1. Are we addressing the ‘right stuff

Consciousness and Cognition 20 (2011) 1059–1083

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Consciousness and Cognition

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If waking and dreaming consciousness became de-differentiated,would schizophrenia result? q

Sue LlewellynFaculty of Humanities, The University of Manchester, Booth Street West, Manchester M15 6PB, UK

a r t i c l e i n f o

Article history:Available online 16 April 2011

Keywords:DreamingWakingConsciousnessSchizophreniaDe-differentiationChaos theoryPhospholipid defects/metabolism

1053-8100/$ - see front matter � 2011 Elsevier Incdoi:10.1016/j.concog.2011.03.022

q This article is part of a special issue of this jConsciousness and Psychosis (Challand Saint Anselm

E-mail address: [email protected]

a b s t r a c t

If both waking and dreaming consciousness are functional, their de-differentiation wouldbe doubly detrimental. Differentiation between waking and dreaming is achieved throughneuromodulation. During dreaming, without external sensory data and with mesolimbicdopaminergic input, hyper-cholinergic input almost totally suppresses the aminergic sys-tem. During waking, with sensory gates open, aminergic modulation inhibits cholinergicand mesocortical dopaminergic suppresses mesolimbic. These neuromodulatory systemsare reciprocally interactive and self-organizing. As a consequence of neuromodulatory rec-iprocity, phenomenologically, the self and the world that appear during dreaming differfrom those that emerge during waking. As a result of self-organizing, the self and the worldin both states are integrated.

Some loss of self-organization would precipitate a degree of de-differentiation betweenwaking and dreaming, resulting in a hybrid state which would be expressed heteroge-neously, both neurobiologically and phenomenologically. As a consequence of progressivede-differentiation, certain identifiable psychiatric disorders may emerge. Ultimately,schizophrenia, a disorganized-fragmented self, may result.

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1. Introduction

This paper elucidates the hypothesis that schizophrenia results from the progressive de-differentiation of waking anddreaming consciousness. In support of this, research is synthesized from several domains which have tended to be discrete:the differentiation of conscious states; phenomenological and neurobiological differences in waking and dreaming;phospholipid metabolism in neuronal membranes; dreaming and memory consolidation and work on the neurobiology, phe-nomenology and heterogeneity of schizophrenia. The methodology is hermeneutic in the sense that a more holistic under-standing of schizophrenia may emerge through considering the interrelationships between these areas of work-essentially,iterative steps of ‘what is the significance of this evidence in this domain in the context of that evidence in that domain’.Keshavan, Tandon, Boutros, and Nasrallah (2008) comment that the accumulating ‘fact-base’ on schizophrenia requiresnew integrative approaches that can generate testable predictions, this particular hypothesis is in this spirit.

Differentiation is achieved between the conscious states of waking and dreaming (see later). If differentiation has to beachieved, it can fail to be achieved, resulting in de-differentiation and a hybrid waking/dreaming state. The mind-brainprocesses that achieve differentiation are complex and, although reciprocally interactive, can vary independently. Therefore,de-differentiation would be expressed heterogeneously. However, one unifying thread is that conscious experience of theworld and the self would both be disrupted in a de-differentiated state. The integrity of waking and dreaming consciousness

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ournal on European Science Foundation EMRC Exploratory Workshop: The Dreaming Mind-Brain,e, Italy, 25th – 28th May 2009).

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1060 S. Llewellyn / Consciousness and Cognition 20 (2011) 1059–1083

underlies the differing experience of the self and the world in the two states. De-differentiation would compromise theintegrity of both states (although not necessarily to the same extent at the same time). The progressive de-differentiationof waking and dreaming consciousness and associated loss of self-organization in both states may gradually result inschizophrenia: a fragmented self. It is argued that understanding of both the heterogeneity of schizophrenia and thedisruption to self-experience can be advanced through this de-differentiation hypothesis.

2. Consciousness, conscious experience and the heterogeneity of schizophrenia

Schizophrenia is a heterogeneous condition. In classic work Bleuler (1911/1950) referred to the ‘group of schizophrenias’.In a recent comment, Carpenter (2008, p. 1003) reiterated that, ‘Schizophrenia has the nosological status of a clinical syn-drome rather than a validated single disease entity. Heterogeneity in clinical presentation and course is routinely observed,and heterogeneity of disease processes is likely’. Tandon, Nasrallah, and Keshavan (2008, p. 1) refer to an ‘. . .admixture ofpositive, negative, cognitive, mood and motor symptoms whose severity varies across patients. . .’. Moreover, there is accep-tance that distinctions between all psychiatric illnesses are fuzzy and symptomatic profiles overlap (Brockington and Leff,1979). Kendall and Jablensky (2003, p. 4) conclude that, ‘. . .there is little evidence that most currently recognized mentaldisorders are separated by natural boundaries. Researchers are increasingly assuming that variation in symptoms is contin-uous’. For example, obsessive-compulsion disorder (OCD) is not infrequently a co-diagnosis with schizophrenia (Krügeret al., 2000). OCD symptoms have been found in up to 50% of patients with schizophrenia (Berman, Merson, Viegner,et al., 1998). In particular, it appears that schizophrenia and bipolar disorder may be closely related, they share the sameetiology (Craddock, O’Donovan & Owen, 2006; Craddock & Owen, 2005; Lichtenstein et al., 2009; Maier, Zobel & Wagner,2006), exhibit symptomatic overlap (Lake, 2008; Lake & Hurwitz, 2006; Pope & Lipinski, 1978), can follow a similar deteri-orating course (Addlington and Addington, 1997; Zuibieta, Huguelet, O’Neil, & Giordani, 2001), involve sleep disturbances(Benson, 2006; Costa e Silva, 2006), can be difficult to distinguish clinically (Craddock & Owen, 2005; Owen & Craddock,2009; Walsh, 2009) and partly share genetic determinants (Craddock, O’Donovan & Owen, 2005, 2006; Lichtenstein et al.,2009). Indeed, the diagnosis of schizoaffective disorder recognizes the overlap between schizophrenia and bipolar disorder.Craddock and Owen (2005) comment on the multidimensional space occupied by functional psychiatric pathologies, ‘Therecent findings are compatible with a model of functional psychosis in which. . . .[there is] susceptibility to a spectrum ofclinical phenotypes. . . .[or indeed]. . . .a multidimensional space [where] in addition to bipolar disorder and schizophreniathere is genetic overlap between the functional psychoses and major depressive disorder – and, indeed, other disorders –with extension into sub-clinical (or normal) variation’. Reviews of population surveys indicate that attenuated psychoticexperiences are reported by 5–8% of respondents (Polanczyk et al., 2010; van Os, Linscott, Myin-Germeys, Delespaul, & Krab-bendam, 2009). Over 10 years, for a representative sample of adolescents and young adults from the general population,Dominguez, Can Saka, Lieb, Wittchen, and van Os (2010) reported a 12% cumulative prevalence rate for both negative/dis-organized and positive psychotic symptoms.

Heterogeneity in presentation and course, overlap with other psychiatric disorders and extension (in attenuated form)into the general population implies difficulty (indeed, most probably, impossibility) in delimiting schizophrenia to a coreconstellation of signs and symptoms. As compared to other illnesses, the diagnosis of schizophrenia has been describedas an art (Eaton, Hall, Macdonald, & McKibben, 2007). One statement that can be definitively made, however, is that schizo-phrenia involves consciousness and disrupts normal conscious experience. As consciousness is a notoriously elusive and con-tested concept (see, for example, Chalmers, 1996), this may not advance matters much unless there is clarification of how‘consciousness’ and ‘conscious experience’ are understood here.

In this paper, ‘Consciousness is the appearance of a world’ (Metzinger, 2009. p. 15). A world appears in both waking anddreaming consciousness (but not in deep dreamless sleep), moreover, when a world becomes present, a self also emerges asa part of this world (Metzinger, 2009, p. 57). The world and the self that appear during waking differ, in certain respects, fromthose that appear during dreaming. (This paper focuses on REM dreaming, rather than the more literal and thought-likeNREM, for a review of the differences see, Nielson, 2003).

‘Conscious experience’ is understood in the sense of a ‘cognitive global workspace’ (Baars, 1988, 1997, 2002). At any pointin time conscious experience focuses on a particular aspect of the world. Conscious experience, ‘. . .resembles a bright spot onthe stage of immediate memory, directed there by a spotlight of attention under executive guidance’ (Baars, 2005, p. 46).Again conscious experience differs in waking and dreaming, although there is a ‘spotlight’ of attention in both, during(non-lucid) dreaming ‘executive guidance’ or the intentional control of that ‘spotlight’ is lacking. Moreover, as working mem-ory is much attenuated in dreaming, the ‘stage of intermediate memory’ dissolves, so, from the perspective of waking con-sciousness, it is unclear why the spotlight is focused where it is in dreaming.

In sum, waking and dreaming consciousness are differentiated both with respect to the world that emerges and the selfthat becomes present. The next section addresses how this differentiation is achieved at the neurobiological level.

3. Achieved differentiation between waking and dreaming consciousness

Achieved differentiation between waking and REM dreaming consciousness can be partly understood through the ‘AIMModel’ (Hobson, 1990, 1992, 1997; Hobson & Stickgold, 1994; Kahn, Pace-Schott, & Hobson, 1997). AIM suggests that allconscious states reflect three processes: the level of brain activation (‘A’); the origin of inputs (‘I’); and dynamic reciprocity

S. Llewellyn / Consciousness and Cognition 20 (2011) 1059–1083 1061

between aminergic and cholinergic neuromodulation (‘M’). Although these processes do tend to vary in concert, they canalso exhibit independent variability (Hobson, Pace-Schott and Stickgold, 2003).

Activation (‘A’) is a measure of conscious experience (the ‘spotlight’ of attention), ‘. . .as reflected in the length, intensityand complexity of subjective reports of mental activity. . .’ (Hobson, Pace-Schott, and Stickgold, 2003, p. 40). Although, phe-nomenologically, reports of conscious experience in dreaming and waking differ in kind (see later), both states are equallyactivated (Hobson, 2002). Indeed, Tononi (2004) argues that during REM dreaming activation may be even higher than inwaking. The origin of inputs (‘I’) reflects the extent to which the brain-mind is making sense either of external sensory dataor internally generated percepts, this difference is driven by both input–output gating of external stimuli and the strength ofinternal data sources (Hobson, Pace-Schott, & Stickgold, 2003). As would be expected from the reported measures of con-scious experience, thalamocortical activation is at normal (waking) levels during REM dreaming (Behrendt, 2006; Paréand Llinás, 1995), so, to achieve differentiation between the two states, external input must be excluded (Hobson, 1999).When sensory stimuli from the external world are blocked, hallucinatory imagery suffuses consciousness (Behrendt,2003; Behrendt & Young, 2004). In contrast, during waking, internal perceptions are gated by sensory afferents so halluci-natory images do not normally arise (Behrendt, 2003; Llinás & Paré, 1991). Fictive hallucinatory movement in dreams iscompelling. Not only are motor commands issued to motor neurons but they are also copied to the sensory system, motoroutput during dreaming is blocked only through postsynaptic inhibition (Hobson, 1999).

Neuromodulation ensures unified, coherent mind/brain responses. In the AIM model, modulation (‘M’) is the ratio ofaminergic (noradrenergic and serotonergic) to cholinergic inputs, the predominance of aminergic modulation during wakingsupports directed thought, insight, judgment, abstract thinking, decision-making, working memory and space–time orienta-tion, the almost total lack of aminergic input to dreaming suppresses these executive functions (Hobson, Pace-Schott, &Stickgold, 2003). Process changes in the three AIM parameters go some way to explaining how the differentiation betweenwaking and dreaming is achieved. However, Hobson, Pace-Schott and Stickgold (2003) recognize that the three dimensionsof ‘AIM’ do not exhaust the conscious state space; indeed, they propose that more dimensions exist. It is suggested here thatto advance understanding of the achieved differentiation between waking and dreaming and, hence, to grasp the conse-quences of a de-differentiated state, a more comprehensive account of ‘M’ is required (to include mesolimbic–mesocorticaldopaminergic modulation) and a self-organization dimension (‘O’), which is dependent upon ‘I’ and ‘M’, should be included.The reasons for these modifications are discussed, in turn, next.

Solms (1999, 2002) argues that the role of dopamine (DA) in directing the dreaming state has been neglected. Indeed heposits that the mesolimbic–mesocortical dopaminergic pathway is crucial for dream generation. Although it is possible thataminergic demodulation may facilitate dopaminergic effects, these DA effects are primary (Solms, 2000). A dynamic recipro-cal relationship between mesocortical and mesolimbic DA projections has been proposed (Davis, Kahn, Ko, & Davidson,1991; Pycock, Kerwin, & Carter, 1980). It has also been shown in rodents that serotonergic systems can modulate the impactof mesolimbic DA (Barr et al., 2004). There is overwhelming evidence that the prefrontal DA inhibits subcortical DA activity(for a review see Guillin, Abi-Dargham, & Laruelle, 2007). Mesocortical DA enables prefrontal neuronal activity whereas mes-olimbic DA has a critical role in motivation and emotion (Mathé, Nomikos, Blakeman, & Svensson, 1999). As discussed below,on the phenomenological level, dreaming is a hyperemotional state where thinking reaches its nadir. Hence, it is intuitivelyplausible that, during dreaming, mesolimbic DA may predominate over mesocortical DA, with the reverse during waking. Asensitized mesolimbic dopaminergic system is correlated with an increase in cholinergic input (Sarter, Nelson, & Bruno,2005). So, during dreaming, increasing mesolimbic DA is associated with increasing cholinergic neuromodulation. Thus, dy-namic reciprocity characterizes not only aminergic/cholinergic systems but also mesocortical/mesolimbic dopaminergic sys-tems and mesolimbic dopaminergic/cholinergic systems.

The combined impact of shifts in ‘I’ and ‘M’ most probably account for the changes in regional activation of the brain thatalso differentiate dreaming and waking (Hobson, Pace-Schott, & Stickgold, 2003). For example, the gating of external stimulialong with the suppression of aminergic and mesocortical DA input may explain the de-activation of the frontal lobe duringREM dreaming. Conversely, the selective activation of the limbic system during REM dreaming may be due to cholinergic andmesolimbic DA stimulation accompanied by strong internally generated percepts. Specifically, Hobson (1999, p. 152) arguesthat dreaming is initiated in the pontine brainstem triggering activation, aminergic demodulation and cholinergic hyperac-tivity which selectively engages the limbic areas. The engagement of the limbic lobe then triggers primary emotions (e.g.fear, elation and rage). These emotions drive dream plot elaboration which is constituted through the visual imagery centresof the associative cortex, the spatial centres of the parietal lobe and the narrative organizing centres of the temporal lobe.Solms (2003) argues that dreaming (unlike REM architecture) is preserved with pontine brain stem lesions whereas a com-plete cessation of dreaming is observed with lesions of the parieto-temporo-occipital (PTO) junction. Despite their differ-ences, both Hobson and Solms agree on certain features of the differential regional activation of the brain during REMdreaming: the dorsolateral prefrontal cortex and the primary visual cortex are deactivated, whereas limbic areas and theoccipitotemporal cortical areas are selectively activated. Normal spatial cognition through the spatial centres of the parietallobe is preserved in both waking and dreaming.

Both waking and dreaming are self-organized mind-brain states (Kahn, Pace-Schott, & Hobson, 1997; Tononi, 2004;Tononi, 2008; Tononi & Edelman, 1998). The mind-brain self-organizes through sensory data and neuromodulation (Free-man, 2005; Singer, 1986). As noted above, although external sensory input is largely ignored during dreaming (Mahowald,Woods & Schenck, 1998) self-organization through neuromodulation and internally generated precepts continues (Kahn,Combs, & Krippner 2002). During waking, self-organization generates a brain ‘forward model mechanism’ that enables


(across all sensory modalities) automatic distinction between external sensory data and internally generated precepts, with-out this mechanism internally generated precepts may be experienced as having external sources (Ford, Roach, Faustman, &Mathalon, 2007). During REM sleep this mechanism does not operate, internally generated precepts are not recognized assuch and if external data is processed (without causing waking) it is co-opted into the internally generated dream narrative.

Self-organization is not stable or fixed but constituted through dynamic processes (Kahn & Hobson, 1993; Kahn, Krippner,& Combs, 2000). These dynamic processes are moulded by ‘attractors’ which enable any self organized state to find its owninherent configurations (Krippner & Combs, 2002). There is a global attractor that leads the mind-brain to settle (albeit,dynamically) at the ‘edge of chaos’ (Goodwin, 1994) or, in other words, in a state of self-organized criticality between orderand disorder (Bak, 1996).

Within every 24 h, two self-organized, highly activated states are achieved: waking and dreaming. Therefore, in the mind-brain, it is intuitively likely that ‘order’ is represented by an achieved differentiation between waking and dreaming and‘chaos’ (or disorder) results from their de-differentiation.

Differentiation between waking and dreaming depends on dynamic reciprocity and is a ‘constantly negotiated compro-mise’ (Hobson, 2002, p. 102). Hence, as is predicted by chaos theory, the achieved differentiation between waking anddreaming is both vulnerable and volatile. Indeed, this is confirmed by the existence of transient dissociated states: luciddreaming; REM sleep disorder; and waking fantasy or ‘daydreaming’ (see Hobson, Pace-Schott and Stickgold, 2003, for a re-view). De-differentiation differs from state dissociations in that de-differentiation would impact upon both waking anddreaming consciousness. Also de-differentiation be an enduring (and sometimes progressively deteriorating, see later),rather than a transient condition.

Systems, such as the mind-brain, that are poised between order and disorder are optimal for complex tasks (Kauffman,1993). If de-differentiation between waking and dreaming occurred then the ability to undertake complex tasks in bothstates would be effected detrimentally. One of the key tenets of chaos theory is uncertainty over the precise ways in whichthese effects would be manifested. In a state of self-organized criticality, a small perturbation in the mind-brain (in thishypothesis a small shift into de-differentiation) can precipitate fluctuations which are largely unpredictable on the basisof initial conditions (Bak, 1996; Orsucci, 2006).

4. How could de-differentiation occur?

The implication of the above arguments is that the heterogeneity associated with schizophrenia (and, possibly, other re-lated psychiatric/neurodevelopmental disorders) may reflect the multifarious possibilities inherent in the process changesthat achieve differentiation between waking and dreaming in the mind-brain. Or, in other words, schizophrenia is a condi-tion of the ‘anomalous dynamics’ (Orsucci, 2006) that can emerge within any system poised at self-organized criticality. Butnot all humans descend into schizophrenia, so the question arises of how these anomalous dynamics are triggered in sus-ceptible individuals.

There is evidence of neuronal cell membrane phospholipid abnormalities in patients with schizophrenia (Glen et al.,1994; Horrobin, Manku, Hillman, Iain, & Glen, 1991; Nuss et al., 2009; Yao & Reddy, 2000; Yao, van Kammen, & Welker,1994). These membrane abnormalities are observed prior to treatment, so they may be trait-related (Jayakumar et al.,2003; Reddy, Keshavan, & Yao, 2004). Schizophrenia may be associated with deficient uptake or excessive breakdown ofmembrane phospholipids (Fenton, Hibbeln, & Knable, 1999). Excessive breakdown may flow from the over-activity of cal-cium-independent phospholipase A2; such over-activity has been demonstrated in schizophrenia (Horrobin, 1996; Macdon-ald et al., 2004; Smesnya et al., 2005). Evidence of abnormal fatty acid metabolism in schizophrenia includes: reduced fattyacid levels in cell membranes; reduced skin flush response to topical niacin; abnormal electroretinogram; increased levels ofcalcium-independent phospholipase A2 in blood and brain; and abnormal 31P magnetic resonance spectroscopy of brainphospholipids (Peet, 2002).

Essential fatty acids (EFAs) are key components of neuronal cell membranes. Eicosapentaenoic acid (EPA) and docosahex-aenoic acid (DHA) are common essential fatty acids in the brain (see, for example, Horrobin, 1998). Supplementation withEPA has been shown to be effective as an adjunct treatment for already medicated patients with schizophrenia (Emsley, My-burgh, Oosthuizen, & van Rensburg, 2002; Peet, Brind, Ramchand, Shah, & Vankar, 2001; Peet & Horrobin, 2002; Shah, Van-kar, Telang, Ramchand, & Peet, 1998). There is indicative evidence that drug-naïve patients may respond too (Puri et al.,2000; Richardson et al., 2000). EPA has also been shown to reduce the risk of psychosis in high-risk individuals (Ammingeret al., 2007), young people with subthreshold psychotic states (Amminger et al., 2010) and enhance treatment response inpatients with a first episode (Berger et al., 2007).

