The Role of Dreaming in Sleep: REM and NREM Sleep Stages and Their Impact on Dreaming, Exercises of Literature

Download The Role of Dreaming in Sleep: REM and NREM Sleep Stages and Their Impact on Dreaming and more Exercises Literature in PDF only on Docsity! 1         Dream Function: Exploring the possibility that dreams protect sleep     Refqah Jassiem and Danyal Wainstein Department of Psychology University of Cape Town Supervisor: Mark Solms Word Count: Abstract: 168 Main Body: 9780 2         ABSTRACT A review of current literature shows that a physiological function for dreaming has not yet been empirically established. Recent developments have resulted in the identification of the neural correlates of dreaming; however, these correlates are yet to be linked with a function for dreaming. Based on the literature, it is reasonable to propose that dreams may function to protect sleep by diverting the disruptive physiological arousal events that naturally occur during sleep. To test this hypothesis, a single-case of dream loss due to bilateral ischemic infarction in the occipital lobes was studied using polysomnographic recordings. The quality and quantity of the patient’s sleep was analysed over two nights in the sleep laboratory in order to verify whether her sleep was significantly more disturbed than the established norms. As predicted, results showed that sleep was significantly more disturbed than the norms, specifically with regard to non-REM sleep stages 1 and 2. The ways in which dreaming may contribute to the protection of sleep are discussed in light of this finding. Keywords: dreaming; dream loss; bilateral occipital lesions; disturbed sleep; polysomnograph 5         humans during REM sleep, within the MC-ML system (Gottesmann, 2004). Finally, recent studies based on the internal measurement of dopamine (through microdialysis and single cell recordings) during the sleep-wake cycle in rats, found a substantial increase in dopamine cell activity and terminal release during REM sleep (Dahan et al., 2007; Lena et al., 2005). In summary, the overall consensus between the clinico-anatomical studies on the one hand, and the neuroimaging and in vivo studies on the other, suggest that the dopaminergic MC-ML system is responsible for the neurogenesis of dreams. REM Sleep and Dreaming are Doubly Dissociable States As previously mentioned, there is a substantial amount of evidence in support of the fact that dreaming and REM sleep are doubly dissociable states. A number of case studies provide evidence for dream cessation occurring while the REM cycle has remained entirely unaltered (Benson & Greenberg, 1969; Bishof & Bassetti, 2004; Brown, 1972; Jus et al., 1973, Poza & Martí Massó, 2006). In other words, the patients ceased to dream while still experiencing entirely normal REM sleep states. Moreover, patients who have suffered lesions to their pontine brainstems, resulting in the elimination of their REM sleep cycles, have still reported experiencing dreams (Solms, 1997). Despite such evidence, many researchers dispute the fact that dreaming and REM actually are doubly dissociable states, because these two phenomena frequently co-occur. In response to this, Solms (2000) explains that although dreaming is highly correlated with REM sleep, this correlation is not due to cholinergic brainstem mechanisms generating dreams, but rather because cholinergic activation provides sufficient cerebral stimulation during sleep for dreaming to occur — dreaming can result from any such cerebral activation. To illustrate this point, Solms (1997, 2000a) draws attention to the occurrence of nightmares during non-REM (NREM) sleep in patients experiencing partial seizures. Furthermore, there is a substantial amount of literature documenting dreaming outside of REM sleep, when cholinergic brainstem mechanisms are silent. Furthermore, numerous studies have documented that some form of dream reports can be obtained from all stages of NREM sleep at rates of up to 50-75% (Foulkes, 1962; Foulkes & Vogel, 1965; Suzuki et al., 2004). Moreover, dream reports from NREM sleep that are indistinguishable from those during REM, have been reported between 5-10% (Hobson, 1988) and 10-30% (Monroe et al., 1965, as cited in Rechtschaffen, 1973) of the time. In particular, Foulkes and Vogel (1965) reported that participants awoken at sleep onset and during N1 sleep often report vivid 6         “dream-like” hallucinatory images with kinaesthetic features, as well as static visual imagery throughout the NREM sleep stages. Recently, functional neuroimaging results have provided further evidence for dream activity during NREM. For example, Hofle et al. (1997) used positron emission tomography (PET) imaging techniques to investigate the changes in regional cerebral blood flow (rCBF) during the progression from relaxed wakefulness through slow wave sleep (SWS). The changes were examined as a function of spindle and delta EEG activities that progressed during NREM sleep. Hofle et al. reported that delta activity and rCBF covaried positively in the primary and secondary visual cortex and the secondary auditory cortex (BA 22). Indeed, this activation is similar to the activation recorded when subjects are asked to lay with their eyes closed and imagine sounds or images (Hofle et al., 1997). In addition, positive covariation between delta activity and rCBF was also found in the left inferior parietal lobule (BA 