Medicine: Psychiatry:

Suicide in Schizophrenia:

Considerations on Communication Pathology

 

by Bernhard J. Mitterauer, MD, Prof. em., University of Salzburg

Volitronics-Institute for Basic Research

Wals, Austria

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Keywords: schizophrenia, suicidal behavior, loss of self-boundaries, communication pathology, pseudo communication.

 

 

The lifetime suicide risk for schizophrenia patients is approximately 5% significantly higher than the general population suicide risk (Ventriglio et al., 2016); Here, I will focus on committed suicides. (Hor and Taylor, 2010). Our understanding of the subjective experience of a patient immediately before self-killing depends on the underlying psychobiological brain model of schizophrenia and the diagnostic methodology (Reeve and Addario-Berry, 2008).

 

I hypothesize that the brain functions of patients with schizophrenia are generalized because of imbalances in tripartite synapses (glial-neuronal synaptic units). Subjectively, the patient exists in an absolute timeless universe. Supposing that schizophrenia is a chronic disease, self-destructive behavior occurs, but a suicidal intent is not at work, since any change of existence may not be relevant in schizophrenia at all. Therefore, the act of self-killing is not communicated as suicidality, but suicidality may represent the interpretation of the observer.

 

Various brain models of schizophrenia as the neurodegenerative model (Pino et al., 2014) with white matter abnormalities (Kochunow and Hong, 2014; Lener et al., 2014) are proposed. My brain model is based on impaired neuro-glial interactions. In normal brain functions glia is modifying information transmission (Volterra, 2013) structuring neuronal networks in distinct time periods, so that the brain is capable of distinguishing subjects and objects in the environment. If information processing in tripartite synapses is imbalanced, a generalization of information processing is generated in the brain (Mitterauer 2005a; 2010; 2015). As experimentally evidenced, (Bauer et al., 2012) an unconstrained flux of neurotransmission in synapses (Mitterauer, 2003) may cause a generalization of information processing in the brain, since oligodendrocyte-axonic information transfer is also affected (Mitterauer and Kofler-Westergren, 2011). This severe impairment of the brain functions makes the patient unable to distinguish between the self and the others. We speak of the loss of self-boundaries in schizophrenia (Mitterauer 2003; 2005b). According to Meltzer (2003) the concept of schizophrenia does not characterize this psychobiological disorder. Is holophrenia (Mitterauer, 2005b) more appropriate?

 

Most importantly, The American Psychiatric Press Textbook (Hales et al.,1999) describes hallucinations and delusions as symptoms that reflect a loss of ego-boundaries and the patient is unable to distinguish between his or her own thoughts and perceptions and those that he obtains by observing the environment. According to DSM - V schizophrenia develops in stages with episodic courses of disease and full remission (Tandem et al., 2013). Contrarily, Zipursky and coworkers (2013) speak of a myth of progressive brain disease in schizophrenia. Currently, the etiopathophysiology of schizophrenia remains unresolved.

 

Phenomenologically, suicide attempts and committed suicides are observable realizing suicidal intentions (Stone and Aldiss, 1999; Stengel 1974). Fundamentally, a person attempting suicide tries to manipulate people in his or her environment in communication-intending behavior, whereas the person absolutely decided to commit suicide avoids other people in the sense of a communication-rejecting behavior (Mitterauer 1989; 2002). However, it is questionable if a suicidal behavior in schizophrenia is communicated by the patient.

 

Representative postmortem studies of patients with schizophrenia indicate that suicidology is faced with limitations, since reliable information of the psychobiological state and suicidal ideation or intent are mostly not available before the act of self- killing ( Pompili, 2016). For instance, suicide notes have not been found (Ishii et al., 2014). In a meta-analysis of 9 representative studies of single case analyses (N= 344) we diagnosed a paranoid psychosis in 68 cases (75%),(37 male, 31 female). At the time of suicide 51 patients were fully remitted and in 17 (25 %) suicides the psychobiological state could not be diagnosed because of a lack of information. The diagnosis of paranoid psychoses compromised all non-organic delusional-hallucinatory diseases including paranoid schizophrenia (Mitterauer,1985). Retrospectively this diagnostic result may not be reliable because of overdiagnoses of paranoid schizophrenia.

 

If we suppose the patients with schizophrenia exist in an absolute subjective and “timeless” universe, to finish their existence may not be an intent at all. However, delusional misinterpretations of the psychosocial situation may cause a self-destructive behavior. Even hallucinations that command self-killing may tend to be impulsive rather than planned (Ishii et al., 2014). From a communication point of view delusions and hallucinations represent a pseudo-communicative behavior (Mitterauer 1980,1983).

 

My proposed model allows interpretation that the act of self-killing in schizophrenia may not be based on suicidal ideation or intention and its communication does not really occur. In conclusion, I suggest that a better understanding of the communication pathology could contribute to programs in schizophrenia research and psycho-bio-social treatment and care.

