Sue Llewellyn suggests that visual imaginative processes akin to those employed in the ancient art of memory (AAOM) underlie all effective mnemonic techniques. Developing this observation, she argues that an unconstrained form of consciousness is necessary for the elaboration of meaningful associations and that the hyperassociative form of visual imagery observed in dreams could reflect the brain's attempt to process emotionally relevant stimuli encountered in wakefulness. In her view, psychosis would emerge if hyperassociational junctions rose to consciousness, possibly through disruptions of spindle activity during non–rapid eye movement (NREM) sleep. Abnormal slow-wave sleep architecture and impaired memory consolidation processes have been linked to the development of psychosis, but the relationship between these phenomena remains largely unknown (Ferrarelli et al. Reference Ferrarelli, Huber, Peterson, Massimini, Murphy, Riedner, Watson, Bria and Tononi2007; Keshavan et al. Reference Keshavan, Montrose, Miewald and Jindal2011; Manoach et al. Reference Manoach, Thakkar, Stroynowski, Ely, McKinley, Wamsley, Djonlagic, Vangel, Goff and Stickgold2010; Seeck-Hirschner et al. Reference Seeck-Hirschner, Baier, Sever, Buschbacher, Aldenhoff and Göder2010).
The striking similarity between dreams and psychosis sparked the interest of many enquirers of the mind throughout history, at least since Aristotle suggested that “the faculty by which, in waking hours, we are subject to illusion when affected by disease, is identical with that which produces illusory effects in sleep” (Aristotle Reference Beare and Beare350 B.C./1941). In both conditions, subjective experience produced by endogenous neural activity is uncritically interpreted as originating in the external environment (Feinberg Reference Feinberg2011). Whereas in healthy subjects the transition from sleep to wakefulness rapidly restores adequate contact with the environment, psychotic patients seemingly experience a continuous loss of touch with reality. Delirious states of consciousness that are traditionally distinguished from so-called functional psychoses for the presence of a recognizable organic cause have been observed to most closely resemble dreams (Hobson Reference Hobson2004). However, several authors have suggested that the progression of knowledge on the neurobiological bases of dream production could shed light on all psychotic disorders, including schizophrenia (D'Agostino et al. Reference D'Agostino, Limosani and Scarone2012; Feinberg Reference Feinberg2011; Gottesmann Reference Gottesmann2006; Perogamvros & Schwartz Reference Perogamvros and Schwartz2012).
Psychosis and dreaming: A common generator?
Deficits in source monitoring and aberrant assignment of significance to irrelevant stimuli are often implicated in current attempts to explain the pathogenesis of psychosis (Corlett et al. Reference Corlett, Taylor, Wang, Fletcher and Krystal2010; Fletcher & Frith Reference Fletcher and Frith2009; Howes & Kapur Reference Howes and Kapur2009). According to these theories, hyperactivity of the mesocorticolimbic dopaminergic system determines abnormal interpretations of subjective experiences by failing to direct attention appropriately to both internal and external stimuli. Whereas hallucinations are hypothesized to derive directly from such dysfunction, delusions are thought to reflect the brain's cognitive effort ultimately to make sense of one's puzzling experience.
The same neural circuitry is strongly linked to the encoding and expression of emotionally salient learning and memory formation in healthy subjects (Laviolette Reference Laviolette2007). Activation of this system and associated limbic structures during REM sleep has been hypothesized to determine prioritization of contents that are reprocessed in dreams (Perogamvros & Schwartz Reference Perogamvros and Schwartz2012). Recent accounts of delusion formation also imply the role of glutamate-dependent synaptic plasticity, whereby incoming information is continuously interpreted on the basis of prior representations because of aberrant prediction error signaling (Corlett et al. Reference Corlett, Taylor, Wang, Fletcher and Krystal2010). According to this mechanism of hierarchical Bayesian learning, dreams analogously arise when “sensory firing is not constrained by top-down prior information and inferences are accepted without question owing to an attenuation of the prediction-error signal from lower to higher levels” (Fletcher & Frith Reference Fletcher and Frith2009, p. 52).
