are individuals with paradoxical insomnia more hyperaroused than individuals with...

International Journal of Psychophysiology 81 (2011) 177–190

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International Journal of Psychophysiology

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Are individuals with paradoxical insomnia more hyperaroused than individuals withpsychophysiological insomnia? Event-related potentials measures at the peri-onsetof sleep

Isabelle Turcotte, Geneviève St-Jean, Célyne H. Bastien ⁎École de psychologie, Université Laval, Québec, Québec, Canada G1K 7P4Laboratoire de neurosciences comportementales humaines, Centre de recherche Université Laval- Robert Giffard, 2525 de la Canardière, Québec, Québec, Canada G1J 2G3

⁎ Corresponding author at: École de psychologie, FBibliothèques, Université Laval, Québec (Qc), CANADA2131x8344; fax: +1 418 656 3646.

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0167-8760/$ – see front matter © 2011 Elsevier B.V. Aldoi:10.1016/j.ijpsycho.2011.06.008

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Article history:Received 25 November 2010Received in revised form 8 June 2011Accepted 11 June 2011Available online 25 June 2011

Keywords:InsomniaInformation processingArousalInhibitionEvent-related potentialswPN

Preliminary QEEG studies suggest that individuals with paradoxical insomnia (Para-I) display higher corticalarousal than those with psychophysiological insomnia (Psy-I). Lately, finer measures, such as event-relatedpotentials, and especially the N1 and P2 components have been used to document arousal processes inindividuals with insomnia. The objective of the present study was to further circumscribe arousal in Psy-I andPara-I using N1, P2 and the waking processing negativity (wPN). N1 and P2 were recorded in the evening, atsleep-onset and in early stage 2 sleep in 26 good sleepers, 26 Psy-I and 26 Para-I. An oddball paradigm wasused and participants received the instruction to ignore all stimuli at all times. Three difference waves (wPNs)were computed to evaluate the transition fromwakefulness to sleep onset, from sleep onset to sleep and fromwakefulness to sleep. Results revealed that N1was smaller duringwakefulness and sleep onset for Psy-I, whileit was larger for Para-I during these same times. P2 was smaller at sleep onset for Psy-I than for Para-I and GS,while P2 duringwakefulness and stage 2 sleepwas larger for Para-I than GS.WPNs revealed that Psy-I showedfewer changes in information processing, while Para-I showed larger changes between recording times. Psy-Iappear to present an inability to inhibit information processing during sleep onset, while Para-I seem topresent overall enhanced attentional processing that results in a greater need for inhibition.

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1. Introduction

Recent epidemiological studies indicate that between 30 and 48%of adults complain of insomnia symptoms (Ohayon, 2002) while closeto 10% suffer of an insomnia syndrome (severe and chronic insomniacomplaints) (Morin et al., 2006). Many precipitating factors (Bastienet al., 2004) and maintaining factors (Morin and Espie, 2003) havebeen suggested as being linked to the appearance or perpetuation ofthe disorder. Nonetheless, the underlying cortical mechanismsassociated with chronic insomnia are just beginning to be betterunderstood (Bastien and Morin, 1998; Bastien et al., 2008; Devotoet al., 2005; Merica et al., 1998; Merica and Gaillard, 1992; Perlis et al.,2001; Sforza and Haba-Rubio, 2006). This study is one of the very fewthat actually measures the extent of information processing ofexternal stimuli in different types of chronic insomnia duringwakefulness, sleep onset and actual sleep.

According to Edinger et al. (2004), individuals with psychophysio-logical (Psy-I) andparadoxical (Para-I) insomniadiffer greatly regardingboth objective and subjective sleep variables. Themain feature of Psy-I isthat they display conditioned sleep difficulty and/or heightened arousalin bed. For example, an inability to initiate sleepwhenwanted, sleepingbetter away from home, intrusive thoughts at night (mind racing),somatic tension, and a difficulty to relax in bed are reported. On theother hand, Para-I severely overestimate their sleep difficulties. Markeddifferences between subjective and objective sleep, more than 6 h ofsleep on polysomnography (PSG) and a sleep efficiency N85% are oftenobserved. Furthermore, ‘normal’ nights are rare, while sleepless nightsand no naps are usually reported on the sleep diary.

Power spectral analysis (PSA) differences in the EEG between goodsleepers (GS) and individuals with insomnia are now well documen-ted (Bastien andMorin, 1998; Merica and Gaillard, 1992; Merica et al.,1998; Krystal et al., 2002; Perlis et al., 2001).While traditional analysesof objective sleep (PSG) do not corroborate the severe sleep difficultycomplaints of Para-I, PSA studies reveal that these individuals appearto display a perturbed microstructure of sleep compared to Psy-I(Edinger and Krystal, 2003; Krystal et al., 2002; Perlis et al., 2001;St-Jean and Bastien, 2008). In that regard, Perlis et al. (2001) haveidentified that during sleep, Para-I displayed greater Beta and Gamma

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178 I. Turcotte et al. / International Journal of Psychophysiology 81 (2011) 177–190

activities (reflecting cortical arousal) than Psy-I. Subsequently, Krystalet al. (2002) have identified an absolute greater amplitude in AlphaandBeta activities in stages 2 and4 of sleep in Para-I compared to Psy-I.These results indicate greater cortical activation in Para-I than in Psy-I,therefore supporting the neurocognitive model of insomnia (Perliset al., 1997) that suggests that high frequency activity is amain featureof chronic insomnia that could interfere with sleep initiation as well assleepmaintenance. Furthermore, this increased cortical arousal wouldalso lead to incompatible sleep activities such as enhanced sensory andinformation processing. However, inhibitory processes or the inabilityto de-arouse or disengage from active wake processing (Espie, 2002)that interferes with the normal initiation of sleep processes inindividuals with insomnia was not taken into account in the previousPSA studies. Furthermore, participants did not specifically correspondto the criteria of Para-I as standardized research diagnostic criteria hadnot yet been established. As such, empirical evidence supportingdeficits in cortical inhibition in insomnia individuals compared to GSare scarce, while the comparison of these processes between thedifferent types of insomnia is non-existent.

Event-related potentials (ERPs) are the electrical responses of thebrain to external sensory stimuli or internal mental events that reflecthow the brain “processes and classifies” stimuli. An external physicalstimulus or internal psychological event elicits small amplitudechanges in the EEG, therefore providing an excellent measure of theextent of information processing within the nervous system. Thelatency and amplitude of the successive positive and negativedeflections following the onset of the stimulus are used to name thedifferent components. As such, a negative component (“N1”), peakingat approximately 75 to 125 ms following the stimulus is followed by apositive component (“P2”), peaking at about 175 to 250 ms. N1 and P2are often elicited in the so-called oddball paradigm in which afrequently occurring ‘standard’ stimulus is presented and at rare andunpredictable times, a feature of the standard stimulus is changed toform a ‘deviant’. Both the standard and deviant elicit N1 and P2components. The N1 and P2 represent early sensory processing,although their amplitude is affected by both exogenous (e.g., stimuluscharacteristics) and endogenous (e.g., attention) factors (Kertesz andCote, 2011). This “N1–P2” complex which is maximum in amplitudeat the Cz site, is a measure of both sensory processing and the extentof attentional processing, since selective attention requires theprocessing of what is relevant (attended) but also the inhibition ofprocessing of what is irrelevant (not attended). Attention allowsindividuals to become conscious of what is relevant, and it is thisattention-related processing that must be inhibited during sleep onsetin order for sleep to occur. Therefore, the transition from wakingconsciousness to sleeping (and in particular, non-REM) unconscious-ness and the necessary inhibition of information processing in orderto fall asleep is reflected by changes in ERPs. Several studies have nowindicated that the amplitude of N1 following an auditory stimuli isvery much reduced, while the amplitude of P2 is increased duringsleep (Cote et al., 2002, Crowley et al., 2002, De Lugt et al., 1996).Those changes are thought to be due, in part, to the removal of a long-lasting negative wave, called waking Processing Negativity (wPN),which occurs because of a disengagement of attention during thesleep onset period (Campbell and Colrain, 2002; Näätänen, 1990). ThewPN is a separate and independent negative-going ERP componentfrom N1 and P2 that represents the additional attention-relatedprocessing of information possible by the individual while awake. It iscomputed by subtracting sleep ERPs from waking ERPs. It reflects thevariation in information processing due to wakefulness and moreprecisely, the extent of inhibition of information processing duringsleep (Campbell et al., 1992). Beginning approximately 25 ms afterstimulus onset, the long-lasting wPN overlaps and summates withboth the N1 and P2 peaks causing them both to become morenegative-going in the waking, attentive state. At sleep onset, with theloss of attention-related processing and the removal of the wPN, N1 is

much reduced but P2 appears to increase in amplitude. Thus, the wPNreflects themarked decrease in the ability to maintain attention to theexternal environment between the alert-waking and the drowsy-sleeping states (De Lugt et al., 1996).