Moreover, EPA, along with DHA, has also been found to be efficacious for bipolar disorder (Stoll, Severus & Freeman, 1999;and unipolar and bipolar depression (Frangou, Lewis, & McCrone, 2006; Freeman et al., 2006). In particular, the therapeuticeffects of EPA have been shown to be equal to fluoxetine in treating major depressive disorder (Jazayeri et al., 2008). Theinclusion of EPA along with other essential fatty acids, vitamins and minerals in the diet of prisoners reduced the incidenceof anti-social behaviour (including violence) by 26.3% (Gesch, Hammond, Hampson, Eves, & Crowder, 2002). The administra-tion of EPA and DHA decreased feelings of anger in substance abusers (Buydens-Branchey & Branchey, 2008). Ultra pureethyl-eicosapentaenoate (E-EPA) diminished aggression and depressive symptoms in women with untreated borderline per-sonality disorder (Zanarini & Frankenburg, 2003). Essential fatty acid deficiencies (with improvements after supplementation)


have been found to be implicated in three developmental disorders which are frequently co-morbid: dyslexia (Richardson,Easton, & Puri, 2000; Richardson & Ross, 2000; Richardson et al., 1999; Richardson et al., 2000a, 2000b; Stordy, 1995; Stordy,1997; Taylor & Richardson, 2000; Taylor et al., 2000), dyspraxia (Richardson & Ross, 2000; Stordy, 1997) and ADHD(Richardson & Puri 2000, 2002; Stevens et al., 1995; Stevens, Zentall, Abate, Kuczek, and Burgess, 1996). In a review, Garlandand Hallahan (2006) concluded that decreased levels of essential fatty acids are implicated in psychiatric conditions charac-terized by disordered impulsivity (ADHD; borderline personality disorder; suicide, deliberate self-harm, aggression andhomicide) and that improvement occurred when deficiencies were corrected. Although these results are preliminary and fur-ther investigation is required, they are indicative of a similar therapeutic role for fatty acid supplementation across a range ofpsychiatric conditions, thereby lending weight to the hypothesis that these conditions are related.

Normal phospholipid metabolism ensures the dynamic fluidity of cell membranes and, thus, preserves multiple neuronalstructures and functions including receptors, ion channels, signal transduction and second messengers, moreover, lipid prod-ucts derived from phospholipid membranes regulate cell signaling systems (Hallahan & Garland, 2005; Kinsella, 1990). Spe-cifically, essential fatty acids are also thought to be associated with dopaminergic and serotoninergic transmission, brainglucose metabolism, eicosanoid synthesis, gene expression, cell growth and may guard against apoptosis (Liperoti, Landi,Fusco, Bernabel, & Onder, 2009). Thus abnormal phospholipid metabolism, associated neuronal cell membrane abnormalitiesand, consequent disrupted neurotransmission may serve as a point of convergence for the generalized dysfunction associ-ated with schizophrenia.

The ‘membrane theory of schizophrenia’ Horrobin, Glen, and Vaddadi (1994) is compatible with disruption to all neuro-transmitter systems. Horrobin et al. (1994, p. 204) comment,’ . . .disruption of the fundamental structure of membranes couldlead to serious brain malfunction, with demonstrable abnormalities of brain histology and abnormalities in the functioningof all neurotransmitter systems: the components of such transmitter systems are all associated with membranes and allfunction through changing membrane behaviour.’ Specifically, membrane abnormalities have been shown to cause disrup-tion to dopaminergic (Malnoe, Milon & Reme, 1990) and cholinergic (Fong & McNamee, 1986) neurotransmitter systems.Reviewing evidence on dietary manipulation of membrane phospholipid composition in rats, du Bois, Deng, and Huang(2005) found impacts on dopamine, serotonin and muscarinic receptor densities; they deduced that there is a tight relation-ship between membrane phospholipid status and normal neurotransmission. In a review, Chalon, Vancassel, Zimmer,Guilloteau, and Durand (2001) concluded that strong links characterize phospholipid status, neurotransmission processesand behavioral disorders. Phospholipid status is determined by genetic markers in conjunction with diet and stress asenvironmental factors, the enzymes that control phospholipid synthesis and breakdown are under genetic control but theessential fatty acids in neuronal membranes cannot be manufactured in the body, they must be included in the diet(Horrobin, 1998). In cross-national studies, there is epidemiological evidence that dietary consumption of essential fattyacids modifies the risk for neuropsychiatric disorders (Hibbeln, 1998; Peet, 2004; Young & Conquer, 2005). Specifically, insuch studies, greater seafood intake was associated with lower incidence of bipolar disorder (30-fold range) and majordepression (50-fold range) (Hibbeln & Salem, 2001).

In addition to effective transmitter-receptor interaction, of particular importance to normal neurotransmission is thescavenging of excess transmitter from the synapse to terminate the signal (Gazzaniga, Ivry, & Mangun, 2002). Moreover,feedback through membrane receptors coordinates the rates of neurotransmitter release with rates of reuptake and ratesof breakdown to ensure the appropriate concentration level for each neurotransmitter in the synapse (Freeman, 1992). Mem-brane abnormalities would impede neurotransmitter-receptor interaction, disrupt the processes that control the concentra-tion of neurotransmitters, interfere with the reuptake and reentry of excess neurotransmitters into the presynaptic neuronand result in a loss of control over neurotransmitter release. Thus the consequence of membrane abnormalities would besome chaotic intermingling of neurotransmitters within the synapse. Ultimately, due to the impact of membrane abnormal-ities and anomalous phospholipid metabolism on multiple transmitter systems, the waking and dreaming states may be-come de-differentiated as some dynamic reciprocity between aminergic/cholinergic/dopaminergic systems is lost. Clearly,this loss of dynamic reciprocity would be a matter of degree. The impact would be slight if membrane abnormalities and/or anomalous metabolism were minimal or considerable if they were grossly aberrant.

Although genetic factors along gene-environment interplay have been shown to contribute 80% to a liability for developingschizophrenia (Tandon, Nasrallah, & Keshavan, 2008), there must be a neurobiological substrate through which this interplayis expressed (Horrobin, 1998). The impact of membrane abnormalities and anomalous phospholipid metabolism on multipletransmitter systems (leading to the de-differentiation of waking and dreaming consciousness) may be, among others, theexpression of this genetic-environmental susceptibility. Why would this be most likely to happen in late adolescence?

Huttenlocher (1979) first reported the 30–40% decline in synaptic density in the frontal cortex during adolescence. Thisfinding has since been confirmed by Glantz, Gilmore, Hamer, Lieberman, and Jarskog (2007) who remark that this decline isconsistent with the superior performance of adults (over children) in frontal cortical-dependent tasks that rely on this prun-ing process to enhance the efficiency of synaptic connectivity. As synaptic elimination occurs at the same developmentalstage as schizophrenia emerges it is intuitively likely that the two are linked in some way. Feinburg (1982) first suggested thatsome pruning defect may cause schizophrenia. EFA metabolism is implicated in synaptic pruning (Crawford, 1992; Richardson& Puri, 2000) so metabolic abnormalities may precipitate pruning defects. However, an alternative (or contributory)explanation is that the 30–40% decline in synaptic density would greatly exacerbate an underlying cumulative (throughoutchildhood) de-differentiation process, as, after pruning, neurotransmission takes place through fewer circuits. The underly-ing cumulative de-differentiation process would, therefore, become manifest as psychiatric symptoms in adolescence.


De-differentiation would be ‘underlying’ as phospholipid status is determined through gene-environment interplay. Dur-ing infancy and childhood this interaction would be expressed differentially due to the impact of diet (including, contempo-rarily, fatty acid supplementation, see above) and stress. As discussed above, phospholipids have highly significant structuraland functional roles in the brain, so phospholipid status would have fundamental consequences for brain development.

It has been proposed that schizophrenia is a neurodevelopmental disorder (Murray & Lewis, 1987; Weinberger, 1986,1987). The earlier onset and more severe form of schizophrenia in men (than women) have been attributed to neurodevel-opmental differences (Castle & Murray, 1991). The ‘membrane theory of schizophrenia’ was developed within the neurode-velopmental paradigm, as gene-environmental interplay influences the way that neurons are laid down, differentiated,culled and re-modelled (Horrobin, 1998). Moreover, although high oestrogen levels have been shown to be protectiveagainst schizophrenia, differences in EFA metabolism may also play a part, as female rats metabolize EFAs more rapidlyand, in the context of EFA deficiency, retain EFAs within membrane phospholipids more readily than males (Horrobin,1998; Marra & de Alaniz, 1989). However, the neurodevelopmental approach is in no way in contradiction with disruptedneurotransmission models of schizophrenia. As argued above, there is a tight relationship between membrane phospholipidstatus and normal neurotransmission. Moreover, disrupted neurotransmission would be a fundamental aspect of the de-dif-ferentiation of waking and dreaming consciousness.

Any adequate understanding of the consequences of de-differentiation must make reference not only to neurobiology butto conscious, lived experience. Phenomenology, as the study of lived experience, is essential to the elucidation of psychopa-thology (Gallagher & Zahavi, 2008; Parnas, Sass, & Zahavi, 2008). If schizophrenia results from the progressive de-differen-tiation of waking and dreaming consciousness, resulting in a hybrid waking/dreaming state, to understand schizophrenia itis necessary to understand the phenomenology of both waking and dreaming.

5. The phenomenology of waking and dreaming

What is experience like during waking and dreaming consciousness? How far does conscious experience differ in the twostates?

The world that appears during dreaming consciousness is completely internally generated in the sense that, as discussedabove, external stimuli are excluded in favour of internal precepts. The world that appears during waking is also entirelyinternally produced but a major aspect of the production is making sense of external sensory data. Waking consciousnessgenerates a strong sense that an external reality exists. To create this outer reality (and a self in this world) the brain-mindsystematically externalizes the sense that ‘I am present in a world outside my brain’ (Metzinger, 2009, p. 23). As a result ofthis externalization, during waking my experience is of a subjective private ‘inner’ world that is present within an objectivepublic ‘outer’ world. During waking I know my subjective world is self-generated whereas the objective external world isnot. Moreover, I experience myself as both a subject and an object in this external world (Legrand, 2007). If I am of a philo-sophical inclination, I accept I have no direct access to the external world except through the representations my brain gen-erates. Nonetheless, in normal waking consciousness, I do not distrust the objective material reality of the external outerworld nor do I doubt that I exist in this domain.

During dreaming consciousness only one world appears, the distinction between subjective and objective worlds is lost,or very much attenuated. Consequently I am not aware that my dreaming world is self-generated. Much follows from this. Inwaking I reflect on and have insight into my own state of mind-brain. I know I am awake and am aware of another possi-bility- dreaming. In contrast, during dreaming I do not attribute a state of mind-brain to myself; also I am unaware that thereis an alternative state-waking. (Only during lucid dreaming is there awareness of the mind-brain state (Voss, Holzmann,Tuin, & Hobson, 2009)). Whilst I am awake I can travel mentally in time. Moreover, I am aware that I am re-visiting the pastor anticipating the future (Metzinger, 2009). During dreaming my situation feels very immediate. I am always present. I donot travel mentally in time. Nor do I think about my situation (Kahn & Hobson, 2005a). Concomitantly, there is loss of sub-jective thinking about the thinking, feeling and situations of those who populate my dreams. So ‘theory of mind’ is muchdiminished (although see, Kahn & Hobson, 2005b) and dreamers are not inclined to empathy. This loss of reflexivity meansthat I do not monitor the actions of self and others. Hence, during dreaming, I do not ponder (‘Am I taking the ‘right’ action?’).So I cannot form flexible responses to situations. I do not think on the causes of my actions nor do I contemplate their con-sequences for self or others. What happens during (non-lucid) dreaming appears not to be under my control; or rather theissue of ‘control’ (like ‘state of mind’, ‘causes’ and ‘consequences’) does not occur to me. I do not run an internal commentaryon external reality. Archer (2003) has termed this commentary the ‘internal conversation’. During waking, in the subjective,private, internal conversation I ‘talk to myself’ as I try to adjust the world to my goals or make sense of ‘what’s going on’externally. In the world that my mind-brain has externalized I may, for example, converse politely with a colleague aboutorganizational politics whilst, in my internal world, I command myself ‘Extricate yourself, you’re going to be late for themeeting at 1400’ or advise myself, albeit from, sometimes, conflicting perspectives, ‘She is looking bored, maybe she actuallydislikes you. . .Do not be stupid, you know that she is on your side’. In sum, during dreaming all executive functions fade,without subjectivity, there is little abstract thinking, decision-making, sustained concentration or applied logic (Dietrich,2003), self-monitoring and the inner conversation are also lost. However, despite (or, arguably, because of) all of these lossesthe authenticity of the dreaming world is not doubted.


Dreaming has been described as remarkably single-minded (Rechtschaffen, 1978). In part, this ‘single-mindedness’ comesabout because the subjective inner ‘evaluating, sense making and advising’ mind is lost. With subjectivity ‘switched off’ thedreamer’s attention is totally caught up in a uni-dimensional, unravelling drama. Loss of reflexivity (including reality mon-itoring, ‘That can’t be true’) allows the dreamer to accept the highly unlikely, indeed, sometimes, the impossible (Nir &Tononi, 2010), the dead return, distinguished and famous public figures become close acquaintances, flying is effortlessand dream characters are sometimes blended (in the sense that aspects of two persons are united into one). Consequently,from the perspective of waking consciousness, dream experiences are often bizarre with a disregard for space/time param-eters (Scarone et al., 2008). The periodic, mundane, habitual behaviours that characterize waking are notably absent (e.g.washing, dressing and grooming). Also lack of self-monitoring implies that this neglect of self-care fails to register. The rel-atively dramatic content of dreaming consciousness (as compared with waking) is driven by primary emotions like anxiety,fear, rage and elation (see Hobson, 1999; Hobson, 2002). More subtle emotions, like serenity, humility and compassion arerare. Although, sustained concentration is negated as dream scenes rapidly appear, shift and dissolve, attention is focusedand perception enhanced -as Leonardo da Vinci’s famous comment about ‘seeing more clearly in dreams’ attests. This fo-cused attention/enhanced perception constitutes another aspect of the ‘single-mindedness’ (Rechtschaffen, 1978) of dreams.

However, during waking, focused attention equates to a spotlight under executive control (Baars, 2005). Such control en-sures that only certain features of any visual scene fall under this spotlight and are, therefore, consciously perceived. Thepeculiarity of this was demonstrated by Simons and Chabis (1999) when, with their attention focused elsewhere, 50% of par-ticipants in their study failed to perceive a man dressed as a gorilla as he crossed their visual field. This is a dramatic illus-tration of the importance of attention to perception. As noted above, executive control is missing in dreaming, so attentioncannot be directed. Directed attention is lost but perception is enhanced in dreams (Hobson, 2002). This may follow from thesparsity of dream scenes. Rather like stage sets, the scenes constructed during dreaming appear edited when compared withthe usual complexity of the waking visual field. Therefore, the significance of directed attention for perception may drop asthere is less to distinguish and assimilate. In a computer simulation Hoffman and McGlashan (1997) showed that perceptionis enhanced when working memory capacity is reduced, as working memory is much diminished in dreaming this may beanother contributory factor to the augmentation of perception in the absence of directed attention.

As thinking reaches its nadir in REM dreaming there is a concomitant peak in visual imagery (Fosse, Stickgold, & Hobson,2001). Dreaming consciousness elaborates internally generated precepts into highly associative narratives dominated by thisvisual imagery (Hobson, 2002). Although the dreamer and other dream characters sometimes speak in (REM) dreams, this isrelatively rare; when attempted, dreamers have difficulty in vocalizing their thoughts (Hobson, 2002). Moreover, the speechis stereotyped and does not form part of a coherent two-way conversation. As deliberate thought is absent these dreamingnarratives cannot be ‘thought about’ as are waking narratives. Hobson (2002) argues that dreaming narratives are driven byemotional salience rather than directed thought, moreover, sensorimotor images dominate. The cholinergic system rendersthe dreaming state of mind ‘hyper-associative’ (Hobson, 2002, pp. 88 and 113), specifically the mind ‘. . .switches from linear-logical to a parallel associative mode. . .’ Hobson, 2002, p. 63). Many concur that associations are ‘looser’ in dreams (Hartmann,1998; Rittenhouse, Broadley, Stickgold, & Hobson, 1993; Stickgold, Scott, Rittenhouse, & Hobson, 1999). Consequently, theform and content of dreaming and waking narratives differs. Although the self that appears in dreaming narratives is veryagential (in the sense of almost always active), these actions are not under intentional control. Moreover, although signifi-cant others often populate my dreams I do not engage with them as I do during waking consciousness. During waking, nonroutine action is almost always ‘. . .reaction to joint action. . .’ (Thift, 2008, p. 7). In dreams, complex interactions with othersare missing. Primary emotions (anxiety, fear, rage and elation) drive dream plots and render my encounters with others lessrestrained, less compassionate, less caring whilst, often, more fraught, more conflictual, more sexually transactional andmore violent. My sense of self is shallow. Even basis self-parameters like age, occupation and marital status are lacking.Consequently, during dreaming, personal identity is diminished. In sum, phenomenologically, waking and dreamingconsciousness do differ both in terms of the world that appears and the self that comes as a part of this world.

On the other hand, as noted above, dreaming- like waking- is a highly activated, self organized state and dreaming -likewaking- feels meaningful. Indeed, one could argue that dreaming consciousness feels more meaningful. I am never bored,depressed, apathetic or fed-up in my dreams. Dreams feel real in the same way that the external world feels real during wak-ing. Dreams do not present meaningless random images, dream material is organized and selective (Revonsuo, 2003). Solms(2003) argues that dream images are actively constructed through complex cognition. Phenomena that arouse motivatedinterest during waking (e.g. people, faces, animals, movement, places and landscapes) also dominate dreaming (Nir & Tononi,2010). In both dreaming and waking, the self surveys a spatially coherent environment (Nielsen & Stenstrom, 2005). Dreamsdo not resemble abstract art. As noted above, dreaming, like waking, is sensorimotor; dreams simulate a very convincingsense of the self moving through space (Hobson, 2002, p. 30). The embodied self is central to waking consciousness(Merleau-Ponty, 2002), similarly, I experience myself as embodied and at the vortex of the unfolding drama that is my dream(Llinás, 2002). Dreaming consciousness, like waking consciousness, is integrated. In both states a conscious scene is unifiedand seamless; hence, a scene cannot be deconstructed into components and is experienced from a private, single point ofview (i.e. during waking one cannot simultaneously perceive both the old witch and the young woman in the visual illusion,similarly, during dreaming there is a single perspective on a scene) (Tononi, 2008; Tononi & Edelman, 1998).

The differences in phenomenology between waking and dreaming are most probably underpinned by shifts in input spec-ificity and neuromodulation (Hobson, 2002), whereas, the similarities are likely to flow from self-organization, integrationand comparable levels of activation. Specifically, the self-organized nature of dreaming, the active, complex, cognitive


processes required for dream construction and this phenomenological data on dream coherence indicate that dreams do notemerge from a disorganized brain.

6. How would de-differentiation be expressed?

Through synthesizing the above evidence on the neurobiology and phenomenology of waking and dreaming conscious-ness, some preliminary observations can be made on how de-differentiation would be expressed. Although, in line withchaos theory, the precise effects would be uncertain, the parameters of de-differentiation will flow from some loss of order(i.e. the diminution of the self-organized integrity of the waking and dreaming states). So the prime characteristic of de-dif-ferentiation will be a degree of disorder. This disorganization would follow from shifts in those parameters that enable thedifferentiation of waking and dreaming (i.e. input specificity and neuromodulation).

Hence any or all of the following may be involved, to a lesser or greater extent. First, shifts in (‘I’) which would equate,during waking, to a loss of focus on external sensory data, accompanied by increasing concern with internal precepts. Duringdreaming shifts in ‘I’ may include disturbed sleep due to increased sensitivity to external sensory data (see later). Second,changes in neuromodulation (‘M’), so that, during waking, cholinergic and mesolimbic dopaminergic modulation rise (andaminergic and mesocortical modulation fall). During dreaming, aminergic and mesocortical dopaminergic modulation wouldrise (and cholinergic and mesolimbic modulation fall). Although both waking and dreaming are activated, in the sense thatlengthy, complex and intense accounts of mental activity can be elicited, ultimately, this activation may not be preserved in aprogressively de-differentiated state.

