PubMed Health⌕ Search

Biomedical subjects

M M Mitler

Publications and source records attributed to M M Mitler.

At least 19 recordsLinked to original sources
PubMed1992

Maintenance of wakefulness test in obstructive sleep apnea syndrome.

The usefulness of a 40-min per trial version of the maintenance of wakefulness test was assessed in 322 patients with obstructive sleep apnea. This test is a variant of the multiple sleep latency test in which patients are asked to remain awake in a quiet darkened room, and then monitored for electroencephalographic sleep onset. The four trials of the test are each stopped after 40 min. The mean sleep latency for all patients was 26.0 +/- 11.8 (SD) min. In a group of 24 patients who underwent treatment with nasal continuous positive airway pressure, the mean sleep latency increased from 18.0 +/- 12.3 to 31.9 +/- 10.4. The strongest nocturnal correlates of the MWT sleep latency were respiratory arousal index (r = -.35), mean oxygen saturation (r = .30), and weight/height ratio (r = -.25). These correlations were comparable to other studies using the MSLT. There were strong intercorrelations among the variables. In the more severe groups, measures of hypoxemia were more strongly correlated with MWT sleep latency. A two-factor analysis of variance using respiratory arousal index and several measures of oxyhemoglobin saturation indicated that both arousals from sleep and degree of hypoxemia contribute interactively to daytime dysfunction in patients with sleep apnea. The MWT appears useful in evaluating disability from daytime sleepiness.

Analysis of Variance↗
PubMed1992

Maintenance of wakefulness test and multiple sleep latency test. Measurement of different abilities in patients with sleep disorders.

The multiple sleep latency test and the maintenance of wakefulness test were administered on the same day to 258 consecutive patients whose clinical presentation required evaluation for excessive sleepiness. While the MSLT is the standard test for assessing excessive daytime sleepiness, the MWT may have some clinical advantage over the MSLT when the assessment of daytime alertness is the primary goal. To explore further the relationship between alertness and sleepiness, we have conducted a thorough analysis of the similarities, differences, and correlations between MWT and MSLT. The results of this study show that the coefficient of correlation between MSLT and MWT (r = 0.41), although statistically significant, accounts for less than 17 percent of the variability between the two tests. Factor analysis suggests that two factors, alertness and sleepiness, account for 91 percent of all variance. Our data demonstrate that patients with diagnosable disorders of excessive somnolence may be discordant on the two tests (eg, having low sleep latency on MSLT but high sleep latency on MWT). Specifically, we found that some patients with abnormally low MSLT scores were able to stay awake when asked to do so on the MWT, and conversely, some patients who failed to stay awake when asked to do so on the MWT were unable to fall asleep quickly on the MSLT. We conclude that the MWT and MSLT measure different abilities and that the MWT may be a useful adjuvant daytime test in many clinical situations.

Adult↗
PubMed1992

Disorders of excessive sleepiness. Treatment improves ability to stay awake but does not reduce sleepiness.

A total of 47 patients with sleep disorder (36 male and 11 female) with a mean age of 47.5 +/- 15 years were evaluated for daytime symptoms with a Multiple Sleep Latency Test (MSLT) and a Maintenance of Wakefulness Test (MWT) given on the same day--once at the time of their diagnostic evaluation and again after one to six months of treatment. The MSLT and MWT data are consistent with the notion that sleep tendency, as measured by the MSLT and ability to remain awake, as measured by the MWT, represent different physiologic processes. Data show a marked treatment-related improvement in ability to stay awake as measured by the MWT and no treatment-related improvement in sleepiness as measured by the MSLT. We conclude that there is a heterogeneous subpopulation of patients with sleep disorders whose symptoms of daytime sleepiness will show no treatment-related improvement in daytime symptoms if they are evaluated only by the MSLT. We suggest that, since ability to stay awake (and not ability to fall asleep) is a requisite for all job-related duties, an objective, physiologically based test such as the MWT should be used to assess the impact of sleep disorders in cases where there is a clinical concern about fitness to drive or work.

Antidepressive Agents, Tricyclic↗
PubMed1991

Relative efficacy of drugs for the treatment of sleepiness in narcolepsy.