In this perspective, both dreams and psychosis depend on a loss of inferential reasoning. Whereas in sleep this loss could serve the function of sustaining elaborative encoding proposed by Llewellyn, in wakefulness it appears to determine a maladaptive circuit of continuous reinforcement of prior mnemonic traces. A genetically based susceptibility to hyperassociative mnemonic encoding during wakefulness could explain the classic positive dimensions of disorganized thought, delusions, and hallucinations that define psychosis. Unlike Llewellyn's view that schizophrenia itself could depend on a dedifferentiation of memory encoding processes in wakefulness and sleep, we suggest this mechanism could reflect a shared neurobiological substrate between dreams and psychotic symptoms found across several different clinical diagnoses.
Bizarreness as a loss of logical constraint
This new theory aims to explain the primarily visual nature of dreams and other well-known peculiarities of this form of consciousness, such as bizarreness. This phenomenon is thought to reflect the spontaneous activity of the brain as a closed system in the absence of environmental inputs and voluntary self-regulation mechanisms (Antrobus Reference Antrobus1991; Mamelak & Hobson Reference Mamelak and Hobson1989; Rechtschaffen Reference Rechtschaffen1978). Indeed, deactivation of the prefrontal cortices – which is also commonly observed during cognitive tasks in schizophrenic patients – is a distinguishing feature of REM sleep, when dream bizarreness is known to reach its peak. Bizarreness can be viewed as a loosening of the formal structure of cognition, suggesting the brain is physiologically prone to the loss of constraint applied by logical reasoning and environmental inputs during wakefulness. Bizarre cognition has recently been shown to clearly differentiate dream and fantasy narratives in healthy subjects but not in acutely psychotic subjects belonging to different diagnostic domains (Limosani et al. Reference Limosani, D'Agostino, Manzone and Scarone2011a). In psychiatry, the correlation of specific brain abnormalities to classic psychopathological symptoms remains elusive, and most research into the neurobiology of psychiatric disorders focuses on a syndromic level. Research into specific transnosographic abnormalities such as the loss of inferential reasoning that accompanies patients' uncritical acceptance of abnormal thoughts and perceptions could hold new promise. Future studies on the neurofunctional correlates of dream bizarreness may help to shed light on such loss, which appears to be crucial for what is commonly described as psychotic patients' loss of touch with reality.
Sue Llewellyn suggests that visual imaginative processes akin to those employed in the ancient art of memory (AAOM) underlie all effective mnemonic techniques. Developing this observation, she argues that an unconstrained form of consciousness is necessary for the elaboration of meaningful associations and that the hyperassociative form of visual imagery observed in dreams could reflect the brain's attempt to process emotionally relevant stimuli encountered in wakefulness. In her view, psychosis would emerge if hyperassociational junctions rose to consciousness, possibly through disruptions of spindle activity during non–rapid eye movement (NREM) sleep. Abnormal slow-wave sleep architecture and impaired memory consolidation processes have been linked to the development of psychosis, but the relationship between these phenomena remains largely unknown (Ferrarelli et al. Reference Ferrarelli, Huber, Peterson, Massimini, Murphy, Riedner, Watson, Bria and Tononi2007; Keshavan et al. Reference Keshavan, Montrose, Miewald and Jindal2011; Manoach et al. Reference Manoach, Thakkar, Stroynowski, Ely, McKinley, Wamsley, Djonlagic, Vangel, Goff and Stickgold2010; Seeck-Hirschner et al. Reference Seeck-Hirschner, Baier, Sever, Buschbacher, Aldenhoff and Göder2010).
The striking similarity between dreams and psychosis sparked the interest of many enquirers of the mind throughout history, at least since Aristotle suggested that “the faculty by which, in waking hours, we are subject to illusion when affected by disease, is identical with that which produces illusory effects in sleep” (Aristotle Reference Beare and Beare350 B.C./1941). In both conditions, subjective experience produced by endogenous neural activity is uncritically interpreted as originating in the external environment (Feinberg Reference Feinberg2011). Whereas in healthy subjects the transition from sleep to wakefulness rapidly restores adequate contact with the environment, psychotic patients seemingly experience a continuous loss of touch with reality. Delirious states of consciousness that are traditionally distinguished from so-called functional psychoses for the presence of a recognizable organic cause have been observed to most closely resemble dreams (Hobson Reference Hobson2004). However, several authors have suggested that the progression of knowledge on the neurobiological bases of dream production could shed light on all psychotic disorders, including schizophrenia (D'Agostino et al. Reference D'Agostino, Limosani and Scarone2012; Feinberg Reference Feinberg2011; Gottesmann Reference Gottesmann2006; Perogamvros & Schwartz Reference Perogamvros and Schwartz2012).