During sleep onset, it is critical in order for sleep to occur, thatawareness of the external environment is inhibited. A possibleproblem for individuals with insomnia may be an inability to inhibitprocessing during sleep onset and within sleep. However, since it isimpossible for individuals to respond verbally or behaviorally whilethey are sleeping, the study of information processing during theprocess of falling asleep and during sleep itself is very limited. ERPsrepresent an ideal technique to investigate the extent of informationprocessing in insomnia participants during those times since the ERPsprotocol used in sleep studies does not require any response from theindividuals. If individuals with insomnia are unable to inhibitinformation processing, it would be expected that the changes fromthe waking ERPs to the sleeping one would be different from what isgenerally observed among GS. Although hyperarousal has alreadybeen investigated using the ERPs techniquewith insomnia individuals(Bastien et al., 2008; Devoto et al., 2005; Kertesz and Cote, 2011; Sforzaand Haba-Rubio, 2006; Yang and Lo, 2007), the inability to inhibitinformation processing during sleep onset aswell as during sleep itselfremains to be clarified. The poor sleep experienced by insomniaindividuals may be the result of an inability to inhibit externalinformation processing of irrelevant stimulus during sleep onset andsleep and this enhanced information processing may result inhyperarousal.

Devoto et al. (2005) suggested a state of hyperarousal in insomniaindividuals compared to GS by using the P300 component amplitudeas a measure of cortical arousal level. Both groups of participantsreceived an oddball task in which they were required to detect a raretarget tone by pressing a button, in a sequence of frequently occurringstandard tones. Individuals with insomnia presented larger P300amplitudes than GS 30 min prior to and following a subjective badnight of sleep. Sforza and Haba-Rubio (2006) measured the amplitudeof N1, P2 and P300 to evaluate the pre-sleep to post-sleep variations inthese ERPs in patients with sleep disorders. The authors did notobserve any between group differences, from evening to morning,when insomnia individuals were compared to GS. On the other hand,Yang and Lo (2007) observed a larger N1 and a smaller P2 inindividuals with insomnia than in GS during the first 5 min ofcontinuous stage 2 sleep, supporting the hyperarousal hypothesis.Recently, our research group (Bastien et al., 2008) recorded ERPs overmultiple nights during wakefulness and sleep onset as an oddballparadigmwas delivered to Psy-I and GS during the 3rd and 4th nightsin the sleep laboratory (in the evening and upon awakening), with theaddition of sleep-onset recordings on the 4th night. All participantsreceived the explicit directive to ignore all auditory stimuli. Duringwakefulness, the amplitude of N1 was larger for Psy-I compared to GSin the evening (on evening 4, following the standard tone, at Pz only)and the morning after evening 4 (following the standard tones, at Czand Pz). On the other hand, the amplitude of N1 recorded at sleeponset and following standard stimuli was smaller for Psy-I than GS (atCz only). Finally, the amplitude of P2 following deviant tones wasgreater in Psy-I than in GS at sleep onset (at Pz only). More recently,Kertesz and Cote (2011) investigated ERPs at sleep onset in Psy-Ipresenting sleep onset complaints specifically. Participants wereadministered an oddball task while awake in the morning andevening, and during repeated sleep-onset attempts. As they fell asleep,they were asked to signal detection of a higher pitch target tone. Aspreviously reported by Yang and Lo (2007), the authors observed asmaller P2 amplitude following the standard stimuli for patients withinsomnia compared to GS, when participants were instructed torespond to targets.

These previous ERPs studies indicate that information processingseems to be altered in insomnia individuals; however, all those studies

179I. Turcotte et al. / International Journal of Psychophysiology 81 (2011) 177–190

were limited to Psy-I and did not investigate information processing inPara-I. The oddball paradigm protocol permits to elicit N1 and P2 byboth standard and deviant stimuli regardless of the nature of theinstructions given to participants (to ignore or to attend to theauditory stimuli). Therefore,we used the oddball paradigmprotocol tocompare Psy-I and Para-I with GS during wakefulness, sleep onset andsleep. In addition, we measured the waking Processing Negativity(wPN) in order to compare the transition fromwakefulness to sleep inPsy-I and Para-I in opposition to GS. To the best of our knowledge, noprevious study has used the wPN to examine the difference in theextent of information processing during the transition from wakeful-ness to sleep in insomnia individuals.

The objectives of the present study were, first, to measure theextent of information processing using the N1 and P2 waves inresponse to both standard and deviant stimuli during wakefulness(evening), sleep-onset and sleep (early stage 2) in individuals withchronic insomnia, Psy-I and Para-I, in comparison to GS. Furthermore,cortical activitywas assessed as irrelevant stimuli were presented, so anon-response oddball paradigm was employed because the instruc-tion to respondmay interfere with the natural sleep onset process andresponses are not possible in late stage 1 and stage 2 sleep. PreviousPSA and ERPs studies revealed that cortical hyperarousal may bepresent at the peri-onset of sleep in insomnia individuals, and thatPara-I appear to show even more signs of cortical arousal than Psy-I.However, the inability to fall asleep and to maintain sleep may alsocome from an inability to inhibit external information processing atthe peri-onset of sleep. Therefore, the general hypotheses were that 1)both types of individuals with chronic insomnia (Psy-I and Para-I) willshow more signs of cortical arousal and less information processinginhibition (larger N1 and a smaller P2 to standard and deviant stimuli)than GS; and 2) Para-I will show even more signs of arousal and lessinformation processing inhibition (larger N1 and a smaller P2 tostandard and deviant stimuli) than Psy-I. The second objective was tocompare thewPN between the 3 groups in order to assess the changesin ERPs amplitudes fromwakefulness to early stage 2 and to evaluate ifthese changes remain the same in Psy-I, Para-I and GS. Wehypothesized that 1) both types of individuals with chronic insomnia(Psy-I and Para-I) will show fewer changes in N1 and P2 fromwakefulness to sleep than GS; and 2) Para-I will show even lesschanges in the wPN than Psy-I since previous studies report greatercortical activation in Para-I than in Psy-I, and that this arousal appearsto persist during sleep. In other words, there would be little differencein information processing between the waking and the sleeping statesin insomnia individuals.

2. Methods

2.1. Recruiting, screening and general procedure

All participants were recruited through newspaper advertise-ments. Following a telephone interview, eligible participants weremailed questionnaires aimed at evaluating the presence of psycho-logical symptoms (BDI; Beck et al., 1988b; BAI; Beck AnxietyInventory; Beck et al., 1988a), sleep (two-weeks of daily sleep diaries)as well as severity of sleep disturbances (ISI; Insomnia Severity Index;Morin, 1993). Upon reception of questionnaires, prospective partici-pants were invited for a clinical interview at the research center. Uponarrival, informed consent was obtained. The Structured ClinicalInterview for DSM-IV (SCID-I; Spitzer et al., 1996) and the InsomniaDiagnostic Interview (IDI; Morin, 1993) were then administered.These evaluations were conducted respectively by a clinical psychol-ogist and a sleep specialist. After the clinical evaluation, includedparticipantswere further invited to undergo four consecutive nights ofPSG recordings at the sleep laboratory. Each participant received anhonorarium for his or her participation in the study.

2.2. Participants

Participants were 78 adults, including 26 individuals sufferingfrom chronic primary psychophysiological insomnia [i.e., 14 men;43 years (9.00)], 26 individuals suffering from chronic primaryparadoxical insomnia [i.e., 6 men; 40 years (9.00)], and 26 self-defined good sleepers [i.e., 10 men; 37 years (9.00)]. The age range forall participants was 25 to 55 years. Participants had a mean educationlevel of 15.0 years (SD=3.0) and were predominantly married(61.5%). The majority of participants were employed (90.8%). Themean duration of insomnia was 10.3 years (SD=8.1) for bothinsomnia groups.

2.2.1. Good sleepers (GS)Participants included in the GS group reported being satisfied with

their sleep and a) did not have subjective complaints of sleepdifficulties, b) did not meet diagnostic criteria for insomnia and c) didnot use sleep-promoting medication. They also had to report a sleepefficiency of 85% or more in the sleep diaries as well as no sleepdifficulty of a higher level then ‘mild’ on the ISI (Morin, 1993) (scoreless than 8 on severity scale).