40). In light of their results, Hofle et al. (1997) hypothesised that the visual and secondary auditory cortex may reveal a possible substrate for dream-like mentation during NREM sleep. These results complement the evidence reviewed above, as the activation of the left inferior parietal lobule corresponds with Solms’s (1997, 2000a, 2000b) clinico- anatomical lesion findings. Furthermore, a functional magnetic imaging (fMRI) study by Portas et al. (2000), that examined auditory processing across the sleep-wake cycle, found that neutral auditory stimuli presented during sleep resulted in activation of the auditory cortex, thalamus and caudate bilaterally; while a meaningful auditory stimulus (e.g. the participant’s name) additionally resulted in higher activation of the middle temporal gyrus and the orbitofrontal cortex bilaterally. As a result, these authors concluded that the brain was able to facilitate external stimuli during sleep. Therefore, it seems that the dreaming mind may retain subliminal contact with reality through the sensory channels, suggesting that “sensory stimuli that reach us during sleep may very well become the sources of dreams” (Freud, 1900/1953, p.23, as cited in Solms, 1997, p.136). Unfortunately, neither of these studies actually investigated whether dreaming was definitely related to the neuronal activation seen during the neuroimaging scans. However, Takeuchi et al. (2001), in a study aimed at exploring the relationship between dreaming during induced Sleep Onset REM Periods (SOREMPs) and regular N1 sleep onset, found that dreaming was more likely to occur in NREM sleep onset when there 7         was increased electroencephalographic (EEG) arousals1 and waking during this time. As a result, the authors concluded that there is a “strong relationship between NREMP Dreams and awakening in our results...we postulate that arousal processes might be related to Dream production during NREM sleep” (p. 50). Therefore, Solms’s (1997) hypothesis, that dreaming throughout the sleep-wake cycle can be activated by various arousing stimuli, some of which are external, is supported by numerous lines of evidence. Consequently, many now agree that dreaming is neither intrinsic to, nor isomorphic with, the REM state (Feinberg, 2000; Vogel, 2000). It would appear that dreaming serves a specific function during sleep, and that it is not merely an epiphenomenon of REM processes. Dreams Protect Sleep As mentioned, the dopaminergic MC-ML system is responsible for generating dreams, and is a partial constituent of what Panksepp (1998) refers to as the SEEKING system. This system motivates nonspecific appetitive behaviours within all mammals, including humans. Several converging lines of evidence have already confirmed that this system is highly active during REM sleep, even more so even than during waking (Dahan et al., 2007; Gottesmann et al., 2004). This evidence has led Solms (1997, 2000a) to hypothesise that because the dorsolateral prefrontal cortex (DLPFC) is deactivated during sleep, the volitional urges which are usually executed in this region during waking (in the form of thoughts and actions with logical consistency, structure and volition) have to be redirected. Therefore, Solms (2000a) argues that these appetitive urges eminating from the highly aroused limbic system are regressively directed toward the PTO region2, where they are represented virtually as dreams.                                                                                                                           1 Arousals can be defined as transient phenomena that result in fragmented sleep without behavioural waking (p. 10). Specifically, an arousal can be scored during REM, N1, N2, or N3 if there is an abrupt shift in the EEG frequency that is characterised by a 3 to 14 second intrusion of alpha, beta, or theta waves (but not spindles or delta). Arousals are expressed as a number per hour (Arousal Index; AI) and in middle aged adults it is normal to have an AI of up to 10 (Chokroverty, 2009). 2 The PTO junction forms an association cortex in the brain; this region is not responsible for primary sensory experiences, but participates in sensory integration and abstract thought processing (Yu, 2007). As mentioned, this region is crucial to dreaming, and damage can result in complete dream loss (Bishoff & Bassetti, 2004; Poza, & Martí Massó, 2006; Solms, 1997). Therefore, it is reasonable to assert that the PTO junction is the perceptual stage upon where dreams are ‘played out’. 10         Aims and Hypotheses While there has been an increased interest in the scientific exploration of dreams in the last few decades, no dream theory has yet been successfully empirically tested. Furthermore, while there have been two cases of total dream loss published (Bischoff & Bassetti, 2004; Poza & Martí Massó, 2006) with full clinical, neuropsychological, neuroimaging and polysomnographic data, the aim of these studies was to fully document a cessation of dreaming simultaneously occurring with regular REM cycles and not to report the effects of dream loss on sleep. However, both cases reported that their patients had experienced disturbed sleep since their dream loss. In light of these results, this study had two primary aims: firstly, we aimed to use polysomnographic recording to comprehensively document dream loss as a distinct neuropsychological dysfunction; and secondly, to focus on the relationship between disturbed sleep and loss of dreaming. For this study, it was predicted that a patient with bilateral occipital lesions would have complete dream loss and that her sleep would subsequently be disturbed. The following hypothesis was examined: H1: A single participant with bilateral occipital lesions will experience significantly disturbed sleep when compared with published norms. 