|dc.description.abstract||The present thesis study is a systematic investigation of information processing at
sleep onset, using auditory event-related potentials (ERPs) as a test of the neurocognitive
model of insomnia. Insomnia is an extremely prevalent disorder in society resulting in
problems with daytime functioning (e.g., memory, concentration, job performance, mood,
job and driving safety). Various models have been put forth in an effort to better
understand the etiology and pathophysiology of this disorder. One of the newer models,
the neurocognitive model of insomnia, suggests that chronic insomnia occurs through
conditioned central nervous system arousal. This arousal is reflected through increased
information processing which may interfere with sleep initiation or maintenance. The
present thesis employed event-related potentials as a direct method to test information
processing during the sleep-onset period.
Thirteen poor sleepers with sleep-onset insomnia and 1 2 good sleepers
participated in the present study. All poor sleepers met the diagnostic criteria for
psychophysiological insomnia and had a complaint of problems with sleep initiation. All
good sleepers reported no trouble sleeping and no excessive daytime sleepiness. Good
and poor sleepers spent two nights at the Brock University Sleep Research Laboratory.
The first night was used to screen for sleep disorders; the second night was used to
investigate information processing during the sleep-onset period. Both groups underwent
a repeated sleep-onsets task during which an auditory oddball paradigm was delivered.
Participants signalled detection of a higher pitch target tone with a button press as they
fell asleep. In addition, waking alert ERPs were recorded 1 hour before and after sleep on
both Nights 1 and 2.As predicted by the neurocognitive model of insomnia, increased CNS activity
was found in the poor sleepers; this was reflected by their smaller amplitude P2
component seen during wake of the sleep-onset period. Unlike the P2 component, the Nl,
N350, and P300 did not vary between the groups. The smaller P2 seen in our poor
sleepers indicates that they have a deficit in the sleep initiation processes. Specifically,
poor sleepers do not disengage their attention from the outside environment to the same
extent as good sleepers during the sleep-onset period. The lack of findings for the N350
suggest that this sleep component may be intact in those with insomnia and that it is the
waking components (i.e., Nl, P2) that may be leading to the deficit in sleep initiation.
Further, it may be that the mechanism responsible for the disruption of sleep initiation in
the poor sleepers is most reflected by the P2 component.
Future research investigating ERPs in insomnia should focus on the identification
of the components most sensitive to sleep disruption. As well, methods should be
developed in order to more clearly identify the various types of insomnia populations in
research contexts (e.g., psychophysiological vs. sleep-state misperception) and the
various individual (personality characteristics, motivation) and environmental factors
(arousal-related variables) that influence particular ERP components. Insomnia has
serious consequences for health, safety, and daytime functioning, thus research efforts
should continue in order to help alleviate this highly prevalent condition.||en_US