„The lunatic is a wakeful dreamer.“
Immanuel Kant was not the first and not the last one hinting at a relationship between mental disorder and dreaming. Others, such as Schopenhauer were more specific in their statements, linking the dream state not to mental disorders in general, but to the condition of psychosis („A dream is a short-lasting psychosis, and a psychosis is a long-lasting dream.“). Several contemporary authors tried to shed light onto the nature of this repeatedly proposed connection between the dreaming state and psychosis, which I want to roll out for you in the following article. To clarify, the used literature mainly refers to the DSM-defined condition of schizophrenia and not to psychosis in general.
Schizophrenia is a severe mental disorder affecting a person’s way of thinking, feeling and acting. Schizophrenic patients seem to have lost the connection to reality. The syndrome consists of more than one subset of symptoms. Besides the subsets of negative symptoms (motivational deficits, social impairment, etc.) and cognitive impairment (hindered executive functioning, attention and memory), the subset probably most strongly associated with the stereotypic phenomenological image of schizophrenia is the set of positive symptoms, consisting of delusions and hallucinations.
Importantly, this text will focus will on the positive or psychotic symptoms.
Phenomenology: Does it feel similar?
Does dreaming feel like a short psychotic episode? Or may it even be one? McCreery, a british psychologist famous for his works on hallucinations, suggests several phenomenological features shared by dreaming and schizophrenia suggesting a strong connection between the concepts: Among others, especially the features of autism (which should not be confused here with the clinical condition of autism), which can be understood as a disconnection from the external environment, lack of insight and delusional beliefs, seem to be of special significance.
The proposed property of autism seems to be evident in dreaming. The state of sleeping is per definition a state, in which the subject is detached from external stimuli. The dreamer is mainly concerned with internal stimulation. According to the Activation-Input-Modulation (AIM) model, dreaming content is elicited by brainstem signals and not by external stimulation reaching sensory cortices. Considerably, there seems to be a phenomenological similarity between the dreaming and the psychotoc state, as schizophrenia-related delusions and hallucinations hint at a disconnection from environment or at least at a misinterpretation of environmental stimuli. The patient is not able to correct his beliefs via environmental feedback, he is also not able to determine the source of auditory hallucinations as being internally generated. Nevertheless, one should be cautious to assume that these two interpretations of autism in the two states are identical.
The autism-feature leads us directly to the delusional experience in psychotic states. Delusional beliefs, such as delusions of persecution or grandiosity bear according to some authors similarities to dream experiences. According to a study (Schredl et al., 2004) the scenario of persecution is a typical dream content. Apart from that, another study (Scarone et al., 2007) using bizarreness as a marker for comparing dreaming and psychotic experience, found similar bizarreness-scores in a psychometric instrument in sleeping control subjects and wakeful patients (Figure 1.).
Another model assumption -contrasting with the AIM-model-predictions- would be, that certain priors -i.e. a-priori internal models of the world – lead to a misinterpretation of external stimuli in schizophrenia and form the basis of the delusional beliefs and in turn function as priors for future perceptions. This assumption denies a complete disconnection of the psychotic subject from the environment (AIM-model), but hints at an erroneous interpretation of the perceived data. False interpretation of external stimuli does also occur in dreaming. McCreery refers to the tale of „Maury’s Guillotine dream“, where the main character Maury dreams of the guillotine at his neck and waking up recognizes it to be the headbord of his bed. While sleeping, Maury changed his position in a way that his neck was not lying on his pillow anymore, but on the headboard. This changed feeling immersed in his dream but with an altered meaning. As a consequence, autism could more be understood as a disconnection in terms of misinterpretation and not of general detachment from external stimuli.
Last but not least, lack of insight is a feature that schizophrenia shares with (non-lucid)-dreaming. When being non-lucid, the dreamer doesn’t know that (s)he is dreaming. Furthermore, the schizophrenic patient has no insight into the delusional character of his beliefs or in the fact that his halluciantions are internally generated, which is one main reason for his pathological condition.
Neurobiology: What about explanations?
A schizophrenia-related finding, which is often cited as an explanation for the lack of inhibitory processes, which might lead to hallucinatory experiences, is the absence of prepulse inhibition (e.g. Kisley et al., 2003). When a healthy subject is confronted with two sensory stimui, the evoked potential of the first stimulus exhibits a N100 property (a negative deflection of the signal 100 msec after the stimulus), whereas the second evoked potential does not (Figure 2). This process is not observed in schizophrenic patients (Figure 2) and is also absent during REM-sleep. REM(rapid-eye-movement)-sleep is a sleep stage that is associated with dreaming experiences in contrast to non-REM-sleep, which is characterized by little to no dreaming. This hints at abnormal stimulus processing in REM-sleep. While this might be functional or at least not harmful during sleep, in the schizophrenic condition this might be a reason for pathological experience.
