties.- Summary.- 5 Neuroendocrinology and Sleep.- Basic Concepts in Neuroendocrinology.- Growth Hormone.- Secretion in Sleep and Waking.- Effect of Alterations in Neurotransmitter Function on GH Secretion.- Locus of Drug Effect.- Somatostatin.- Secretion of GH in Psychiatric Patients.- Secretion of GH in Disease.- Aging and GH.- Effects of GH Administration.- The Pituitary-Adrenal Axis.- Relation to the Sleep-Waking Cycle.- Sleep-Related Cortisol Secretion in Disease.- Effects of Cortisol and ACTH on Sleep.- Prolactin.- Relation of PRL to Other Hormones.- Drugs and Sleep-Related PRL Secretion.- Sleep-Related PRL Secretion in Disease.- Follicle-Stimulating Hormone and Luteinizing Hormone.- Relation of LH and FSH Secretion to Sleep.- Relation of Testosterone Secretion to Sleep.- Effects of Sex Hormones on Sleep.- Sleep-Related FSH and LH Secretion in Disease.- Thyroid-Stimulating Hormone.- TSH Secretion and Sleep.- Sleep in Hyperthyroidism and Hypothyroidism.- Central Nervous System Actions of TRH.- Antidiuretic Hormone and Renin.- ADH and Renin Secretion during Sleep.- Effects of ADH on Sleep.- Melatonin.- Summary.- II Pathology of Sleep.- 6 Sleep-Related Breathing Disorders.- Snoring.- Incidence of Sleep Apnea Syndromes.- Regulation of Respiration in Sleep.- Methods of Recording and Measuring Sleep-Related Respiration.- Clinical Syndromes.- Obstructive Sleep Apnea.- Central Sleep Apnea.- Mixed Apneas.- Hypoventilation Syndromes.- Treatment.- Obstructive Sleep Apnea.- Central Sleep Apnea.- Adjunctive Treatment and Precautions.- Questions for the Future.- Summary.- 7 Narcolepsy and Disorders of Excessive Sleepiness.- Definition.- Excessive Daytime Sleepiness and Sleep Attacks.- Cataplexy.- Sleep Paralysis.- Hypnogogic and Hypnopompic Hallucinations.- Disordered Nocturnal Sleep.- Automatic Behavior.- Psychosocial Consequences.- Performance Deficits.- Disordered Physiology.- Natural History.- Epidemiology and Genetics.- Etiology.- Animal Models of Narcolepsy.- Diagnosis.- Sleep Laboratory Findings.- Narcolepsy with Other Sleep Disorders.- Clinical Evaluation.- Other Disorders of Excessive Daytime Sleepiness.- Idiopathic Central Nervous System Hypersomnolence.- Sleep Drunkenness.- Insufficient Sleep Syndrome.- Hypersomnolence Associated with Medical or Toxic Conditions.- "Secondary Narcolepsy".- Excessive Sleepiness in Depression.- Pharmacotherapy of Narcolepsy.- Stimulants.- Antidepressants.- Monoamine Oxidase Inhibitors.- Serotonin Antagonists and Agonists.- Gamma-Hydroxybutyrate.- Propranolol.- Opiates.- Other Treatments.- Summary.- 8 Alcohol, Alcoholism, and the Problem of Dependence.- Animal Studies.- Ethanol and the Sleep EEG.- Effects of Prior Exposure to Ethanol.- Behavioral Measures of Sleep in Long- and Short-Sleeping Mice.- Ethanol and Neurotransmitters.- Ethanol in Normal Human Subjects.- Effects of Ethanol in Chronic Alcoholics.- Sleep in "Dry" Alcoholics.- Response to Ethanol.- Sleep during Acute Withdrawal.- REM Sleep Rebound.- Experimental Approaches to Ethanol Toxicity and Withdrawal.- Ethanol and Hypnotics.- Ethanol and Sleep Apnea.- Summary.- 9 Affective Disorders.- Observations of Patients.- Symptomatic Depressed Patients Compared to Controls.- Longitudinal Studies.- Sleep and the Switch Process in Bipolar Patients.- Theories of Sleep in Depression.- REM Deprivation.- Extended Sleep and Sleep Satiety.- Circadian View of Depression.- Implications of the Two-Process Model.- Reciprocal Interaction Model.- Pharmacological Models.- Manipulations of Sleep as Treatments for Depression.- REM Sleep Deprivation.- Total Sleep Deprivation.- Partial Sleep Deprivation.- Advance of the Sleep-Wake Cycle.- Summary.- 10 Circadian Rhythms and Sleep.- Background.- Models of Sleep-Wake Regulation.- Disorders of the Sleep-Wake Schedule.- Transient Disturbance.- Persistent Disturbance.- Pharmacology.- Use of Hypnotics in Acute Phase Shifts.- Circadian Rhythm Alteration by Drugs.- Summary.- 11 Nocturnal Myoclonus and the Restless Legs Syndrome.- Nocturnal Myoclonus.- Prevalence.- Relation to Sleep Disturbance.- Drugs Associated with Myoclonus.- Differential Diagnosis.- Treatment.- Restless Legs Syndrome.- Clinical Features.- Treatment.- Summary.- 12 Chronic Insomnia.- Persistent Psychophysiological DIMS.- Subjective DIMS without Objective Findings.- Other Forms of Chronic Insomnia.- Qualities Associated with Insomnia.- Daytime Sleepiness.- Daytime Performance.- Sleep Studies of Insomniacs.- The Subjective Experience of Insomniacs.- Is Poor Sleep the Same as "Light" Sleep?.- Insomniacs' Perception of Habitual Sleep.- Treatment of Insomnia.- Nonpharmacological Techniques.- Sleep Hygiene.- A Program for Patients.- Summary.