These neurobiological shifts will, naturally, result in phenomenological changes. If the degree of de-differentiation wasslight then, for example, during waking there could be merely some ‘dreaminess’ through an increased focus on internal pre-cepts. Or a modest increase in anxiety, as anxiety is the predominant emotion in dreaming (Hobson, 2002). Equally, asdreaming is a hyperemotional state characterized by primary emotions allied with a loss of executive control, waking prob-lems with managing rage or controlling aggression may emerge. Or relationship difficulties may present themselves, as dur-ing dreaming there is little empathic connection with others. Or psychomotor control in waking may be affected as motoroutputs are blocked in dreaming. Or difficulties with sustained concentration may be experienced, as concentration is notmaintained during dreaming. Or thinking during waking may become less linear-logical and more highly associative, asdreaming is a hyper-associative state. If such shifts remain modest then the results of de-differentiation would hard to dis-tinguish from ordinary functioning. Indeed, as any conscious state is a ‘constantly negotiated compromise’ (Hobson, 2002, p.102) between waking and dreaming, it could be argued that such shifts are the essence of normality. That this is a matter ofdebate, however, is evidenced in the current draft of DSM-5 (see, www.dsm5.org), where new syndromes (e.g. temper dys-regulation disorder with dysphoria) proliferate, this has elicited the criticism that under DSM-5 ‘normality’ will become ahighly restricted zone (Wykes & Callard, 2010).

Leaving this debate aside, if the intrusion of an aspect of dreaming into waking becomes more pronounced and/orwaking consciousness takes on multiple facets of dreaming, then various disorders may emerge. Slight anxiety may pro-gress to ‘anxiety disorder’. Or if a lack of sustained concentration becomes combined with impulsivity (due to a disregardfor consequences – another aspect of dreaming) this may progress into ‘attention deficit hyperactivity disorder’. Or ifmood became highly reactive with a notable increase in impulsive aggression ‘borderline personality disorder’ may bethe result.

As discussed earlier, as with all non-linear complex systems, a small disturbance in the mind-brain can give rise to largefluctuations which are unpredictable on the basis of initial conditions (Bak, 1996; Orsucci, 2006). Hence a small disturbance(equating to a minor neuronal membrane defect and/or metabolic abnormality) could give rise to any of the above possibil-ities. On the other hand, a small disturbance only implies some loss of self-organization. Moreover, it has been shown that themind/brain strives towards self-organization (Cicchetti & Tucker, 1994; Fingelkurts & Fingelkurts, 2004; Goodwin, 1994).Any self organized state finds its own inherent configurations (Krippner & Combs, 2002). So, when understood in the termsof chaos theory, the progression (or not) of de-differentiation would depend upon complex dynamics. For example, a modestincrease in anxiety could stabilize or may progress to ‘anxiety disorder’ whereupon a new stable configuration may bereached. So the progression of any disease process would depend upon the extent of the loss of self-organization as, onlymodest losses would enable new stable, albeit anomalous (e.g. anxiety disorder) configurations.

At the neurobiological level, minor neuronal cell membrane phospholipid abnormalities (which may impact on only alimited number of neurotransmitters) would limit the possibilities for disease progression. However, as discussed earlier,gross neuronal membrane defects and associated metabolic abnormalities could precipitate a chaotic intermingling of neu-rotransmitters in the synapse with the progressive loss of self-organization and subsequent on-going de-differentiation ofwaking and dreaming consciousness. Ultimately, as more and more aspects of dreaming consciousness become incorporatedin the waking state, identifiable psychiatric disorders (including psychosis) may emerge. Such a situation would not, how-ever, equate precisely to ‘dreaming during waking’. A de-differentiated state would be a hybrid one, not dreaming nor wak-ing but an anomalous ‘in-between’ condition. As argued earlier, this ‘inbetween’ state could be expressed in a myriad ofdifferent ways and would be a matter of degree.

The paper will now assess how far de-differentiation can explain the positive, disorganized/cognitive, motor and mood as-pects of schizophrenia on a phenomenological level, before considering if this de-differentiation hypothesis is compatible with

http://www.dsm5.org


the neurobiology of schizophrenia. Negative symptoms will be discussed later. These particular dimensional distinctions (po-sitive, disorganized/cognitive, motor, mood and negative) are those suggested in Tandon et al. (2008), cited earlier in this paper.

6.1. Positive symptoms

As argued above, internally generated precepts are the very essence of dreaming and the dreamer readily accepts the impos-sible. Many have noted that with regard to hallucinations (perceptions without external stimulus) and delusions (false, fixedbeliefs about reality) there are connections between psychosis and dreaming. In The Interpretation of Dreams Freud quotes fromKant, Krauss, Schopenhauer, Hagen and Wundt to this effect. The idea continues to convince (see for example, Koresko, Snyder,& Feinberg, 1963; Rechtschaffen, Schulsinger, & Mednick, 1964). More recently, Hobson (2004) suggested that the dream is amodel for (psychotic) madness. Similarly, Gottesmann (2006) proposed that REM sleep is a useful model for schizophrenia.

Whilst this de-differentiation hypothesis predicts similarities between psychosis and dreaming it departs from the idea ofdreaming as a model for psychosis. Rather, this paper will argue that both waking and dreaming are functionally adaptive (seelater). Similarities between psychosis (positive symptoms) and dreaming do not imply equivalence between the two states;dreaming is self-organized, whereas psychosis is disordered. As noted earlier, to achieve a dreaming state of mind-brainthere must be cholinergic suppression of aminergic neuromodulation, mesolimbic dominance over mesocortical dopaminer-gic function, sensory gates must be closed, the prefrontal cortex de-modulated and so on. Clearly all of these conditions arenot met in psychosis which is a condition that occurs during waking. Although their performance may be defective, patientswith psychosis do retain some frontal lobe functionality and are still processing external data. However erroneous their con-clusions may be, such patients are trying to make sense of their experience. During dreaming, dreamers do not engage insense making. Therefore, phenomenologically, the experience of psychosis will differ in from that of dreaming.

For example, although hallucinations characterize both dreaming and psychosis, dreaming is totally hallucinated,whereas, in psychosis, hallucinations only emerge sporadically and do not take up the whole visual field, Collerton, Perry,and McKeith (2005) argue against the case for hallucinations as dream intrusions, in part on the grounds that dreams occupythe whole visual field whereas hallucinations do not. However, during dreaming the sensory gates are closed and the frontalcortex de-modulated whereas in a de-differentiated state there would still be some aminergic input, with the sensory gatesonly partially closed, sensory input would diminish so there would only be an increase in the possibility for hallucinatoryimagery to emerge (see Behrendt, 2003, 2006; Behrendt & Young, 2004).

Dreaming is essentially visually hallucinated, whereas auditory hallucinations predominate in psychosis (see, for exam-ple, Schiffer, Rao, & Fogel, 2003). Although speculative, this may also be explained through considering psychosis as a hybridstate. As argued earlier, during waking consciousness, the brain-mind systematically externalizes the sense of an externalworld (Metzinger, 2009). As a result of this process, in waking there is experience of a subjective private ‘inner’ world thatis present within an objective public ‘outer’ world. Moreover, during waking, the mind-brain makes a distinction betweenthese worlds, without this distinction, internally generated precepts may be experienced as having external sources (Fordet al., 2007). During dreaming consciousness there is no externalization of the sense of an outer world and, therefore, thedistinction between the internal subjective world and the external world is lost. During psychotic waking the externalizationprocess would still be present (at least to some extent) but the distinction between an external ‘public’ world and internal‘private’ precepts is being eroded due to the partial intrusion of the dreaming state (which conflates the external and internalworlds). Therefore, in a de-differentiated state, when waking has incorporated some (not all) of the characteristics of dream-ing it is unsurprising that internal precepts become experienced as external reality.

During waking, as argued earlier, the main internal ‘running commentary’ on the external world is not visual but takes theform of an ‘internal conversation’ (Archer, 2003). During this internal conversation, sometimes based on my fears, I advisemyself over what to do next. For example, ‘Hurry up, slowcoach, you are getting old, you’re going to miss the train’, some-times, I equivocate giving rise to multiple internal ‘voices’, ‘Don’t have chocolate, you’ll get fat, you are supposed to be on adiet. . .Oh, go on, it’s Ok if you only have a small piece’. Due to the externalization process, along with some loss of self-mon-itoring (owing to the partial de-activation of the frontal cortex), in a de-differentiated state, this internal advice may be expe-rienced as external threats or commands. Based on evidence from functional magnetic resonance imaging, Lawrie et al.(2002) conclude that auditory hallucinations emerge consequent upon the defective monitoring of inner speech processedin temporal areas which are unconstrained by prefrontal inputs. Auditory hallucinations in schizophrenia are either voicesconversing amongst themselves or voices commanding, threatening or commenting on the patient (Tandon et al., 2008). Inmost cases, auditory hallucinations are whole phases or sentences and are often not in responses to external speech (Hoff-man and McGlashan, 1997). Internal advice to oneself is also in sentences and often not in response to the speech of others.Increases in anxiety and fear due to the carry over of such primary emotions from the dreaming state (see mood disorderslater) would tend to pitch this ‘internal advice experienced as external commands’ more negatively.

Similarly, although delusions characterize psychosis and dreaming, their nature differs in the two states. Persecutory delu-sions and delusions of body/mind control are most common in schizophrenia (see, for example, Appelbaum, Robbins, & Roth,1999). Paranoia and feelings of body/mind control do not pervade dreaming. As argued above, the more or less complete loss ofexecutive functions in dreaming implies that the dreamer does not consider the issue of control. In a de-differentiated state thepartial intrusion of some phenomenal aspects of dreaming means that some loss of intentional control may be experienced dur-ing waking. Sufficient prefrontal functioning would be retained, however, for awareness of this loss to be registered. If one’sactions are not under the control of the self then it would be a reasonable sense making assumption that they may be under


the control of another. During dreaming, emotions such as fear and anxiety are tied to the dream plot (Hobson, 2002). If in-creases in fear and anxiety from the dreaming state start to permeate everyday waking situations (where such emotions areinappropriate and non-explicable in terms of on-going events) then the fear and anxiety appears free-floating and in need ofalternative explanation. In a de-differentiated state the presence of free-floating fear and anxiety may arouse suspicion that,in turn, may give rise to an inference of concealed threats thus fuelling a paranoia which would tend to be augmented byany felt experience of loss of control.

Particularly at an early stage, people with schizophrenia often become highly religious (Mohr & Huguelet, 2004). Moreoverreligiosity can persist; religious delusions are one of the least well understood phenomena in schizophrenia (Brüne, 2009). Againreligious delusions are not common in dreaming. As argued above, chaos theory predicts that when a degree of self-organizationis lost the consequent state fluctuations are unpredictable. In a de-differentiated state where felt loss of intentional control is notaccompanied by increased fear and anxiety, this loss may be interpreted benignly as, for example, well intended guidance froman (unknown) external source. This more positive interpretation could then precipitate not paranoia but religiosity.

In sum, although psychosis and dreaming do have striking parallels there are also significant differences. It is argued thatpsychosis as a de-differentiated, hybrid state (where only variable aspects of dreaming consciousness are incorporated inwaking and to a greater or lesser degree) accounts better for these differences than the thesis that dreaming is a modelfor understanding psychosis.

6.2. Cognitive/disorganized symptoms

As some self-organization has been lost, a de-differentiated state would, by definition, be a disorganized one. Cognitive/disorganized symptoms include: positive formal thought disorders (e.g. pressure of speech, tangentiality, derailment, inco-herence, and illogicality), poverty of the content of speech, alogia, bizarre behaviour, difficulty in abstract thinking, poorattention, unusual thought and poor insight (see, for example, Hardy-Baylé, Sarfati & Passerieux, 2003). As argued earlier,thinking reaches its nadir in REM dreaming (Fosse et al., 2001) so some thought disorder would be anticipated in a de-differentiated state. Dreaming is, of course, a highly associative visual (rather than a spoken) mode where the dreameroften engages in bizarre behaviour. As noted earlier, although dreamers do sometimes speak in dreams, this is relativelyinfrequent and when attempted, dreamers struggle to vocalize their thoughts (Hobson, 2002). Working memory alongwith other executive functions (abstract thinking, decision-making, sustained concentration and applied logic) are greatlysuppressed in dreaming (Dietrich, 2003). During (non-lucid) dreaming insight is lost (Voss et al., 2009). If waking con-sciousness has encompassed some aspects of dreaming many of these cognitive/disorganized symptoms could beexplained.

Motor output is blocked in dreaming and thinking is greatly suppressed but, in a hybrid state, unusual thought mayoccur and bizarre urges may be acted out. Whilst bizarre impulses are activated in psychosis, normal routines are ne-glected (or poorly performed) in schizophrenia. The disorganization syndrome is associated with poor self care (Liddle,1987) and inappropriate attire (Tandon et al., 2008). Routine, habitual self-care activities are rarely undertaken duringdreaming, so in a hybrid state these may be neglected. Difficulty in abstract thinking, poor insight and poor attention(as sustained concentration) would follow from the suppression of executive functions in dreaming. ‘Loosening of associ-ations’ has been seen as fundamental to schizophrenia since Bleuler (1911/1950). During dreaming, linear-logic is lost to aloosely parallel associative, rapidly changing visual narrative, the details of which are not vocalized. If this non-linear-lo-gic, very loosely associative, rapidly changing mode started to drive waking thought and was vocalized, from the point ofview of the audience, there would be pressure of speech with illogicality, tangentiality and derailment. Working memorydeficits would exacerbate these difficulties. If the degree of penetration of the dreaming state into waking was even great-er then vocalization may become incoherent, there may be poverty of speech content, lack of unprompted speech and,even, ultimately, alogia.

Uhlhaas and Mishara (2007) argue that in the literature on the cognitive/disorganization syndrome, changes in basicperception have been neglected. They report that patients with schizophrenia experience a fragmentation of the normallyintegrated perceptual field. Moreover, patients focus only on details of a scene to the neglect of the wider background,rendering relatively unimportant features accentuated and hyper-significant. In a hybrid dreaming–waking state the sen-sory gates would be partially closed with some loss of self-organization and visual integration, so perceptual anomalieswould be anticipated. In addition, as argued earlier, the world that appears during dreaming is relatively sparse (comparedto the one that materializes in waking) with an enhanced perception of these limited phenomena. So in a de-differentiatedwaking state some loss of scene background (or context) may be experienced with an unusual accentuated focus on spe-cific details. In waking an appreciation of context is essential to make sense of ‘what’s going on’. So, in a de-differentiatedstate, perceptual anomalies could only exacerbate sense making difficulties consequent upon the diminution of executivefunctions.

A cardinal aspect of schizophrenia is lack of insight (Carroll et al., 1999). As argued above in a de-differentiated state therewould be a partial de-activation of the frontal lobes, this would result some loss of self-monitoring. Moreover, the reality ofwhat conscious experience is ‘telling one’ is not questioned in either dreaming or waking. So this sense of the authenticity ofexperience would be likely to be preserved in a de-differentiated state. Thus, in a de-differentiated state, both some loss ofself-monitoring and a preserved sense of authenticity would mitigate against insight.


6.3. Motor symptoms

Some inhibition of psychomotor function is present in schizophrenia (see Morrens, Hulstijn, & Sabbe, 2007, for a review).As motor output is blocked during dreaming, de-differentiation could result in some slowing of movement during waking.Morrens, Hulstijn, Lewi, De Hert, and Sabbe (2006) suggest that the repetitive, purposeless motor activity seen in schizophre-nia may be the result of impaired executive function due to reduced activity in the dorsolateral prefrontal cortex. As arguedabove, the frontal lobe is deactivated during REM dreaming, with an associated suppression of executive functions, so theexistence of stereotypy would also be compatible with the de-differentiation thesis. Only the oculomotor pathway functionsduring the eponymous REM dreaming (see, for example, Hobson & McCarley, 1977); these rapid eye movements are not un-der intentional control. Some carryover of rapid eye movements in a de-differentiated state may account for both pursuit andantisaccade abnormalities. Goldman (2000) reports that 80% of patients with schizophrenia (who are not medicated) exhibitabnormally jerky saccadic eye movements when their eyes pursue a moving target. Over and above this pursuit abnormality,people with schizophrenia also have an antisaccade abnormality (see, for example, Turetsky et al., 2007).

6.4. Mood symptoms, bipolar disorder and autopoiesis

Anxiety is a prominent feature of the early stages of schizophrenia (Chapman, 1966). Social anxiety is highly prevalent inout-patients with schizophrenia, their social anxiety scores did not differ from those of subjects with social anxiety as theirprimary diagnosis (Pallanti, Quercioli, & Hollander, 2004). This indicates that the social anxiety suffered in schizophreniadoes not differ in kind from that in social anxiety syndrome. As argued above, anxiety is the most common emotion indreaming and as social interaction is attenuated in dreaming, it may be anticipated that in a de-differentiated state socialsituations would precipitate anxiety.

Depression is common in schizophrenia (Tandon et al., 2008). Depression does not characterize dreaming. However,depression is, of course, integral to bipolar disorder. As noted earlier, although modern psychiatric practice continues to rec-ognize and diagnose two major psychiatric conditions (schizophrenia and bipolar disorder), there is current debate onwhether they are indeed distinct (Craddock, O’Donovan & Owen, 2005, 2006; Craddock & Owen, 2005). Disturbances to affec-tive experience and expression are fundamental aspects to schizophrenia, particularly in the early stages (Yung & McGorry,1996). Altered prefrontal function characterizes not only schizophrenia but also affective disorders (Stoll, Renshaw, Yurge-lun-Todd, & Cohen, 2000). The formal thought disorder (including a loosening of associations) that occurs in schizophreniaalso characterizes mania (Solovay, Shenton, & Holzman, 1987). Even auditory hallucinations arise in 15% of patients withmood disorders (Hoffman, 2003). Auditory hallucinations occur in between 50–70% of patients diagnosed with schizophre-nia (Andreasen & Flaum, 1991; Sartorious, Shapiro, & Jablonsky, 1974). Keshavan et al. (2008) provide a review on the manyareas of neurobiological overlap between affective disorder and schizophrenia.

Some light may be shred on the relationship between schizophrenia and bipolar disorder through considering the conceptof autopoiesis. ‘Autopoiesis’ expresses the idea of holistic self-producing systems (Maturana & Varela, 1980; Varela, Matur-ana, & Uribe, 1974) The mind-brain is such a system, it produces itself as a unitary, bounded entity. Autopoiesis accounts forthe holistic ‘feel’ of both waking and dreaming, both are experienced as unified. Self-producing systems are also self-orga-nizing ones, ‘. . .an autopoietic system has a domain in which it can compensate for perturbations through the realization ofits autopoiesis, and in this domain it remains a unity’ (Varela et al., 1974, p. 188). This implies that if ‘perturbed’ the mind-brain (as an autopoietic, self-organizing system) can reconstitute itself– such organizing potential is inherent in the produc-tion of a coherent whole from constituent parts. As Goodwin (1994, p. 169) puts it, ‘. . .complex non-linear dynamic sys-tems. . .. tend to settle dynamically at the edge of chaos. If it [the system] moves too far into the chaotic regime it willcome out again of its own accord; and if it strays too far into the ordered regime it will tend to ‘melt’ back into dynamicfluidity where there is a rich but labile order, one that is inherently unstable and open to change’. If, as argued earlier, orderin the mind-brain is represented by an achieved differentiation between waking and dreaming and ‘chaos’ or disorder(schizophrenia) results from their de-differentiation, then bipolar disorder may equate to autopoietic attempts to restoreself-organization (Llewellyn, 2009).

