Once a person has one sleep problem, they are less able to cope with another one. For example, persons with obstructive sleep apnea are less able to cope with the demands of shift work.
A. Vakulin and colleagues pubished "Effects of Alcohol and Sleep Restriction on Simulated Driving Performance in Untreated Patients With Obstructive Sleep Apnea" in this months issue of Annals of Internal Medicine. This study compared patients with untreated OSA and matched controls on a driving simulator. The study found that "Patients with OSA are more vulnerable than healthy persons to the effects of alcohol consumption and sleep restriction on various driving performance variables. "
Showing posts with label alcohol. Show all posts
Showing posts with label alcohol. Show all posts
Sunday, October 11, 2009
Sunday, October 04, 2009
Alcohol, Sleep, and Pregnancy
Below is a small excerpt from the article "Sleep disorders associated with alcohol use and abuse," available at Medlink Neurology:
Alcohol use should be avoided during pregnancy. The potential adverse physical and neurocognitive effects, including fetal alcohol syndrome, of maternal alcohol consumption on the developing fetus have been extensively reviewed (Wattendorf and Muenke M 2005). Recent research has clarified the effects of prenatal alcohol consumption on the child’s postnatal sleep. Maternal prenatal consumption of alcohol results in infant postnatal sleep fragmentation as well as the suppression of spontaneous movements during sleep, at 6 to 8 weeks of age (Troese et al 2008). In utero alcohol exposure results in altered neonatal autonomic control during sleep, possibly increasing the risk of Sudden Infant Death Syndrome (Fifer et al 2009).
References:
Wattendorf DJ, Muenke M. Fetal alcohol spectrum disorders. Am Fam Physician 2005;72(2):279-82, 285.
Troese M, Fukumizu M, Sallinen BJ, Gilles AA, Wellman JD, Paul JA, Brown ER, Hayes MJ. Sleep fragmentation and evidence for sleep debt in alcohol-exposed infants. Early Hum Dev 2008;84(9):577-85.
Fifer WP, Fingers ST, Youngman M, Gomez-Gribben E, Myers MM. Effects of alcohol and smoking during pregnancy on infant autonomic control. Dev Psychobiol 2009;51(3):234-42.
Alcohol use should be avoided during pregnancy. The potential adverse physical and neurocognitive effects, including fetal alcohol syndrome, of maternal alcohol consumption on the developing fetus have been extensively reviewed (Wattendorf and Muenke M 2005). Recent research has clarified the effects of prenatal alcohol consumption on the child’s postnatal sleep. Maternal prenatal consumption of alcohol results in infant postnatal sleep fragmentation as well as the suppression of spontaneous movements during sleep, at 6 to 8 weeks of age (Troese et al 2008). In utero alcohol exposure results in altered neonatal autonomic control during sleep, possibly increasing the risk of Sudden Infant Death Syndrome (Fifer et al 2009).
References:
Wattendorf DJ, Muenke M. Fetal alcohol spectrum disorders. Am Fam Physician 2005;72(2):279-82, 285.
Troese M, Fukumizu M, Sallinen BJ, Gilles AA, Wellman JD, Paul JA, Brown ER, Hayes MJ. Sleep fragmentation and evidence for sleep debt in alcohol-exposed infants. Early Hum Dev 2008;84(9):577-85.
Fifer WP, Fingers ST, Youngman M, Gomez-Gribben E, Myers MM. Effects of alcohol and smoking during pregnancy on infant autonomic control. Dev Psychobiol 2009;51(3):234-42.
Saturday, June 02, 2007
Treatment of Alcohol-related sleep disorders
The following is from an article I wrote for Medlink Neurology on "Sleep disorders associated with alcohol use and abuse." It is copyrighted by Medlink Neurology:
For the sleep disorders occurring during alcohol intake, cessation of alcohol use is often the only necessary treatment. Treatment of the sleep apnea exacerbated by alcohol requires avoidance of alcohol intake at least for 4 hours to 6 hours before going to bed. If the apnea does not resolve with alcohol cessation, then standard treatments for obstructive sleep apnea, such as nasal continuous positive airway pressure, are required. The hypersomnia that can occur with alcohol use is usually eliminated after 1 day or 2 days without alcohol, but insomnia may actually worsen for the first 2 weeks to 7 weeks off alcohol. It is important not to restart the alcohol even at a low dose to ameliorate this problem; similarly, use of hypnotics is contraindicated because of the cross-tolerance with alcohol and the potential for both abuse and dependence. Sedating antihistamines or low doses of sedating antidepressants can be used for temporary relief when insomnia episodes are particularly severe. Patients should be reassured that in most cases the insomnia gradually gets better.
Behavioral treatments for insomnia with good sleep hygiene, relaxation training, desensitization, or sleep restriction should be used during the withdrawal period. If evidence develops for depression then a sedating antidepressant (eg, amitriptyline or mirtazapine) may be helpful for both sleep and depression.