2.2.2. Individuals with insomnia (INS)All participants suffering from insomnia were further divided into

psychophysiological and paradoxical subgroups based on their PSGdata and their sleep diaries obtainedduring their stay at the laboratory.For the purpose of this study, we decided to categorize participants inthe appropriate subgroup if theymet the diagnostic criteria for Night 2or Night 3, since Night 1 was the adaptation night and they receivedauditory stimulations all through Night 4. Only two insomniaparticipants could not be categorized as psychophysiological orparadoxical since they did not meet the required criteria of eithersubgroup. Therefore, they were excluded from the study and only 26participants were retained in each subgroup.

2.2.3. Psychophysiological insomnia participants (Psy-I)Individuals suffering from chronic psychophysiological insomnia

met the following inclusion criteria: (a) presence of a subjectivecomplaint of insomnia, defined as difficulty initiating (i.e., sleep-onsetlatency N30 min) and/or maintaining sleep (i.e., time awake aftersleep-onset N30 min) present at least three nights per week;(b) insomnia duration of at least six months; (c) insomnia or itsperceived consequences causing marked distress or significantimpairment of occupational or social functioning; and (d) presenceof a subjective complaint of at least one negative daytime consequenceattributed to insomnia. These participants also corresponded to thecriteria set forward by Edinger et al. (2004) for ‘psychophysiological’insomnia.

2.2.4. Paradoxical insomnia participants (Para-I)In addition to the mentioned chronic primary insomnia criteria,

paradoxical insomnia participants had (a) a total sleep time of morethan 6 h 30 min and a sleep efficiency greater than 85% on nocturnalPSG; (b) showed marked discrepancies between subjective andobjective sleep measures (i.e. a difference of 60 min or more for totalsleep time, or a difference of at least 15% between subjective andobjective measures of sleep efficiency). The following observation wasalso common: complaint of severe sleep difficulties most of the time(sleepless nights on sleep diaries being an indicator of severedifficulties). These criteria for paradoxical insomnia categorizationwere derived from Edinger et al. (2004). The retained thresholdsappeared reasonable in light of the previous literature regardingparadoxical insomnia.

Exclusion criteria for all participants were: (a) presence of asignificant current medical or neurological disorder that compromisessleep; (b) presence of a major psychopathology; (c) alcohol or drug


abuse during the past year; (d) evidence of another sleep disordersuch as sleep apnea (apnea-hypopnea index N15) or periodic limbmovements during sleep (myoclonic index with arousal N15); (e) ascore of 23 or higher on the BDI (Beck et al., 1988b); (f) use ofpsychotropic or othermedications known to alter sleep; and (g) use ofa sleep-promoting agent. For the participants with insomnia, thecriteria are consistent with those of the DSM-IV (American Psycho-logical Association, 1994) for chronic and primary insomnia. Partic-ipants in the insomnia group that used a sleep-promoting medicationon occasional basis (twice a week or less often) were enrolled in thestudy after a two-week withdrawal period.

2.3. Material

2.3.1. Insomnia Diagnostic Interview (Morin, 1993)The IDI is conducted in a semi-structured format and assesses the

presence of insomnia and potential contributing factors. It is designedto identify (a) the nature of the complaint, (b) the sleep–wakeschedule, (c) insomnia severity, (d) daytime consequences, (e) thenatural history of insomnia, (f) environmental factors, (g) medicationuse, (h) sleep hygiene factors, (i) the presence of other sleep disorders,(j) the patient's medical history and general health status, and (k) afunctional analysis for antecedents, consequences, precipitating andperpetuating factors.

2.3.2. Sleep diaryThe Sleep diary (SD) (Morin, 1993) is a daily journal used to assess

subjective sleep quality. The various sleep–wake parameters derivedfor this study were sleep-onset latency (SOL); wake after sleep-onset(WASO); total sleep time (TST); time in bed (TIB); and finally, sleepefficiency (SE), defined as the ratio of TST divided by TIB, expressed asa percentage. The SD is completed upon arising each morning for a2-week baseline period in order to provide a stable index of sleepcomplaints (Morin, 1993). In addition, our participants completed theSD eachmorning upon awakening in the sleep laboratory. Ameanwascalculated for each of the derived variables.

2.3.3. Insomnia Severity IndexThe ISI (Morin, 1993) is a reliable and valid brief self-report

instrument that yields a quantitative index of perceived insomniaseverity (Bastien et al., 2001). The ISI comprises seven items targetingthe severity of sleep disturbances, the satisfaction relative to sleep, thedegree of impairment of daytime functioning caused by the sleepdisturbances, the noticeability of impairment attributed to the sleepproblem as well as the degree of distress and concern related to thesleep problem. Each item is rated on a 5-point Likert scale and thetotal score ranges from 0 to 28. A higher score reveals more severeinsomnia. The ISI partly reflects the diagnostic criteria outlined in theDSM-IV (American Psychological Association, 1994).

2.4. Polysomnographic (PSG) and Event-Related Potentials (ERPs)recordings

Participants spent four consecutive nights in the sleep laboratory.They were instructed to arrive at around 8:00 pm each night forelectrode montage and preparation. Participants were asked to refrainfromalcohol, drugs, excessive caffeine andnicotinebefore coming to thelaboratory. Bedtime and time in bed were determined according toreported time on the SD. For all participants, lights-out was initiatedafter a bio-calibration, with no less than a fixed 8 h of PSG recordings.

A standard PSG montage was used, including electroencephalo-graphic (EEG; including C3, C4, O1, O2, Fz, Cz, Pz), electromyographic(EMG; chin) and electro-oculographic (EOG; left and right: supra-orbital ridge of one eye and the infra-orbital ridge of the other)recordings. This placement allowed for the recording of horizontaland vertical eye movement artifacts and blinks to be subtracted from

on-going EEG (Gratton et al., 1983). Electrodeswere referred to linkedmastoids with a forehead ground and interelectrode impedance wasmaintained below 5 kΩ. In addition, respiration and tibialis EMGweremonitored during the first night of PSG recording in order to rule outsleep apnea and periodic limb movements. Participants diagnosedwith another sleep disorder were excluded and referred to anappropriate sleep specialist. A Grass Model 15A54 amplifier system(Astro-Med Inc., West Warwick, USA; gain 10,000; band pass 0.3–100 Hz) was used. While PSG signals were digitized at a sampling rateof 512 Hz using commercial software product (Harmonie, StellateSystem, Montreal, Canada), ERPs environment was controlled withthe InstEP Systems™ (V4.2) using the same sampling rate. Sleeprecordings were scored visually (Luna, Stellate System, Montreal,Canada) by qualified technicians according to standard criteria(Rechtschaffen and Kales, 1968) using 20-second epochs. Sleepstaging was carried out using central and occipital EEG leads.Reliability checks were conducted by an independent scorer to insurea minimum of 85% inter-scorer agreement. In addition of being thescreening night for sleep disorders other than insomnia, Night 1constituted an adaptation night. Clinical sleep data were derived fromNights 2 and 3. Auditory stimuli were presented right before going tobed and 15 min after awakening on the 3rd and 4th PSG nights, as wellas at sleep-onset and all night long on the 4th night. The present studyreports data on wakefulness (evening), sleep-onset and sleep (earlystage 2) ERPs recordings of Night 4 only.

Objective measures of sleep included sleep onset latency (SOL)(defined as the interval from lights off with the intention to sleep tothe first uninterrupted minute of stage 2), wake after sleep-onset(WASO), total sleep time (TST), sleep efficiency (SE), and proportion(%) as well as time spent (min) in stages 2, 3, 4 and rapid eyemovement (REM). For ERPs classification purposes, the sleep onsetperiod was defined as relaxed wakefulness (as subjects attempted tofall asleep) and stimulus presentation was halted upon the appear-ance of K-Complexes, a sign of definitive stage 2 sleep (Campbell andColrain, 2002).

2.5. ERP protocol

For the pairing of individuals as well as for calibration purposes,each participant received an audiometric evaluation establishingnormal hearing levels (15 dB ISO; 500, 1000, 2000 and 4000 Hz). Briefduration auditory stimuli were presented by ER-3A transducersthrough a 25 cm plastic tube and foam inserts were placed in theear canal. The generation of auditory stimuli was controlled by thePresentation Software™ (Neurobehavioral Sciences).