Psychosis and dreaming: A common generator?
Deficits in source monitoring and aberrant assignment of significance to irrelevant stimuli are often implicated in current attempts to explain the pathogenesis of psychosis (Corlett et al. Reference Corlett, Taylor, Wang, Fletcher and Krystal2010; Fletcher & Frith Reference Fletcher and Frith2009; Howes & Kapur Reference Howes and Kapur2009). According to these theories, hyperactivity of the mesocorticolimbic dopaminergic system determines abnormal interpretations of subjective experiences by failing to direct attention appropriately to both internal and external stimuli. Whereas hallucinations are hypothesized to derive directly from such dysfunction, delusions are thought to reflect the brain's cognitive effort ultimately to make sense of one's puzzling experience.
The same neural circuitry is strongly linked to the encoding and expression of emotionally salient learning and memory formation in healthy subjects (Laviolette Reference Laviolette2007). Activation of this system and associated limbic structures during REM sleep has been hypothesized to determine prioritization of contents that are reprocessed in dreams (Perogamvros & Schwartz Reference Perogamvros and Schwartz2012). Recent accounts of delusion formation also imply the role of glutamate-dependent synaptic plasticity, whereby incoming information is continuously interpreted on the basis of prior representations because of aberrant prediction error signaling (Corlett et al. Reference Corlett, Taylor, Wang, Fletcher and Krystal2010). According to this mechanism of hierarchical Bayesian learning, dreams analogously arise when “sensory firing is not constrained by top-down prior information and inferences are accepted without question owing to an attenuation of the prediction-error signal from lower to higher levels” (Fletcher & Frith Reference Fletcher and Frith2009, p. 52).
In this perspective, both dreams and psychosis depend on a loss of inferential reasoning. Whereas in sleep this loss could serve the function of sustaining elaborative encoding proposed by Llewellyn, in wakefulness it appears to determine a maladaptive circuit of continuous reinforcement of prior mnemonic traces. A genetically based susceptibility to hyperassociative mnemonic encoding during wakefulness could explain the classic positive dimensions of disorganized thought, delusions, and hallucinations that define psychosis. Unlike Llewellyn's view that schizophrenia itself could depend on a dedifferentiation of memory encoding processes in wakefulness and sleep, we suggest this mechanism could reflect a shared neurobiological substrate between dreams and psychotic symptoms found across several different clinical diagnoses.
Bizarreness as a loss of logical constraint
This new theory aims to explain the primarily visual nature of dreams and other well-known peculiarities of this form of consciousness, such as bizarreness. This phenomenon is thought to reflect the spontaneous activity of the brain as a closed system in the absence of environmental inputs and voluntary self-regulation mechanisms (Antrobus Reference Antrobus1991; Mamelak & Hobson Reference Mamelak and Hobson1989; Rechtschaffen Reference Rechtschaffen1978). Indeed, deactivation of the prefrontal cortices – which is also commonly observed during cognitive tasks in schizophrenic patients – is a distinguishing feature of REM sleep, when dream bizarreness is known to reach its peak. Bizarreness can be viewed as a loosening of the formal structure of cognition, suggesting the brain is physiologically prone to the loss of constraint applied by logical reasoning and environmental inputs during wakefulness. Bizarre cognition has recently been shown to clearly differentiate dream and fantasy narratives in healthy subjects but not in acutely psychotic subjects belonging to different diagnostic domains (Limosani et al. Reference Limosani, D'Agostino, Manzone and Scarone2011a). In psychiatry, the correlation of specific brain abnormalities to classic psychopathological symptoms remains elusive, and most research into the neurobiology of psychiatric disorders focuses on a syndromic level. Research into specific transnosographic abnormalities such as the loss of inferential reasoning that accompanies patients' uncritical acceptance of abnormal thoughts and perceptions could hold new promise. Future studies on the neurofunctional correlates of dream bizarreness may help to shed light on such loss, which appears to be crucial for what is commonly described as psychotic patients' loss of touch with reality.