Biomedical subjects

Yaron Dagan

Publications and source records attributed to Yaron Dagan.

16 recordsLinked to original sources

PubMed2006

Autonomic changes during wake-sleep transition: a heart rate variability based approach.

Autonomic function during sleep and wakefulness has been extensively investigated, however information concerning autonomic changes during the wake to sleep transition is scarce. The objective of the present study was to non-invasively characterize autonomic function and additional physiologic changes during sleep onset in normal and abnormal sleep. The estimation of autonomic function was based on time-frequency analysis of the RR interval series, using the power components in the very-low-frequency range (0.005-0.04 Hz), low-frequency (0.04-0.15 Hz), and high-frequency range (0.15-0.5 Hz). The ratio of low to high frequency power represented the sympathovagal balance. Thirty-four subjects who underwent whole night polysomnography were divided into 3 groups according to their complaints and study results: normal subjects, apneic patients (OSAS), and subjects with various sleep disorders (VSD). The results indicated a significant increase in RR interval during sleep onset, although its variability decreased; respiratory rate did not change, yet respiration became more stable; EMG amplitude and its variability decreased with sleep onset. Very-low-frequency power started to decrease significantly 2 min before sleep onset in all groups; low-frequency power decreased and high-frequency power did not change significantly in all groups, accordingly their ratio decreased and reflected a shift towards parasympathetic predominance. Although autonomic function displayed similar behavior in all subjects, OSAS and VSD patients presented a higher sympathovagal balance reflecting enhanced sympathetic predominance in those groups compared to normal subjects, both before and after sleep onset. All parameters reached a nadir at a defined time point during the process of falling asleep. We conclude that the wake-sleep transition period represents a transitional process between two physiologically different states; this transition starts with a decrease in the very slow oscillations in heart rate that anticipates a step-change resetting of autonomic function, followed by a decrease in sympathovagal balance towards the end of the process.

Adolescent↗

PubMed2006

Cognitive performance during sustained wakefulness: A low dose of caffeine is equally effective as modafinil in alleviating the nocturnal decline.

Cognitive performance at night exhibits a substantial drop, typically before dawn. One of the means of dealing with this phenomenon, as well as with the accompanying sleepiness during sustained wakefulness, is the administration of stimulants. The most widely used and well-documented stimulants are caffeine, amphetamines, and modafinil. Of these, amphetamines are the least recommended, as they may severely affect behavior. Caffeine and modafinil seem to produce relatively milder side effects and usually only at high doses. Previous comparison studies have revealed equal efficacy of both the stimulants in maintaining alertness and performance during sustained wakefulness. However, these studies used relatively high, and thus not completely safe, doses of these drugs (600 mg caffeine and 400 mg modafinil). Therefore, the aim of the present study was to assess the efficacy of a low and medically safe dose of caffeine (200 mg) and modafinil (200 mg) in maintaining cognitive performance during sustained wakefulness. A flight simulation task was chosen for the assessment of the stimulants in a counter-balanced, within-subject design under four different conditions: baseline (no drugs), placebo, caffeine (200 mg), and modafinil (200 mg). The equal effectiveness of both drugs in abolishing the nocturnal drop in cognitive performance, as well as of oral temperature and blood pressure, supported the use of low doses of caffeine and modafinil for the maintenance of alertness in healthy subjects during sustained wakefulness.

Adult↗

PubMed2006

Body Mass Index (BMI) as a first-line screening criterion for detection of excessive daytime sleepiness among professional drivers.