A survey was conducted on 10 polysomnographic studies on the pharmacologic treatment of the sleepiness of narcolepsy. Three studies employed the MSLT and 7 employed the MWT as their polygraphic measure of sleep tendency. Statistically and clinically significant therapeutic changes were apparent for pemoline, modafinil, dextroamphetamine and methylphenidate. Codeine, ritanserin and protriptyline did show statistically significant effects. The common feature among the drugs that did produce clinically significant improvements seems to be facilitatory action on central catecholaminergic transmission. Within this group of drugs, only methylphenidate and dextroamphetamine brought MWT sleep latencies to approximately 70% of normal levels.

Adult↗
PubMed1990

Narcolepsy.

Narcolepsy is a neurological condition with a prevalence of up to 1 per 1,000 that is characterized by irresistible bouts of sleep. Associated features include the pathological manifestations of rapid-eye-movement (REM) sleep: cataplexy, sleep paralysis, hypnagogic hallucinations, and abnormal sleep-onset REM periods and disturbed nocturnal sleep. The condition is strongly associated with the HLA-DR2 and DQw1 phenotype. The phenomenology of narcolepsy is discussed, and diagnostic procedures are reviewed. Treatment modalities involving central nervous system stimulants for somnolence and tricyclic drugs for REM-sleep abnormalities are discussed. Sleep laboratory studies on the treatment efficacy of methylphenidate, pemoline, dextroamphetamine, protriptyline, and viloxazine are presented. Data suggest that: (1) methylphenidate and dextroamphetamine objectively improve somnolence; (2) pemoline, at doses up to 112.5 mg, is less effective in controlling somnolence but may improve certain aspects of performance; and (3) protriptyline and viloxazine are effective anticataplectic agents that produce little improvement in somnolence.

Adult↗
PubMed1988

HLA-DR2 association with excessive somnolence in narcolepsy does not generalize to sleep apnea and is not accompanied by systemic autoimmune abnormalities.

Recent reports that nearly all patients with narcolepsy have the HLA-DR2 phenotype suggest that autoimmunity may underly the etiology or pathogenesis of this disorder. Of 11 narcoleptic patients in the present study, 9 were HLA-DR2, confirming the strong association with this class II antigen but indicating that this is not an obligatory phenotype. In contrast only 3/10 patients with sleep apnea were HLA-DR2, suggesting that this form of excessive somnolence has a different etiopathogenesis. Significant levels of rheumatoid factor, antinuclear antibodies or autoantibodies to native DNA, denatured DNA, histones, Sjogren's syndrome B antigen, or Smith antigen were undetectable in sera from narcoleptic patients. Antibodies to rodent brain, primate brain stem, and neurocytotoxic antibodies were also not found. These results along with the absence of laboratory signs and clinical features of a systemic inflammatory process indicate that if narcolepsy is an autoimmune disease, the underlying lesion or pathologic condition may be confined to the central nervous system.

Adult↗
PubMed1988

Bedtime ethanol increases resistance of upper airways and produces sleep apneas in asymptomatic snorers.

Nasal continuous positive airway pressure (nasal CPAP) and polysomnography were used to analyze the time course of the effect of bedtime ethanol on resistance of upper airways and on the number of respiratory pauses during sleep. On one night, six asymptomatic nonalcoholic male snorers drank 2 ml/kg of 100 proof vodka mixed in orange juice (ethanol dose, 0.79 gm/kg, giving a peak blood alcohol level of 71.8 +/- 33.3 mg/dl). On a second night they received a placebo (1-2 drops of vodka floated on top of the orange juice). We measured (a) the minimum nasal (CPAP) required to eliminate snoring, (b) the number of hypopneas and apneas during each hour of sleep and (c) the arterial oxygen saturation (SaO2) by ear oximetry. On the alcohol night there was a significant increase in the CPAP pressure required to eliminate snoring (placebo 4.8 +/- 1.7 cm H2O, alcohol 6.2 +/- 1.5 cm H2O). The number of respiratory events per hour of sleep (apnea index) was 7.5 +/- 2.1 for ethanol nights versus 3.8 +/- 2.7 for placebo nights (p less than 0.0125). An apnea index of greater than 5 is generally considered abnormal. There was no significant difference in the number of desaturation events (declines of 4% or more in the SaO2) or in the mean SaO2, but the minimum SaO2 was significantly lower on the ethanol night (placebo 89.8% +/- 1.6, alcohol 86.8% +/- 2.7, p less than 0.05). The effect of this dose of alcohol on airway resistance was most pronounced during the first 2 hr after ingestion.

Adult↗
PubMed1988

Hypersomnia and the perception of sleep-wake states: some preliminary findings.