Self-organizing occurs though the brain’s modulatory systems (Kahan, LaBerge, Levitan, & Zimbardo, 1997; Singer, 1986)so any autopoietic response would also be expected to occur through neuromodulation. As argued earlier, de-differentiationwould result in cholinergic and mesolimbic dopaminergic modulation rising (and aminergic and mesocortical modulationfalling) during waking. During dreaming, de-differentiation would cause aminergic and mesocortical dopaminergic modula-tion to rise (and cholinergic and mesolimbic modulation to fall). If an autopoietic response to correct these ‘imbalances’ oc-curred, mania/hypomania may flow from self-organizing to produce a ‘purer’ waking state (through aminergic hyperactivityand cholinergic hypoactivity). In contrast, depression may result from autopoeitic attempts to induce a ‘purer’ dreamingstate (through cholinergic hyperactivity and aminergic hypoactivity). If psychosis predominated (with the waking state moreaffected) then it would be predicted that bipolar disorder would begin with a manic episode. Alternatively, if the dreamingstate were more affected, the first episode would be more likely to be a depressive one. Or both aminergic and cholinergichyperactivity could alternate (resulting in rapid cycling bipolar ‘disorder’). Evidence is suggestive of this possibility.

Classic cholinergic–adrenergic imbalance theories of mania and depression have been proposed (Janowsky, El-Yousef,Davis, Hubbard et al., 1972; Janowsky, El-Yousef, Davis, & Sekerke, 1972; Janowsky, Risch, & Gillin, 1983). Over-activity ofcatecholamine neurotransmission may explain mania/hypomania, whereas depletion of amines may account for depression


(Donaldson, 1998). Cholinergic reversal of manic symptoms has been demonstrated (Janowsky, El-Yousef, Davis, Hubbardet al., 1972; Janowsky, El-Yousef, Davis, & Sekerke, 1972). People with depression exhibit shorter REM latency and height-ened REM density, which may be interpreted as hyper-cholinergic activity (Riemann et al., 1994). Mahmood and Silverstone(2001) found that central serotonergic activity is reduced in depression and reported similar findings in euthymia but failedto consistently substantiate an increase in mania. Selective serotonin reuptake inhibitors can precipitate mania (Breggin,2004; Peet, 1994).

Once established, schizophrenia tends to be chronic but characterized by remissions, albeit that these are incomplete(Tandon et al., 2008). Such a trajectory is, at least, suggestive of some autopoietic response. If schizophrenia and bipolar dis-order are mutually implicated, so that the latter can be an attempt to restore order to the former, then this may partly ex-plain the uncertain trajectory of schizophrenia. It has been noted that schizophrenia is potentially reversible in the prodromestage (Lee, McGlashan, & Woods, 2005). If an autopoietic response to incipient schizophrenia started early and was success-ful, then the de-differentiation process may be arrested. On the other hand, a more severe form of schizophrenia may inducemore dramatic manic and depressive symptoms- precipitating classic bipolar disorder. Observations from clinical practicenote a sometime temporal progression from classic bipolar disorder to schizophrenia, with the reverse being rare (Walsh,2009). This would be the case if bipolar disorder was an autopoietic response but, in some cases, ultimately failed.

This hypothesis that bipolar ‘disorder’ may be an autopoietic attempt to restore order to schizophrenia does not excludethe possibility that bipolar disorder could also be expressed as an independent condition of anomalous neuro-dynamics.

7. How does ‘de-differentiation’ compare with current thinking on the neurobiology of schizophrenia?

Clearly it is not possible here to review all possible relevant research findings on schizophrenia but some comparisons aremade with classic and continuing areas of work. In psychiatry, thinking on schizophrenia has been dominated by the ‘dopa-mine hypothesis’. The early hyperdopaminergic theory of schizophrenia was superseded by one positing (implicitly, in thewaking state) hyper-mesolimbic dopamine and hypo- cortical dopamine (Carlsson, 1988; Davis et al., 1991; Weinberger,1987; Weinberger, Aloia, Goldberg, & Berman, 1994). Howes and Kapur (2009) have recently argued, however, that the pic-ture on schizophrenia is more complex than this mesolimbic–mesocortical DA imbalance hypothesis implies. They state thatwhile DA imbalance may account well for psychosis, it does not explain the totality of schizophrenia, reasoning that multipletransmitter systems are likely to be involved in negative symptomatology and cognitive deficits. Such arguments reflectthose of others. Multiple ‘imbalance’ hypotheses have been suggested. Schizophrenia (as observed in the waking state) ischaracterized by serotonergic and noradrenergic demodulation and cholinergic hypermodulation (Bymaster, McKinzie, &Felder, 2004; Gottesmann, 2006; Sarter et al., 2005). Sarter and Bruno (1999) have argued that both hyper- and hypo-cho-linergic activity characterizes a broad range of neuropsychiatric conditions including schizophrenia. Noradrenergic instabil-ity has been suggested in schizophrenia (Van Kammen & Gelernter, 1987). Cholinergic–dopaminergic interactions have beenimplicated in the expression of positive and negative symptoms (Tandon et al., 1999). Dysfunctions in both serotoninergicand dopaminergic systems have been proposed, with the serotoninergic mediating negative symptomatology and dopami-nergic precipitating the positive symptoms (Bleich, Brown, Kahn, & van Praag, 1988). Tandon et al. (1999) suggest that al-tered balance between DA and one or more other transmitter systems are likely to be involved in schizophrenicsymptoms. In a more recent review, Keshavan et al. (2008) argue for the implication of dopamine, glutamate, GABA, acetyl-choline and serotonin (although they conclude that the evidence for 5-HT involvement is indirect).

Second, there has also been a substantial body of research exploring frontal lobe dysfunction (see, for example, Berman,Zec, & Weinberger, 1986; Buchsbaum, 1990; Weinberger, Berman, & Zec, 1986). Weinberger et al., 1994 point out that thiswork can be traced back to Kraepelin; they argue that, although there is evidence of prefrontal dopaminergic deafferentation,this is likely to be secondary to a failure of prefrontal activation. Functional brain imaging of patients with schizophreniaconfirms the lack of activation of the dorsolaternal prefrontal cortex when confronted with cognitive tasks (Berman &Meyer-Lindenberg, 2004). Such failure results in impairment on tests of ‘executive’ functions involving abstract thoughtand working memory. Frontal lobe dysfunction has not been clearly linked to any structural pathology, however (Bilder &Goldberg, 1987; Goldberg & Bilder, 1987).

Disturbed information processing and attentional dysfunctions constitute a third major area of work with a long history(Braff, 1993). Sensory gating deficits are well documented in schizophrenia (Adler et al., 1982; Hirano et al., 2010; Judd,McAdams, Budnick, & Braff, 1992; Potter, Summerfelt, Gold, & Buchanan, 2006; Venables, 1964). These gating failures resultin people with schizophrenia being unable to filter out irrelevant data, all sensory signals tend to be perceived as equallysignificant hence, sensory overload is the consequence. Judd et al. (1992) suggest that there is a tendency for gating deficitsto be more prominent in frontal areas. Specificity on attentional and gating deficits has been gained through studies on eventrelated potentials. Mismatch negativity (MMN) represents the pre-attentive phase of auditory information processing; MMNis disturbed in schizophrenia, a finding that has been consistently replicated (Umbricht & Krljes, 2005). The P300 waveformhas been seen as the neuro-correlate of a working memory update on environmental changes. Blunted amplitude of the audi-tory P300 response to salient stimuli is present in schizophrenia (Bramon, Rabe-Hesketh, Sham, Murray, & Frangou, 2004;Jeon & Polich, 2003). Although the data is not as consistent as for P300 (possibly due to methodological differences), P50suppression (the normal decrease in P50 amplitude when the second of two paired auditory stimuli is presented) is dis-rupted in schizophrenia (Bramon et al., 2004; de Wilde, Bour, Dingemans, Koelman, & Linszen, 2007; Patterson et al.,


2008). Pre-pulse inhibition (which is implicated in sensory gating) is reduced in schizophrenia (Braff & Light, 2005; Geyer,Krebs-Thomson, Braff, & Swerdlow, 2001).

Work on frontal lobe dysfunction and research into disturbed information processing/sensory gating deficits both linkinto the disconnectivity hypothesis of schizophrenia. Friston (2002, p. 66) defines this, ‘Schizophrenia can be understoodin cognitive terms, and in terms of pathophysiology as a failure of functional integration within the brain.’ Friston and Frith(1995) proposed that there may be disruption of fronto-temporal interactions; they also note work which has highlightedsome abnormal integration of prefrontal activity with that in subcortical, limbic and temporal structures. Lawrie et al.(2002) implicate reduced frontotemporal connectivity with auditory hallucinations in schizophrenia. Keshavan et al.(2008) suggest that P50 gating deficits in schizophrenia may reflect frontal–hippocampal miscommunication.

Clearly there are some convergences between this de-differentiation thesis and neurobiological findings in schizophrenia.Both ‘de-differentiation’ and current thinking on schizophrenia implicate not only mesolimbic–mesocortical DA imbalancebut altered balance between other transmitter systems. Differentiation implies both hyper-cholinergic input into wakingand hypo-cholinergic into dreaming, both are thought to characterize schizophrenia. The de-differentiation of waking anddreaming consciousness would disrupt reciprocity between dopaminergic/serontonergic/noradrenergic/cholinergic systems.Current thinking on schizophrenia is moving towards implicating multiple and interacting imbalances between modulatorysystems (Carlsson, Waters, Waters, & Carlsson, 2000; du Bois et al., 2005).

Input–output gating dysfunctions would characterize de-differentiation in a similar manner to those seen in schizophre-nia. De-differentiation would result in diminution of sensory input during waking (due to sensory gates being ‘partiallyclosed’). This may intensify the hallucinatory positive symptoms induced by heightened mesolimbic DA. De-differentiationwould result in fewer sensory signals being registered; those that are processed may induce the ‘sensory overload’ seen inschizophrenia- as the dreaming state is non-adaptive for the processing of external sensory information. Moreover, as dreamscenes are sparse compared to waking ones, it appears that there is less of a requirement to filter information (compared towaking) so, in a de-differentiated state, filtering problems may emerge.

As argued earlier, during dreaming the dorsolateral prefrontal cortex and the primary visual cortex are deactivated,whereas limbic areas and the occipitotemporal cortical areas are selectively activated. De-differentiation would be expectedto reduce frontal lobe activation and impair frontal lobe functionality during waking. As the regional activation of the brainvaries between waking and dreaming, resulting in two different functionally integrated states, it would be anticipated thatde-differentiation would engender a loss of functional integration in both cognitive and physiological terms in a similar wayto that outlined in the disconnection hypothesis.

8. Negative symptoms and sleep disturbances

The above sections have outlined the possible implications of the de-differentiation of waking and dreaming conscious-ness for the functionality of the waking state. The discussion has also considered the compatibility of the de-differentiationthesis with the neurobiology of schizophrenia but, implicitly this has also been in terms of impact in the waking state.But if the de-differentiation idea has any validity then effects on dreaming consciousness and sleep would also be antici-pated. De-differentiation involves some loss of dynamic reciprocity between neuromodulatory systems. This loss is not abso-lute, however, but a matter of degree. So, for example, the retention of some dynamic reciprocity between neuromodulatorysystems would imply that if aminergic and mesocortical dopaminergic input decline during waking, they would rise in REMdreaming and also during other sleep stages. An increase in aminergic and/or mesocortical dopaminergic modulation duringsleep (and dreaming) would be expected to disrupt sleep. As noted earlier, schizophrenia and bipolar disorder are both char-acterized by sleep disturbances (Benson, 2006; Costa e Silva, 2006). Ferrarelli et al. (2007) report reduced spindle density inschizophrenia. In a review Monti and Monti (2005) conclude that sleep-onset and maintenance insomnia is a fundamentalfeature of schizophrenia, regarding of medication status or whether the clinical phase is chronic or acute. They also remarkthat most studies show that stage 4 sleep is reduced, as is REM latency, but REM sleep duration remains unchanged. More-over, it would be expected that the partial projection of waking into dreaming would partly disinhibit motor function duringsleep. Restless legs syndrome in sleep has been found to be higher in patients with schizophrenia than normals (Kang et al.,2007).

Studies on whether dreaming consciousness (as opposed to REM sleep) is disrupted in schizophrenia face clear difficul-ties. First, in neuroscience there is profound split between those ‘. . .holding that the dream is a mere random byproduct ofREM sleep physiology, and [those holding] that the dream is an organized subjective experience that performs a specificfunction.’ (Ardito, 2003). If the conscious experience of dreaming serves no function, then disruption has no consequence.Second, the idea (discussed earlier) that dreaming is a model for psychosis (or schizophrenia) has tended to mask the pos-sible functions of dreaming. Third, experimental approaches to studying the functionality of dreaming are hard to design andexecute. If dreaming does have a function, could the loss of this functionality be linked to the negative symptoms ofschizophrenia?

Negative symptomology (social withdrawal, diminished affect, loss of motivation and apathy) is generally accepted to bemore debilitating (Andreasen, 1990) and less curable, being resistant to pharmacological approaches (Erhart, Marder, & Car-penter, 2006; Samuelian, 1996). Indeed, it has been argued that the anti-psychotic medications currently used to treat po-sitive symptoms may induce negative symptomatology, engendering a loss of interest in the world (Breggin, 1980; Charlton,


2006; Panksepp, 1985). This would be expected under the de-differentiation thesis as blocking mesolimbic dopamine mayresult in a rise of mesocortical DA, due to some retained reciprocity between these modulatory systems (Davis et al., 1991;Guillin et al., 2007; Pycock et al., 1980). This would improve both positive and disorganized symptoms during waking butmay exacerbate negative symptoms due to the impact of less mesolimbic and more mesocortical DA during dreaming, asdescribed in 8.1 below. Thus the efficacy of anti-psychotic medication would depend upon the balance of positive and neg-ative symptoms, which would, in turn, be contingent on the relative impact of de-differentiation on the waking and dream-ing states. Specifically, if de-differentiation affects the waking state more than the dreaming one then anti-psychotics wouldbe of more benefit. In contrast, if the dreaming state is more negatively affected, then anti-psychotics would be less effica-cious, indeed, as described above, they may exacerbate the negative syndrome.

The intrusion of some aspects of dreaming into waking (as discussed above) may have implications for negative symp-toms, for example, motion slowing may be linked to apathy and/or loss of intentional control and inability to make senseof waking experience may lead to a loss of motivation. But these possibilities seem insufficient to account for the devastatingimpact of negative symptoms. Would the intrusion of some physiological and phenomenological of waking into dreamingcause problems? Admittedly, this is highly speculative but this paper will go onto explore the idea that dreaming conscious-ness may be functional for emotionally salient memories. Indeed, that a dream may be a mnemonic device for such mem-ories. If this is the case, then the intrusion of aspects of waking into dreaming may result in pathologies, indeed, specifically,may have implications for negative symptomatology.

8.1. Is dreaming functionally adapted to support imaginative association and memory?

Hartley (1749) proposed that perceptions of an integrated, meaningful world emerge from ‘joint impression’ or associa-tion. He also believed that personally meaningful psychological associations create a sense of self. He held that this funda-mental principle of association works at the level of the brain and the mind (Buckingham & Finger, 1997). Dreaming is anactivated, conscious, cyclically periodic brain/mind state; this suggests that dreaming has some function. Indeed dreamingconsciousness may be complementary to waking (Hobson, 2009). Association may be the source for self-organizing and inte-gration (a unified experience from a single perspective) in both waking and dreaming consciousness. The basis for associa-tion in the two states may be different, however. Freud contended that dreams reflect ‘free’ or loose association. This idea hasproved a robust one. Stickgold (2003) argues that, during dreaming, the brain ignores predictable associations, instead novelconnections are sought out and strengthened as appropriate. Strengthening associations, particularly novel ones, is integralto long term potentiation and the enhancement of memory (see, for example, Lynch, 2004; Malenka & Bear, 2004).

Throughout Classical Antiquity and into the Early Middle Ages, memory was recognized to be a creative process wherematerial to be remembered (in current terms, ‘encoded’ and ‘stored’ in long term memory) was made memorable throughimaginative, personal association. In this ancient art of memory (AAOM) personally significant events/people/emotions wereinterlinked in ways that did not reflect how these events/people/emotions had actually been related in day-to-day experi-ence but how they were meaningfully, emotionally associated from a personal point of view (Bolzoni, 2001; Carruthers,2008; Yates, 1966) The aim of AAOM (incorporating the method of loci) was to produce memory cues or ‘. . .chains of asso-ciation that regenerate memories.’ (Bolzini, 2001:xviii). The more bizarre, dramatic and absurd is the cue, the more resilientis the memory to which the cue has been associated (Hughes, 1997). As compared to replay or rehearsal, AAOM can still pro-duce extraordinary memory ‘feats’ during waking (Wilding & Valentine, 1997). But with sensory gates closed, and witharound 2 h each day devoted to the task, REM dreaming consciousness may self-organize specifically to support associativemnemonic functioning and, hence, be much superior to waking in this respect. Some indicative evidence of this is providedby Sprenger et al. (2010) who demonstrated that REMs, when imagining vivid scenes in dreaming, were similar to eye move-ments with open eyes when imagining remembered scenes during waking.

Memory is not unitary but multi-faceted. Classic work in psychology recognizes six types of memory. Memory is tradi-tionally divided into declarative (explicit) and non-declarative (implicit) categories, declarative memory can be further di-vided into episodic and semantic, non-declarative is sub-divided into procedural/skill, conditioning, non-associative andpriming, such a division gives six categories of memory (although sometimes autobiographical memory is seen as a subsetof episodic, on some schema it is considered an independent category). Sleep is implicated in all of these six types of memoryand there is no known memory category for which sleep does not provide benefit (Stickgold, 2009). Stickgold (2009) calcu-lates that with six different kinds of memory, five different stages of sleep and six stages of post-encoding memory process-ing, there are 144 distinct sub-questions involved! This paper, however, is not directly concerned with all of the complexquestions that the relationship between sleep and memory raises.

Rather this section of the paper is focused on this question,’ If dreams are functional for memory, what kind of memorymight dreams enable?’ Clearly we need to remember what is important to us – concerns. Concerns include some episodicand autobiographical memories but are not limited to them. Concerns also encompass projects – things to accomplish inthe future (from writing a paper on dreaming consciousness to meeting a friend for coffee next week). In relation to ourown concerns and projects, we need to remember our interactions and conversations with significant others, as thesemay converge with or cut across our plans. In relation to our own thoughts, intentions and goals, memory is not only aboutthe past, ‘. . .memory pulls us forward. . .’ (Robinson, 2005, p. 192) as memory helps us decide what to do next. Concerns areemotionally salient. We cogitate on our concerns. So, we need to remember waking thoughts about concerns. Concerns drivepersonal identity. Archer (2000, p. 10) argues that personal identities are formed by the way that concerns are monitored and


prioritized. So if projects, emotional responses to concerns, waking thoughts about concerns and, even, the nature of con-cerns are forgotten, personal identity is eroded. In terms of this paper, there is no exact fit between the classic memory def-initions in psychology and the type of memory that may be enhanced in dreaming consciousness. ‘Episodic’ memory is theclosest to ‘emotional concern memory’ but, as discussed above, the latter is much wider than the former.

8.1.1. A possible example of bizarre, creative dream association and memory enhancementNielsen and Stenstrom (2005) suggest that the links between dreaming and memory will only be elucidated when sub-

jects are able to identify the non-obvious source memories for their dreams; they also propose that self-identification ofthese sources, in the mode of Freud, William James and others, may yet prove to be the most productive method. In thisspirit, I narrate the following dream fragment as an example of bizarre, absurd and creative dream association.

I dream I am having my eyes tested and instead of the normal chart the ophthalmologist uses ‘Bagpuss’. In my dream, the usual‘chart’ letters are apparent under Bagpuss’s fur, I fail the test because I can’t see them.

‘Bagpuss’ is an old, fat, saggy cloth cat-a 1970’s UK children’s TV character. I often get my eyes tested because I am veryshort-sighted. The Bagpuss dream occurred shortly after a recent test for glaucoma. Instead of my normal optometrist I wasreferred to the hospital I used to be taken to as a child. I was most certainly worried, even afraid. What did the occasion meanto me? Well, I was very conscious of the hospital visits I made as a child when I feared that the stronger and stronger spec-tacles I was being prescribed indicated that I was going blind. Now many years later I was returning to this same hospital fora test for glaucoma- which can cause blindness and is quite common in the elderly. So, for me, the visit had associations ofboth being young and growing old. Bagpuss is old, not to mention fat and saggy! And Bagpuss is for the young- he is a chil-dren’s TV character. But this does not seem enough, does it? Why associate Bagpuss with a test for glaucoma? Glaucomastarts with a loss of peripheral vision. Bagpuss is always in scenes which shade out into hazy, lost, blankness (see ‘Bagpuss’on youtube). Predictably, I always disliked Bagpuss without ever analyzing the reason why. For me, in my dreams, Bagpuss isassociated with being young, growing old and fear of blindness through glaucoma.