OBJECTIVES: Obstructive sleep apnea (OSA) is the main predisposing factor of excessive daytime sleepiness (EDS), and, therefore, increases the risk of road crashes. However, it is difficult to rely on medical intake for OSA or fatigue since drivers' symptoms reports are not reliable. On the other hand, direct measurement of EDS among large numbers of drivers carries serious practical drawbacks. Obstructive sleep apnea, in turn, is strongly related to obesity, and elevated body mass index (BMI) is considered one of the major risk factors for OSA. Thus, it could be postulated that BMI may carry predictive value for EDS proneness. METHODS: The present study examined the interrelation between BMI, degree of OSA, as measured with Respiratory Distress Index (RDI), and the degree of EDS, as measured with the mean sleep onset latency in the Multiple Sleep Latency Test (MSLT) among obese (BMI = 32) professional drivers. The drivers went through polysomnography followed by the five sessions of MSLT in the next day. RESULTS: In accordance with prior studies, we have found strong correlation between BMI and the degree of OSA on the one hand, and between the degree of OSA and EDS on the other hand. OSA was detected among 77.7% of the drivers, 47.1% were sleepy, 19% had severe sleepiness [mean sleep latency [MSL < or = 5 min.], 28.1% had moderate sleepiness [MSL < or = 10 min.]. None of the drivers complained about any sleep problem, including snoring, and all reported that they do not experience excessive daytime sleepiness. Thus, there was no correlation between their subjective report and objective findings. CONCLUSIONS: Obese drivers with BMI above 32 are highly prone to be sleepy during the day. Their subjective reports of OSA or fatigue symptoms are not reliable. Therefore it is highly recommended to screen them easily by weight and height measure for further sleep study and decision about their driving abilities.

Adult↗

PubMed2006

Melatonin treatment in adolescents with delayed sleep phase syndrome.

This retrospective study describes the effects of long-term treatment with melatonin in 33 adolescents (age range, 10-18 years) with delayed sleep phase syndrome (DSPS). Patients were treated with oral melatonin, 3 to 5 mg/day for an average period of 6 months. During the treatment, sleep onset was advanced and sleep duration was longer. Treatment was also associated with a decrease in the proportion of patients reporting school difficulties. No adverse effects of melatonin were noted. This study indicates that long-term treatment with melatonin can be beneficial for adolescents with DSPS in terms of sleep-wake schedule and school performance.

Administration, Oral↗

PubMed2006

[A chronobiological approach in treatment of sleep disturbances in Alzheimer's dementia patients].

Alzheimer's dementia (AD) is a neurodegenerative disease that is often accompanied by severe sleep disturbances. The manifestation of the sleep disturbances is twofold: nighttime hyperarousal sometimes accompanied by irritability and agitation, and daytime excessive sleepiness. Thus, although treatment with sedatives or hypnotics may offer some relief to the nighttime hyperarousal, the daytime excessive sleepiness remains mostly unresolved. Recently, however, more promising results in relief of excessive daytime sleepiness, as well as nighttime hyperarousal, are offered by the chronobiological approach. This approach attributes the sleep problems of AD patients to a dysfunction in a broader neuronal mechanism, namely the biological clock, that paces various physiological functions, among which is the sleep-wake cycle. The biological clock, situated in the suprachiasmatic nuclei (SCN) of the hypothalamus, receives environmental light input via neuronal signals from the retina. The SCN, in turn, innervates the pineal gland, that is responsible for the production and release of melatonin. Light stimulus causes the attenuation of melatonin secretion from the pineal gland; whereas the cessation of light increases melatonin secretion. In diurnal mammals, the dim light melatonin onset (DLMO) is in accordance with sleep onset. The chronobiological approach offers two main treatments to the sleep problems in AD patients: morning exposure to bright light and evening administration of melatonin, both of which show at least moderate success in restoring the sleep-wake cycle in AD patients, that is more marked in the early stages of the disease.

Alzheimer Disease↗

PubMed2005

Dysregulation of circadian rhythms following prolactin-secreting pituitary microadenoma.