2.5.1. OddballTheN1 and P2waveswere recordedwith auditory stimuli consisting

of standard anddeviant tones. Standard stimuli had an intensity of 70 dBSPL; a duration of 50 ms, a rise-and-fall time of 2 ms, a frequency of2000 Hz and a probability of .85. Deviant stimuli had an intensity of90 dBSPL; adurationof 50 ms, a rise-and-fall timeof 2 ms, a frequencyof1500 Hz and a probability of .15. The deviant stimulus varied infrequency, intensity and probability of occurrence. Because itwas louderand rarer than the standard, it was expected to elicit larger N1 and P2 inthewaking state. The interstimulus intervalwas kept constant at 2 s. Theoddball paradigmconsistedof 3blocks of 180 auditory stimuli. Oneblocklasted 6 min, for a total of about 18 minof stimulus presentation for the 3blocks. For some participants, the sleep onset period did not permit thedelivery of 3 full blocks of stimuli (shorter sleep onset latency).Nonetheless, at least one full block of auditory stimuli was deliveredduring the transition from wakefulness to sleep. Participants thatreceived just one block of stimuli (135 standard tones and 45 devianttones) during sleep onset still received a sufficient number of devianttones. According to Picton et al. (2000), aminimumof 20deviant tones isrequired in order toobtain a statistically stable average that is considered

Table 1Means and standard deviations of sociodemographic and clinical data for good sleepers(GS), individuals with psychophysiological insomnia (Psy-I) and individuals withparadoxical insomnia (Para-I).

GS Psy-I Para-I

n=26 n=26 n=26

Age (years)M 37.04 (9.04) 42.65 (8.53) 40.42 (9.04)

GenderFemale 16 12 20Male 10 14 6

Insomnia duration (months)M 120.61 (99.14) 126.85 (97.45)

ISIM 1.92ab (2.90) 16.63 (3.20) 17.61 (2.92)

BDIM 2.58ab (3.42) 7.35 (5.62) 6.95 (3.65)

BAIM 1.85ab (2.62) 5.94 (5.00) 8.10 (6.88)

Note: a) GSdifferent fromPsy-I, b) GSdifferent fromPara-I, c) Psy-I different fromPara-I.


reliable and consistent. Time between blocks varied between 15 s to2 min. Again, during the presentation of tones, participants wereinstructed to ignore the tones. While awake, participants were allowedto read a book/magazine during the presentation of the auditory stimuli.If excessive eye movements were displayed, the participants wereinstructed to stare at a fixed red line on the wall.

2.5.2. Data analysisContinuous EEG (Fz, Cz and Pz sites) was recorded and stored for

off-line analysis. ERPs collected during wakefulness, sleep-onset andearly stage 2 were averaged separately. Each ERP trial was binnedaccording to stimulus category (standard and deviant) and thenaveraged accordingly. Sweeps of 550 ms were reconstructed with50 ms prior to stimulus onset (baseline) and 500 ms post stimulusonset for the detection of ERPs.

The amplitude and latency of N1 and P2 were measured for eachblock of sound presentation for each stimulus (standard and deviant) ateach timeperiod. N1was defined as themost negative peak between 70and 150 ms after stimulus-onset while P2 was defined as the mostpositive peak between 150 and 250 ms after stimulus-onset. ThreewPNdifference waves were computed: 1) the wPNa wave was measured bysubtracting the sleep onset from the waking evoked potentials (wake–sleeponset), 2) thewPNbwavewasmeasuredbysubtracting the stage 2from sleep onset evoked potentials (sleep onset — stage 2) and 3) thewPNc wave was measured by subtracting the stage 2 from the wakingevoked potentials (wake — stage 2). N1 and P2 data were scored at Cz,since all studied ERPs are usuallymaximal in amplitude at this site. Datawere rejected if either the EEG or EOG exceeded ±100 μV, effectivelyremoving artifacts resulting from large eye blinks and/or movements.Digitalfilteringwas conductedwith a bandpass of 0.01–30 Hz for 12 dB.EOG correction/rejection was applied (Gratton et al., 1983). At sleep-onset, any sweep containing high amplitude waves (e.g. vertex sharpwaves), movement time or any sign of stage 2 sleep was excluded fromfurther analysis andonly artifact-free sweepswere included. Inaddition,trials containing K-complexeswere removed from the analyses. All datawere examined for outliers.

2.6. Statistical analyses

One-wayANOVAsandChi-squarewereused in order to compare the3 groups on sociodemographic variables and sleep characteristics. Twomixed model ANOVAs including 2 within-subject factors (recordingtime, 3 levels; auditory stimuli, 2 levels) and one between-subjectindependent factor (group, 3 levels) were computed onmeasures of N1and P2 (amplitude and latency). Post-hoc pairwise comparisons werealso performed to identify significant differences between groups. Inorder to allow for multiple comparisons, the Bonferroni correctionmethodwas applied to post hoc analyses.When significant interactionswere found, simple effects tests were performed. However, one majorproblem with the ANOVA procedure is that it is very conservative.Previous literature has consistently demonstrated changes in N1 and P2from the waking to sleeping states. Thus, more liberal statisticalprocedures were also employed. Therefore, one-tailed t-tests werecomputed on the N1 and P2 amplitude and latency data in order toinvestigate between group differences. Finally, one-way ANOVAs werealso computed on wPNa, wPNb and wPNc in order to assess thepresence of any groupdifferences. Followupone-tailed t-testswere alsorun on wPNs.

3. Results

3.1. Characteristics of participants

Table 1 shows sociodemographic data and clinical variables for thethree groups of participants. Statistical analyses showed that thegroups were similar according to age, F(2, 75)=2,64, pN .05, and

gender, χ2 (2, N=78)=5.20, pN .05. Predictably, both groups of poorsleepers had higher scores on the ISI, F(2, 70)=214.02, pb .01,revealing greater severity of insomnia symptoms in these groups. Assuch, both groups of insomnia individuals reported similar severity ofsleep difficulties. Although all participants remained under the clinicalthreshold for psychiatric syndrome, both groups of poor sleepersdisplayed more depressive symptoms, F(2, 67)=9.21, pb .01, on theBDI and more anxious symptoms, F(2, 61)=9.52, pb .01, on the BAIthan GS.

3.2. Subjective and objective sleep parameters

Between group differences: Table 2 shows mean subjective andobjective sleep laboratory parameters for Nights 2, 3 and 4 for thethree groups of participants.

3.2.1. Night 2Analyses revealed significant differences among groups on all

subjective measures; SOL, F(2, 74)=11.75, pb .01 , WASO, F(2, 71)=42.57, pb .01, TST, F(2, 72)=24.81, pb .01 , and SE, F(2, 72)=41.34,pb .01 for Night 2. Specifically, compared to GS and Psy-I, Para-Ireported taking longer to fall asleep. However, the three groups weresignificantly different from each other onWASO, TST and SEmeasures.More precisely, Para-I reported spending the longest time awake aftersleep onset, sleeping the less time and having the lowest sleepefficiency, while GS reported spending the less time awake, sleepingthe longest time and having the highest sleep efficiency of the threegroups. With regard to the objective sleep variables during Night 2,significant differences among groups were found on SE, F(2, 75)=6.28, pb .01 and WASO, F(2, 75)=6.29, pb .01. Both groups ofinsomnia individuals had a lower sleep efficiency and spent moretime awake after sleep onset than GS. Differences among groupswere also observed for percentage, F(2, 75)=3.74, pb .05, and timespent, F(2, 75)=3.49, pb .05, in stage 3 and percentage, F(2, 75)=5.55, pb .01, and time spent, F(2, 75)=5.14, pb .01, in stage 4.Specifically, Psy-I had a lower percentage and spent less time in stage 3than Para-I, while Para-I had a higher percentage and spentmore timein stage 4 than GS and Psy-I.

3.2.2. Night 3For Night 3, significant differences among groupswere found again

for all subjective sleep variables; SOL, F(2, 74)=13.63, pb .01, WASO,F(2, 75)=25.53, pb .01, TST, F(2, 75)=26.78, pb .01, and SE, F(2, 75)=38.27, pb .01. Although GS and Psy-I did not differ on these measures,Para-I reported taking longer to fall asleep, spending more time

Table2

Mea

nsan

dstan

dard

deviations

oflabo

ratory

slee

ppa

rametersforGS,

Psy-Ia

ndPa

ra-I

grou

ps.