Another line of research deals with alterations in global connectivity patterns in the brain – i.e. differences in how brain regions are interconnected – between schizophrenic patients and healthy subjects. Several studies indeed suggest altered cortical connectivity patterns in schizophrenics. Zhang and colleagues showed that the efficiency of information transfer and integration is decreased in brains of patients. Small-Worldness is a theoretical property of networks, which is mainly characterized by low path lengths between network locations (nodes) with a minimum number of connections. Apart from the average path length in the network, also nodal centrality of node N – the number of shortest paths between two nodes A and B that runs through N – is a useful marker for network efficiency. Both, average path length and nodal centrality were decreased in patients compared to healthy subjects. Also, during the REM-sleep stage altered connectivity patterns are found. However, research suggests that in REM-sleep there is neither a pattern of global disconnectivity, nor altered topological organization within temporal or frontal areas, but a functional segregation of the fronto-central from the posterior network, the connectome is split into two strongly connected components. This result differs clearly from the schizophrenia-related results mentioned above.
A third line of research is concerned with neurochemistry. One of the most influential neurochemical theories of schizophrenia is the dopamine hypothesis. Roughly, it states, that decreased prefrontal dopamine circulation is linked to negative symptomatology, while increased dopamine activity in the midbrain (mainly nucleus accumbens) is associated with positive symptoms. A tendency for both activity alterations is also observed during REM-sleep. This could explain some phenomenological similarites, such as bizarreness of experience and lack of insight. Another molecule related to schizophrenia is the excitatory neurotransmitter glutamate being negatively associated with psyhcotic symptomatology and vivid dreaming (e.g. Wong & Van Tol, 2003). A decreased glutamatergic release in nucleus accumbens has been reported both in REM-sleep and schizophrenia. Several authors (e.g. Skrzypinska & Szmigielska, 2013) suggest that midbrain-glutamate-release is connected to glutamate release in hippocampus, amygdala and the prefrontal cortex and that glutamatergic hypoactivity in the nucleus accumbens leads to impaired glutamate functioning in the prefrontal cortex.
Arriving at a conclusion
What can we distill from these findings about the quotes relating schizophrenia and dreaming? Has Kant anticipated recent findings? I would argue that this is not the case. Two important limitations come up immediately, that strongly question the proposed link. First, only part of the schizophrenic symptoms (lack of insight, delusions) are related to dreaming. Second, most research on this topic compares schizophrenia to REM-sleep, the fact that dreaming also occurs during non-REM-sleep is mostly neglected.
Furthermore neurobiological findings at best hint at same tendencies in parts of schizophrenia and REM-sleep. To conclude that dreaming might function as a model for schizophrenia, as some authors do, is at the current point of the research process an exaggerating extrapolation.
So, are we at least a little bit psychotic every night? Probably, that is just a nightmare.
2 thoughts on “Is psychosis just a dream? Links between schizophrenia and dreaming”
Insightful people who have made the observation that the “schizophrenia” syndrome and psychosis in general have strong similarities to somnolent states are not as far off the mark as this author is suggesting. Analyses like these is why research on so-called schizophrenia is in such a state of latency. What the author did in this article is to try to test the theoretical model (which is not the same as a biological model) by taking what science knows about the electro-neurochemistry of somnolence to set up a comparison to what is known about the electro-neurochemistry of so-called schizophrenia. This is a pitfall and a failure of analysis. First of all, science understands so little about the sleep state of consciousness and the same goes for so-called schizophrenia in particular and “psychosis” in general. I consider exacerbated states of “psychosis” (neurogenic dysmentation) to be a disordered state of consciousness which is not as reductive and specific as modeling after sleep. This kind of analysis is similar to what is seen in fuctional MRI. Researchers may be able to see parts of the brain light up, so to speak, but do they really understand what is happening in the brain – the answer is no. I also do not call “schizophrenia” a mental disorder, I call it a brain disorder and lean toward calling it an ideopathic encephalopathy…it is hubris and nonsense for medical science to reserve that term to what psychiatry strangely calls “general medical” conditions.
One first thing: I like your idea of schizophrenia as a disorder state of consciousness, which might not be properly modelled by the sleep state, I would aggree with you on that point. However, it was not the scope of this article to find an optimal frame for embedding the condition of schizophrenia, but just a theoretico-empirical collection and concatenation guided by the modelling assumption of the sleep state. So, I would consider your criticism too general, because it does not adress inherent fallacies in my argumentation. Also your further comments (schizophrenia is not a mental disorder; fMRI data cannot be interpreted as unambiguously as one might wish) relate to much more general discussions (concepts of disorder, interpretatbility of data) which i would locate in a ‘scientific theory’-environment, which is far beyond the scope of this article.