11         METHODS Sample Mrs P was a 65-year-old dextral female. She was a homemaker with 10 years of formal education, and no previous medical or psychiatric history. The selection criteria for the case included loss of dreaming (a complete lack of subjective dream recall), accompanied by specific posterior lesions to the PTO junction. Mrs P was the first patient found to meet these criteria. Any patients with any other sleep or neurological disorder that could confound the results, were not considered for the study. Mrs P was referred by a neurologist from Groote Schuur Hospital. Healthy Age-Matched Controls. In order to understand specifically what effects dream loss may have on sleep, it is important to exclude natural changes in sleep that are related to age. Age has been found to have disruptive effects on sleep organisation and architecture (Chokroverty, 2009; Feinberg, 1973). For this reason, a study by Boselli et al. (1998) comprised of 10 participants (5 females, 5 males) over 60 years of age, was used as a control group. Boselli et al. recruited healthy individuals with no daytime complaints, good sleep quality and regular life habits. Moreover, the participants’ sleep macrostructure was compatible with widely accepted quantitative norms (Ohayon et al., 2004). Chronic Stroke Controls. In addition to age, stroke has been found to have an impact on the quality of sleep (Bassetti & Aldrich, 2001; Chokroverty & Montagna, 2009; Korner et al., 1986; Vock et al., 2002). In order to exclude the effects of stroke on Mrs P’s sleep quality and quantity, published sleep macrostructure means for a group of patients with ischemic hemispheric lesions have been used for comparison (Vock et al., 2002). Since our case was in the post-chronic phase after stroke (>5 years), Vock et al.’s study was suitable to use for comparison. Measures Case History Mrs P’s case history was taken directly from her medical records, and her case information has been duplicated here in accordance with the APA guidelines for confidentiality and anonymity (American Psychiatric Association, 2005). As such, certain 12         identifying information has been excluded, albeit not to the extent that the information provided has been distorted in any way Dream Recall Mrs P was asked to give a subjective account of her dreaming, or lack thereof, since her stroke in 2006. Specifically, she was asked whether she still dreamt or if she remembered any dreams she may have had in the past 5 years. In addition, semi-spontaneous nocturnal REM sleep interviewing, during the first night in the sleep laboratory, was used to verify dream loss. This interview consisted of briefly asking Mrs P, during unprompted REM awakening, if she was dreaming, and about what was going through her mind prior to being awoken. Neuropsychological Tests A range of neurocognitive tests were chosen for this study, focusing primarily on higher visual and spatial perception, visual and verbal short-term memory, and visual and audio-verbal long-term memory — the necessary neuropsychological functions required for intact dream recall (Appendix A). The constellation of neuropsychological subtests and scoring systems used in this study are widely recognised and internationally established standard measures, and are being used on an ongoing basis in the daily clinical neurocognitive assessments of the neuropsychologists at Groote Schuur Hospital (Strauss, Sherman & Spreen, 2006). Visuo-spatial perception. For the assessment of visuo-spatial perception, the subtests chosen were from Luria’s Neuropsychological Investigation for higher visual perception and integration included: 1) object recognition; 2) visual recognition of letters, words and phrases; 3) calculations; 4) colours and faces; 5) language (Christensen, 1974). In addition, the Judgement of Line Orientation Test (Benton et al., 1994); Benton’s Facial Recognition Test (Benton et al., 1994); and the Boston Naming Test (BNT; which doubles as a language test), were also used (Kaplan, Goodglass & Weintraub, 2001). Constructional praxis. The WAIS-III Blocks were chosen for assessing perceptual organization and constructional praxis (The Psychological Corporation, 1997). In addition, the Rey-Osterrieth Complex Figure was also utilised for this purpose (ROCF; Rey, 1941; Osterrieth, 1944). 