Disease relevance of Disorders of Excessive Somnolence

• NADPH oxidase mediates hypersomnolence and brain oxidative injury in a murine model of sleep apnea [1].
• We hypothesized that long-term intermittent hypoxia activates brain NADPH oxidase and that this enzyme serves as a critical source of superoxide in the oxidation injury and in hypersomnolence [1].
• We have also advanced data indicating that the hypersomnia, hyperphagia, lethargy, fatigue, and relative apathy of the syndrome of atypical depression are associated with concomitant hypofunctioning of the CRH and LC-NE systems [2].
• Paradoxical response to nitrazepam in a patient with hypersomnia secondary to nocturnal myoclonus [3].
• Cerebrospinal fluid homovanillic acid and 5-hydroxyindoleacetic acid in hypersomnia with periodic apneas or idiopathic hypersomnia: preliminary results [4].

Psychiatry related information on Disorders of Excessive Somnolence

• Narcolepsy and idiopthic hypersomnia: biogenic amines and related compounds in CSF [5].
• Although the cumulative increases in wakefulness were statistically equivalent, METH, but not modafinil, produced subsequent rebound hypersomnolence [6].
• Hypocretin ligand deficiency appears not to be the major cause for other hypersomnias, with a possible continuum in the pathophysiology of narcolepsy without cataplexy and idiopathic hypersomnia [7].
• As a group, the anti-68/48 kDa-positive CFS patients presented more frequently with hypersomnia (P<0.005), short-term amnesia (P<0.07) or difficulty in concentration (P<0.05) than those CFS patients without the antibodies [8].
• CSF hypocretin-1 levels in narcolepsy, Kleine-Levin syndrome, and other hypersomnias and neurological conditions [7].

High impact information on Disorders of Excessive Somnolence

• In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations [9].
• The hypersomnia of SCN-ablated squirrel monkeys is unique in magnitude, but is not incompatible with a role for the SCN pacemaker in actively promoting sleep [10].
• Higher levels of depression, hypersomnia, and leaden paralysis were noted in the patients who received haloperidol than in those who received phenelzine and those who received placebo [11].
• Desipramine in the treatment of hypersomnolence following abrupt cessation of cocaine use [12].
• These data suggest that the loss of 5-HT neurons of the DRN and the SCN is associated with the presence of hypersomnia in MyD [13].

Chemical compound and disease context of Disorders of Excessive Somnolence

• When ovulation was inhibited by a combination of ethinylestradiol and lynestrenol, an oral contraceptive pill, the hypersomnia ceased [14].
• Our findings indicate that modafinil significantly alleviates hypersomnolence (p < 0.05) in the bulldog, as evidenced by dramatically decreased mean total sleep time (from a control value of 50.5% to 8.3% with the drug) and increased mean sleep latency (from a control value of 71.0 minutes to a value of 346.6 minutes with the drug) [15].
• Pigs injected I.C.V. with 50 ng/kg TNF-alpha showed anorexia, hypersomnia, and an abrupt increase in plasma cortisol concentration [16].
• Physicians concerned with daytime hypersomnolence in PD patients treated with dopamine agonists and receiving high levodopa dosage equivalents should consider polysomnographic monitoring for impaired daytime sleep latency [17].
• An important point is emphasized in our case in which the patient reacted unfavorably to Ritalin, becoming sexually aroused, although his hypersomnia improved [18].

Biological context of Disorders of Excessive Somnolence

• First-degree relatives were also at higher risk for idiopatic hypersomnia (OR: 23.0), obstructive sleep apnea syndrome (OR: 6.8), adjustment sleep disorder (OR: 4.0), insufficient sleep syndrome (OR: 7.0), circadian rhythm disorders (OR: 2.5), REM behavior disorder (OR: 4.4), and sleep talking (OR: 2.0) [19].
• To gain new insights into the pathophysiology of MD, we determined whether the antiarrhythmic drug hydroquinidine would ameliorate slow saccadic eye movements (SEMs), apathy and hypersomnia in MD patients [20].

Anatomical context of Disorders of Excessive Somnolence

• A new hypothesis claims that, in women with winter SAD, decreased levels of estradiol in the ventromedial hypothalamus are associated with the occurrence of atypical symptoms of depression, including increased daytime sleepiness and hypersomnia during the winter [21].

Gene context of Disorders of Excessive Somnolence

• An 11-year-old boy with Kearns-Sayre syndrome developed hypersomnia associated with bithalamic lesions and had complete absence of sleep spindles on a nocturnal polysomnogram [22].
• The role of cerebrospinal fluid hypocretin measurement in the diagnosis of narcolepsy and other hypersomnias [23].
• The hypersomnolence was associated with marked elevations in the serum prolactin level [24].
• These observations imply an intrinsic hypersomnolence sometimes accompanied by abnormal REM pressure may be an integral part of EDS in DM1 patients [25].
• BACKGROUND: Patients with major depressive disorder (MDD) and atypical features have reactive mood plus at least two symptoms: hypersomnia, hyperphagia, leaden paralysis or a lifetime sensitivity to rejection [26].

References