Figueredo-Rodríguez P, Río-Portilla Y, Sánchez-Romero JI, Pérez-Ortiz A, Corsi-Cabrera M

Language: Spanish
References: 48
Page: 59-67
PDF size: 166.31 Kb.

ABSTRACT

Difficulty in sleep initiation, with or without objective signs, is one of the most frequent complaints in primary insomniacs. The electroencephalographic (EEG) activity characteristic of waking (beta and alpha oscillations) is gradually replaced by the EEG signs of sleep (sleep spindles and theta/delta waves) during the sleep onset period (SOP) in normal subjects. The decrease in fast oscillations occurs at the first signs of stage 1, whereas theta and delta increase occurs later, indicating that waking promoting mechanisms are turned off before sleep-promoting mechanisms are fully started. It could be therefore hypothesized that difficulty in sleep initiation in insomniacs might be due to either a hyperactivation of waking promoting systems, a weakness of sleep promoting mechanisms or an imbalance between them. Quantitative EEG analysis has revealed higher beta during wakefulness, as well as during sleep and lower slow (delta) activity in insomniacs. The presence of alpha activity during cognitive information processing, especially of slow alpha activity in relation to attention, as well as in some pathologies associated to sleep disturbances, has suggested that alpha activity during sleep is a sign of activation; however, alpha activity during sleep has been less studied in insomniacs. Only broad bands have been considered in all of the aforementioned studies, and in almost all of them the analyses were restricted to central regions. It is therefore important to study the entire frequency spectrum of EEG activity in insomniacs. Sleep initiation does not occur simultaneously over the entire cortex but starts as a local process which gradually invades the rest of the cortex, in which the frontal lobes play a crucial role. Frontal and parietal regions are part of an important network involved in attention and conduction of thought. Thus, quantitative analysis of narrow EEG bands and their distribution in the cerebral cortex may contribute to a better understanding of neural mechanisms compromised in etiology of sleep initiation in primary insomnia. The main objective of the present investigation was, therefore, to analyze the spectral power of narrow EEG bands in the 19 derivations of the 10-20 International System during SOP in primary insomniacs with difficulty in sleep initiation. Given that one of the main complaints of insomniacs is the difficulty to initiate sleep and that hyperarousal is one of the factors proposed to be involved in the etiology of insomnia, EEG activity during SOP of the first night in the laboratory was analyzed to control activating effects of surrounding circumstances and isolate permanent EEG characteristics.Subjects were 19-34 years old, right-handed with primary sleep insomnia, which were thoroughly screened via structured psychiatric, medical and sleep interviews and scales. Subjects were younger and the age range was narrower than in other EEG frequency spectral content studies of primary insomniacs to avoid confounding effects of changes in sleep architecture or in EEG generated by development. All patients met the criteria for primary insomnia with sleep onset difficulty and impaired daytime function on three or more nights per week for at least six months and with no medical, psychiatric or neurological conditions; they were not medicated and had no other sleep disorders. Participants taking sleep medications or other drugs (urine test), respiratory or sleep disorders such as apnea and periodic limb movements (PSG) were excluded. The control group (n=9) was matched for age and dexterity, but had no complaints of insomnia and reported their sleep as restorative and satisfactory. All participants underwent a single night of standard polysomnography (EEG, EOG and EMG) in the laboratory. In addition, the 19 electrode sites of the 10-20 International System referred to ipsilateral earlobes, oral-nasal airflow and anterior tibialis EMG were recorded. PSG was scored in 30 sec epochs, blind to the subject group according to Rechtschaffen and Kales criteria.EEG from SOP (lights out to consolidate sleep), defined as 3 consecutive minutes of delta sleep, was digitized at 1024 Hz with 12 bits resolution and filter settings of 0.03-70 Hz. EEG was segmented into two-sec non-overlapping epochs and inspected for artifacts. All artifact-free epochs were Fast Fourier Transformed and absolute (AP) and relative power (RP: AP in each Hz bin/total spectrum power x 100) was obtained for 1 Hz bins. AP and RP was logtransformed before statistical analysis, and was averaged over each derivation and sleep stage of SOP. Group differences were compared by means of Student’s t tests and probability level was set at p‹0.05.In contrast with healthy controls, insomniac patients exhibited higher alpha RP (7 and 8 Hz) over all frontal derivations during stage 2 of SOP and higher RP of isolated beta and gamma frequencies during wakefulness. PSG of both groups showed the «first night effect» with decreased total sleep time, decreased sleep efficiency index and REM sleep percentage compared to normal values for the 20-30 age decade; PSG variables were not significantly different between the two groups except for wakefulness percentage during SOP. Insomniacs did differ from controls in subjective estimation of sleep quality and continuity in spite of similar PSG. The absence of significant differences between insomniacs and controls in sleep EEG activity (delta, theta and sigma frequencies) suggests that sleep homeostatic function is preserved in insomniacs, which agrees with results obtained in other studies after partial sleep deprivation. The absence of a stronger promoting effect of insomnia in the insomniac group by the first recording night indicates that EEG characteristics found in this group cannot be attributed to external stimuli nor surrounding circumstances and rather suggests a more stable alteration; however, further studies of larger groups and other age spans are needed to confirm present results. The evidence mentioned above suggests an imbalance between waking and sleep promoting mechanisms in primary insomniacs with difficulty in sleep initiation and sleep perception. Attention depends not only on vigilance level, but also on frontal regions which, together with posterior association areas, conform an essential network for purposive endogenously guided attention. The presence in insomniacs of alpha activity in frontal regions, which is a sign of top-down control of attention, and its absence in posterior regions during stage 2 suggests the persistence of a certain level of endogenous attention during stage 2 of SOP, which contributes in turn to the subjective perception of sleep onset difficulties and bad sleep quality.

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