15         scores into z-scores (Zcalc) which were then compared to the critical z-values (Zcrit) in order to determine whether the null hypotheses were rejected. Specifically, the critical z-values used were: Zcrit = ± 2.58 ( = 0.01; [two-tailed test]); Zcrit = 2.32 ( = 0.01, [one-tailed test]; Durrheim, 2002). Neurocognitive Tests. The neuropsychological tests were analysed by way of the hypothetical-deductive approach, as used by the neuropsychologist at Groote Schuur Hospital in their everyday clinical practice. Specifically, we used Mrs P’s test scores to confirm or reject informal hypothesis about her neurocognitive functioning. For example, we hypothesized that Mrs P’s memory would be intact, and used the scores from her tests to either accept or reject this conclusion. Scoring of the neuropsychological tests was done according to the standard procedures outlined with each test. Procedure The neuropsychological testing took place at Groote Schuur Hospital, where a quiet room, free of distractions, was used as an assessment setting. The sleep study was completed at the Cape Sleep Centre at Gatesville Medical Centre—an approved AASM sleep Laboratory — where the PSG recording was professionally monitored by a qualified sleep technologist. Sleep Study Mrs P was monitored in the Gatesville sleep laboratory for two consecutive nights. On both nights full-night PSG recordings from her were obtained. The first night was an adaptation night, to help Mrs P become familiar with the laboratory setting, as well as to confirm her basic sleep/dream activity. The second night Mrs P was left to sleep without interruption in order to determine the quality and quantity of her sleep. Mrs P was thoroughly informed of the main purpose of the study and the procedures, and a consent form was signed before data collection began (Appendix D). Furthermore, she was told that she was free to withdraw from the study at any time without consequence, should she wish to do so. Night 1. Mrs P arrived at the Gatesville Medical Centre at approximately 22:00; she arrived late because she had mistakenly thought that the sleep study was being done at Groote Schuur Hospital, and had gone there first. After being asked to lie down in the sleep laboratory bed, electrodes were attached to her as per the 10-20 system of placement (see 16         measures). Mrs P was then asked to sleep as she normally would in her home environment. Polysomnograph recording started at 22:53; Lights Off (LO) occurred at 23:27; and Sleep Onset (SO) was at 01:15 the following morning. During Mrs P’s two REM cycles she awoke without being prompted, and these awakenings were used as an opportunity for dream recalls: she was briefly questioned as to whether she was dreaming and then left to go back to sleep. Polysomnograph recording ended 06:01. Mrs P was asked for a subjective account of her sleep, was thanked for participating in the study, and asked to come back the following night. Night 2. Mrs P arrived at Gatesville Medical Centre at approximately 19:00. She was asked to lie down in the sleep laboratory bed and electrodes were attached as per the previous night. She was then asked to sleep as she normally would in her home environment. Polysomnograph recording started at 20:21; LO occurred at 20:31; and SO was at 20:58. Mrs P was not interrupted or disturbed and was left to sleep as naturally as possible. Polysomnograph recording ended at 06:01 and the lights were switched on. Mrs P was debriefed and asked whether she had dreamt and whether she felt that her quality of sleep in the laboratory was comparable to the quality of her sleep at home. Finally, Mrs P was thanked for taking part in the study and compensated in accordance with her participation agreement. 17         RESULTS History of stroke In late February 2006, Mrs P was admitted to hospital following the sudden onset of blindness and a severe headache while she was shopping (history obtained from her family members). It was reported that her vision returned partially within a few minutes, but that her headache persisted and was accompanied by severe dizziness. Mrs P was put on medication as a secondary stroke prevention measure. In early March 2006, Mrs P was sent for neurological evaluation because she remained confused. Neurologically, Mrs P was found to have the following problems: an abnormal mental state characterised by axial amnesia; persistent disorientation to time; difficulties with problem solving and complexity; and labile mood. However, neuropsychological testing indicated that no visual agnosia (inability to recognise objects/images ); aphasia (difficulty in producing or comprehending, spoken or written language); impulse control; or word generation symptoms were present, and that Mrs P’s general judgement was preserved. Additionally, Mrs P’s report indicated that she had visual cortical dysfunction, which resulted in a left superior quadrantanopia (partial defect in her visual field). Also, a mildly ataxic gait (unstable balance) was observed, but no other focal localising signs were present. Mrs P only regained her memory 7 days after her initial stroke. She was also found to be photophobic (sensitive to light) and her blurred vision remained a consistent complaint. Magnetic Resonance Imaging Results Routine magnetic resonance imaging (MRI) done 14 days after Mrs P’s stroke in 2006, and was used to identify structural neuropathological changes (Appendix E). Overall, the scans revealed acute infarcts in both occipital lobes (larger on the right) and right cerebellar hemisphere. In addition, a small ischemic lesion was noted in the left thalamus. Furthermore, Computed Tomography (CT) angiogram demonstrated that Mrs P’s extracranial vasculature was normal, and no features of dissection were noted. Moreover, no haemorrhaging was indicated by the gradient echo sequences. 20         Time  (hours)     Figure  1.  Sleep  hypnogram  for  the  second  sleep  laboratory  night,  derived  from  the  EEG  recordings.     Horizontal  axis  measured  in  hours.  W  =  waking;  R=  REM  sleep;  N1  =  stage  1  sleep;  N2  =  stage  2  sleep;   N3  =  stage  3  sleep.  