In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.
J Bruce, L Tamarkin, C Riedel, S Markey and E Oldfield
Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Journal of Clinical Endocrinology & Metabolism, Vol 72, 819-823, Copyright © 1991 by Endocrine Society
Friday, May 2, 2008
Melatonin - Circadian Cycle - Delayed sleep phase syndrome
Main article: Circadian rhythm sleep disorder
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers,[28] and the effect of modern lighting practice on endogenous melatonin has been proposed as a contributory factor to the larger overall incidence of some cancers in the developed world.
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland
J. GORSKI, D. KAJDANIUK, J. GLOGOWSKA-SZELAG, Z. OSTROWSKA, M. NOWAK, B. BUNTNER
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
procarbazine
Sensitivity to procarbazine
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
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