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Authors' reply

Published online by Cambridge University Press:  02 January 2018

Naoto Adachi
Affiliation:
Adachi Mental Clinic, Kitano 7-5-12, Kiyota, Sapporo 004-0867, Japan. Email: adacchan@tky2.3web.ne.jp
Nozomi Akanuma
Affiliation:
Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, Kodaira, and Department of Neuropsychiatry, School of Medicine, Tokyo Medical and Dental University, Tokyo
Masaaki Kato
Affiliation:
Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, Kodaira
Masumi Ito
Affiliation:
Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, Kodaira
Tsunekatsu Hara
Affiliation:
Komagino Hospital, Hachioji
Yasunori Oana
Affiliation:
Department of Neuropsychiatry, School of Medicine, Tokyo Medical University, Tokyo
Masato Matsuura
Affiliation:
Department of Neuropsychiatry, Nihon University School of Medicine, Tokyo
Yoshiro Okubo
Affiliation:
Department of Neuropsychiatry, School of Medicine, Tokyo Medical and Dental University, Tokyo
Teiichi Onuma
Affiliation:
Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, Kodaira, Japan
Corresponding
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Abstract

Type
Columns
Copyright
Copyright © Royal College of Psychiatrists, 2010 

We thank Professors Craddock and Owen for the insightful comments on the possible molecular genetic basis of the relation between epilepsy and psychosis. In most clinical studies of psychosis in patients with epilepsy, individual psychotic vulnerabilities are rarely concerned compared with epilepsy-related factors. However, several large studies have recently demonstrated genetic vulnerabilities to psychosis even in patients with epilepsy. Reference Adachi, Matsuura, Hara, Oana, Okubo and Kato1,Reference Qin, Xu, Laursen, Vestergaard and Moriensen2 Our recent work Reference Adachi, Akanuma, Ito, Kato, Hara and Oana3 also demonstrated various factors (i.e. genetic, organic, and epilepsy-related) associated with the development of interictal psychosis in patients with epilepsy.

Psychoses in patients with any central nervous system (CNS) adversity, not only epilepsy but also other brain disorders, can be diagnosed as organic psychosis. The international criteria for mental disorders, either the ICD–10 or the DSM–IV, recognise the traditional dichotomy, i.e. functional and organic psychosis. However, since such CNS adversities are not invariably associated with the development of psychotic states, other additional conditions are required to generate psychotic symptoms. It is known that psychoses after brain injury occur more frequently in people with a family loading of psychoses. Reference Corcoran and Malaspina4 Thus, individual (possibly constitutional) vulnerability to psychosis can be considered as a contributing factor to the development of organic psychosis and its severity.

As for classification systems for mental disorders, many limitations of the Kraepelinian dichotomy between schizophrenia and affective disorders have been discussed. Reference Craddock and Owen5 Likewise, there appear to be limitations to the dichotomous view of organic and non-organic. The concept of organic psychosis has been useful to classify and treat patients, but it appears too simplistic to explain complex pathogenesis in such patients. It may be time to reconceptualise psychoses in patients with or without diagnosable brain disorders.

Footnotes

Edited by Kiriakos Xenitidis and Colin Campbell

References

1 Adachi, N, Matsuura, M, Hara, T, Oana, Y, Okubo, Y, Kato, M, et al. Psychoses and epilepsy: are interictal and postictal psychoses distinct clinical entities? Epilepsia 2002; 43: 1574–82.CrossRefGoogle ScholarPubMed
2 Qin, P, Xu, H, Laursen, TM, Vestergaard, M, Moriensen, PB. Risk for schizophrenia and schizophrenia-like psychosis among patients with epilepsy: population based cohort study. BMJ 2005; 331: 23–5.CrossRefGoogle ScholarPubMed
3 Adachi, N, Akanuma, N, Ito, M, Kato, M, Hara, T, Oana, Y, et al. Epileptic, organic and genetic vulnerabilities for timing of the development of interictal psychosis. Br J Psychiatry 2010; 196: 212–6.CrossRefGoogle ScholarPubMed
4 Corcoran, C, Malaspina, D. Traumatic brain injury and risk for schizophrenia. Int J Mental Health 2001; 30: 1732.CrossRefGoogle Scholar
5 Craddock, N, Owen, MJ. The Kraepelinian dichotomy – going, going … but still not gone. Br J Psychiatry 2010; 196: 92–5.CrossRefGoogle Scholar
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