Night

2Night

3Night

4

GS

Psy-I

Para-I

GS

Psy-I

Para-I

GS

Psy-I

Para-I

Subj

mea

sures

SOL

12.19b

(11.80

)23

.96c

(23.37

)45

.96(3

5.29

)8.19

b(6

.18)

23.65c

(20.15

)45

.00(3

8.78

)12

.73b

(13.51

)25

.46c

(20.40

)48

.80(3

6.09

)W

ASO

17.92a

b(1

8.75

)60

.29c

(43.61

)12

6.46

(55.70

)15

.65b

(18.25

)52

.99c

(51.91

)14

5.58

(103

.17)

15.54a

b(1

6.16

)57

.52c

(46.50

)13

3.50

(72.72

)TS

T44

4.65

ab(4

6.79

)40

1.20

c(6

2.46

)31

5.79

(83.55

)43

3.95

b(4

9.60

)39

3.58

c(6

0.22

)28

1.42

(110

.02)

420.92

b(4

9.87

)37

8.35

c(6

2.36

)27

4.96

(105

.41)

SE(%

)93

.53a

b(5

.91)

82.84c

(10.53

)65

.12(1

5.27

)94

.83a

b(4

.52)

84.36c

(10.08

)60

.88(2

2.22

)92

.63a

b(5

.72)

81.87

c(1

2.39

)59

.28(2

1.93

)PS

Gda

taSO

L6.35

(4.54)

10.50(9

.88)

11.73(1

3.85

)5.60

(4.55)

8.14

(7.33)

8.08

(7.48)

4.60

ab(3

.57)

9.99

(8.35)

10.80(8

.11)

WASO

23.98a

b(2

2.06

)56

.25(4

0.90

)52

.77(4

1.59

)20

.26a

(17.65

)45

.43(3

7.52

)36

.04(3

1.91

)25

.74a

b(2

2.70

)55

.12(3

6.10

)58

.44(4

0.95

)TS

T42

8.58

(52.16

)40

1.88

(49.09

)41

0.99

(40.71

)40

3.88

(56.40

)40

4.90

(44.53

)40

6.60

(37.25

)41

1.08

(46.24

)38

4.68

(44.01

)38

6.35

(44.81

)SE

(%)

92.35a

b(5

.07)

85.00(8

.89)

85.96(9

.66)

93.12a

(4.08)

87.68(7

.59)

89.46(7

.02)

92.04a

b(5

.03)

85.00(8

.10)

84.04(9

.47)

Stag

e1time(m

in)

14.72(9

.61)

18.47(1

3.20

)12

.42(7

.07)

11.51(8

.63)

17.08(1

1.88

)19

.67(5

1.15

)15

.37(8

.26)

17.59(9

.69)

15.35(9

.57)

Prop

ortion

(%)

3.50

(2.32)

4.67

(3.26)

3.08

(1.79)

2.94

(2.33)

4.26

c(2

.93)

2.38

(2.18)

3.81

(2.17)

4.63

(2.52)

4.12

(2.72)

Stag

e2time(m

in)

278.60

(40.10

)26

2.42

(39.81

)25

3.23

(51.31

)26

0.07

(47.30

)25

8.59

(48.58

)24

9.22

(39.15

)26

1.12

(48.49

)24

3.60

(47.59

)24

4.91

(40.50

)Prop

ortion

(%)

65.03(5

.01)

65.39(6

.94)

61.25(9

.36)

64.31(6

.28)

63.79(8

.28)

61.54(9

.22)

63.15(7

.46)

63.22(9

.12)

63.41(7

.28)

Stag

e3time(m

in)

26.53(1

7.00

)21

.39c

(18.28

)36

.72(2

7.15

)25

.16(1

8.15

)24

.46(2

0.16

)36

.78(2

9.63

)23

.59(1

7.90

)25

.68(2

0.47

)26

.65(1

9.86

)Prop

ortion

(%)

6.14

(3.94)

5.37

c(4

.76)

9.16

(6.74)

6.46

(4.83)

6.25

(5.33)

8.94

(7.18)

5.94

(4.79)

6.88

(5.40)

7.07

(5.28)

Stag

e4time(m

in)

4.37

b(6

.08)

2.38

c(4

.58)

12.03(1

8.34

)3.08

b(5

.35)

3.34

c(6

.41)

12.15(1

5.98

)2.97

(6.72)

4.83

(8.67)

8.10

(13.33

)Prop

ortion

(%)

1.01

b(1

.40)

0.59

c(1

.13)

3.00

(4.49)

0.77

b(1

.31)

0.89

c(1

.75)

2.92

(3.83)

0.75

(1.67)

1.27

(2.20)

2.11

(3.54)

REM

time(m

in)

104.38

(24.39

)97

.22(2

7.29

)96

.59(2

1.43

)10

4.05

(28.68

)10

1.43

(28.61

)98

.95(2

1.61

)10

8.03

b(2

3.64

)92

.97(2

6.11

)91

.33(2

5.41

)Prop

ortion

(%)

24.32(4

.81)

23.98(5

.17)

23.52(4

.51)

25.52(5

.33)

24.94(6

.14)

24.22(4

.21)

26.16(4

.47)

24.00(5

.48)

23.29(5

.64)

Note:

SOL=

Slee

p-on

setlatenc

y,W

ASO

=W

akeafterslee

pon

set,TS

T=

Totals

leep

time,

SE=

Slee

pefficien

cy.

a)GSdifferen

tfrom

Psy-I,b)

GSdifferen

tfrom

Para-I,c)Psy-Id

ifferen

tfrom

Para-I.


awake and having a shorter total sleep time than the two othergroups. However, the three groups were different on sleep efficiencywith Para-I reporting the lowest efficiency and GS reporting thehighest. Objectively, the analysis revealed significant differencesamong groups for SE, F(2, 74)=4.80, pb .05, WASO, F(2, 74)=4.57,pb .05, percentage, F(2, 74)=3.81, pb .03 of stage 1 and percentage,F(2, 74)=5.83, pb .01, and time spent, F(2, 74)=6.31, pb .01, instage 4. Psy-I had a lower sleep efficiency and spent more timeawake after sleep onset than GS. They also had a higher percentageof stage 1 than Para-I, while Para-I had a higher percentage andspent more time in stage 4 than GS and Psy-I.

3.2.3. Night 4During Night 4, the results were quite similar as in Night 2 for all

subjective sleep measures, except for TST, where Para-I reportedhaving less total sleep time than the 2 other groups. For objectivesleep variables, significant differences among groups were observedon SE, F(2, 75)=8.24, pb .01, SOL, F(2, 75)=5.96, pb .01 and WASO,F(2, 75)=7.22, pb .01. Precisely, GS had a higher sleep efficiency,took less time to fall asleep, and spent less time awake than the othertwo groups. GS also spent more time in REM sleep F(2, 75)=3.50,p=.04 than Para-I.

In summary, Para-I reported sleeping worse than Psy-I and GS onevery night, while GS reported sleeping the better. Objectively, GSslept better than both groups of insomnia individuals. However, thedata in Table 2 also reveal that our group of Psy-I did not presentextremely severe sleep disturbances, even though all participants inthis group met the chronic primary insomnia diagnosis criteria.

Within groups differences: Paired sample t-tests were computedbetween objective sleep variables of Night 3 and Night 4 for each groupin order to evaluate for possible differences that could be attributed tothe presentation of auditory stimuli duringNight 4. For theGS group, nosignificant differences were found for objective sleep variables betweenNight 3 and Night 4. Among Psy-I, significant differences were found forthe TST, t (23)=2.56, pb .05 and the total amount of time spent in stage2, t (23)=2.03, pb .05. This group slept longer and spent more time instage 2 during Night 3 than during Night 4. For the Para-I group,betweennights comparisonswere significant for the followingobjectivesleep variables: SE, t (25)=2.51, pb .05, WASO, t (25)=−2.35, pb .05,percentageof stage1, t (25)=−3.13, pb .01, total amountof stage3 andpercentageof stage3, t (25)=2.57, pb .05, t (25)=2.76, pb .01 and totalamount of stage 4, t (25)=2.18, pb .05. Specifically, Para-I had a bettersleep efficiency, spent less time awake after sleep onset, had a lowerpercentage of stage 1, a higher percentage and total amount of timespent in stage 3 aswell as a higher total amount of time spent in stage 4during Night 3 compared to Night 4.

3.3. ERPs measures

See Table 3 for means and standard deviations and Fig. 1 for anillustration of the grand average ERPs for all three groups ofparticipants. Fig. 2 illustrates the grand average ERPs recorded duringwakefulness, sleep onset and stage 2 within each group.

3.3.1. N1Mixed model ANOVAs revealed no significant difference among

groups for N1 amplitude F(2, 66.9)=1.84, pN .05. However, maineffects of recording time F(2, 255.3)=148.00, pb .01 and auditorystimuli F(1, 239.6)=92.62, pb .01 were found. Furthermore, theRecording Time X Auditory Stimuli interaction was significant. Simpleeffects tests showed that the amplitude of N1 was larger for thestandard stimuli in wakefulness and during sleep onset than duringstage 2. For the deviant stimuli, the N1 amplitude was also largerduring wakefulness and sleep onset than during stage 2.

For N1 latency, no significant difference among groups was foundF(2, 65.8)=.90, pN .05, but amain effect of recording time F(2, 263.5)=

Table 3Mean latency (in ms) and amplitude (in uV) of N1 and P2 (and standard deviation) measured at Cz for GS, Psy-I and Para-I groups.