A patient who developed an irregular sleep-wake pattern following prolactin-secreting pituitary microadenoma is described. The patient reported difficulties in sleep onset and awakening at the desired time, which caused major dysfunction in his daily life activities. Despite these difficulties, the sleep-related complaints of the patient remained unrecognized for as long as three yrs. Statistical analyses of the patient's rest-activity patterns revealed that the disruption of the sleep-wake circadian rhythm originated from a disharmony between ultradian (semicircadian) and circadian components. The circadian component displayed shorter than 24 h periodicity most of the time, but the semicircadian component fluctuated between longer and shorter than 12 h periods. Additionally, desynchrony in terms of period length was found in the tentative analyses of the rest-activity pattern, salivary melatonin, and oral temperature. While the salivary melatonin time series data could be characterized by a best-fit cosine curve of 24 h, the time series data of oral temperature was more compatible with 28 h best-fit curve. The rest-activity cycle during the simultaneous measurements, however, was best approximated by a best-fit curve of 21 h. The dysregulation of circadian rhythms occurred concomitantly, but not beforehand, with the onset of pituitary disease, thus suggesting an association between the two phenomena. This association may have interesting implications to the modeling of the circadian time-keeping system. This case also highlights the need to raise the awareness to circadian rhythm sleep disorders and to consider disruptions of sleep-wake cycle in patients with pituitary adenoma.

Adenoma↗

PubMed2005

Case study: psychiatric misdiagnosis of non-24-hours sleep-wake schedule disorder resolved by melatonin.

This case study describes a 14-year-old male suffering from significant academic and personal difficulties, who has been diagnosed with depression, schizotypal personality disorder, and learning disabilities. Because of excessive sleepiness, assessment for a potential sleep disorder was performed. An overnight polysomnographic study revealed no primary sleep disorders. Wrist actigraphy revealed a non-24-hour sleep-wake pattern. Delay in temperature rhythm and dissociation with melatonin rhythms were also noted. Treatment with oral melatonin restored normal sleep-wake schedule. In a follow-up psychiatric evaluation, none of the above diagnoses were present. Greater awareness of sleep disorders may prevent psychiatric misdiagnosis of treatable sleep-wake schedule disorders.

Adolescent↗

PubMed2005

Behavioral and psychiatric consequences of sleep-wake schedule disorders.

Circadian rhythm sleep disorders (CRSDs) arise when an individual's sleep-wake rhythm mismatches the environmental 24-h schedule. Physiological data and genetic studies in patients with CRSDs suggest that these disorders result from abnormal functioning of the circadian timing system. Diagnosis involves recognition of the characteristics of CRSDs, which can be achieved by clinical interview and actigraphic monitoring of rest-activity patterns. Bright-light therapy and melatonin administration have proved to be the most effective treatment modalities of CRSDs. In psychiatric practice, CRSDs can be encountered on various occasions. Some evidence indicates that a deviant sleep-wake schedule might be a predisposing factor to personality disorders. CRSDs can emerge as an iatrogenic effect of certain psychoactive drugs, such as haloperidol and fluvoxamine. It is not uncommon that the daytime functional difficulties that accompany CRSDs are misinterpreted as symptoms of psychopathology. Recognition and awareness of these disorders should prevent years of erroneous diagnosis and treatment in these patients.

Circadian Rhythm↗

PubMed2004

The ineffectiveness of magnotherapy in a patient with obstructive sleep apnea syndrome and cardiovascular comorbidity.

Obstructive sleep apnea syndrome (OSAS) is associated with mild to severe cardiovascular risks. The most common standard treatment for OSAS, continuous positive airway pressure, was found to have beneficial effects on cardiovascular sequelae of OSAS. Additionally, commercial companies promote nonprescription treatments for OSAS. These products frequently lack scientific support for their efficacy and need further research. We report an objective test of magnetic therapy, one such product, in a patient with OSAS and cardiovascular comorbidities. Two nights of polysomnographic recording using the split-night protocol did not reveal any consistent differences in OSAS symptoms whether the patient slept with or without the magnetic equipment. It was concluded that magnetic treatment was unsuccessful in reducing OSAS symptoms in our patient and may even increase possible cardiovascular and stroke risks by preventing the patient from pursuing an adequate medical treatment, such as continuous positive airway pressure.