35 hypersomniacs (20 with obstructive sleep apnea and 15 with narcolepsy) and 15 controls estimated sleep latency during systematic trials of attempting to remain awake during the day. The error in subjective assessment of sleep latency was more variable for both patient groups than for controls. In addition, narcoleptics could not provide a determination of sleep latency or differentiate sleep-wake states on nearly 23% of all trials. Ratings on a subjective sleepiness scale did not covary with objective sleep latency for any hypersomniac. The findings suggested that patients with either sleep apnea or narcolepsy had difficulty differentiating sleep and quiet wakefulness during the day.

Adult↗
PubMed1988

Effect of triazolam on sleep and arterial oxygen saturation in patients with chronic obstructive pulmonary disease.

We compared the effects of a placebo with 0.125 and 0.25 mg of triazolam (Halcion) on sleep quality, oximetry, and respiratory events during sleep in ten stable outpatients with chronic obstructive pulmonary disease. The subjects had a forced expiratory volume in 1 s ranging from 17% to 76% of the predicted value (mean +/- SD, 38.1% +/- 19%) and a waking arterial oxygen pressure from 46 to 84 mm Hg (mean +/- SD, 67 +/- 12 mm Hg). Polysomnography was done on three nights within a two-week period after the patients received on a "blinded" basis either placebo or 0.125 or 0.25 mg of triazolam. Triazolam produced improvements in total sleep duration, time spent in stage 2 nonrapid eye movement (NREM) sleep, and subjective of sleep quality. For most patients, there was a nighttime drop in arterial oxygen percentage of saturation (SaO2) in the placebo condition, but triazolam did not cause a significant worsening, of the mean SaO2, minimum SaO2, or the number of apneic and hypopneic events. Across all experimental conditions, we documented little desaturation during wakefulness (mean low, 87.2% +/- 10.2%), more during NREM sleep (mean low, 83.2% +/- 12.6%), and most desaturation in REM sleep (mean low, 80.1% +/- 15.7%). We conclude that single-night use of triazolam improved the quality and duration of sleep in patients with chronic obstructive pulmonary disease. In patients without severe waking hypoxemia and without carbon dioxide retention, triazolam did not increase either nocturnal hypoxemia or respiratory events during sleep.

Aged↗
PubMed1987

When people die. Cause of death versus time of death.

A sample of 4,920 disease-related deaths from New York City for 1979 (8.7 percent of all relevant data from New York City's files) showed a 60 percent rise in death rate beginning at 2 A.M. and reaching a peak at 8 A.M. A smaller peak was also noted at 6 P.M. The rise in human mortality beginning at 2 A.M. and peaking at 8 A.M. might be explained by: artifact of deaths occurring anytime during the night that are discovered after daybreak, effect of less efficient health care between 2 A.M. and 8 A.M., and disease processes that somehow increase risk of death between 2 A.M. and 8 A.M. An attempt was made to differentiate among these possibilities by comparing time of death for various subsamples. The bimodal pattern appeared only in the temporal distribution of deaths of persons over 65 years of age; deaths of persons under 65 did not show significant temporal concentration. There were also prominent differences in the distribution of deaths for different reported causes of death. Ischemic heart disease, which numerically accounted for over 50 percent of the sample, showed peak mortality at 8 A.M. for both males and females. Hypertensive disease showed a significant peak in mortality at 1 A.M. for females only. Cerebrovascular disease peaked significantly at 6 A.M. with a significant peak only for males. The age and disease specificity of the 2 A.M. to 8 A.M. rise in death is consistent with a disease-related explanation for the bimodal circadian pattern in mortality. The quality and efficiency of health care could be improved with more precise information on peak periods of risk for specific morbid conditions.

Aged↗
PubMed1987

Narcolepsy. Diagnosis, treatment, and management.

Narcolepsy is a syndrome of unknown origin characterized by the irresistible urge to sleep. Other important features are disturbed nocturnal sleep and abnormal manifestations of REM sleep such as cataplexy, sleep paralysis, and abnormal sleep-onset REM periods. Narcolepsy is not a rare condition. With a prevalence between 2 and 10 per 10,000 individuals, it is about as common as multiple sclerosis. Like multiple sclerosis, narcolepsy can be disabling and have profound consequences for job capability, public safety, sense of self-worth, and social image.

Animals↗
PubMed1987

A historical perspective on sleep disorders medicine.