Comparison of polysomnography and sonography for assessing regularity of respiration during sleep in adenotonsillar hypertrophy.

Abstract: Increasing awareness of the role of adenotonsillar hypertrophy in the etiology of chronic airway obstruction and disturbed respiration during sleep has created interest in the diagnostic methods available to assess the effects of obstruction. This study evaluates and compares simultaneously-obtained recordings of polysomnography and sleep sonography in children obstructed by adenotonsillar hypertrophy. Four hundred sixty-five 4-minute samples obtained from 18 patients in a clinical studies unit were analyzed and rated as to severity. Agreement between polysomnography and sleep sonography was very high in scoring the respiratory pattern (r = 0.79) and detecting apnea (r = 0.89). These findings demonstrate that sleep sonography is a reliable method for evaluating patients with upper airway obstruction due to adenotonsillar hypertrophy.

Ingestion of Either Scotch or Vodka Induces Equal Effects on Sleep and Breathing of Asymptomatic Subjects

Abstract: • Polysomnography was performed on 13 asymptomatic men and four women on three consecutive nights in our sleep laboratory. In random order, the subjects ingested either orange juice alone or the equivalent of 1 mL of 100-proof alcoholic beverage (scotch or vodka) per pound of body weight in 1.5 hours or less. All subjects ingested a different beverage on each of the three nights. Blood alcohol level in the subjects before sleep was, for vodka, 73 mg/100 mL, and, for scotch, 74 mg/100 mL. On control nights the subjects showed significantly more time in bed, sleep period time, and total sleep time, and more rapid eye movement sleep. On the scotch and vodka nights, oxygen saturation was significantly lower; there were more episodes of oxygen desaturation in which there was greater than 4% decrease in saturation, more desaturation to levels of less than 90%, and more hypopnea. Comparison of data of scotch with vodka nights showed no significant differences in any variable. Both scotch and vodka ingestion in equal dosage induced sleep-disordered breathing and nocturnal oxygen desaturation in asymptomatic volunteers, and the beverages had equal effects. ( Arch Intern Med 1987;147:1145-1147)

Sleep apnoea and organic solvent exposure

Abstract: Fifteen patients referred for the evaluation of possible organic solvent encephalopathy were studied by clinical polysomnography. Seven had more than 30 apnoeas per night and an apnoea index of higher than 5, thus fulfilling the commonly used criteria of the sleep apnoea syndrome. Another group of eight workers exposed to trichlorethane, examined without prior knowledge of their individual symptoms, showed a significantly elevated number of sleep apnoeas compared with nine controls. The results indicate that organic solvent exposure can cause sleep apnoea.

Nasal occlusion during sleep in normal and near-miss for sudden death syndrome infants.

Abstract: Obligatory nasal breathing has been suggested in the past as a contributor to sudden infant death syndrome (SIDS): nasal obstruction would result in death as infants were unable to breathe orally. To test this hypothesis, we studied 55 normal and 14 near-miss for SIDS infants during a whole-night polysomnography. On several occasions, the infant nares were gently occluded by the fingertips of the investigator. Infants continued to make respiratory efforts against the occluded nose for a variable time (apnoea time), then opened the mouth and started to breathe through it. Mean apnoea time in normal infants was 4.76 +/- 3.41 s (means +/- SD), and 6.54 +/- 4.25 s in near-miss for SIDS ones. These figures were not significantly different. Analysis according to sleep stage (quiet sleep: 4.08 +/- 3.24 s in normals and 6.50 +/- 4.18 s in near-miss for SIDS ones; active sleep: 6.54 +/- 3.67 s in normals and 6.58 +/- 4.76 s in near-miss for SIDS ones) did not disclose any significant difference between groups. There was no significant relationship between apnoea time and age in either group. In many cases, an arousal preceded the resumption of (oral) flow. However, in almost half of the occlusions, oral breathing was initiated during continuing sleep. We conclude: 1) infants are not obligatory nasal breathers, and 2) the nasal obstruction hypothesis should be discarded in the etiology of SIDS.

Treatment of the obstructive sleep apnea syndrome.

Abstract: The obstructive sleep apnea syndrome is a disorder of sleep and breathing that is being recognized with increasing frequency. The pathophysiologic consequences range from mild sleepiness to life-threatening cardiovascular and respiratory decompensation. The primary forms of treatment are directed at modifying the upper airway with either an operation or continuous positive airway pressure. Aside from tracheostomy, which is virtually always successful, other forms of treatment have met with varying results. Ancillary therapy, including oxygen, weight loss and drugs, is often helpful but seldom curative. Follow-up sleep studies are necessary to evaluate the effectiveness of treatment. Selecting therapy for a patient with obstructive sleep apnea requires a comprehensive evaluation including polysomnography, special examinations of the upper airway and assessing the cardiopulmonary status. Therapy is based on the severity of disease and must be tailored to each patient.

[Dangerous snoring. Sleep-apnea syndrome].

Abstract: Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.