Cardiovascular Diseases↗

PubMed2004

Sleep apnea as a risk factor for hypertension.

PURPOSE OF REVIEW: High blood pressure and obstructive sleep apnea are closely related, and the latter is considered to induce hypertension. The primary underlying mechanism is sympathetic activation triggered by apneic episodes. This type of hypertension is difficult to treat. The purpose of this review is (1) to evaluate the epidemiological data in view of the current focus on preclinical sleep apnea and prehypertension, (2) to examine additional factors that might contribute to high blood pressure, and (3) to indicate the best therapeutic strategy for treatment of hypertension in these patients. RECENT FINDINGS: Cardiovascular effects of sleep apnea can be detected early in the course of the disease, and young subjects are particularly susceptible to its deleterious effect. Blood pressure profiles in these patients show higher diastolic blood pressure and no nocturnal dipping. The renin-angiotensin axis in conjunction with other vasoactive hormones add to the sympathetic activation in elevating blood pressure in sleep apnea. Pro-inflammatory cytokines further contribute to the atherosclerotic consequences that primarily affect the heart and brain, and spare the kidneys. Mounting evidence indicates that treatment of sleep apnea using positive airway pressure, palato-nasal surgery and weight reduction correct the associated hypertension. Conversely, antihypertensive therapy is less effective. SUMMARY: Even the early stages of sleep apnea are associated with high blood pressure and cardiovascular consequences. Despite our knowledge of the role of the sympathetic activation and vasoactive hormones, no specific antihypertensive therapy is superior, and the optimal way of controlling hypertension is to treat sleep apnea and associated obesity.

Humans↗

PubMed2003

Diastolic blood pressure is the first to rise in association with early subclinical obstructive sleep apnea: lessons from periodic examination screening.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is associated with long-term cardiovascular morbidity. Little is known about these relations at early stages. We conducted a case-control study in which we analyzed the clinical characteristics of young adults who underwent a periodic health examination and were screened for, and eventually found to experience, OSAS. METHODS: We identified 121 subjects newly diagnosed in a sleep study as having OSAS, and 229 matched control subjects in which screening for OSAS was negative. All had a medical interview, physical examination, and routine laboratory tests. RESULTS: Subjects who had OSAS had a higher, body mass index (3-kg/m(2) difference) and a higher diastolic blood pressure (4-mm Hg difference) value, without elevation in systolic blood pressure. There was no metabolic difference (lipids profile and fasting glucose levels) between groups. CONCLUSIONS: Diastolic blood pressure is higher early in the course of OSAS. Long term follow-up may determine effects of prevention and early intervention in OSAS and associated hypertension.

Adult↗

PubMed2002

The effects of coffee consumption on sleep and melatonin secretion.

BACKGROUND: In this study we examined the effects of caffeine on sleep quality and melatonin secretion. Melatonin is the principal hormone responsible for synchronization of sleep. Melatonin secretion is controlled by neurotransmitters that can be affected by caffeine. METHODS: In the first part of the study, six volunteers drank either decaffeinated or regular coffee in a double-blind fashion on one day, and the alternate beverage 7 days later. Sleep parameters were assessed by actigraphy. In the second part of the study, the subjects again drank either decaffeinated or regular coffee, and they then collected urine every 3h for quantitation of 6-sulphoxymelatonin (6-SMT), the main metabolite of melatonin in the urine. RESULTS: We found that drinking regular caffeinated coffee, compared to decaffeinated coffee, caused a decrease in the total amount of sleep and quality of sleep, and an increase in the length of time of sleep induction. Caffeinated coffee caused a decrease in 6-SMT excretion throughout the following night. CONCLUSIONS: The results of our study confirm the widely held belief that coffee consumption interferes with sleep quantity and quality. In addition, we found that the consumption of caffeine decreases 6-SMT excretion. Individuals who suffer from sleep abnormalities should avoid caffeinated coffee during the evening hours.