Cz N1 P2

Standard Deviant Standard Deviant

LatencyWakefulness GS 112.55 (12.77) 118.58 (14.82) 200.19 (14.99) 216.52 (18.87)

Psy-I 115.48 (15.56) 113.88 (13.23) 222.90 (19.05) 219.35 (17.09)Para-I 117.77 (12.75) 121.09 (9.34) 205.08 (23.25) 216.15 (21.93)

Sleep onset GS 118.30 (15.24) 118.65 (13.82) 218.95 (15.21) 223.88 (18.53)Psy-I 116.67 (10.53) 122.49 (11.32) 216.14 (16.35) 205.36 (19.30)Para-I 121.87 (12.19) 121.35 (11.29) 210.94 (20.32) 213.28 (19.85)

Stage 2 GS 115.00 (22.86) 124.66 (14.08) 214.13 (19.46) 220.28 (18.61)Psy-I 122.16 (15.40) 122.26 (18.67) 211.29 (20.42) 213.09 (22.37)Para-I 125.98 (14.98) 126.64 (20.39) 216.62 (20.20) 226.56 (19.78)

AmplitudeWakefulness GS −4.71 (2.75) −8.53 (3.14) 2.72 (2.38) 6.13 (4.09)

Psy-I −4.01 (1.78) −6.89 (2.21) 3.43 (1.97) 5.93 (4.71)Para-I −5.22 (2.68) −8.94 (3.72) 4.16 (2.30) 5.69 (2.89)

Sleep onset GS −3.58 (2.59) −7.71 (1.98) 5.03 (3.14) 8.33 (4.41)Psy-I −3.66 (1.73) −6.01 (2.74) 3.43 (2.15) 5.67 (3.61)Para-I −5.11 (2.26) −7.93 (4.08) 5.40 (2.64) 8.17 (4.15)

Stage 2 GS −.76 (1.45) −1.27 (2.51) 2.79 (2.17) 8.57 (4.19)Psy-I −1.24 (2.14) −2.44 (4.83) 4.03 (3.14) 9.73 (8.30)Para-I −1.50 (2.70) −2.44 (4.83) 4.75 (2.43) 12.03 (6.36)

Note: a) GS different from Psy-I, b) GS different from Para-I, c) Psy-I different from Para-I.


5.17, pb .01 was observed. Post-hoc pairwise comparisons showed asignificant difference between the N1 latencies recorded while awake(evening) and those recorded during early stage 2. The latency of N1 gotlonger from wakefulness to sleep.

3.3.2. P2For P2 amplitude, again, no significant difference among groups

was observed F(2, 66.8)=.73, pN .05, but main effects of recordingtime F(2, 249.0)=12.29, pb .01 and auditory stimuli F(1, 233.8)=126.46, pb .01 were found. In addition, Group×Recording Time andRecording Time×Auditory Stimuli interactions were found. Thesimple effects test performed on the Group×Recording Time interac-tion showed that the amplitude of P2 differed between GS and Para-Ionly during stage 2 sleep F(2, 121.4)=4.03, pb .05. Indeed, Para-Ipresented larger P2 amplitude than GS for this recording time. Thesimple effects tests also revealed that the P2 amplitude was larger forthe deviant stimuli during stage 2 than in wakefulness and duringsleep onset. However, no significant differencewas found between therecording times for the P2 amplitude for the standard stimuli.

Analyses on P2 latency, revealed no significant difference amonggroups F(2, 68.6)=.12, pN .05. However, significant main effects ofauditory stimuli as well as a significant Group×Recording Time andGroup×Auditory Stimuli interactions were found. Simple effects testsrevealed that for theGS, theP2 latencywas longerduring sleeponset thanduringwakefulness,while for the Para-I, the P2 latencywas longer duringstage 2 than in wakefulness. The Group×Auditory Stimuli interactionshowed that the P2 latencywas longer for the deviant stimuli than for thestandardone, but only forGS andPara-I. Therefore, theP2 latencydifferedbetween the different recording times and auditory stimuli within thegroups but no differences were present among the groups.

3.3.3. wPNsIn order to evaluate the difference between information processing

due to wakefulness and the extent of inhibition in informationprocessing during sleep, a one-way ANOVA was conducted on thethreewPNs. ThewPNsweremeasured at two time points correspondingto the latencies of N1 and P2. The difference scores were obtained bysubtracting ERPs amplitudes derived from sleep onset from thoseobtainedwhile awake (wPNa), theERPs amplitudesderived fromstage2sleep from those obtained at sleep onset (wPNb) as well as the ERPsamplitudes derived from stage 2 sleep from those obtained during

wakefulness recordings (wPNc). Tables 3 and 4 show the means andstandard deviations of the wPNs measured at two time pointscorresponding to the latencies of N1 and P2 at Cz for the three groups.The one-wayANOVA revealed only one difference among groups for thewPNb wave F(2, 34)=3.84, pb .05. Post-hoc test revealed that thetransition from sleep onset to stage 2 sleep for the time pointcorresponding to the latency of P2 (deviant stimuli) was differentbetweenGSandPara-I. Indeed, Para-I presented amuch largerdifferencewave following the deviant stimuli than GS when the ERPs amplitudesderived from stage 2 sleep were subtracted from those obtained duringsleep onset. Figs. 3 and 4 illustrates the wPNs measured at two timepoints corresponding to the latencies of N1 and P2 at Cz for all groups.

3.4. One tailed t tests for N1 and P2

Analyses performed on the ERPs amplitudes revealed that the N1amplitude recorded during sleep onset, t (28)=−1.96, pb .05 wassmaller following the deviant stimuli for Psy-I than for GS. The P2amplitudewasalsodifferentduring sleeponset among these twogroups,for both the standard stimuli t (32)=1.69, pb .05 and the deviant one,t (28)=1.79, pb .05, with Psy-I again presenting a smaller amplitudethan GS. The N1 amplitude recorded during sleep onset, t (39)=2.02,pb .05 was larger following the standard stimuli for Para-I than for GS.Differences among GS and Para-I were also observed for the P2amplitude resulting from the standard tones recorded during wakeful-ness, t (34)=−1.84, pb .05, but also for the P2 amplitude during earlystage 2 for both the standard, t (42)=−2.82, pb .01 and the deviantstimuli, t (39)=−2.09, pb .05. The P2 component was larger in Para-Iwhen compared to GS for these two recording times. Finally, significantdifferences were identified among Psy-I and Para-I during wakefulnessfor the N1 amplitude resulting from the deviant stimuli, t (26)=1.74,pb .05, as well as for the N1 amplitude during sleep onset, t (33)=2.07,pb .05 for the standard tonewhichwas significantly larger in Para-I thanin Psy-I. The P2 amplitude was also larger in Para-I than in Psy-I duringthe sleep onset, for both the standard, t (33)=−2.36, pb .01 and thedeviant stimuli, t (27)=−1.72, pb .05.

Analyses also revealed that the P2 latencywas longer for Psy-I thanGS duringwakefulness t (30)=−3.75, pb .01 for the standard stimuli,but that it was shorter for Psy-I than GS during sleep onset, t (28)=2.68, pb .01 for the deviant stimuli. The N1 latency was shorter for GSthan Para-I during early stage 2, t (42)=−2.00, pb .05 for the

WakefulnessStandard

Wakefulness Deviant

Sleep OnsetStandard

Early Stage 2Standard

Sleep OnsetDeviant

Early Stage 2Deviant

500 ms 500 ms

500 ms 500 ms

500 ms 500 ms

N1N1

N1

N1

N1

N1

P2

P2

P2

P2

P2

P2 GS

Psy-IPara-I

µV µV

GSPsy-I

Para-I

GSPsy-I

Para-I

GSPsy-I

Para-I

GSPsy-I

Para-I

GSPsy-I

Para-I

Fig. 1. Grand averages ERPs at Cz to standard and deviant stimuli during wakefulness, sleep onset and definitive sleep (stage 2). Note: The grand average does not always reflect theN1 and P2 means that were scored for individual subjects.


standard tones. Psy-I presented shorter latency than Para-I for the N1resulting from deviant stimuli during wakefulness, t (26)=−1.68,pb .05, and the P2 latency during early stage 2 t (36)=−1.96, pb .05for the deviant stimuli. Alternately, the P2 latency resulting from thestandard tones during wakefulness was shorter among Para-I thanPsy-I, t (34)=2.47, pb .01.