 

References:

 

Bauer, M., Praschak-Rieder, N., Kasper, S., and Willeit, M. (2012). Is dopamine neurotransmission altered in prodromal schizophrenia? A review of evidence. Cuor. Pharm. Des. 18, 1568-79.

 

Hales, R.E., Yudofsky, S.C., and Talbott, J.A. (Eds.). (1999). The American Psychiatric Press Textbook of Psychiatry. American Psychiatric Press, Washington.

 

Hor, K., and Taylor, M. (2010). Suicide and schizophrenia: a systematic review of rates and risk factors. J. Psychopharmacol. 24, 81-90.

 

Ishii, T., Hashimoto, E., Ukai, W. Kakutani, R., et al. (2014). Characteristics of attempted suicide with schizophrenia compared with those with mood disorders: a case-controlled study in Northern Japan. PLOS One 9, e 96272. doi: 10.1371/ journal.pone. 0096272.

 

Kochunov, P., and Hong, L.E. (2014). Neurodevelopmental and neurogenerative models of schizophrenia: white matter at the center stage. Schizophr. Bull. doi: 10.1093/schbul/sbre 070.

 

Lener, M.S., Wong, E., Tang, C.Y, Byne, W., et al. (2015). White matter abnormalities in schizophrenia and schizotypical personality disorder. Schizophr. Bull. 41, 300-310.

 

Meltzer, H. (2003). Multiple neurotransmitters involved in antipsychotic drug action. In: Kapur, S., and Lecrubier, Y. (eds.), dopamine in the pathophysiology and treatment of schizophrenia. Martin Dunitz, London, pp.177-205.

 

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Mitterauer, B. (1989). Das suizidale Zuwendungs-/Abwendungssyndrom. Schweizer Archiv für Neurologie und Psychiatrie 140, 125-146.

 

Mitterauer, B. (2002). Comunicazione e anticomunicazione nel comportamento suicidario. In: De Riso, S., and Sarchiapone, M. (eds.). Il Suicidio. Aspetti biologici, psicologici e sociali. Masson, Milano, pp. 97-105.

 

Mitterauer, B. (2003). The loss of self-boundaries: towards a neuromolecular theory of schizophrenia. Bio Systems 72, 209-215.

 

Mitterauer, B. (2005a). Nonfunctional glial proteins in tripartite synapses: a pathophysiological model of schizophrenia. Neuroscientist 11, 192-198.

 

Mitterauer, B. (2005b). Verlust der Selbst-grenzen. Entwurf einer interdisziplinären Theorie der Schizophrenie. Springer, Wien, New York.

 

Mitterauer, B. (2010). Synaptic imbalances in endogenous psychoses. Bio Systems 100, 113-121.

 

Mitterauer, B.J. (2015). Balancing and imbalancing effects of astrocytic receptors in tripartite synapses. Common pathophysiological model of mental disorders and epilepsy. MEHY 84, 315-320.

 

Mitterauer, B.J., and Kofler-Westergren, B. (2011). Possible effects of synaptic imbalances on oligodendrocyte- axonic interactions in schizophrenia: a hypothetical model. front. psychiatry. doi: 10.3389/ fpsyt 2011 00015.

 

Pino, O., Guilera, G., Gomez-Benito, J., Najas-Garcia, A., et al. (2014). Neurodevelopment or neurodegeneration: review of theories of schizophrenia. Actas Esp. Psiguiatr. 42, 185-195.

 

Pompili, M., Mancinelli, I., Ruberto, A., Kotzalidis, G.D., and Tatarelli, R. (2005). Where schizophrenic patients commit suicide: a review of suicide among patients and former inpatients. In. J. Psychiatry. Med. 35, 171-190.

 

Reeve, P., and Addario-Berry, L. (2008). Mental health: maybe human troubles don’t fit into set categories. Nature 454, 824.

 

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Tandon, R., Gaebel, W., Barch, D.M., Bustillo, J. et al. (2013). Definition and description of schizophrenia in the DSM-5. Schizophren. Res. 150, 3-10.

 

Ventriglio, A., Gentile, A., Bonfitto, I, Stella, E., et al. (2016). Suicide in the early stage of schizophrenia. Front. Psychiatry http://dx.doi.org/10.3389/fpsyt. 2016. 00116.

 

Volterra, A. (2013). Astrocytes: modulation of synaptic function and network activity. In: Kettenmann, H., and Ransom, B.R. (eds). Neurologia, Oxford, Oxford University Press, pp.481-493.

 

Zipursky, R.B., Reilly, T.J., and Murray, M. (2013). The myth of schizophrenia as a progressive brain disease. Schizophr. Bull. 39, 1363-1372.

 



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