Journal Article↗

PubMed2002

Circadian rhythm sleep disorders (CRSD).

Circadian Rhythm Sleep Disorders (CRSD) are a group of sleep disorders characterized by a malsynchronization between a person's biological clock and the environmental 24-h schedule. These disorders can lead to harmful psychological and functional difficulties and are often misdiagnosed and incorrectly treated due to the fact that doctors are unaware of their existence. In the following review we describe the characteristics of CRSD, diagnosis, treatment as well as their relationship to psychopathology, psychotropic drugs and head trauma.

Antipsychotic Agents↗

PubMed2002

Case study of circadian rhythm sleep disorder following haloperidol treatment: reversal by risperidone and melatonin.

A patient with Gilles de la Tourette syndrome treated with haloperidol, ingested once daily after awakening from sleep, exhibited an irregular sleep-wake pattern with a free-running component of approximately 48 h. Transfer to risperidone, ingested once daily after awakening from sleep, was beneficial resulting in a sleep-wake cycle more synchronized at the appropriate phase to the external zeitgebers, and fewer nocturnal disturbances. The circadian sleep-wake schedule was fully synchronized when the patient had been subsequently treated with melatonin at 21:00h, before intended nocturnal sleep, in addition to risperidone in the morning. Restoration of the sleep-wake circadian pattern was accompanied by the patient's subjective report of significant improvement in his quality of life, social interactions, and occupational status. This observation suggests that circadian rhythm sleep disorders can be related to the typical neuroleptic haloperidol and restored by the atypical neuroleptic risperidone. Similar findings reported in patients suffering from other disorders support the hypothesis that the described disruption of the sleep-wake schedule is medication rather than illness-related. Therefore, it is very important to realize that circadian rhythm sleep disorders may be a side effect of neuroleptics.

Adult↗

PubMed2002

Circadian Rhythm Sleep Disorders (CRSD) in psychiatry--a review.

Circadian Rhythm Sleep Disorders (CRSD) are a group of sleep disorders characterized by a de-synchronization between a person's biological clock and the environmental 24-hour schedule. There are four main types of CRSD, namely, Delayed Sleep Phase Syndrome (DSPS) (the most common), Advanced Sleep Phase Syndrome (ASWD), Non-24-hour Sleep-Wake Syndrome (Free-Running Pattern) and Irregular (or Disorganized) Sleep Wake Pattern. These disorders lead to harmful psychological and functional difficulties and certain personality disorders may also be related to them. It has been found that psychotropic drugs, SSRI and haloperidol can cause CRSD, and this is also true for some cases of minor head trauma. They are often misdiagnosed and incorrectly treated due to the fact that many doctors are unfamiliar with them. This review describes the disorders, their consequences and available treatment.

Antipsychotic Agents↗

PubMedDate not supplied

Sleep disturbances in adolescents with symptoms of attention-deficit/hyperactivity disorder.

We evaluated 32 nonmedicated male adolescents diagnosed with attention-deficit/hyperactivity disorder (ADHD) in childhood, 35 male adolescents similarly diagnosed who were receiving methylphenidate (MPH), and 77 control boys. Both ADHD groups completed self-report questionnaires assessing sleep disturbances; weekday and holiday sleep duration; and symptoms of ADHD, anxiety, and depression. Parents and teachers rated the severity of the participants' ADHD. The control group completed self-report questionnaires assessing sleep disturbances. We found that nonmedicated participants and controls did not differ in the severity of sleep disturbance. In contrast, the medicated participants demonstrated a significantly greater severity of sleep disturbance compared with the nonmedicated participants and reported elevated levels of symptoms of ADHD, anxiety, and depression. Specific analyses showed that depressive symptoms contributed significantly to the degree of sleep disturbance when controlling for ADHD diagnosis and MPH treatment. These findings suggest that among adolescents with ADHD symptoms, the severity of symptoms of depression may contribute to the degree of sleep disturbance in addition to the effect of their primary disorder and MPH treatment.

Adolescent↗