If, in waking consciousness, I was asked for a personally meaningful, strikingly bizarre, visual image that was associatedwith glaucoma, being young and growing old. I think it highly unlikely I would be able to come up with anything. But, in mydreams, I easily make an imaginative, associative ‘leap’ across 35 years to connect blindness with a saggy, old cloth cat.Dreaming may differ from waking consciousness primarily because it forges more imaginative, more bizarre and lesstime/space bound associations. Such associations may act to enhance memory. Lake (2008) has demonstrated that looseassociation or ‘flight of ideas’ in schizophrenia becomes explicable if the patient is able to narrate the personal associationsthat link the ideas. Similarly here, the association between Bagpuss and ophthalmology in my dream is understandable in thelight of my past history. This suggests that ‘flight of ideas’ in schizophrenia may emerge consequent upon the intrusion ofloose associations from the dreaming state.

8.1.2. Other phenomena that both enhance memory and characterize dreamingAlong with association, dreaming has several characteristics that have been shown to aid memory. First, dreaming creates

sequential visual imagery; visualization improves recall (Bower, 1970). Pictorial representation, particularly when theimages are interacting, also enhances memory (Richardson, 1980). Second, dreams are frequently more dramatic and emo-tionally driven than everyday waking experience. Unusual, dramatic and emotionally salient events are more memorable(Dutta & Kanungo, 1975; Hunt, 2008; Rubin & Friendly, 1986; Rusting, 1998). This memory effect is exemplified and ex-tended in ‘flashbulb memory’; as the name suggests, what is surprising about this phenomenon is not that dramatic eventsare easily recalled but that the personal circumstances surrounding unusual occurrences are also vividly remembered(Brown & Kulik, 1977). This may suggest that, in dreams, introducing emotionally charged, bizarre and dramatic events im-proves recall of this content but also aids memories for the more ordinary, but connected, personal context. Third, dreamsportray organized scenes (for example, the sky is always above the characters, the ground always below). And these scenesform a narrative. Organization and narration support memory (Mandler, 1984). Finally, in my dreams, I am embodied andfeel I am living out the events. Embodied memories are the most resilient (Merleau-Ponty, 2002).

8.2. Evidence on the relationship between dreaming and memory

This evidence will be addressed through discussing work on how and why dreams embed memories and reviewingneurobiological data indicating that mnemonic processes function during dreaming.

Freud (1999) thought that all dream material relates in some way to remembered experience, this he asserted as undis-puted knowledge. Similarly, Stickgold (2002) argues that with sensory signals excluded, memories along with derived sym-bols and meanings are the only possible sources for dreams. Hall and Van de Castle (1966) found extensive support forFreud’s proposal that recent events are the basis for dream plot elaboration. The new associative links forged during dreamsmay be vital for understanding the meaning of events as they unfold (Stickgold, 2002). Dreams do not replay whole episodicmemories but around 65% of content can be clearly traced to memory fragments of waking experiences (Fosse, Fosse,Hobson, & Stickgold, 2003). The presence of new and bizarre associations may account for the 35% of dream content thatis not readily traceable to waking experiences. For example, at first I am unlikely to understand the connection betweena saggy old cloth cat and my visit to the ophthalmologist but on reflection I may see the connection. If dream content is


entirely composed of meaningfully associated memory fragments, everything in dreams is relevant to the dreamer. Duringwaking emotional salience (or relevance) has to be discerned from a myriad of sensory signals, it may be that duringdreaming consciousness emotional salience can be assumed.

During memory ‘encoding’ the hippocampus enables the creation of novel meaningful associations (Achim & Lepage,2005; Davachi & Wagner, 2002; de Vogelaere, Santens, Achten, Boon, & Vingerhoets, 2010; Henke et al., 1999). Activity inthe hippocampus is increased during REM dreaming compared to both waking and NREM (Nielsen & Stenstrom, 2005). Re-cent memories may be stored in the hippocampus temporarily and then reactivated during dreams (Hobson, 2002). Indreams, access to remote memories is also enhanced (Hobson, 2002). Evidence is consistent with the processing of emotion-ally charged memory traces during REM sleep, limbic areas, especially the amygdala, are activated (Revonsuo, 2003). Wag-ner, Gais, and Born (2001) demonstrated that recall of emotional charged (but not neutral) text was significantly enhancedfollowing REM enriched late night sleep. Similarly, Rauchs et al. (2004) reported improvement for episodic declarative mem-ories after REM enriched late night sleep. Nielsen and Stenstrom (2005) suggest that, during dreaming, memories may berelocated from the hippocampus to be ‘stored’ in the associative neocortex. In sum, this physiological evidence is, at least,suggestive of the dream as a hyper-associative mnemonic narrative that embeds memory ‘fragments’ to form chains of asso-ciation that can regenerate whole memories.

However, it may be objected that dreams are forgotten, so how can they have a mnemonic function? Dreams are not gen-erally recalled into waking consciousness- this does not prove that they are forgotten. It has been suggested that 95% of cog-nition is unconscious (Lakoff & Johnson, 1999; Thift, 2008). Joordens, Wilson, Spalek, and Paré (2010) state there is nowgeneral agreement that memories have both conscious and unconscious influences; moreover, they produce experimentaldata indicating that conscious and unconscious processes operate independently. So there would be nothing surprisingabout dreams functioning mnemonically at an unconscious level. The Penfield experiments lend intuitive support to thisidea; stimulation of the exposed cortex of patients elicited reports of dream-like memories. Indeed, if dreams embed person-ally meaningful associative cues that are not easily understood in waking consciousness it is clear that the cues must kept out ofthe waking mind. To return again to the Bagpuss example, if whenever I go to the ophthalmologist I consciously associatethis with Bagpuss without knowing the reason why I am making the association I will be confused. If psychosis is ‘dreaminghallucination partially projected into waking’ then in a psychotic state I may hallucinate Bagpuss when visiting the ophthal-mologist. Behrendt (2005) comments that, ‘. . .what we see in a hallucination or dream is usually expected unconsciously.’This would be the case if waking hallucinations, like dreams, are constituted from memory fragments associated in ways thatresonate at an unconscious level but are not readily understood in waking consciousness.

The ‘continuity hypothesis’ suggests that dreams portray concerns and experiences from waking life (Domhoff, 1996;Hartmann, 1998; Schredl, 2003). Revonsuo (2003) argues there is overwhelming evidence that dreams incorporate wakingconcerns. But such suggestions have to be supplemented with clarification of why -in dreams- our concerns and experiencesappear (from the perspective of waking consciousness) in such a fragmented and, sometimes, bizarre and dramatic way. Theidea of the dream as a mnemonic associative narrative that conflates memory fragments could explain this. Payne, Stickgold,Swanberg, and Kensinger (2008) have demonstrated that sleep preferentially enhances memory for the emotional (but notthe neutral) components of waking scenes. Only the emotional essence (or essential ‘fragment’) of personally significantwaking experiences may feature in dreams. Also dreaming experiences always differ from the ‘same’ waking experiencesbecause they always form part of a chain of association. For example, Bagpuss was not present at my recent visit to the oph-thalmologist nor was there an ophthalmologist around in my remote memory of seeing Bagpuss on TV. Bagpuss and oph-thalmology are not related in any logical, linear, cause and effect way. But they are related in an emotionally salient way.The ‘Bagpuss’ dream conflates the two memory fragments because it expresses what the visit to the ophthalmologist meansto me- glaucoma and fear.

Foster (2009, p. 30) states that ‘. . .information in long term memory is thought to be stored primarily in terms of themeaning of the information’, moreover, Solms and Turnbull (2002, pp. 173 and 174) suggest that long term memories arestored, organized and connected in very different ways to the ‘rational’ memory forms that are retrieved into waking con-sciousness. This paper suggests that dreams are both the media for associating recent and remote memories and the waythat long term memories are ‘stored’ and organized – as chains of emotionally associated memory ‘fragments’. Crick andMitchison (1983) point out that the richly interconnected assemblies of the neocortex could serve to store associations;however, they postulate that such an associative net may become overloaded and produce bizarre associations. Theirhypothesis is that dreams rid the net of such incongruities. But AAOM shows that it is precisely those bizarre associationsthat make memories more memorable. The more absurd and striking the cue – the more resilient the memory to whichthe cue is associated. Bizarre associations have high mnemonic functionality. Hebbian principles (Hebb, 1949) dictate, first,that a memory ‘fragment’ can elicit a more complete memory and, second, a memory with a particular element can invokeother memories with that element. This is possible through chains of association. Korsakoff proposed that the accessibility ofa memory is dependent not only on the strength of the trace but also on the number of associations made (Banks, 1996).Habitual actions (for example, visits to an ophthalmologist) are particularly resilient because script memories are available(Mandler, 1984). In the Bagpuss dream, there is little detail of the routine events that constitute eye-testing. However, thisfragment could trigger the appropriate associated script memory (drops, dilation, examination and discussion). The presenceof Bagpuss ‘tells me’ what kind of variant occurred on the routine eye examination – a test for glaucoma.

Such suggestions are congruent with the reconstruction of memories on retrieval (Bartlett, 1932; Neisser, 1962; Schach-tel, 1947). Declarative memories are also dynamic (Paller & Voss, 2004) and labile, not only before encoding, but also upon


retrieval (Maquet, 2001; Nader, 2003). Lability is necessary, first, for the meaningful ‘updating’ of memories as new relatedexperiences are assimilated and, second, as remote memories influence the meaning and significance attributed to recentexperiences. Stickgold (2009) propose that memories evolve over time but ‘evolution’ may be a slightly misleading meta-phor. For example, as a child my memory of visits to the ophthalmologist were characterized by fear, followed by a long per-iod of time when they evoked only mild anxiety, now fear has returned as the possibility of glaucoma looms. Whilst it maybe said that my memory ‘evolved’, this evolution was not driven by random events but personal emotional salience.

If dreaming is particularly functional for ‘emotional concern memory’ and, ultimately, personal identity then the partialintrusion of aspects of the dreaming state into waking along with the partial intrusion of aspects of the waking state intodreaming will start to erode memory, concerns and over time, personal identity will diminish. For example, as argued earlier,if dreaming incorporates memory fragments, when dreaming is partially projected into waking, some personal memory frag-ments (which function as bizarre memory cues in dreams) will start to appear during waking experience. At first, these mayonly present as puzzling intrusive thought associations but, if psychosis emerges, they may develop into visual or auditoryhallucinations (e.g. a Bagpuss hallucination during a visit to the ophthalmologist). Badcock, Waters, Maybery, and Michie(2005) found that, in schizophrenia, the presence of auditory hallucinations was associated with an inability to suppressmemories that were not relevant to the on-going situation. To an external observer, Bagpuss seems totally irrelevant to avisit to the ophthalmologist, but, to me, on an unconscious level (that can become conscious), Bagpuss is emotionally salient(in the ways described above).

Hallucinations are very emotionally salient, so memories will be formed of them. Consequently, during dreaming in psy-chotic patients, associative memory cues will be forged to what are already associative memory cues (e.g. Bagpuss). Thus afalse memory (Bagpuss actually was heard or seen at the ophthalmologist) will be formed and strengthened. This processwould allow a hallucination to become delusion (a fixed false belief). If the association–hallucination–delusion process oc-curred in connection with a fairly commonplace event in the life of the patient then a particular delusion may come to dom-inate consciousness.

Moreover, as argued earlier, the projection of aspects of dreaming into waking will inter alia impair working memory, im-pede abilities to filter out irrelevant non-emotionally salient data and, hence, diminish focus on new truly emotionally sali-ent material. So memories will be formed of non-salient data and, over time, memories of emotionally salient concerns willdiminish. Although it is possible to form associative emotionally charged memory cues during waking, this paper has arguedthat dreaming is functionally adapted to this task and, therefore, performs at a much superior level. Hence, the projection ofaspects of waking consciousness into dreaming will curtail the ability to form chains of imaginative, personally associativememory cues. In consequence, over time memories for concerns (even delusional ones) will fade and personal identity willbe eroded. The loss of memory for concerns and the erosion of personal identity may be expressed in the clinically manifestnegative symptoms of de-motivation, apathy and social withdrawal.

Solms and Turnbull (2002, p. 312) observed that patients who do not dream become ‘aspontaneous, inert and apathetic’.This is predictable if dreams forge the associative cues that are necessary to remember concerns/projects and, thus, maintainthe coherent identity that enables (in waking) the imagining and planning of a future. Patients with schizophrenia woulddream but, over time, the partial projection of aspects of waking physiology and cognitive into dreaming would result indreams losing mnemonic functionality. People with pronounced negative schizophrenic symptomology would, therefore,come to resemble those who do not dream.

9. Is this congruent with findings on memory impairments in schizophrenia?

In sum, the above discussion presents indicative evidence that phenomena are selected for memory formation duringwaking consciousness but are strengthened, organized and re-organized during dreaming consciousness, through beingassociated to personal emotionally salient cues. The de-differentiation of waking and dreaming consciousness would, there-fore, have a negative impact on memory selection, formation, strengthening/enhancement (‘consolidation’), organizationand reorganization.

There is a history of experimental research into memory impairment in schizophrenia that is consistent with this thesis,in the sense that it shows generalized dysfunction across a wide range of memory tasks (see, for example, Aleman, Hijman,de Haan, & Kahn, 1999; Calev, 1984; Clare, McKenna, Mortimer, & Baddeley, 1993; Gold, Randolph, Carpenter, Goldberg, &Weinberger, 1992; Goldberg, Weinberger, Pliskin, Berman, & Podd, 1989; Manoach & Stickgold, 2009; McKay et al., 1996;Stickgold, 2005; Tamlyn et al., 1992). Experimental testing during schizophrenia for loss of emotional concern memoriesdue to disrupted dream-dependent consolidation processes is clearly fraught with difficulty. There has been interest, how-ever, in the specific relationships between emotionally charged memories, personal identity and schizophrenia.

To be functional, memory has to be selective. Concern memories are formed of emotionally salient events/people/places.Dopamine mediates the emotional salience of both external events and internal representations (Kapur, 2003). Linked todopamine dysfunction, during waking, schizophrenia is characterized by aberrant salience; false significance is attributedto irrelevant phenomena, whilst, at the same time, there is adaptive failure to discern truly emotionally salient events (Kapur,Mizrahi, & Li, 2005; Roiser et al., 2009). Such dysfunction may lead to memories being fashioned from insignificant stimuli,whilst memories of salient events fail to be formed. Moreover, in support of the iterative scenario outlined above, Roiser et al.(2009) found that aberrant salience correlated with both delusions and negative symptoms in schizophrenia. As mentioned


earlier, Badcock et al. (2005) report that auditory hallucinations in schizophrenia are related to the intrusion of activatedmemory representations. Thus aberrant salient in schizophrenia is explicable through the de-differentiation idea.

Conscious recollection of episodic memories is significantly impaired in schizophrenia and it is argued that this dysfunc-tion results from encoding failures (Danion, Huron, Vidailhet, & Berna, 2007; Gold et al., 2000; Neumann, Blairy, Lecompte, &Philippot 2007). Achim and Lepage (2005) argue that people with schizophrenia may use less associative encoding strategies.This would be congruent with the disruption of personal associative memory processes, if waking is partially projected intodreaming, consequent upon de-differentiation. Conscious recollection involves mentally re-living events, such reflection isvital for rethinking the past and projecting into the future. If the thread that connects the present self with the past is broken,a meaningful life narrative cannot be sustained. Without a meaningful life narrative, the future cannot be envisaged and en-acted. In schizophrenia the loss of conscious recollection of past experiences leads to an erosion of the sense of the presentself being continuous with the past self (Danion et al., 2007). People with schizophrenia have difficulty in re-living the pastand find it even harder to imagine the future (D’Argembeau, Raffard & Van der Linden, 2008). They also have difficulty indiscerning the meaning in what should be personal self-defining memories (Raffard et al., 2009). To argue that personal iden-tity is eroded (Blairy et al., 2008; Riutort, Cuervo, Danion, Peretti, & Salamé, 2003) hardly captures the devastation, unlikehaving an illness, schizophrenia is something a person can become (Estroff, 1989). Although ‘person with schizophrenia’ isnow used rather than ‘schizophrenic’ as this language is thought to be less alienating and stigmatizing, there may be animportant sense in which this understanding does not adequately reflect the way in which the condition transforms the self(Sass, 2007).

10. If waking and dreaming consciousness became de-differentiated, would schizophrenia result? Concludingcomments

If waking and dreaming consciousness became de-differentiated, would schizophrenia result? Based on the arguments ofthis paper, the answer is: ‘possibly’. Whether schizophrenia emerged would depend upon the degree of de-differentiationwhich, in turn, would be contingent upon the extent of membrane defects and abnormalities in phospholipid metabolism.The extent and nature of phospholipid aberration would drive the extent and nature of neurotransmitter imbalance and theconsequent phenomenological expression of psychiatric symptoms. Susceptibility to these symptoms would depend upongene-environment interplay (including diet and stress) which predict the impact of phospholipid aberrations on multipletransmitter systems.

If membrane defects and/or abnormalities in phospholipid metabolism were less serious and transmitter systems lessdisrupted, rather than schizophrenia, such conditions as anxiety syndrome, ADHD or borderline personality disorder mayresult. However, in the mode predicted by chaos theory, more severe phospholipid abnormalities may precipitate a processthat, ultimately, leads to unpredictable dynamic fluctuations between interacting neuromodulatory systems, as some reci-procity between these systems is lost. Two related and sometimes intertwined possibilities, emergent from this flux, wouldbe schizophrenia and bipolar disorder.

The progression of the schizophrenia may be partly dependent upon the efficacy of bipolar disorder as an autopoietic,self-organizing response and partly driven by the iterative processes of memory formation during waking and memory orga-nization/consolidation during dreaming. As suggested in 8.2, in a de-differentiated state, the first psychotic episode mayemerge when some personal memory fragments (which function as bizarre memory cues in dreams) become conscious,externalized, visual hallucinations- through being triggered by unconscious association during waking. Or, as suggested inSection 6.1, auditory hallucinations may start to appear during waking experience when inner ‘voices’ (or speech memories)are externalized. Whether visual or auditory, these hallucinations (as emotionally salient phenomena) will be selected formemory formation to the possible neglect of truly (in relation to concerns) emotionally salient material. Diminished func-tionality for memory organization/consolidation during dreaming would lead to further diminution in emotionally, mean-ingful memories. Iterations of this process may result in a more or less complete loss of the personally meaningfulassociations that create and sustain a sense of self (Hartley, 1749).

This de-differentiation thesis should be testable. For example, Voss et al. (2009) were successful in using EEG to demon-strate the physiological correlates of lucid dreaming. As yet, imaging techniques cannot capture the dynamics of neuromod-ulation, but this should change as the field matures. Nahas (2010) pinpoints multimodal imaging techniques and cross-validations with genetic studies as the way forward.

Although schizophrenia is a heterogeneous condition, one unifying focus is the fragmentation of the self (see, for example,Frith, 1992; Parnas et al., 2008; Sass & Parnas, 2003). The self that appears during dreaming is rather different from the onethat emerges in waking. The dreaming self does not do much thinking, and does not think about this loss of thinking. Thedreaming self is driven by primary emotions. The engagement between the dreaming self and others in dreams is less em-pathic. The dreaming self does not inhabit a private subjective realm within a public objective world. But, because of theselosses, the dreaming self may be able to make more imaginative hyper-associative connections between personally mean-ingful memories to consolidate and organize these in long term memory. The waking self does think and can cogitate uponthis thinking, is able to engage with others in meaningful joint endeavour, and does dwell in a private inner space whilstexperiencing the sense of an embodied self within an externalized world, but may be less able to achieve leaps of associativeimagination.


Some of the strangest phenomena in schizophrenia may be explained by the de-differentiation of these two disparateselves. For example, an incomplete or discontinuous externalization of the sense of a self who inhabits an external worldmay give rise to an uncertain sense of existing. A loss of the distinction between the private internal realm and the externalworld may lead to a failing sense of the privacy of the inner world and/or aspects of the self may begin to feel like externalobjects. Diminishing self awareness and self-monitoring may precipitate feelings of anonymity. Such experiences sometimescharacterize schizophrenia (Parnas et al., 2008; Sass & Parnas, 2003) As pointed out earlier, personally meaningful psycho-logical associations create a sense of self (Hartley, 1749). If the personally meaningful associations which may be forged inboth waking and dreaming dissolve due to de-differentiation then the sense of self may fragment. Bleuler (1911/1950) be-lieved that the core deficit in schizophrenia is the loss of experience of an integrated, continuous sense of self.

