Disease relevance of Arousal

• GER, however is likely to be important in the pathogenesis of arousals, but there is no evidence that it is involved in the pathogenesis of apneas [1].
• Cortical arousals were significantly less frequent in the victims who would succumb to SIDS in the future than in the control infants during both REM and non-REM sleep (p = 0.039) [2].
• One reason for this higher mortality may be that apnea-related hypoxia and arousals from sleep can increase sympathetic nervous system activity (SNA), as manifested by increases in overnight urinary and daytime plasma norepinephrine concentrations ([UNE] and [PNE], respectively) [3].
• Bupropion SR reduces periodic limb movements associated with arousals from sleep in depressed patients with periodic limb movement disorder [4].
• Cheyne-Stokes respiration (CSR) is common in patients with congestive heart failure (CHF) and is associated with significant nocturnal O2 desaturation, arousals and sympathetic activation [5].

Psychiatry related information on Arousal

• Data from sleep questionnaires and polysomnography showed that the two week course of melatonin did not influence sleep parameters, including total sleep time, sleep latency, sleep efficiency, sleep onset latency, arousals, duration of stages 1-4, rapid eye movement (REM) sleep, and REM onset latency [6].
• Depressed adolescents showed increased baseline phasic REM sleep measures, increased arousals, a trend toward reduced slow-wave sleep, and a greater difference in the change of first REM period density on the scopolamine night versus placebo night compared to controls [7].
• A significant decrease in the number of sleep stage transitions, arousals, and awakenings longer than 3 minutes was found only with lormetazepam [8].
• In summary, nefazodone, an effective antidepressant, decreases arousals and wakefulness during sleep and reduces light non-REM sleep [9].
• 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 [10].

High impact information on Arousal

• During the night LES relaxation and GER occurred only during transient arousals from sleep or when the subjects were fully awake, but not during stable sleep [11].
• Antireflux therapy (nizatidine) reduced arousals but not apnea-hypopnea index in patients with OSA [1].
• Each patient was used as his own control and periods with blood glucose concentration less than 3 mmol/l were compared to exactly the same periods in nights with blood glucose level over 5 mmol/l. During hypoglycaemia the amount of deep sleep was reduced and replaced by superficial sleep and arousals of short duration [12].
• Respiratory disturbances, sleep profile, and arousals improved significantly with both modes (AHI: baseline, 35.1 +/- 26/h; APAP(FOT), 5.0 +/- 5.2; CPAP, 4.3 +/- 6.3; p < 0.001 baseline versus each mode) [13].
• When comparing a 16-channel PSG montage with that of a seven-channel cardiorespiratory montage, we found that 84% of all movement/arousals could be detected using the abbreviated montage [14].

Chemical compound and disease context of Arousal

• Compared with the baseline nights, plasma cortisol significantly increased immediately after continuous arousals were started or the subject was awakened and remained awake [15].
• Fluoxetine increased light Stage 1 sleep, the number of arousals and rapid eye movement (REM) density [16].
• Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals [17].
• Propoxyphene had marginal benefit and significantly decreased arousals and mildly decreased leg movements for leg activity monitoring, but not for PLM on the polysomnograms [18].
• American Academy of Sleep Medicine arousal criteria applied to central leads and to frontal leads allowed detection of an additional 24% respiratory event-related arousals by frontal leads than by conventional leads [19].

Biological context of Arousal

• The fluoxetine group experienced a lower-average sleep efficiency index (SEI) and significantly more eye movements and arousals during non-REM sleep than the control group [20].
• The hypothesis that raising blood pressure (BP) during human sleep, by intravenous administration of angiotensin II, causes arousals was tested [21].
• Among the variables studied, including such previously reported predictors as serum albumin level, urea reduction ratio, and hematocrit, only the PLMS index (PLMSI), arousing PLMSI (APLMSI), and total number of arousals per hour of sleep significantly predicted mortality [22].

Anatomical context of Arousal

• DISCUSSION: Together with paroxysmal arousals and nocturnal paroxysmal dystonia, ENWs has been considered as a manifestation of the nocturnal frontal lobe epilepsy [23].
• A high level of TNF production in macrophages of ground squirrel is observed over the active period and during arousals in winter [24].

Gene context of Arousal

• No association was found between stimulation of ventilation and the occurrence of arousals; the respiratory analeptic effect of CRH thus appears to be specific.(ABSTRACT TRUNCATED AT 250 WORDS)[25]
• Many of the PLMS in the children with ADHD were associated with arousals [26].
• In addition, NCPAP suppressed the presence of cyclic alternating pattern (CAP) in REM sleep and induced an impressive rebound of arousals and of certain CAP variables-i.e., CAP rate, CAP time, number of CAP cycles-which dropped well below the physiologic values expressed by controls [27].
• These criteria were modified for the purposes of this study because it was noticed that, at the age of the group under analysis, most electroencephalogram arousals, often accompanied by electromyogram activation, are expressed at the level of the electroencephalogram by theta frequencies and not alpha or higher frequencies [28].
• However, more than 50% of COPD patients also have sleep complaints characterised by longer latency to falling asleep, more frequent arousals and awakenings, and/or generalised insomnia [29].

Analytical, diagnostic and therapeutic context of Arousal

• We describe 14 hypersomniac patients whose polysomnographic recordings revealed abnormal EEG patterns consisting of paroxysmal epileptic discharges during stages 2 and 3 of NREM sleep, associated with arousals, fragmentation of sleep, and reduction in sleep efficiency, particularly REM sleep [30].
• Patients on polypharmacy and phenobarbital therapy slept more, phenytoin patients had very short sleep latency but more wakefulness and less sleep efficiency; those taking clonazepam were also awake more and had lower sleep efficiency, while arousals during sleep were more frequent in patients on valproate and carbamazepine [31].

References