As mentioned above, sleep abnormalities in alcoholics can persist for several years after alcohol cessation; this sleep disturbance may contribute to relapse of alcoholism. Various medications and psychotherapy techniques have been used to treat this sleep disturbance. Gabapentin, at doses of 300 mg to 1800 mg at bedtime, is useful in treating insomnia in abstinent alcohol-dependent outpatients and appears to be more effective than trazodone (Karam-Hage and Brower 2003). Although quetiapine is of potential benefit for this condition (Monnelly et al 2004; Sattar et al 2004), the risk of tardive dyskinesia and metabolic abnormalities associated with the use of atypical antipsychotics suggests that they should be used cautiously, if at all, for insomnia. Cognitive-behavioral treatments, including stimulus control, sleep restriction, and cognitive restructuring, have been shown to improve subjective sleep quality in recovering alcoholics (Currie et al 2004).
The melatonin receptor agonist Ramelteon (Rozerem-Takeda) is an option for treating insomnia in recovering alcoholics, though controlled trials are lacking. Ramelteon is not a controlled substance, and has essentially no abuse liability (Anonymous 2005; Griffiths and Johnson 2005). It is approved for the treatment of insomnia characterized by difficulty with sleep onset (Laustsen and Andersen 2006). The standard dose is 8 mg, taken within 30 minutes of going to bed. It is metabolized by cytochrome p450 enzyme 1A2 but does not appear to inhibit or induce this enzyme (Laustsen and Andersen 2006). It should not be used in combination with fluvoxamine, a strong 1A2 inhibitor (Takeda Pharmaceuticals 2005).
Acamprosate (Campral- Forest Pharmaceuticals) is a glutamate modulator that is FDA-approved for the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation (Forest Pharmaceuticals 2005). A recent parallel double-blind placebo-controlled study found that acamprosate improved sleep quality during early abstinence (Staner et al 2006).
disclaimer: this is not the final edited version that will appear in Medlink Neurology. I encourage you to check out the website for Medlink Neurology for the full version of this article as well as numerous other articles about sleep (a few written by me).
For the sleep disorders occurring during alcohol intake, cessation of alcohol use is often the only necessary treatment. Treatment of the sleep apnea exacerbated by alcohol requires avoidance of alcohol intake at least for 4 hours to 6 hours before going to bed. If the apnea does not resolve with alcohol cessation, then standard treatments for obstructive sleep apnea, such as nasal continuous positive airway pressure, are required. The hypersomnia that can occur with alcohol use is usually eliminated after 1 day or 2 days without alcohol, but insomnia may actually worsen for the first 2 weeks to 7 weeks off alcohol. It is important not to restart the alcohol even at a low dose to ameliorate this problem; similarly, use of hypnotics is contraindicated because of the cross-tolerance with alcohol and the potential for both abuse and dependence. Sedating antihistamines or low doses of sedating antidepressants can be used for temporary relief when insomnia episodes are particularly severe. Patients should be reassured that in most cases the insomnia gradually gets better.
Behavioral treatments for insomnia with good sleep hygiene, relaxation training, desensitization, or sleep restriction should be used during the withdrawal period. If evidence develops for depression then a sedating antidepressant (eg, amitriptyline or mirtazapine) may be helpful for both sleep and depression.
As mentioned above, sleep abnormalities in alcoholics can persist for several years after alcohol cessation; this sleep disturbance may contribute to relapse of alcoholism. Various medications and psychotherapy techniques have been used to treat this sleep disturbance. Gabapentin, at doses of 300 mg to 1800 mg at bedtime, is useful in treating insomnia in abstinent alcohol-dependent outpatients and appears to be more effective than trazodone (Karam-Hage and Brower 2003). Although quetiapine is of potential benefit for this condition (Monnelly et al 2004; Sattar et al 2004), the risk of tardive dyskinesia and metabolic abnormalities associated with the use of atypical antipsychotics suggests that they should be used cautiously, if at all, for insomnia. Cognitive-behavioral treatments, including stimulus control, sleep restriction, and cognitive restructuring, have been shown to improve subjective sleep quality in recovering alcoholics (Currie et al 2004).
The melatonin receptor agonist Ramelteon (Rozerem-Takeda) is an option for treating insomnia in recovering alcoholics, though controlled trials are lacking. Ramelteon is not a controlled substance, and has essentially no abuse liability (Anonymous 2005; Griffiths and Johnson 2005). It is approved for the treatment of insomnia characterized by difficulty with sleep onset (Laustsen and Andersen 2006). The standard dose is 8 mg, taken within 30 minutes of going to bed. It is metabolized by cytochrome p450 enzyme 1A2 but does not appear to inhibit or induce this enzyme (Laustsen and Andersen 2006). It should not be used in combination with fluvoxamine, a strong 1A2 inhibitor (Takeda Pharmaceuticals 2005).
Acamprosate (Campral- Forest Pharmaceuticals) is a glutamate modulator that is FDA-approved for the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation (Forest Pharmaceuticals 2005). A recent parallel double-blind placebo-controlled study found that acamprosate improved sleep quality during early abstinence (Staner et al 2006).
disclaimer: this is not the final edited version that will appear in Medlink Neurology. I encourage you to check out the website for Medlink Neurology for the full version of this article as well as numerous other articles about sleep (a few written by me).
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