Significant differences were found among GS and Psy-I for the P2amplitude from the wPNa, t (22)=−2.50, pb .01. and the wPNb,t (28)=1.76, pb .05, for the standard tones, as well as for the N1amplitude from wPNb, t (24)=−1.94, pb .05 for the deviant stimuli.For all those wPNs, GS presented a larger difference than Psy-I in theERPs components. Para-I presented significant larger differences thanGS for the following: the P2 amplitude from the wPNb, for both thestandard t (31)=1.82, pb .05 and the deviant tones, t (44)=3.57,pb .01; and the P2 amplitude from the wPNc resulting from thedeviant tones, t (24)=2.28, pb .05. Finally, Para-I presented largerdifferences than Psy-I for the N1 amplitude from the wPNb for thedeviant stimuli, t (20)=2.06, pb .05, and the P2 amplitude from thewPNc for the standard, t (30)=1.95, pb .05 and the deviant tones,t (22)=1.92, pb .05.

4. Discussion

4.1. Sleep variables

As expected, differences between groups were observed onsubjective measures of sleep, with Para-I reporting more complaintsand sleep difficulties on all measures when compared with the othertwo groups. Significant differences were also found on objective sleepvariables of latency to sleep onset, wake after sleep onset and sleepefficiency, as well as percentage and amount of time spent in differentstages during the laboratory nights. Most differences were observedbetween Psy-I and GS, with a few exceptions. These results confirmthat our categorizing procedure for Para-I appears to be quitesensitive and reflect the criteria set forth by Edinger et al. (2004).

4.2. Event-related potentials

A maximum peak deflection algorithm was used to score N1 andP2. It is important to mention that a limit of this scoring procedure isthat the maximum peak deflection procedure might mistakenly

Standard Deviant

500 ms

Standard Deviant

Standard Deviant

N1

P2

500 ms

WakefulnessSleep onset

Stage 2

µV µV

GS

Psy-I

Para-I

500 ms

500 ms500 ms

500 ms

P2

N1

N1

P2

N1

P2

N1

P2


Stage 2


Stage 2


Stage 2


Stage 2


Stage 2

Fig. 2. Grand averages ERPs at Cz to standard and deviant stimuli for GS, Psy-I and Para-I. Note: The grand average does not always reflect the N1 and P2 means that were scored forindividual subjects.

Table 4wPNs means and standard deviations at Cz for GS, Psy-I and Para-I groups.

Amplitude N1 P2

Standard Deviant Standard Deviant

Wake — Sleep onset (wPNa) GS −.96 (2.40) −1.13 (2.36) −1.48a (2.25) −.97 (4.73)Psy-I −.61 (1.64) −1.26 (1.02) .60 (1.74) −.73 (1.45)Para-I −.22 (1.81) −1.42 (3.45) −1.00 (3.27) −2.52 (4.81)

Sleep onset — stage 2 (wPNb) GS −3.09 (1.76) −6.59a (4.36) 1.75ab (2.89) −.25b (4.81)Psy-I −2.83 (2.18) −3.51c (3.45) .02 (2.38) −2.17 (8.27)Para-I −3.62 (2.55) −6.68 (3.77) −.01 (2.66) −6.65 (4.07)

Wake — stage 2 (wPNc) GS −4.01 (2.51) −6.87 (4.89) −.15 (1.95) −2.74b (4.83)Psy-I −3.79 (2.58) −5.49 (3.09) .68c (2.23) −2.68c (6.66)Para-I −3.69 (3.27) −6.53 (3.96) −1.06 (2.69) −7.86 (6.59)

Note: a) GS different from Psy-I, b) GS different from Para-I, c) Psy-I different from Para-I.


wPNa wPNb wPNc

GS

Psy-I

Para-I

Wake SO

SO Stage 2

Wake Stage 2

Wake SO

SO Stage 2

Wake Stage 2

Wake SO

SO Stage 2

Wake Stage 2

500 ms sm005sm005

sm005sm005sm005

sm005sm005sm005

µVµVµV

Fig. 3. Grand average ERPs at Cz to standard stimuli for GS, Psy-I and Para-I. The gray zone represents the difference in information processing between the two recording times.


identify noise as a true signal, particularly during the sleep period. It islikely that this could account for the differences between the meandata and the grand averages.

Themixedmodel ANOVA results indicate no significant differencesfor the N1 amplitude and latency between the three groups. Thestimulus type had an effect on the amplitudes of either N1 or P2 peaks,

wPNa wPNb wPNc µVµVµV

GS

Psy-I

Para-I

sm005sm005sm005

sm005sm005sm005

sm005sm005sm005

Wake SO

SO Stage 2

Wake Stage 2

Wake SO

SO Stage 2

Wake Stage 2

Wake SO

SO Stage 2

Wake Stage 2

Fig. 4. Grand average ERPs at Cz to deviant stimuli for GS, Psy-I and Para-I. The gray zone represents the difference in information processing between the two recording times.


since the deviant tone elicited larger amplitudes than the standardone. The recording time also had an impact on the amplitudes of N1and P2. As expected, the amplitude of N1 decreased fromwakefulness

to sleep, while the amplitude of P2 increased. These findings areconsistent with other studies (Campbell et al., 1992; Crowley andColrain, 2004; Kertesz and Cote, 2011). Finally, the recording time also


influenced the latencies of both N1 and P2, as they got longer fromwakefulness to sleep. It has been shown that the latency of N1 and P2tend to become prolonged as the individual becomes increasinglydrowsy and finally enters definitive sleep (Campbell et al., 1992; DeLugt et al., 1996).

On the other hand, when one tailed t-tests were performed on theERPs data, between groups differences emerged. The N1 amplituderecorded during sleep onset was the largest for Para-I while it was thesmallest for Psy-I. During wakefulness, N1 was also larger for Para-Ithan for Psy-I. The larger N1 amplitude observed in Para-I during sleeponset supports the neurocognitive model of insomnia (Perlis et al.,1997) that suggests that high frequency activity is a main feature ofchronic insomnia that could interfere with sleep initiation. This modelalso states that increased cortical arousal would also lead toincompatible sleep activities such as enhanced sensory and informa-tion processing which could be reflected by the larger N1 amplitudealso observed in Para-I during wakefulness before going to sleep.Although we did not find significant larger N1 amplitude for the Psy-Igroup, our previous study (Bastien et al., 2008) revealed that theypresent larger N1 upon awakening in the morning. Thus, it is possiblethat the degree of arousal level varies during the day according toother factors. In that regard, Turcotte and Bastien (2009) investigatedthe relation between objective sleep parameters and the amplitudesand latencies of ERPs components N1 and P2 among Psy-I and GS.Pearson's correlation analyses were conducted between objectivesleep measures and the amplitude and latency of N1 and P2 recordedduring the evening, sleep onset and upon awakening. They showedthat the increase in N1 and P2 amplitude observed for Psy-I seems tobe directly linked to objective sleep quality while sleep quality seemsto be directly associated to the larger ERPs amplitudes observed thenext morning. Therefore, the extent of attentional processing could bewaxing andwaning with objective sleep quality. It is also possible thatthe stresses of daily activities (stress at work, taking care of the kids)influenced information processing. While the ERPs protocol used inthis study relied only on a one night assessment, which does notpermit to evaluate for stability, further studies should focus onmultiple assessments over several nights and days in order to monitorthe influence of sleep quality and daily activities on variation ofattentional processing levels among insomnia individuals.

Regarding the P2 amplitude, one tailed t-tests also revealed morebetween groups differences than the mixed model analyses. Duringwakefulness, the P2 amplitude was larger in Para-I than GS. Duringsleep onset, the P2 amplitude was smaller in Psy-I compared to GS,while it was larger in Para-I than in GS during stage 2 sleep. Again,these results provide support to the neurocognitivemodel of insomnia(Perlis et al., 1997).We hypothesized that insomnia individuals wouldpresent a smaller P2 as they would lack the ability to inhibit externalstimulations. Therefore, the smaller P2 observed during sleep onset inPsy-I could reflect an inability to inhibit non-pertinent stimuli whiletrying to fall asleep. These results corroborate those obtained byKertesz and Cote (2011) and indicate that Psy-I have not successfullydisengaged or inhibited to the same extent as GS. On the other hand,the larger P2 observed among the Para-I across all recording timesraises an interpretation challenge. The underlying neurologicalcorrelates or functional significance of the P2 is still poorly understood(Crowley and Colrain, 2004). In light of our previous results showingthat Para-I appeared to be the group that was the most disturbed bythe auditory tones delivered during the night according to theirobjective PSG parameters, it is possible to argue that the need forgreater inhibition might come from the fact that they are more easilydisturbed by the stimulations. Crowley and Colrain (2004) suggestedthat the amplitude of P2 following standard tones appears to increasewith age (just like sleep fragmentation), therefore an enhanced P2might represent an inability to inhibit or withdraw attention fromirrelevant stimuli. A growing body of evidence suggests that corticalarousal is present in insomnia individuals. Insomnia being multifac-

eted, it is likely that other factors act to maintain sleep difficulties (e.g.repeated negative events, emotional arousal). Usually, Para-I produceseemingly normal PSGs (when not bothered by stimulations), whichdo not represent their sleep complaints. However, in this study, thePara-I group presented larger P2 amplitude during wakefulness andsleep than GS and larger P2 amplitude during sleep onset than Psy-I.While Turcotte and Bastien (2009) linked objective sleep quality withevening, morning and sleep onset ERPs components, they did notevaluate a possible association between N1, P2 and subjective sleepvariables, neither did they have a Para-I group. Therefore, it is possiblethat enhanced P2 amplitude might be related to subjective sleepquality among this subgroup of insomnia individuals, since they alsoreported poor sleep efficiency on this night. It is also possible that thegreater need for inhibition reflected by the larger P2 might come inresponse to the larger N1 also observed in this group. Therefore, theincreased inhibition might be in response to compensate for theenhanced attentional processing.