Arrows  indicate  REM  sleep  stages.     Table 1. REM Cycles Total Cycle REM start REM 1 8.5 171.5 23:10:45 REM 2 43.5 168.5 01:27:45 REM 3 24.0 185.5 04:52:45 Note. All values are measured in minutes, except REM start, which is an indication of time. Table 2 Analysis of Sleep Stages per Fraction First Second Third 190 min 190 min 190 min W 53.5 78.5 69.0 N3 63.0 25.0 29.0 REM 8.5 43.0 24.0 Note. All values are measured in minutes. W = waking; Sl ee p   St ag es   21         N3 = stage 3 non-REM sleep; REM = rapid eye movement. Table 3 Comparison of Sleep Parameters Between the Mrs P and Healthy Age-matched Controls Mrs P Controls (n=10) Zcalc SL 27.5 12 (7) 2.21 TST 369 406 (42) -0.88 SE 64.7 81 (8) -2.04 WASO 173.5 68 (45) 2.34* N1 44.5 32 (16) 0.78 N2 132 234 (31) -3.29** N3 117 54 (16) 3.94** REM 75.5 86 (23) -0.46 REML 159.5 82 (32) 2.42* Note. All values are measured in minutes, except for SE which is a percentage. SL = Sleep Latency; TST = Total sleep time (R + N1 + N2 + N3); W = waking; WASO= Waking after sleep onset; TW = Total waking; REMS = Rapid Eye Movement Sleep; NREMS = Non-Rapid Eye Movement sleep; N1 = NREM stage 1; N2 = NREM stage 2; N3 = NREM stage 3 (Also referred to as Slow Wave Sleep [SWS]); REML = REM Latency. *Zcrit = ±2.32, α = 0.01, one-tailed test; **Zcrit = ± 2.58, α = 0.01, two-tailed test. Comparison of Means for Mrs P and the Normative Control Groups Figure 2 shows a visual display of the sleep parameter means (in minutes) for Mrs P, the healthy age-matched control (HAC) group, and the chronic stroke control (CSC) group. The differences in Mrs P’s sleep parameters when compared with the HAC and CSC groups were most apparent for WASO, REML, N2 and N3 sleep. Both Mrs P and the CSCs tended to have slightly less REM and more N1 than the HACs. Waking After Sleep Onset. There was a noticeable difference between the WASO means for Mrs P, the HACs and the CSCs. Waking after sleep onset only accounted for 6.13% of the TSE (473 minutes) in the CSC group and 13.93% of the TSE (488 minutes) in the HAC group, as shown by Figure 3. However, WASO accounted for 29.9% of Mrs P’s TSE (526.5 minutes). 22           Figure  2.  Comparison  of  Sleep  Parameter  means  for  Mrs  P,  the  healthy  age-­‐matched  controls,  and   the  chronic  stroke  controls.  All  values  are  measured  in  minutes.  WASO  =  waking  after  sleep  onset;  SL   =  sleep  latency;  REML  =  REM  latency;  REM  =  rapid  eye  movement;  N1  =  stage  1  sleep;  N2  =  stage  2   sleep;  N3  =  stage  3  sleep.           WASO   SL   REML   REM   N1   N2   N3   ParYcipant   174   28   160   76   45   132   117   Healthy   68   12   82   86   32   234   54   Chronic   29   23   99   69   52   253   21   0   50   100   150   200   250   300   Ti m e (m in ut es ) Sleep Parameters 25         DISCUSSION As predicted, our study confirmed preserved REM sleep in a case with deep bilateral occipital lobe damage resulting in total dream loss. Polysomnographic recording clearly indicated that Mrs P experienced REM sleep on both nights in the sleep laboratory, while dream recall established that she did in fact have complete dream loss. Therefore, Mrs P is the third comprehensively documented case of dream loss as a distinct neuropsychological dysfunction. Furthermore, the results of this case study confirmed the hypothesis: the PSG data verified that the patient’s sleep was significantly more disturbed than published normative controls. Based on the previous literature, it was predicted that dreaming could protect sleep by diverting activity from the SEEKING system, as well as EEG arousals. While Mrs P did experience disturbed sleep, the results were not consistent for both of these ideas. The exact ways in which our study confirms that dreaming protects sleep are elaborated on below. Neuropsychological Testing The neuropsychological testing of Mrs P focused on excluding the presence of specific neurocognitive deficits which might jeopardize her ability to recall her dreams. Specifically, the basic preservation of visual and verbal short-term memory function, visual and verbal long-term memory function, and spatial cognition (visuo-spatial perception and recognition and constructional praxis), are all necessary requirements for dream recall. In addition, other more obvious neurocognitive deficits such as aphasia, also needed to be ruled out. The neurocognitive assessment revealed that, firstly, Mrs P does not display a short- term memory deficit in either the verbal or visual sphere. This is despite her relatively poor performance on the WMS III Visual Reproduction I task, which may be accounted for by her mild constructional apraxia (see below). Testing of Mrs P’s verbal long-term memory found that although she struggled somewhat with complexity, she was clearly able to lay down new memories and retain the overall content and structure of the newly-learnt material. With respect to her visual long- term memory, Mrs P proved that she did not display a major memory deficit through her ability to recall all of Luria’s Complex Scenes accurately. Her performance on the Rey- Osterrieth Complex Figure (ROCF), suggested that Mrs P’s visual memory was impaired. However, this test lacked construct validity due to the fact that Mrs P had primary visual 26         difficulties that made pen and paper tests difficult to complete. In particular, she suffered from blurred vision and photophobia, and often