Of all the puzzling things about schizophrenia, one of the most perplexing is the question of why, given the majority ofpeople with schizophrenia do not marry or have children, the condition persists, another is that, although full-blown schizo-phrenia is so disabling, some people with an attenuated form are highly talented (for example, James Joyce and Isaac Newtonhad psychopathological symptoms, John Nash was diagnosed with schizophrenia, Bertrand Russell and Albert Einstein hadfirst degree relatives with the condition), both the persistence of schizophrenia and the relationship to creativity suggest thata predisposition to schizophrenia may convey some benefit (Andreasen, 2000). Redfield-Jamison (1994) has investigated therelationship between artistic creativity and bipolar disorder, many distinguished poets, artists, writers and musicians (e.g.Blake, Byron, Van Gogh, Woolf and Schumann), although not usually diagnosed as such at the time, seem to have experi-enced either bipolar disorder or schizophrenia or both. This link to creativity may be explained as a small degree of de-dif-ferentiation may be of advantage. If the linear-logic of normal waking consciousness became interspersed with the highlyassociative leaps of imagination that characterize dreaming then cognition, problem-solving and creativity would beaugmented.

Waking and dreaming consciousness are both utterly normal states of mind-brain. Why two conscious states? Why notjust one? If schizophrenia is the devastating possibility inherent in the dynamic neuromodulation that enables the achieve-ment of two differing states of consciousness, then this suggests that both these conscious states are necessary and, indeed,may be complementary. Moreover, this de-differentiation thesis can explain why in persons with talents and abilities, just a‘touch of schizophrenia’ may enhance their contribution to scientific endeavour and artistic creativity.

Acknowledgments

I wish to thank Allan Hobson and Silvio Scarone for their encouragement with regard to this work.

References

Achim, A. M., & LePage, M. (2005). Episodic memory-related activation in schizophrenia: Meta-analysis. British Journal of Psychiatry, 187, 500–509.Addlington, J., & Addington, D. (1997). Attentional vulnerability indicators in schizophrenia and bipolar disorder. Schizophrenia Research, 23, 197–204.Adler, L. E., Pachtman, E., Franks, R. D., Pecevich, M., Waldo, M. C., & Freeman, R. (1982). Neurophysiological evidence for a defect in neuronal mechanisms

involved in sensory gating in schizophrenia. Biological Psychiatry, 17, 639–654.Aleman, A., Hijman, R., de Haan, E. H. F., & Kahn, S. (1999). Memory impairment in schizophrenia: A meta-analysis. The American Journal of Psychiatry, 156,

1358–1366.Amminger, G., Schäfer, M. R., Papageorgiou, K., Becker, J., Mossaheb, N., Harrigan, S. M., et al (2007). Omega-3 fatty acids reduce the risk of early transition to

psychosis in ultra-high risk individuals: A double-blind randomized placebo-controlled treatment study. Schizophrenia Bulletin, 33(Suppl), 418–419.Amminger, G., Schäfer, M. R., Papageorgiou, K., Klier, C. M., Cotton, S. M., Harrigan, S. M., et al (2010). Long-chain x-3 fatty acids as indicated prevention of

psychotic disorders. Archives General Psychiatry, 67, 146–154.Andreasen, N. C. (1990). Positive and negative symptoms: Historical and conceptual aspects. Modern Problems Pharmacopsychiatry, 24, 1–42.Andreasen, N. C. (2000). Schizophrenia: The fundamental questions. Brain Research Reviews, 31, 106–112.Andreasen, N. C., & Flaum, M. (1991). Schizophrenia: The characteristic symptoms. Schizophrenia Bulletin, 7, 27–50.Appelbaum, P. S., Robbins, P. C., & Roth, L. H. (1999). Dimensional approach to delusions: Comparison across types and diagnosis. American Journal of

Psychiatry, 156, 1938–1943.Archer, M. S. (2000). Being human: The problem of agency. Cambridge: Cambridge University Press.Archer, M. S. (2003). Structure, agency and the internal conversation. Cambridge: Cambridge University Press.Ardito, R. B. (2003). Dreaming as an active construction of meaning. In E. F. Pace-Schott, M. Solms, M. Blagrove, & S. Harnad (Eds.), Sleep and dreaming:

Scientific advances and reconsiderations (pp. 118–119). New York: Cambridge University Press (first published in the December 2000 Special Issue ofBehavioural and Brain Sciences).

Baars, B. J. (1988). A cognitive theory of consciousness. New York: Cambridge University Press.Baars, B. J. (1997). In the theater of consciousness: The workspace of the mind. New York: Oxford.Baars, B. J. (2002). The conscious access hypothesis: Origins and recent evidence. Trends Cognitive Science, 6, 47–52.Baars, B. J. (2005). Global workspace theory of consciousness: Toward a cognitive neuroscience of human experience? Progress in Brain Research, 150, 45–53.Badcock, J., Waters, F., Maybery, M., & Michie, P. (2005). Auditory hallucinations: Failure to inhibit irrelevant memories. Cognitive Neuroscience, 10, 125–136.Bagpuss. <http://www.youtube.com/watch?v=Ga23iSxyXO4>.Bak, P. (1996). How nature works: The science of self-organized criticality. New York: Springer.Banks, W. P. (1996). Korsakoff and amnesia. Consciousness and Cognition, 5, 22–26.Barr, A. M., Lehmann-Masten, V., Paulus, M., Gainetdinov, R. R., Caron, M. G., & Geyer, M. A. (2004). The selective serotonin-2A receptor antagonist M100907

reverses behavioral deficits in dopamine transporter knockout mice. Neuropsychopharmacology, 29, 221–228.Bartlett, F. C. (1932). Remembering: A study in experimental and social psychology. Cambridge: Cambridge University Press.Behrendt, R. P. (2003). Hallucinations: Synchronisation of thalamocortical gamma oscillations underconstrained by sensory input. Consciousness and

Cognition, 12, 413–451.Behrendt, R. P. (2005). Open peer commentary. Attentional deficit versus impaired reality testing: What is the role of executive dysfunction in complex

visual disorders? Behavioral and Brain Sciences, 28, 758–759.

http://www.youtube.com/watch?v=Ga23iSxyXO4


Behrendt, R. P. (2006). Dysregulation of thalamic sensory transmission in schizophrenia: Neurochemical vulnerability to hallucinations. Journal ofPsychopharmacology, 20, 356–372.

Behrendt, R. P., & Young, C. (2004). Hallucinations in schizophrenia, sensory impairment, and brain disease: A unifying model. Behavioral and Brain Sciences,27, 771–787.

Benson, S. L. (2006). Sleep in schizophrenia: Impairments, correlates and treatment. Psychiatric Clinics of North America, 29, 1033–1045.Berger, G. E., Proffitt, T.-M., McConchie, M., Yeun, H., Wood, S. J., Amminger, G. P., et al (2007). Ethyl-eicosapentaenoic acid in first-episode psychosis: A

randomized placebo-controlled trial. Journal of Clinical Psychiatry, 68, 1867–1875.Berman, I., Merson, A., Viegner, B., et al (1998). Obsessions and compulsions as a distinct cluster of symptoms in schizophrenia: A neuropsychological study.

Journal Nervous Mental Disorders, 186, 150–156.Berman, K., & Meyer-Lindenberg, A. (2004). Functional brain imaging studies in schizophrenia. In D. S. Charney & E. J. Nestler (Eds.), Neurobiology of Mental

Illness (2nd ed., pp. 311–323). Oxford: Oxford University Press.Berman, K. F., Zec, R. F., & Weinberger, D. R. (1986). Physiologic dysfunction of dorsolateral prefrontal cortex in schizophrenia II: Role of neuroleptic

treatment, attention and mental effort. Archives General Psychiatry, 43, 126–135.Bilder, R. M., & Goldberg, E. (1987). Motor perseverations in schizophrenia. Archives Clinical Neuropsychology, 2, 195–214.Blairy, S., Neumann, A., Nutthais, F., Pierret, L., Collet, D., & Philippot, P. (2008). Improvements in autobiographical memory in schizophrenia patients after a

cognition intervention. Psychopathology, 41, 388–396.Bleich, A., Brown, S.-L., Kahn, R., & van Praag, H. M. (1988). The role of serotonin in schizophrenia. Schizophrenia Bulletin, 14, 297–315.Bleuler, E. (1911/1950). Dementia praecox or the group of schizophrenias. In J. Zinkin (Transl.). New York: International Universities Press.Bolzoni, L. (2001). The gallery of memory. In Parzen, J. (Transl.). Toronto: University of Toronto Press.Bower, G. H. (1970). Analysis of a mnemonic device. American Scientist, 58, 496–510.Braff, D. L. (1993). Information processing and attention dysfunctions in schizophrenia. Schizophrenia Bulletin, 19, 233–259.Braff, D. L., & Light, G. A. (2005). The use of neurophysiological endophenotypes to understand the genetic basis of schizophrenia. Dialogues in Clinical

Neuroscience, 7, 125–135.Bramon, E., Rabe-Hesketh, S., Sham, P., Murray, R. M., & Frangou, S. (2004). Meta-analysis of the P300 and P50 waveforms in schizophrenia. Schizophrenia

Research, 70, 315–329.Breggin, P. R. (1980). Brain-disabling therapies. In E. Valenstein (Ed.), The psychosurgery debate (pp. 467–492). New York: Freeman.Breggin, P. R. (2004). Suicidality, violence and mania caused by selective serotonin reuptake inhibitors (SSRIs): A review and analysis. International Journal of

Risk & Safety in Medicine, 16, 31–49.Brockington, I. F., & Leff, J. P. (1979). Schizo-affective disorder: Definitions and incidence. Psychological Medicine, 9, 91–99.Brown, R., & Kulik, J. (1977). Flashbulb memories. Cognition, 5, 73–99.Brüne, M. (2009). On shared psychological mechanisms of religiousness and delusional beliefs. In E. Voland & W. Schiefenhövel (Eds.), The biological

evolution of religious mind and behaviour (pp. 217–228). Berlin: Springer.Buchsbaum, M. S. (1990). Frontal lobes, basal ganglia, temporal lobes – Three sites for schizophrenia? Schizophrenia Bulletin, 16, 377–378.Buckingham, H. W., & Finger, S. (1997). David Hartley’s psychobiological associationism and the legacy of Aristotle. Journal of the History of Neurosciences, 6,

21–37.Buydens-Branchey, L., & Branchey, M. (2008). Long-chain n-3 polyunsaturated fatty acids decrease feelings of anger in substance abusers. Psychiatric

Research, 157, 95–104.Bymaster, F. P., McKinzie, D. L., & Felder, C. C. (2004). New evidence for the involvement of muscarinic cholinergic receptors in psychoses. In I. Silman, H.

Soreq, L. Anglister, D. Michaelson, & A. Fisher (Eds.), Cholinergic mechanisms: Function and dysfunction (pp. 331–343). London: Taylor and Francis.Calev, A. (1984). Recall and recognition in chronic nondemented schizophrenics: Use of matched tasks. Journal of Abnormal Psychology, 93, 172–177.Carlsson, A. (1988). The current status of the dopamine hypothesis of schizophrenia. Neuropsychopharmacology, 1, 179–186.Carlsson, A., Waters, N., Waters, S., & Carlsson, M. L. (2000). Network interactions in schizophrenia – Therapeutic implications. Brain Research Reviews, 31,

342–349.Carpenter, W. T. (2008). A few methodologic issues of note. Schizophrenia Bulletin, 34, 1003–1005 (618).Carroll, A., Fattah, S., Clyde, Z., Coffey, I., Owens, D. G. C., & Johnstone, E. C. (1999). Correlates of insight and insight change in schizophrenia. Schizophrenia

Research, 35, 247–253.Carruthers, M. (2008). The book of memory: A study of memory in medieval culture (2nd ed.). Cambridge: Cambridge University Press.Castle, D. J., & Murray, R. M. (1991). The neurodevelopmental basis of sex differences in schizophrenia. Psychological Medicine, 21, 565–575.Chalmers, D. (1996). The conscious mind: In search of a fundamental theory. Oxford: Oxford University Press.Chalon, S., Vancassel, S., Zimmer, L., Guilloteau, D., & Durand, G. (2001). Polyunsaturated fatty acids and cerebral function: Focus on monoaminergic

neurotransmission. Lipids, 36, 937–944.Chapman, J. (1966). The early symptoms of schizophrenia. British Journal of Psychiatry, 112, 225–251.Charlton, B. G. (2006). Why are doctors still prescribing neuroleptics? QJM: An international Journal of Medicine, 99, 417–420.Cicchetti, D., & Tucker, D. (1994). Development and self-regulatory structures of the mind. Development and Psychopathology, 6, 533–549.Clare, L., McKenna, P. J., Mortimer, A. M., & Baddeley, A. D. (1993). Memory in schizophrenia: What is impaired and what is preserved? Neuropsychologia, 31,

1225–1241.Collerton, D., Perry, E., & McKeith, I. (2005). Why people see things that are not there: A novel Perception and Attention Deficit model for recurrent complex

visual hallucinations. Behavioral and Brain Sciences, 28, 737–757.Costa e Silva, J. A. (2006). Sleep disorders in psychiatry. Metabolism, 55, S40–44.Craddock, N., O’Donovan, M. C., & Owen, M. J. (2005). The genetics of schizophrenia and bipolar disorder: Dissecting psychosis. Journal of Medical Genetics,

42, 193–204.Craddock, N., O’Donovan, M. C., & Owen, M. J. (2006). Genes for schizophrenia and bipolar disorder? Implications for psychiatric nosology. Schizophrenia

Bulletin, 32, 9–16.Craddock, N., & Owen, M. J. (2005). The beginning of the end for the Kraepelinian dichotomy? British Journal of Psychiatry, 186, 364–366.Crawford, M. A. (1992). Essential fatty acids and neurodevelopmental disorder. In N. G. Bazan (Ed.), Neurobiology of essential fatty acids (pp. 307–314). New

York: Plenum Press.Crick, F., & Mitchison, G. (1983). The function of dream sleep. Nature, 304, 111–114.Danion, J.-M., Huron, C., Vidailhet, P., & Berna, F. (2007). Functional mechanisms of episodic memory impairment in schizophrenia. The Canadian Journal of

Psychiatry, 52, 693–701.D’Argembeau, A., Raffard, S., & Van der Linden, M. (2008). Remembering the past and imagining the future in schizophrenia. Journal Abnormal Psychology,

117, 247–251.Davachi, L., & Wagner, A. D. (2002). Hippocampal contributions to episodic encoding: Insights from relational and item-based learning. Journal

Neurophysiology, 88, 982–990.Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine in schizophrenia: A review and reconceptualization. American Journal of Psychiatry, 148,

1474–1486.de Vogelaere, F., Santens, P., Achten, E., Boon, P., & Vingerhoets, G. (2010). Hippocampal activation during face-name associative memory encoding: Blocked

versus permuted design. Neuroradiology, 52, 25–36.de Wilde, O. M., Bour, L. J., Dingemans, P. M., Koelman, J. H., & Linszen, D. H. (2007). A meta-analysis of P50 studies in patients with schizophrenia and

relatives: Differences in methodology between research groups. Schizophrenia Research, 97, 137–151.


Dietrich, A. (2003). Functional neuroanatomy of altered states of consciousness: The transient hypofrontality hypothesis. Consciousness and Cognition, 12,231–256.

Domhoff, G. W. (1996). Finding meaning in dreams: A quantitative approach. Plenum Press.Dominguez, M. G., Can Saka, M., Lieb, R., Wittchen, H.-U., & van Os, J. (2010). Early expression of negative/disorganized symptoms predicting psychotic

experiences and subsequent clinical psychosis: A 10-year study. American Journal of Psychiatry, 167, 1075–1082.Donaldson, D. (1998). Psychiatric disorders with a biochemical basis. UK: Parthenon.du Bois, T. M., Deng, C., & Huang, X.-F. (2005). Membrane phospholipid composition, alterations in transmitter systems and schizophrenia. Progress in Neuro-

Psychopharmacology & Biological Psychiatry, 29, 878–888.Dutta, S., & Kanungo, R. N. (1975). Affect and memory: A reformulation. Oxford: Pergamon Press.Eaton, W. W., Hall, A. L., Macdonald, R., & McKibben, J. (2007). Case identification in psychiatric epidemiology: A review. International Review of Psychiatry,

19, 497–507.Emsley, R., Myburgh, C., Oosthuizen, M. B., & van Rensburg, S. J. (2002). Randomized, placebo-controlled study of ethyl-eicosapentaenoic acid as

supplemental treatment in schizophrenia. American Journal of Psychiatry, 159, 1596–1598.Erhart, S. M., Marder, S. R., & Carpenter, W. T. (2006). Treatment of schizophrenia, negative symptoms: Future prospects. Schizophrenia Bulletin, 32, 234–237.Estroff, S. E. (1989). Self, identity, and subjective experiences of schizophrenia: In search of the subject. Schizophrenia Bulletin, 15, 189–196.Feinburg, I. (1982). Schizophrenia: Caused by a fault in programmed synaptic elimination during adolescence? Journal of Psychiatric Research, 17, 319–334.Fenton, W. S., Hibbeln, J., & Knable, M. (1999). Essential fatty acids, lipid membrane abnormalities, and the diagnosis and treatment of schizophrenia.