While no significant difference among groups was found concern-ing the latency of N1 and P2 in the results from the mixed modelanalyses, the one tailed t-tests revealed some. When compared to GS,a delayed P2 during wakefulness was observed among Psy-I, while adelayed N1 during stage 2 was found in Para-I following standardtones. According to previous studies (Bastuji and Garcia-Larrea, 1999;Colrain et al., 2000; Cote et al., 2002; Harsh et al., 1994), a latencydelay in ERPs usually indicates slowed processing speed. However,during sleep onset, Psy-I showed faster P2 latency following deviantstimuli than GS. Although these results seem contradictory, it ispossible to argue that insomnia individuals (Psy-I and Para-I) appearto present an alteration in information processing speed.

The current research is novel in investigating the wPN, this longlasting negative difference wave that overlaps both the N1 and P2peaks causing themboth to becomemore positive as an individual fallsasleep. We hypothesized that both types of chronic insomnia wouldshow fewer changes inN1 and P2 amplitude thanGS fromwakefulnessto sleep, since previous studies reported that hyperarousal seems to beconstant and persistent. Part of this hypothesis was confirmed withPsy-I showing less difference than GS in the N1 amplitude from sleeponset to sleep for the deviant stimuli and in the P2 amplitude fromwakefulness to sleep onset and sleep onset to sleep for the standardstimuli. At sleep onset, the ability to successfully disengage attentionfrom the external stimulations usually concurswith the removal of thewPN, therefore causingN1 to get smaller and P2 to get larger amongGS(Muller-Gass and Campbell, 2002; Näätänen, 1990). However, thesmaller changes observed in Psy-I during these transition times appearto indicate that they have trouble disengaging attention or inhibitingstimulations coming from the external environment in order to sleep.These results provide support to Espie's insomnia model (2002) thatstates that inhibitory processes or the inability to de-arouse ordisengage from active wakefulness processing interferes with thenormal initiation of sleep processes in insomnia individuals. Theseresults also corroborate a previous study byNofzinger et al. (2004) thatcompared individuals with primary insomnia with GS using positionemission tomography. They found that insomnia participants showedgreater global cerebral glucose metabolism during sleep and whileawake and a smaller decline in relative metabolism from waking tosleep states in wake-promoting regions. The authors concluded thatthe inability to fall asleep in insomnia individuals may be related to afailure of arousal mechanisms to decline in activity from waking tosleep.

Alternately, the larger changes observed in the Para-I group for theN1 amplitude from sleep onset to sleep for the deviant stimuli and theP2 amplitude fromwakefulness to sleep for both types of stimuli whencompared to Psy-I, as well as the larger difference in the P2 amplitudefrom sleep onset to sleep, for both stimuli, and the P2 amplitude fromwakefulness to sleep for deviant tones when compared to GS, appearmore challenging to interpret. These results indicate a large amount of


variation in the extent of information processing during sleep onsetand sleep. Therefore, inhibition processes necessary to fall asleep arevery different in Para-I and this group might have to show greaterinhibition in order to close channels to irrelevant stimulations.Furthermore, this group reported taking longer to fall asleep thanPsy-I and GS on this particular night, while this complaint was onlypartially corroborated by PSG. This suggests, once again, that the P2amplitude might be associated with the subjective sleep perception.Moreover, between night comparisons revealed that GS were notaffected by the presentation of stimuli all through the fourth night,while Para-I appeared to be the group that was the most disturbed bythe auditory tones according to their objective sleep parameters. Theseresults appear to contradict a study by Haynes et al. (1985) thatinvestigated arousal thresholds in sleep-onset insomnia, Para-I, andGS. In this study, all three groups showed similar auditory arousalthresholds and no differences between groups were found insensitivity to nocturnal auditory stimuli. However, at this time, nocriteria had yet been established to subdivide insomnia individuals inPsy-I or Para-I, so only the objective sleep onset latency was used toseparate these groups. Furthermore, Haynes et al. (1985) onlyrecruited sleep-onset insomnia participants and they measured onlythe sleep onset latency, the number of awakenings and the latency toreturn to sleep after awakening as objective sleep variables. Hayneset al. (1985) presented a 1000-Hz tone with intervals of 13 s betweentone presentations over a speaker suspended 42 cm above the bed.Decibel levelswere increased 4–5 dBwith each tone presentationuntilthe subject acknowledged hearing the most recent tone presented. Inour protocol, participants received standard (70 dB, 2000 Hz) anddeviant (90 dB, 1500 Hz) stimuli through ear inserts and theinterstimulus interval was kept constant at 2 s. Therefore, our protocolappears to bemore intrusive and it is possible that in these conditions,the auditory arousal threshold might differ in Para-I and that theauditory stimuli disturbed or disrupted sleep and this disturbance wasevidenced by other objective sleep variables.

4.3. Insomnia subtypes

Considering the variability in sleep patterns of insomnia in-dividuals, it can be difficult to categorize these individuals into Para-Ior Psy-I subtype even with a standard set of criteria like the onesprovided by Edinger et al. (2004). Our protocol required thatparticipants spend four nights at the sleep laboratory, so multipleobjective and subjective sleep recordings were obtained. While thediagnostic criteria put forward by Edinger et al. (2004) are certainlyuseful, they offer few indications regarding how many nights shouldbe taken into account before categorizing insomnia participants asparadoxical or which cut-offs should be used to quantify thediscrepancies between subjective estimates and objective measures.For the purpose of this study, we decided to categorize participants asindividuals with paradoxical insomnia if they met the diagnosticcriteria during Night 2 or Night 3. We also decided to use a 15% cut-offbetween subjective and objective measures of sleep efficiency, and adifference of 60 min or more for total sleep time. In light of the resultsobtained for the paradoxical insomnia group in this study, thecombination of the standard set of criteria provided by Edinger et al.(2004) and the thresholds we decided to retain to quantify thediscrepancies between subjective estimates and objective measuresappears to be strongly justified.

5. Conclusion

While individuals with psychophysiological insomnia showed aninability to inhibit information processing during sleep onset, in-dividuals with paradoxical insomnia presented enhanced attentionalprocessing and/or a greater need for inhibition during wakefulness,sleep onset and sleep. This group was also the most disturbed,

according to objective sleep parameters from the presentation ofauditory tones. Individuals with psychophysiological insomniashowed fewer changes in information processing from wakefulnessto sleep onset and from sleep onset to sleep, while the paradoxicalgroup presented larger changes in information processing during thetransition from sleep onset to sleep and during wakefulness to sleep.ERPs and PSA studies are beginning to reveal that these 2 subgroupsappear to present distinct cortical activity related to informationprocessing characteristics. Obviously, these results highlight the factthat brain activity in individuals with paradoxical insomnia requiresmuch more investigation since information processing seems to bereally altered in this group during transitional conscious to uncon-scious states and we currently are only beginning to clarify whatmight be happening in this group of sleepers in which the severity ofsleep complaints does not reflect actual sleep. Also, further studiesusing multiple assessments and ERPs recordings during the nightwhile also monitoring for subjective sleep quality and/or dailyactivities, and to another extent personality, could be informativeon the degree of interference of these factors on informationprocessing. Furthermore, studies evaluating the relationship betweenERPs and the degree of misperception or discrepancy amid objectiveand subjective sleep variables might provide more information onvariations in information processing and its link to a potentialobjective/subjective sleep difficulty continuum. Finally, it is notewor-thy to mention that the definition of the sleep onset period is slightlydifferent among studies according to the measured variables (i.e., EEGbased or behavioral) and that it is possible that the amplitude of thewPN waves vary according to this definition. Therefore, studiesfocusing on the sleep onset period in insomnia individuals and thedifference in information processing possible during this period isworthy of future investigation. The repeated sleep onset recordingprocedure previously used by researchers (Cote et al., 2002; Kerteszand Cote, 2011; Ogilvie et al., 1991) to investigate this critical periodshould be prioritized.

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