asked for us to close the curtains because the light ‘hurt her eyes’. Furthermore, she has a mild constructional apraxia (see below) that hindered her ability to successfully complete the ROCF test. This observation is supported by the fact that she was able to recall visual images from Luria’s Neuropsychological Investigation successfully. The real-world images depicted in Luria’s Complex Scenes were less abstract and more meaningful than the ROCF, and did not require intact higher visuo- constructional ability. Additionally, Mrs P was subsequently able to recall in some detail the room where her PSG was done, thereby adding additional confirmation that her visual long- term memory was largely intact (Appendix G). Overall, no amnesic syndrome was present. The WAIS-III Blocks Design and the ROCF, aside from testing Mrs P’s visual short- term memory, also indicated that she had a mild constructional apraxia. This impairment may have accounted for her poor visual memory performance scores. Furthermore, Mrs P had normal visuo-spatial perception, and no prosopagnosia or agnosia was present. If she had been dreaming she would not have been incapable of recounting them due to visuo-spatial impairments. Her BNT performance also verified that she was not aphasic, further confirming that her lack of subjective dream recall was not due to an inability to verbally communicate her dreams or to understand questions/instructions given to her. In summary, the overall neuropsychological testing of Mrs P confirmed that her dream loss was not better accounted for by short or long-term memory deficits, visuo-spatial impairments or problems with visual recognition. Furthermore, even if Mrs P was experiencing visual memory impairment, a range of findings have confirmed that impaired memory in no way provides sufficient explanation for a total lack of awareness of dream experience (Solms 1997; Yu, 2007). Even patients with profound memory deficits are able to effectively report dream recall and awareness. The retrieval of personal dream experience through multiple channels makes it highly unlikely that dream content would be forgotten, even if there is a memory disturbance in specific modalities (e.g. visuospatial or audioverbal memory; Flexser & Tulving, 1978). Therefore, we are confident that memory loss was not a confounding factor in this study. Dream Loss and Non- REM Sleep Although our findings replicate those of Bischof and Bassetti (2004) and Poza and Martí Massó (2006) in terms of dream loss accompanied by disturbed sleep, neither of the aforementioned authors provided specific data as to exactly how their patients’ sleep was 27         disturbed. However, it is perhaps too simplistic to conclude that dreams prevent the disruption of sleep generally, and we propose that dreaming protects sleep in a very definite way. Specifically, our results indicated that dream loss may have affected Mrs P’s sleep architecture — which consists of the various sleep stages — in numerous ways (Appendix B). Compared with HACs, Mrs P had significantly more WASO, higher N3, and decreased N2. Further analysis ruled out the possible influences of age and general complications due to stroke: the two control groups, the healthy age-matched controls (HAC) and the chronic stroke controls (CSC), followed a similar trend with regards to their sleep stages, which differed from Mrs P. Interestingly, there was more discrepancy between the CSCs and Mrs P, than between the HACs and Mrs P, further excluding the possibility that damage due to stroke (other than dream loss) led to Mrs P’s sleep disturbances. This is an important finding, considering that frequent dream mentation has been reported to occur during the N1 and N2 sleep stages, and warrants further discussion. Looking at Mrs P’s sleep hypnogram (Figure 2) it is clear that she struggled to enter N1 sleep, as well as enter and maintain N2 sleep, throughout the night: her N2 sleep is continuously fragmented and often resulted in waking. Indeed, her two longest waking periods (> 1 hour each) both emerged from disrupted N2 sleep. Moreover, after these periods of wakefulness Mrs P had difficulty going back to sleep, and increased N1 and N2 sleep fragmentation is apparent here as well. In addition, Mrs P experienced 132 sleep stage shifts during the second night, which indicates that switching between sleep stages was problematic. Furthermore, the majority of these sleep stage shifts emerged from her N2 sleep disruptions. Mrs P’s difficulty in falling asleep may also have been due to ineffective N1 sleep, as N1 is increased with inter-sleep wakefulness because it facilitates the transition from wakefulness into sleep (Hirshkowitz & Sharafkhaneh, 2009). However, Mrs P did not have increased N1 (to account for her increased WASO) when compared with the HACs. Therefore, Mrs P’s continuous sleep stage shifts may have been an inability to efficiently progress between sleep stages, due to her disrupted N1 sleep. It would therefore appear that because Mrs P was unable to dream, she was unable to maintain and enter N1 and N2 sleep effectively. Further evidence for this conclusion comes from comparing Mrs P’s EEG arousals with those of the HACs. As reported by Boselli et al. (1998), elderly participants experienced substantially more EEG arousals than young and middle aged adults (F(3, 36), p < 0.0001) and had an average NREM arousal index (AI) of 30.7 arousals per