Biological Psychiatry, 47, 8–21.Ferrarelli, F., Huber, R., Peterson, M. J., Massimini, M., Murphy, M., Riedner, B. A., et al (2007). Reduced sleep spindle activity in schizophrenia patients. The

American Journal of Psychiatry, 164, 483–492.Fingelkurts, A. A., & Fingelkurts, A. A. (2004). Making complexity simpler: Multivariability and metastability in the brain. International Journal of

Neuroscience, 114, 843–862.Fong, T. M., & McNamee, M. G. (1986). Correlation between acetylcholine receptor function and the structural properties of membranes. Biochemistry, 25,

830–840.Ford, J. M., Roach, B. J., Faustman, W. O., & Mathalon, D. H. (2007). Synch before you speak: Auditory hallucinations in schizophrenia. American Journal of

Psychiatry, 164, 458–466.Fosse, M. J., Fosse, R., Hobson, J. A., & Stickgold, R. J. (2003). Dreaming and episodic memory: A functional dissociation. Journal of Cognitive Neuroscience, 15,

1–9.Fosse, R., Stickgold, R., & Hobson, J. A. (2001). Brain-mind states: Reciprocal variation in thoughts and hallucinations. Psychological Science, 12, 30–36.Foster, J. K. (2009). Memory. UK: Oxford University Press.Frangou, S., Lewis, M., & McCrone, P. (2006). Efficacy of ethyl-eicosapentaenoic acid in bipolar depression: Randomised double-blind placebo-controlled

study. British Journal Psychiatry, 188, 46–50.Freeman, W. J. (1992). Chaos in psychiatry. Biological Psychiatry, 31, 1079–1081.Freeman, W. J. (2005). NDN, volume transmission, and self-organization in brain dynamics. Journal of Integrative Neuroscience, 4, 407–421.Freeman, M. P., Hibbeln, J. R., Wisner, K. L., Davis, J. M., Mischoulon, D., Peet, M., et al (2006). Omega-3 fatty acids: Evidence basis for treatment and future

research in psychiatry. Journal Clinical Psychiatry, 67, 1954–1967.Freud, S. (1999). The interpretation of dreams. In J. Crick (Transl.). Oxford: Oxford University Press.Friston, K. J. (2002). Dysfunctional connectivity in schizophrenia. World Psychiatry, 1(2), 66–71.Friston, K. J., & Frith, C. D. (1995). Schizophrenia: A disconnection syndrome? Clinical Neuroscience, 3, 89–97.Frith, C. D. (1992). The cognitive neuropsychology of schizophrenia. Sussex UK: Lawrence Erlbaum.Gallagher, S., & Zahavi, D. (2008). The phenomenological mind. London: Routledge.Garland, M. R., & Hallahan, B. (2006). Essential fatty acids and their role in conditions characterized by impulsivity. International Review of Psychiatry, 18,

99–105.Gazzaniga, M. S., Ivry, R. B., & Mangun, G. R. (2002). Cognitive neuroscience (2nd ed.). London: W.W. Norton & Company.Gesch, C. B., Hammond, S. M., Hampson, S. E., Eves, A., & Crowder, M. J. (2002). Influence of supplementary vitamins, minerals and essential fatty acids on the

antisocial behaviour of young adult prisoners. British Journal of Psychiatry, 181, 22–28.Geyer, M. A., Krebs-Thomson, K., Braff, D. L., & Swerdlow, N. R. (2001). Pharmacological studies of prepulse inhibition models of sensorimotor gating deficits

in schizophrenia: A decade in review. Psychopharmacology, 156, 117–154.Glantz, L. A., Gilmore, J. H., Hamer, R. M., Lieberman, J. A., & Jarskog, L. F. (2007). Synaptophysin and PSD-95 in the human prefrontal cortex from mid-

gestation into early adulthood. Neuroscience, 149, 582–591.Glen, A. I., Glen, E. M., Horrobin, D. F., Vaddadi, K. S., Spellman, M., Morse-Fisher, N., et al (1994). A red cell membrane abnormality in a sub-group of

schizophrenic patients: Evidence for two diseases. Schizophrenia Research, 12, 53–61.Gold, J. M., Randolph, C., Carpenter, C. J., Goldberg, T. E., & Weinberger, D. R. (1992). Forms of memory failure in schizophrenia. Journal of Abnormal

Psychology, 101, 487–494.Gold, J. M., Rehkemper, G., Binks, S. W., Carpenter, C. J., Fleming, K., Goldberg, T. E., et al (2000). Learning and forgetting in schizophrenia. Journal of Abnormal

Psychology, 109, 534–538.Goldberg, E., & Bilder, R. M. (1987). The frontal lobes and hierarchical organization of cognitive control. In E. Perecman (Ed.), The frontal lobes revisited

(pp. 159–187). New York: IRBN Press.Goldberg, T. E., Weinberger, D. R., Pliskin, N. H., Berman, K. F., & Podd, M. H. (1989). Recall memory deficit in schizophrenia: A possible manifestation of

prefrontal dysfunction. Schizophrenia Research, 2, 251–257.Goldman, H. H. (2000). Review of general psychiatry (5th ed.). USA: McGraw-Hill.Goodwin, B. (1994). How the leopard changed its spots: The evolution of complexity. Great Britain: Phoenix.Gottesmann, C. (2006). The dreaming sleep stage: A new neurobiological model of schizophrenia? Neuroscience, 140, 1105–1115.Guillin, O., Abi-Dargham, A., & Laruelle, M. (2007). Neurobiology of dopamine in schizophrenia. International Review of Neurobiology, 78, 1–39.Hall, C. S., & Van de Castle, R. L. (1966). The content analysis of dreams. New York: Appleton-Century-Crufts.Hallahan, B., & Garland, M. R. (2005). Essential fatty acids and mental health. British Journal of Psychiatry, 186, 275–277.Hardy-Baylé, M. C., Sarfati, Y., & Passerieux, C. (2003). The cognitive basis of disorganization symptomatology in schizophrenia and its clinical correlates:

Toward a pathogenetic approach to disorganization. Schizophrenia Bulletin, 29, 459–471.Hartley, D. (1749). Observations on Man, his Frame, his Duty, and his Expectations (Vol. 2). Bath and London: Samuel Richardson.Hartmann, E. (1998). Dreams and nightmares: The new theory on the origin and meaning of dreams. Berlin: Plenum Press.Hebb, D. O. (1949). The organization of behavior: A neuropsychological theory. New York: Wiley.Henke, K., Kroll, N. E. A., Behniea, H., Amaral, D. G., Miller, M. B., Rafal, R., et al (1999). Memory lost and regained following bilateral hippocampal damage.

Journal of Cognitive Neuroscience, 11, 682–697.Hibbeln, J. R. (1998). Fish consumption and major depression (letter). Lancet, 351, 1213.Hibbeln, J. R., & Salem, N. (2001). Omega-3 fatty acids and psychiatric disorders: Current status of the field. In D. Mostofsky, S. Yehuda, & N. Salem (Eds.),

Fatty acids: Physiological and behavioral functions (pp. 311–330). Totowa, NJ: Humana Press.Hirano, Y., Hirano, S., Maekawa, T., Obayashi, C., Oribe, N., Monji, A., et al (2010). Auditory gating deficit to human voices in schizophrenia: A MEG study.

Schizophrenia Research, 117, 61–67.


Hobson, J. A. (1990). Activation, input source and modulation: A neurocognitive model of the state of the brain-mind. In J. F. Kihlstrom, D. L. Schacter, & R. R.Bootzin (Eds.), Sleep and cognition. US: American Psychological Association.

Hobson, J. A. (1992). A new model of the brain-mind state: Activation level, input source and mode of processing (AIM). In J. S. Antrobus & M. Bertini (Eds.),The neuropsychology of sleep and dreaming. US: Erlbaum.

Hobson, J. A. (1997). Consciousness as a state-dependent phenomenon. In J. Cohen & J. Schooler (Eds.), Scientific approaches to the question of consciousness.US: Erlbaum.

Hobson, J. A. (1999). Consciousness. New York: W.H. Freeman and Company.Hobson, J. A. (2002). Dreaming: An introduction to the science of sleep. Oxford: Oxford University Press.Hobson, J. A. (2004). A model for madness. Nature, 430, 21.Hobson, J. A. (2009). REM sleep and dreaming: Towards a theory of protoconsciousness. Nature Reviews Neuroscience, 10, 803–813.Hobson, J. A., & McCarley, R. W. (1977). The brain as a dream state generator: An activation-synthesis hypothesis of the dream process. American Journal of

Psychiatry, 134, 1335–1348.Hobson, J. A., Pace-Schott, E. F., & Stickgold, R. (2003). Dreaming and the brain: Toward a neuroscience of conscious states. In E. F. Pace-Schott, M. Solms, M.

Blagrove, & S. Harnad (Eds.), Sleep and dreaming: Scientific advances and reconsiderations (pp. 1–50). New York: Cambridge University Press (firstpublished in the December 2000 Special Issue of Behavioural and Brain Sciences).

Hobson, J. A., & Stickgold, R. (1994). The conscious state paradigm: A neurocognitive approach to waking, dreaming and sleeping. In M. S. Gazzaniga (Ed.),The cognitive neurosciences. US: MIT Press.

Hoffman, R. E. (2003). Auditory hallucinations: What’s it like hearing voices?. <http://www.healthyplace.com/thought-disorders/articles/auditory-hallucinations-whats-it-like-hearing-voices/menu-id-64/> Accessed 08.11.10.

Hoffman, R. E., & McGlashan, T. H. (1997). Synaptic elimination , neurodevelopment, and the mechanism of hallucinated ‘‘voices’’ in schizophrenia. AmericanJournal of Psychiatry, 154, 1683–1689.

Horrobin, D. F. (1996). A possible relationship between dyslexia and schizophrenia, two disorders in which membrane phospholipid (PL) metabolism isdisturbed. Schizophrenia Research, 18(1), 156.

Horrobin, D. F. (1998). The membrane phospholipid hypothesis as a biochemical basis for the neurodevelopmental concept of schizophrenia. SchizophreniaResearch, 30, 193–208.

Horrobin, D. F., Glen, I. M., & Vaddadi, K. (1994). The membrane hypothesis of schizophrenia. Schizophrenia Research, 13, 195–207.Horrobin, D. F., Manku, M. S., Hillman, H., Iain, A., & Glen, M. (1991). Fatty acid levels in the brains of schizophrenics and normal controls. Biological

Psychiatry, 30, 795–805.Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III – The final common pathway. Schizophrenia Bulletin, 35, 549–562.Hughes, T. (1997). Introduction: Memorising poems. In T. Hughes (Ed.), By heart: 101 poems to remember. London: Faber and Faber.Hunt, R. R. (2008). Does salience facilitate longer-term retention? Memory, 17, 49–53.Huttenlocher, P. R. (1979). Synaptic density in human frontal cortex – Developmental changes and effects of aging. Brain Research, 163, 195–205.Janowsky, D. S., El-Yousef, M. K., Davis, J. M., Hubbard, B., & Sekerke, H. J. (1972b). Cholinergic reversal of manic symptoms. Lancet, 299, 1236–1237.Janowsky, D. S., El-Yousef, M. K., Davis, J. M., & Sekerke, H. J. (1972a). A cholinergic–adrenergic hypothesis of mania and depression. Lancet, 300, 632–635.Janowsky, D. S., Risch, S. G., & Gillin, J. C. (1983). Adrenergic–cholinergic balance and the treatment of affective disorders. Progress Neuropsychopharmacology

Biological Psychiatry, 7, 297–307.Jayakumar, P. N., Gangadhar, B. N., Subbakrishna, D. K., Janakiramaiah, N., Srinivas, J. S., & Keshavan, M. S. (2003). Membrane phospholipids abnormalities in

never-treated schizophrenia: A 31P magnetic resonance spectroscopy study. Biological Psychiatry, 54, 491–494.Jazayeri, S., Tehrani-Doost, M., Keshavarz, S. A., Hosseini, M., Djazayery, A., Amini, H., et al (2008). Comparison of the therapeutic effects of omega-3 fatty

acid eicosapentaenoic acid and fluoxetine, separately and in combination, in major depressive disorder. Australian and New Zealand Journal of Psychiatry,42, 192–198.

Jeon, Y. W., & Polich, J. (2003). Meta-analysis of P300 and schizophrenia: Patients, paradigms and practical implications. Psychophysiology, 40, 684–701.Joordens, S., Wilson, D. E., Spalek, T. M., & Paré, D. E. (2010). Turning the process-dissociation procedure inside-out: A new technique for understanding the

relation between conscious and unconscious influences. Consciousness and Cognition, 19, 270–280.Judd, L. L., McAdams, L., Budnick, B., & Braff, D. L. (1992). Sensory gating deficits in schizophrenia: New results. The American Journal of Psychiatry, 149,

488–493.Kahan, T. L., LaBerge, S., Levitan, L., & Zimbardo, P. (1997). Similarities and differences between dreaming and waking cognition: An exploratory study.

Consciousness and Cognition, 6, 132–147.Kahn, D., Combs, A., & Krippner, S. (2002). Dreaming as a function of chaos-like stochastic processes in the self-organizing brain. Nonlinear Dynamics,

Psychology, and Life Sciences, 6, 311–321.Kahn, D., & Hobson, J. A. (1993). Self-organization theory of dreaming. Dreaming, 3, 151–178.Kahn, D., & Hobson, J. A. (2005a). State-dependent thinking: A comparison of waking and dreaming thought. Consciousness and Cognition, 14, 429–438.Kahn, D., & Hobson, J. A. (2005b). Theory of mind in dreaming: Awareness of feelings and thoughts of others in our dreams. Dreaming, 15, 48–57.Kahn, D., Krippner, S., & Combs, A. (2000). Dreaming and the self-organized brain. Journal of Consciousness Studies, 7, 4–11.Kahn, D., Pace-Schott, E. F., & Hobson, J. A. (1997). Consciousness in waking and dreaming: The roles of neuronal oscillation and neuromodulation in

determining similarities and differences. Neuroscience, 78, 13–38.Kang, S. G., Lee, H. J., Jung, S. W., Cho, S. N., Han, C., Kim, Y. K., et al (2007). Characteristics and clinical correlates of restless legs syndrome in schizophrenia.

Progress Neuropsychopharmacological Biological Psychiatry, 31, 1078–1083.Kapur, S. (2003). Psychosis as a state of aberrant salience. A framework linking biology, phenomenology and pharmacology in schizophrenia. American

Journal of Psychiatry, 160, 13–23.Kapur, S., Mizrahi, R., & Li, M. (2005). From dopamine to salience to psychosis-linking biology, pharmacology and phenomenology of psychosis.

Schizophrenia Research, 79, 59–68.Kauffman, S. A. (1993). The origins of order: Self-organization and selection in evolution. Oxford: Oxford University Press.Kendall, R., & Jablensky, A. (2003). Distinguishing between the validity and utility of psychiatric diagnoses. American Journal of Psychiatry, 160, 4–12.Keshavan, M. S., Tandon, R., Boutros, N. N., & Nasrallah, H. A. (2008). Schizophrenia, ‘‘just the facts’’: What we know in 2008 part 3: Neurobiology.

Schizophrenia Research, 106, 89–107.Kinsella, J. E. (1990). Lipids, membrane receptors, and enzymes: Effects of dietary fatty acids. Journal of Parenteral and Enteral Nutrition, 14, 200S–217S.Koresko, R., Snyder, F., & Feinberg, I. (1963). ‘‘Dream time’’ in hallucinating and non-hallucinating schizophrenic patients. Nature, 199, 1118–1119.Krippner, S., & Combs, A. (2002). A systems approach to self-organization in the dreaming brain. Kybernetes, 31, 1452–1462.Krüger, S., Braeunig, P., Hoefer, J., Shugar, G., Boerner, I., & Langkraer, J. (2000). Prevalence of obsessive–compulsive disorder in schizophrenia and

significance of motor symptoms. The Journal of Neuropsychiatry and Clinical Neurosciences, 12, 16–24.Lake, C. R. (2008). Disorders of thought are severe mood disorders: The selective attention defect in mania challenges the Kraepelian Dichotomy – A review.

Schizophrenia Bulletin, 34, 109–117.Lake, C. R., & Hurwitz, N. (2006). Schizoaffective disorders are psychotic mood disorders: There are no schizoaffective disorders. Psychiatry Research, 143,

255–287.Lakoff, G., & Johnson, M. (1999). Philosophy in the flesh: The embodied mind and its challenges to western thought. US: Basic Books.Lawrie, S. M., Buechel, C., Whalley, H. C., Frith, C. D., Friston, K. J., & Johnstone, E. C. (2002). Reduced frontotemporal functional connectivity in schizophrenia

associated with auditory hallucinations. Biological Psychiatry, 51, 1008–1011.Lee, C., McGlashan, T. M., & Woods, S. W. (2005). Prevention of schizophrenia: Can it be achieved? CNS Drugs, 19, 193–206.

http://www.healthyplace.com/thought-disorders/articles/auditory-hallucinations-whats-it-like-hearing-voices/menu-id-64/

http://www.healthyplace.com/thought-disorders/articles/auditory-hallucinations-whats-it-like-hearing-voices/menu-id-64/


Legrand, D. (2007). Subjectivity and the body: Introducing basic forms of self-consciousness. Consciousness and Cognition, 16, 577–582.Lichtenstein, P., Yip, B. H., Björk, C., Pawitan, T., Sullivan, P. F., & Hultman, C. M. (2009). Common genetic determinants of schizophrenia and bipolar disorder

in Swedish families: A population-based study. The Lancet, 373, 234–239.Liddle, P. F. (1987). The symptoms of chronic schizophrenia: A re-examination of the positive–negative dichotomy. British Journal of Psychiatry, 151,

145–151.Liperoti, R., Landi, F., Fusco, O., Bernabel, R., & Onder, G. (2009). Omega-3 polyunsaturated fatty acids and depression: A review of the evidence. Current

Pharmaceutical Design, 15, 4165–4172.Llewellyn, S. (2009). Is ‘bipolar disorder’ the brain’s autopoietic response to schizophrenia? Medical Hypotheses, 73, 580–584.Llinás, R. R. (2002). I of the vortex: From neurons to self. US: MIT Press.Llinás, R. R., & Paré, D. (1991). Of dreaming and wakefulness. Neuroscience, 44, 521–535.Lynch, M. (2004). Long term potentiation and memory. Physiological Reviews, 84, 87–136.Macdonald, D. J., Boyle, R. M., Glen, A. C. A., Ross, B. M., Glen, A. I. M., Ward, P. E., et al (2004). The investigation of cytosolic phospholipase A2 using ELISA.

Prostaglandins Leukotrienes, Essential Fatty Acids, 70, 377–381.Mahmood, T., & Silverstone, T. (2001). Serotonin and bipolar disorder. Journal of Affective Disorders, 66, 1–11.Mahowald, M. W., Woods, S. R., & Schenck, C. H. (1998). Sleeping dreams, waking hallucianations and the central nervous system. Dreaming, 8, 89–102.Maier, W., Zobel, A., & Wagner, M. (2006). Schizophrenia and bipolar disorder: Differences and overlaps. Current Opinion Psychiatry, 19, 165–170.Malenka, R. C., & Bear, M. F. (2004). LTP and LTD: An embarrassment of riches. Neuron, 44, 5–21.Malnoe, A., Milon, H., & Reme, C. (1990). Effect of in vivo modulation of membrane docosahexaenoic acid levels on the dopamine-dependent adenylate

cyclase activity in the rat retina. Journal of Neurochemistry, 55, 1480–1485.Mandler, J. (1984). Stories, scripts and scenes: Aspects of schema theory. US: Lawrence Erlbaum Associates.Manoach, D. S., & Stickgold, R. (2009). Does abnormal sleep impair memory consolidation in schizophrenia? Frontiers in Human Neuroscience, 3, 1–8.Maquet, P. (2001). The role of sleep in learning and memory. Science, 294(5544), 1048–1054.Marra, C. A., & de Alaniz, M. J. (1989). Influence of testosterone administration on the biosynthesis of unsaturated fatty acids in male and female rats. Lipids,

24, 1014–1019.Mathé, J. M., Nomikos, G. G., Blakeman, K. H., & Svensson, T. H. (1999). Differential actions of dizocilpine (MK-801) on the mesolimbic and mesocortical

dopamine systems: Role of neuronal activity. Neuropharmacology, 38, 121–128.Maturana, H. R., & Varela, F. J. (1980). Autopoiesis and cognition: The realization of the living. Holland: D. Reidel Publishing.McKay, A. P., McKenna, P. J., Bentham, P., Mortimer, A. M., Holbery, A., & Hodges, J. R. (1996). Semantic memory is impaired in schizophrenia. Biological

Psychiatry, 39, 929–937.Merleau-Ponty, M. (2002). Phenomenology of perception (Transl. 1958). In: Routledge, Kegan Paul (Transl.). London: Routledge Classics.Metzinger, T. (2009). The ego tunnel. New York: Basic Books.Mohr, S., & Huguelet, P. (2004). The relationship between schizophrenia and religion and its implications for care. Swiss Medical Weekly, 134, 369–376.Monti, J. M., & Monti, D. (2005). Sleep disturbances in schizophrenia. International Review of Psychiatry, 17, 247–253.Morrens, M., Hulstijn, W., Lewi, P. J., De Hert, M., & Sabbe, B. G. C. (2006). Stereotypy in schizophrenia. Schizophrenia Research, 84, 397–404.Morrens, M., Hulstijn, W., & Sabbe, B. (2007). Psychomotor slowing in schizophrenia. Schizophrenia Bulletin, 33, 1038–1053.Murray, R. M., & Lewis, S. W. (1987). Is schizophrenia a neurodevelopmental disorder? British Medical Journal, 295, 681–682.Nader, K. (2003). Memory traces unbound. Trends in Neuroscience, 26, 65–72.Nahas, Z. (2010). The frontiers on brain imaging and neuromodulation: A new challenge. Frontiers in Psychiatry, 1, 1–2.Neisser, U. (1962). Cultural and cognitive discontinuity. In T. E. Gladwin & W. Sturtevant (Eds.), Anthropology and human behaviour (pp. 54–71). Washington,

DC: Anthropological Society of Washington.Neumann, A., Blairy, S., Lecompte, D., & Philippot, P. (2007). Specificity deficit in the recollection of emotional memories in schizophrenia. Consciousness and

Cognition, 16, 469–484.Nielsen, T. A., & Stenstrom, P. (2005). What are the memory sources of dreaming? Nature, 437, 1286–1289.Nielson, T. A. (2003). A review of mentation in REM and NREM sleep: ‘‘Covert’’ REM sleep as a possible reconciliation of two opposing models. In E. F. Pace-

Schott, M. Solms, M. Blagrove, & S. Harnad (Eds.), Sleep and dreaming: Scientific advances and reconsiderations (pp. 59–84). New York: CambridgeUniversity Press (first published in the December 2000 Special Issue of Behavioural and Brain Sciences).