The recent development of sleep disorders medicine traces its origins to the increased understanding of basic human sleep physiology gained over the past 30 years. The primary tool for diagnosis and management is the long-term polygraphic recording of multiple physiologic variables (polysomnography). A "style" of practice is emerging that is multidisciplinary and often institutionally-based in sleep disorders centers. High patient and physician satisfaction in this field indicate that rapid growth will continue.

History of Medicine↗
PubMed1986

Fibromyalgia. 1. Review of a common rheumatologic syndrome.

Fibromyalgia is a nonarticular rheumatic syndrome of unknown cause characterized by diffuse musculoskeletal aching, pain and stiffness, easy fatigability, multiple discreet tender points, emotional distress, and often, light and restless sleep with intensification of symptoms upon awakening. Symptoms are modulated by environmental, physiologic, and psychological factors. Generally, findings from laboratory tests and roentgenograms are normal. In primary fibromyalgia, no underlying rheumatic or other systemic organic disease is present. Secondary fibromyalgia is a manifestation of underlying disease.

Fibromyalgia↗
PubMed1986

Fibromyalgia. 2. Management guidelines and research findings.

Treatment of fibromyalgia includes various forms of therapy--physical, behavioral, psychological, and pharmacologic. No drug therapy has proved uniformly successful, but some drugs provide temporary relief from pain. After an initial therapy program has been established, patients can assume the major responsibility for management. Research studies aimed at defining the cause of fibromyalgia have linked it to sleep disorders, neurogenic mediators, immune mechanisms, muscle disease, and psychological disturbances.

Brain↗
PubMed1986

Forty-eight-hour polysomnographic evaluation of narcolepsy.

Eleven narcoleptic and 11 control subjects completed five multiple sleep latency test (MSLT) procedures with instructions to "fall asleep" while supine and five maintenance of wakefulness test (MWT) procedures with instructions to "remain awake" while comfortably sitting. Narcoleptic subjects had a shorter sleep latency and a higher frequency of sleep onset REM periods (SOREMPs) on both daytime tests than controls. Each group had a longer sleep latency on the MWT than MSLT. For patients with narcolepsy, the differences between the two daytime procedures suggest the tests measure distinct aspects of sleep-wake tendency. Sleep latency on the MSLT did not correlate with sleep latency on the MWT for narcoleptic subjects. Furthermore, the number of SOREMPs during the MSLT for narcoleptic subjects did not correlate with the number of SOREMP during the MWT. Measures of nocturnal REM sleep for narcoleptic subjects correlated with sleep latency on the MSLT. In particular, REM latency at night was highly predictive of the magnitude of hypersomnia for patients with narcolepsy. Sleep latency at night tended to relate to sleep latency on the daytime tests for controls. Patients with narcolepsy had a shorter sleep latency, more frequent arousals, and a shorter REM latency than control subjects across the 2 nights of study.

Adult↗
PubMed1986

Treatment of narcolepsy: objective studies on methylphenidate, pemoline, and protriptyline.

Methylphenidate, pemoline, and protriptyline were studied for their treatment efficacy in narcolepsy. A low, intermediate, and high dose level of each drug was studied for 1 week. For methylphenidate the doses were 10, 30, or 60 mg/day; for pemoline, 18.75, 56.25, or 112.5 mg/day; and for protriptyline 10, 30, or 60 mg/day. The order of dose levels was random from subject to subject and the daily dose was divided into thirds and taken in identically appearing capsules morning, noon, and afternoon. Subjects were 6 narcoleptic patients studied on methylphenidate (5 women and 1 man; mean age 54.5 + 11.7 years), 7 narcoleptic patients studied on pemoline (5 women and 2 men; mean age 43.0 + 7.1 years), and 4 narcoleptic patients studied on protriptyline (2 women and 2 men; mean age 42.5 + 16.9 years). Testing consisted of day-long sessions occurring at the end of each dose level and involving a clinical status questionnaire as well as maintenance of wakefulness, Wilkinson addition, and Digit-Symbol Substitution tests. Results were compared with 9 control subjects with no sleep disorder (5 women and 4 men; mean age 39.2 + 8.4 years) who were given placebo that was purported to be a "stimulant drug" and tested in a similar manner. Results demonstrated profound differences in ability to stay awake and perform between narcoleptic patients and controls. Data also suggested that methylphenidate significantly improves ability to stay awake. Pemoline seems to improve ability to perform. Protriptyline does not significantly alter ability to stay awake or to perform.

Adult↗