hour. Moreover, the HACs 30         However, it is important to note that Mrs P’s REM was not completely normal, as her third REM period was shorter than her second (Table 1), and usually REM periods increase as the night progresses (Hirshkowitz & Sharafkhaneh, 2009). Mrs P’s disorganised REM periods may be related to her inability to enter N2 sleep, when emerging from N3 sleep. Indeed, the natural progression in sleep stages during the night work as follows: N3 usually leads briefly into N2 and then is followed by REM (Hirshkowitz & Sharafkhaneh, 2009). Therefore, because Mrs P may have been unable to enter REM sleep, this may have accounted for her decreased REM throughout the night, as well as her increased REM latency (the time it took her to enter her first REM period; Table 1). However, these conclusions are only speculative and need further investigation. One last point concerning Mrs P’s REM sleep that should be noted is the fact that she was experiencing a REM rebound effect on her second night in the sleep laboratory, due to an insufficient amount of REM the previous night. REM rebound is known to cause an increased amount of REM in the night following the disturbance, and this may have made Mrs P’s REM periods longer and deeper than usual (Chokroverty, 2009). This is a confounding factor that limits what we can deduce from Mrs P’s REM results and is a flaw in the design of the study. The findings of this study provide tentative evidence that dreaming is able to protect sleep by effectively diverting physiological EEG arousals that emerge from both internal and external sources, consequently aiding the successful transition between sleep stages, as well as between wakefulness and sleep. Limitations and Future Directions We have already referred to the fact that general brain damage due to ischemic hemispheric stroke often disrupts sleep (Bassetti & Aldrich, 2001; Chokroverty & Montagna, 2009; Korner et al., 1986; Vock et al., 2002). This is especially true during the acute (1-8 days) and subacute (9-35 days) periods after stroke. It has been reported that REM sleep is drastically reduced in the first few days after stroke and only recovers 1 – 3 weeks afterwards (Giubilei et al., 1992, as cited in Vock et al., 2002). However, since our study is only the third case of dream loss that has been comprehensively documented using PSG recording, it is reasonable to assume that none of the literature on hemispheric stroke and sleep has considered the possibility that some of the sleep disturbance in patients who have suffered stroke may be due to a loss of dreaming. Indeed, if it has been considered it has not been reported, and to our knowledge there is no literature on ischemic hemispheric stroke that 31         addresses this issue. Therefore, future research could explore the extent to which some of known disturbances of sleep following hemispheric stroke may be related to dream loss. Moreover, and unlike many other dream studies, our findings highlight the importance that dreaming may have during NREM sleep. This should encourage future research to focus on dreaming outside of REM sleep. However, it is important to remember that any investigation into NREM dreaming needs to account for the fact that dreaming during this sleep stage is highly idiosyncratic between people, and does not occur as reliably as REM dreaming (Foulkes & Vogel, 1965). According to our results, this may be because NREM dreaming occurs as needed, in order to facilitate the transition of sleep, and these needs may differ drastically between people. We concede that the whole issue needs further investigation, and that our answers here are only tentative. Additionally, because this study was unreliable with regards to our findings during REM sleep, future research will need to address whether dreaming may also have a protective function during REM sleep. However, our results indicate that a disruption in NREM may have led to increased REM latencies, and subsequently disorganised REM periods. Therefore, any disturbance in sleep that is related to dream loss may disrupt the entire balance of the sleep stages. Ultimately, it may be more productive for dream research to do away with the REM/ NREM dichotomy and study the effects that dream loss may have throughout the sleep cycle. A limitation of this study was that we were unable to analyse a matched control. This limitation was primarily due to the scarcity of ischemic bilateral occipital lesion cases. Indeed, a control participant would have enabled more reliable conclusions to be made. However, what we have observed from Mrs P in comparison to normative controls from the literature thus far, has allowed us to propose a promising new hypothesis for future research: Dreams protect sleep by diverting external and internal arousals during NREM sleep, therefore facilitating the transition between sleep stages. Conclusion The hypothesis that dreams protect sleep was investigated using PSG recording in a single-case with dream loss due to bilateral occipital lesions. Mrs P was found to have significantly disturbed sleep compared to normative controls from the literature. Although most of the literature on dreaming focuses on REM sleep, Mrs P’s NREM was found to be the most disturbed, especially N1 and N2. Therefore, our results point to an important function for dreaming during NREM sleep, potentially contributing to a more comprehensive 32         understanding of the dream process throughout the sleep-wake cycle. Furthermore, this conclusion is in line with those of other dream specialists such as Solms (1997, 2000a) and Freud (1953), and marks the first occasion in which a function for dreams has been successfully empirically tested, as well as the first time that the psychoanalytic theory of dreams has been able to be empirically tested. 