Nir, Y., & Tononi, G. (2010). Dreaming and the brain: From phenomenology to neurophysiology. Trends in Cognitive Sciences, 14, 88–100.Nuss, P., Tessier, C., Ferreri, F., De Hert, M., Peuskens, J., Trugnan, G., et al (2009). Abnormal transbilayer distribution of phospholipids in red blood cell

membranes in schizophrenia. Psychiatry Research, 169, 91–96.Orsucci, F. F. (2006). The paradigm of complexity in clinical neurocognitive science. Neuroscientist, 12, 390–397.Owen, M. J., & Craddock, N. (2009). Diagnosis of functional psychoses: Time to face the future. The Lancet, 373, 190–191.Pallanti, S., Quercioli, L., & Hollander, E. (2004). Social anxiety in outpatients with schizophrenia: A relevant case of disability. American Journal of Psychiatry,

161, 53–58.Paller, K. A., & Voss, J. L. (2004). Memory reactivation and consolidation during sleep. Learning & Memory, 11, 664–670.Panksepp, J. (1985). Mood changes. In P. Vinken, G. Bruyn, & H. Klawans (Eds.). Handbook of clinical neurology (Vol. 45). UK: Elsevier.Paré, D., & Llinás, R. (1995). Conscious and pre-conscious processes as seen from the standpoint of sleep-waking cycle neurophysiology. Neuropsychologia,

33, 1155–1168.Parnas, J., Sass, L. A., & Zahavi, D. (2008). Recent developments in the philosophy of psychopathology. Current Opinion Psychiatry, 21, 578–584.Patterson, J. V., Hetrick, W. P., Boutros, N. N., Jin, Y., Sandman, C., Stern, H., et al (2008). P50 sensory gating ratios in schizophrenics and controls: A review

and data analysis. Psychiatric Research, 158, 226–247.Payne, J. D., Stickgold, R., Swanberg, K., & Kensinger, E. A. (2008). Sleep preferentially enhances memory for emotional components of scenes. Psychological

Science, 19, 781–788.Peet, M. (1994). Induction of mania with selective serotonin re-uptake inhibitors and tricyclic antidepressants. The British Journal of Psychiatry, 164,

549–550.Peet, M. (2002). Essential fatty acids: Theoretical aspects and treatment implications for schizophrenia and depression. Advances in Psychiatric Treatment, 8,

223–229.Peet, M. (2004). International variations in the outcome of schizophrenia and the prevalence of depression in relation to national dietary practices: An

ecological analysis. British Journal of Psychiatry, 184, 404–408.Peet, M., Brind, J., Ramchand, C. N., Shah, S., & Vankar, G. K. (2001). Two double-blind placebo controlled pilot studies of eicosopentaenoic acid in the

treatment of schizophrenia. Schizophrenia Research, 49, 243–251.Peet, M., & Horrobin, D. F. (2002). A dose-ranging exploratory study of the effects of ethyleicosapentaenoate in patients with persistent schizophrenic

symptoms. Journal of Psychiatric Research, 36, 7–18.Polanczyk, G., Moffitt, T. E., Arseneault, L., Cannon, M., Ambler, A., Keefe, R. S., et al (2010). Etiological and clinical features of childhood psychotic symptoms:

Results from a birth cohort. Archives General Psychiatry, 67, 328–338.Pope, H. G., & Lipinski, J. F. (1978). Diagnosis in schizophrenia and manic-depressive illness, a reassessment of the specificity of ‘‘schizophrenic’’ symptoms

in the light of current research. Archives General Psychiatry, 35, 811–828.Potter, D., Summerfelt, A., Gold, J., & Buchanan, R. W. (2006). Review of clinical correlates of P50 sensory gating abnormalities in patients with

schizophrenia. Schizophrenia Bulletin, 32, 692–700.


Puri, B. K., Richardson, A. J., Horrobin, D. F., Easton, T., Saeed, N., Oatridge, A., et al (2000). Eicosapentaenoic acid treatment in schizophrenia associated withsymptom remission, normalisation of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes. InternationalJournal of Clinical Practice, 54, 57–63.

Pycock, C. J., Kerwin, R. W., & Carter, C. J. (1980). Effect of lesion of cortical dopamine terminals on subcortical dopamine receptors in rats. Nature, 286,74–77.

Raffard, S., D’Argembeau, A., Lardi, C., Bayard, S., Boulenger, J.-P., & Van Der Linden, M. (2009). Exploring self-defining memories in schizophrenia. Memory,26–38.

Rauchs, G., Bertran, F., Guillery-Girard, B., Desgranges, B., Kerrouche, N., & Denise, P. (2004). Consolidation of strictly episodic memories mainly requiresrapid eye movement sleep. Sleep, 27, 395–401.

Rechtschaffen, A. (1978). The single-mindedness and isolation of dreams. Sleep, 1, 97–109.Rechtschaffen, A., Schulsinger, F., & Mednick, S. (1964). Schizophrenia and psychological indices of dreaming. Archives of General Psychiatry, 10, 89–93.Reddy, R. D., Keshavan, M. S., & Yao, J. K. (2004). Reduced red blood cell membrane essential polyunsaturated fatty acids in first episode schizophrenia at

neuroleptic-naive baseline. Schizophrenia Bulletin, 30, 901–911.Redfield-Jamison, K. (1994). Touched with fire: Manic depressive illness and the artistic temperament. USA: Free Press.Revonsuo, A. (2003). The contents of consciousness during sleep: Some theoretical problems. In E. F. Pace-Schott, M. Solms, M. Blagrove, & S. Harnad (Eds.),

Sleep and dreaming: Scientific advances and reconsiderations (pp. 207–208). New York: Cambridge University Press (first published in the December 2000Special Issue of Behavioural and Brain Sciences).

Richardson, J. T. E. (1980). Mental imagery and human memory. London: Macmillan.Richardson, A. J., Calvin, C. M., Clisby, C., Schoenheimer, D. R., Montgomery, P., Hall, J. A., et al (2000a). Fatty acid deficiency signs predict the severity of

reading and related difficulties in dyslexic children. Prostaglandins, Leukotrienes, Essential Fatty Acids, 63, 69–74.Richardson, A. J., Easton, T., & Puri, B. K. (2000). Red cell plasma fatty acid changes accompanying symptom remission in a patient with schizophrenia

treated with eicosapentaenoic acid. European Neuropsychopharmacology, 10, 189–193.Richardson, A. J., Easton, T., McDaid, A. M., Hall, J. A., Montgomery, P., Clisby, C. & Puri, B. K. (1999). Essential fatty acids in dyslexia: Theory, experimental

evidence and clinical trials. In Glen, A.I.M., Peet, M. & Horrobin, D.F. (Eds.), Phospholipid Spectrum Disorder in Psychiatry (pp. 225–241). Carnforth: MariusPress.

Richardson, A. J., McDaid, A. M., Calvin, C. M., Higgins, C. J., & Puri, B. K. (2000b). Reduced behavioural and learning problems in children with specificlearning difficulties after supplementation with highly unsaturated fatty acids. European Journal of Neuroscience, 12(Suppl. 11), 296.

Richardson, A. J., & Puri, B. K. (2000). The potential role of fatty acids in Attention Deficit/Hyperactivity Disorder (ADHD). Prostaglandins Leukotrienes,Essential Fatty Acids, 63, 79–87.

Richardson, A. J., & Puri, B. K. (2002). A randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fattyacids on ADHD-related symptoms in children with specific learning difficulties. Progress in Neuropsychopharmalogical & Biological Psychiatry, 26,233–239.

Richardson, A. J., & Ross, M. A. (2000). Fatty acid metabolism in neurodevelopmental disorder: A new perspective on associations between ADHD, dyslexia,dyspraxia and the autistic spectrum. Prostaglandins Leukotrienes, Essential Fatty Acids, 63, 1–9.

Riemann, D., Hohagen, F., Bahro, M., Lis, S., Stadm}uller, G., Gann, H., et al (1994). Cholinergic neurotransmission, REM sleep and depression. Journal ofPsychosomatic Research, 38, 15–25.

Rittenhouse, C. S., Broadley, D., Stickgold, R., & Hobson, J. A. (1993). Increased semantic priming upon awakenings from REM sleep. Sleep Research, 22, 97.Riutort, M., Cuervo, C., Danion, J.-M., Peretti, S., & Salamé, P. (2003). Reduced levels of specific autobiographical memories in schizophenia. Psychiatry

Research, 117, 35–45.Robinson, M. (2005). Housekeeping. UK: Faber and Faber.Roiser, J. P., Stephan, K. E., den Ouden, H. E. M., Barnes, T. R. E., Friston, K. J., & Joyce, E. M. (2009). Do patients with schizophrenia exhibit aberrant salience?

Psychological Medicine, 39, 199–209.Rubin, D. C., & Friendly, M. (1986). Predicting which words get recalled: Measures of free recall, availability, goodness, emotionality and pronunciability for

925 nouns. Memory & Cognition, 14, 79–94.Rusting, C. L. (1998). Personality, mood, and cognitive processing of emotional information: Three conceptual frameworks. Psychological Bulletin, 124,

165–196.Samuelian, J. C. (1996). Incidence of the deficit form in refractory schizophrenia. Encephale, 22, 19–23.Sarter, M., & Bruno, J. P. (1999). Abnormal regulation of corticopetal cholinergic neurons and impaired information processing in neuropsychiatric disorders.

Trends Neuroscience, 22, 67–74.Sarter, M., Nelson, C. L., & Bruno, J. P. (2005). Cortical cholinergic transmission and cortical processing in schizophrenia. Schizophrenia Bulletin, 31, 117–138.Sartorious, N., Shapiro, R., & Jablonsky, A. (1974). The international pilot study of schizophrenia. Schizophrenia Bulletin, 1, 21–35.Sass, L. A. (2007). ‘Schizophrenic person’ or ‘Person with schizophrenia’?: An essay on illness and the self. Theory and Psychology, 17, 395–420.Sass, L. A., & Parnas, J. (2003). Schizophrenia, consciousness, and the self. Schizophrenia Bulletin, 29, 427–444.Scarone, S., Manzone, M. L., Gambini, O., Kantzas, I., Limosani, I., D’Agostino, A., et al (2008). The dream as a model for psychosis: An experimental approach

using bizarreness as a cognitive marker. Schizophrenia Bulletin, 34, 515–522.Schachtel, E. (1947). On memory and childhood amnesia. Psychiatry, 10, 1–26.Schiffer, R.B., Rao, S.M. & Fogel, B.S. (2003). Neuropsychiatry (2nd ed.). UK: Lippincott, Williams & Wilkins.Schredl, M. (2003). Dream research: Integration of physiological and psychological models. In E. F. Pace-Schott, M. Solms, M. Blagrove, & S. Harnad (Eds.),

Sleep and dreaming: Scientific advances and reconsiderations (pp. 213–215). New York: Cambridge University Press (first published in the December 2000Special Issue of Behavioural and Brain Sciences).

Shah, S., Vankar, G. K., Telang, S. D., Ramchand, C. N., & Peet, M. (1998). Eicosapentaenoic acid (EPA) as an adjunct in the treatment of schizophrenia.Schizophrenia Research, 29, 158.

Simons, D. J., & Chabris, C. F. (1999). Gorillas in our midst: Sustained inattentional blindness for dynamic events. Perception, 28, 1059–1074.Singer, W. (1986). The brain as a self-organizing system. European Archives of Psychiatry and Neurological Sciences, 236, 4–9.Smesnya, S., Kindera, D., Willhardtb, I., Rosburga, T., Laschb, J., Bergerc, G., et al (2005). Increased calcium-independent phospholipase A2 activity in first but

not in multiepisode chronic schizophrenia. Biological Psychiatry, 57, 399–405.Solms, M. (1999). The interpretation of dreams and the neurosciences. <http://www.psychanalysis.org.uk/solms4.htm> Accessed 01.04.08.Solms, M. (2000). Dreaming and REM sleep are controlled by different brain mechanisms. Behavioral and Brain Sciences, 23, 843–850.Solms, M. (2002). Dreaming: cholinergic and dopaminergic hypotheses. In E. Perry, H. Ashton, & A. Young (Eds.), Neurochemistry of consciousness

(pp. 123–131). Philadelphia: Benjamins.Solms, M., & Turnbull, O. (2002). The brain and the inner world. New York: Other Press.Solovay, M. R., Shenton, M. E., & Holzman, P. S. (1987). Comparative studies of thought disorder: 1Mania and schizophrenia. Archives General Psychiatry, 44,

13–20.Sprenger, A., Lappe-Osthege, M., Talamo, S., Gais, S., Kimmig, H., & Helmchen, C. (2010). Eye movements during REM sleep and imagination of visual scenes.

Neuroreport, 21, 45–49.Stevens, L. J., Zentall, S. S., Abate, M. L., Kuczek, T., & Burgess, J. R. (1996). Omega-3 fatty acids in boys with behaviour, learning and health problems.

Physiology & Behaviour, 59, 915–920.Stevens, L. J., Zentall, S. S., Deck, J. L., Abate, M. L., Watkins, B. A., Lipp, S. R., et al (1995). Essential fatty acid metabolism in boys with attention-deficit

hyperactivity disorder. American Journal of Clinical Nutrition, 62, 761–768.

http://www.psychanalysis.org.uk/solms4.htm


Stickgold, R. (2002). EMDR: A putative neurobiological mechanism of action. Journal Clinical Psychology, 58, 61–75.Stickgold, R. (2003). Inclusive versus exclusive approaches to sleep and dream research. In E. F. Pace-Schott, M. Solms, M. Blagrove, & S. Harnad (Eds.), Sleep

and dreaming: Scientific advances and reconsiderations (pp. 223–225). NewYork: Cambridge University Press (first published in the December 2000Special Issue of Behavioural and Brain Sciences).

Stickgold, R. (2005). Sleep-dependent memory consolidation. Nature, 427, 1272–1278.Stickgold, R. (2009). How do I remember? Let me count the ways. Sleep Medicine Reviews, 13, 305–308.Stickgold, R., Scott, L., Rittenhouse, C., & Hobson, J. A. (1999). Sleep-induced changes in associative memory. Journal of Cognitive Neuroscience, 11, 182–193.Stoll, A. L., Renshaw, P. F., Yurgelun-Todd, D. A., & Cohen, B. M. (2000). Neuroimaging in bipolar disorder: What have we learnt? Biological Psychiatry, 48,

505–517.Stoll, A. L., Severus, W. E., Freeman, M. P., Rueter, S., Zboyan, H. A., Diamond, E., et al (1999). Omega-3 fatty acids in bipolar disorder. Archives General

Psychiatry, 56, 407–412.Stordy, B. J. (1995). Benefit of docosahexaenoic acid supplements to dark adaptation in dyslexia. Lancet, 346, 385.Stordy, B. J. (1997). Dyslexia, attention deficit hyperactivity disorder, dyspraxia – Do fatty acids help? Dyslexia Review, 9, 1–3.Tamlyn, D., McKenna, P. J., Mortimer, A. M., Lund, C. E., Hammond, S., & Baddeley, A. D. (1992). Memory impairment in schizophrenia: Its extent, affiliations

and neuropsychological character. Psychological Medicine, 22, 101–115.Tandon, R., Nasrallah, H. A., & Keshavan, M. S. (2008). Schizophrenia, ‘‘just the facts’’ 4. Clinical features and conceptualization. Schizophrenia Research, 110,

1–23.Tandon, R., Taylor, S. F., DeQuardo, J. R., Eiser, A., Jibson, M. D., & Goldman, M. (1999). The cholinergic system in schizophrenia reconsidered.

Neuropsychopharmacology, 21, 189–202.Taylor, K. E. T., Higgins, C. J., Calvin, C. M., Hall, J. A., Easton, T., McDaid, A. M., et al (2000). Dyslexia in adults is associated with clinical signs of fatty acid

deficiency. Prostaglandins, Leukotrienes & Essential Fatty Acids, 63, 75–78.Taylor, K. E. T., & Richardson, A. J. (2000). Visual function, fatty acids and dyslexia. Prostaglandins, Leukotrienes & Essential Fatty Acids, 63, 89–93.Thift, N. (2008). Non-representation theory. London: Routledge.Tononi, G. (2004). An information integration theory of consciousness. BMC Neuroscience, 5(42), 1–22 (open access).Tononi, G. (2008). Consciousness as integrated information: A provisional manifesto. Biological Bulletin, 215, 216–242.Tononi, G., & Edelman, G. M. (1998). Consciouness and complexity. Science, 282, 1846–1851.Turetsky, B. I., Calkins, M. E., Light, G. A., Olincy, A., Radant, A. D., & Swerdlow, N. R. (2007). Neurophysiological endophenotypes of schizophrenia.

Schizophrenia Bulletin, 33, 69–94.Uhlhaas, P. J., & Mishara, A. L. (2007). Perceptual anomalies in schizophrenia: Integrating phenomenology and cognitive neuroscience. Schizophrenia Bulletin,

33, 142–156.Umbricht, D., & Krljes, S. (2005). Mismatch negativity in schizophrenia: A meta-analysis. Schizophrenia Research, 76, 1–23.Van Kammen, D. P., & Gelernter, J. (1987). Biochemical instability in schizophrenia: The norepinephrine system. In H. Y. Meltzer (Ed.), Psychopharmacology:

The third generation of progress. New York: Raven Press.van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P., & Krabbendam, L. (2009). A systematic review and meta-analysis of the psychosis continuum:

Evidence for a psychosis proneness–persistence–impairment model of psychotic disorder. Psychological Medicine, 39, 179–195.Varela, F. G., Maturana, H. R., & Uribe, R. (1974). Autopoiesis: The organization of living systems. Its characterization and a model. Biosystems, 5, 187–196.Venables, P. H. (1964). Input dysfunction in schizophrenia. In B. Maher (Ed.), Progress in experimental personality research (pp. 1–47). New York: NY Academic

Press.Voss, U., Holzmann, R., Tuin, I., & Hobson, J. A. (2009). Lucid dreaming: A state of consciousness with features of both waking and non-lucid dreaming. Sleep,

32, 1191–1200.Wagner, U., Gais, S., & Born, J. (2001). Emotional memory formation is enhanced across sleep intervals with high amounts of rapid eye movement sleep.

Learning and Memory, 8, 112–119.Walsh, D. (2009). The unitary nature of functional psychoses. The Lancet, 373, 809.Weinberger, D. R. (1986). The pathogenesis of schizophrenia: A neurodevelopmental theory. In H. A. Nasrallah & D. R. Weinberger (Eds.), The neurology of

schizophrenia (pp. 387–405). Amsterdam: Elsevier.Weinberger, D. R. (1987). Implications of normal brain development for the pathogenesis of schizophrenia. Archives of General Psychiatry, 44, 660–669.Weinberger, D. R., Aloia, M. S., Goldberg, T. E., & Berman, K. F. (1994). The frontal lobes and schizophrenia. Journal of Neuropsychiatry, 6, 419–427.Weinberger, D. R., Berman, K. F., & Zec, R. (1986). Physiologic dysfunction of dorsolateral prefrontal cortex in schizophrenia, I. Regional cerebral blood flow

evidence. Archives General Psychiatry, 43, 114–124.Wilding, J., & Valentine, E. (1997). Superior memory: Essays in cognitive psychology. UK: Psychology Press.Wykes, T., & Callard, F. (2010). Diagnosis, diagnosis, diagnosis: towards DSM-5. Journal of Mental Health, 19, 301–304.Yao, J. K., & Reddy, R. (2000). Fatty acids and psychiatric disorders. In C. K. Chow (Ed.), Fatty acids in foods and their health implications (pp. 995–1012). New

York, NY: Marcel Dekker.Yao, J. K., van Kammen, D. P., & Welker, J. A. (1994). Red blood cell membrane dynamics in schizophrenia: II. Fatty acid composition. Schizophrenia Research,

13, 217–226.Yates, F. (1966). The art of memory. London: Routledge and Kegan Paul.Young, G., & Conquer, J. (2005). Omega-3 fatty acids and neuropsychiatric disorders. Reproduction, Nutrition, Development, 45, 1–28.Yung, A. R., & McGorry, P. D. (1996). The prodromal phase of first episode psychosis. Schizophrenia Bulletin, 22, 353–370.Zanarini, M. C., & Frankenburg, F. R. (2003). Omega-3 fatty acid treatment of women with borderline personality disorder: A double-blind, placebo-

controlled pilot study. American Journal of Psychiatry, 160, 167–169.Zuibieta, J. K., Huguelet, P., O’Neil, R. L., & Giordani, B. J. (2001). Cognitive function in euthymic bipolar 1 disorder. Psychiatry Research, 102, 9–20.

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1. Are we addressing the ‘right stuff