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The multiple choice administration of this test is used to measure a participant’s visual recognition. The Babcock Story Test. This test was used for the evaluation of long-term verbal memory (Babcock, 1930; Babcock & Levy, 1940). A detailed story was narrated to the participant and she was then required to recall the details she could remember immediately after. The same story was then read a second time and the participant was again required to repeat all the story to the best of her ability. The Bicycle Drawing Test. The BDT was included for the purpose of assessing revisualisation, and the participant was asked to draw a bicycle from memory, without the aid of a copy (Lezak, 1995).   41         Appendix B: Standard Definitions for Sleep Macro- and Microstructure Measurements Sleep Macrostructure Based on the American Association of Sleep Medicine (AASM) standard criteria, sleep is divided into two states with independent functions and controls: Non-REM and REM sleep (Chokroverty, 2009). Ideally, NREM and REM alternate in cycles that last 90-110 minutes on average. Furthermore, a sleep cycle is defined by the end of a REM period. In middle-aged adults, 4-6 sleep cycles are usually present in a normal sleep period; however, in elderly adults (>65 years) there may be as few as three sleep cycles in a sleep period of the same length. Normally, the first two sleep cycles mostly contain N3 sleep, which is reduced or absent in subsequent sleep cycles (Chokroverty, 2009). In contrast, REM sleep is increased from the first to the last sleep cycles, with the longest REM period dominating the last sleep cycle. Non-REM Sleep. NREM sleep accounts for 75-80% of sleep time in adults. According to the AASM scoring manual, on the basis of electroencephalographic (EEG) criteria, NREM sleep can be subdivided into three stages: N1, N2 and N3. Stage 1 sleep (N1) occupies 3-8% of total sleep time; Stage 2 sleep (N2) occupies 45-55%; and Stage 3 sleep (Slow wave sleep; N3) comprises 15-20% of totals sleep time. Stage 1 sleep facilitates the transition from wakefulness to sleep, and is identified when alpha rhythm diminishes to less than 50% of an epoch (30 seconds of polysomnographic recording time), that is intermixed with slower theta and beta waves. After approximately 12 minutes Stage 2 (N2) begins and lasts for about 30- 60 minutes, before slow wave sleep (SWS; N3) occurs. Slow wave sleep then briefly returns to N2 sleep before progressing to REM (Chokroverty, 2009). REM Sleep.REM sleep accounts for 20-25% of a person’s total sleep time. Physiologically, it is characterised by “bursts of [rapid eye movements] in all directions... phasic swings in blood pressure and heart rate, irregular respiration, spontaneous middle ear muscle activity, myoclonic twitching of the facial and limb muscle, and tongue movements” (Chokroverty, 2009, p. 8). In addition, EEG recordings consist of a low amplitude, fast pattern of beta waves, mixed with a small amount of theta. The first REM period lasts a few minutes and then progresses to N2, which is followed by N3, before the next REM period commences. 42         Sleep Microstructure The microstructure phenomena that are important to this study are arousals. Indeed, arousals can be defined as transient phenomena that result in fragmented sleep without behavioural waking (p. 10). Specifically, an arousal can be scored during REM, N1, N2, or N3 if there is an abrupt shift in the EEG frequency that is characterised by a 3 to 14 second intrusion of alpha, beta, or theta waves (but not spindles or delta). Arousals are expressed as a number per hour (Arousal Index; AI) and in middle aged adults it is normal to have an AI of up to 10 (Chokroverty, 2009). However, it should be noted that in the elderly arousals are more prevalent and an AI of 15 is considered normal (Boselli et al., 1998). 45         Appendix E: Magnetic Resonance Images Figure 1. Axial magnetic resonance images (A - D) show acute infarcts in the lingual, fusiform and parahippocampal gyri bilaterally, more extensive and deep on the right. Specifically, BA 17, 18 and 27 have been affected in the left hemisphere and BA 17, 18, 19 and 27 in the right hemisphere. Images E – F also show a lacune in the posterior nucleus of the left thalamus. 46         A B                     C     D             C D         E F E F 47         Appendix F: Transcripts for Subjective Dream Recall during REM The dialogue during the first semi-spontaneous REM awakening (4:34 am) went as follows: Researcher: “Hello.” Participant: “Mmm..” R: “What were you dreaming about?” P: “Hmmm....nothing.” R: “Were you dreaming?” P: “No, uh uh.” R: “No dreams?” P: “No.” R:”Ok, you go back to sleep.” The second semi-spontaneous awakening was at 5.42 am, and went as follows: Researcher : “Hello.” Participant : (eyes open). R : “What were you thinking about?” P : (shakes head) R : “Nothing?” P : “Hmmm...” R : “Were you dreaming?” P : “(shakes head) R : “No?” P : “No.” R : “Ok, go back to sleep.”