The neurobiology of relapse in schizophrenia

Gary Remington, George Foussias, Ofer Agid, Gagan Fervaha, Hiroyoshi Takeuchi, Margaret Hahn

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Dopamine's proposed role in psychosis proved a starting point in our understanding of the neurobiology of relapse, fitting given the central role positive symptoms play. This link is reflected in early work examining neurotransmitter metabolite and drug (e.g. amphetamine, methylphenidate) challenge studies as a means of better understanding relapse and predictors. Since, lines of investigation have expanded (e.g. electrophysiological, immunological, hormonal, stress), an important step forward if relapse per se is the question. Arguably, perturbations in dopamine represent the final common pathway in psychosis but it is evident that, like schizophrenia, relapse is heterogeneous and multidimensional. In understanding the neurobiology of relapse, greater gains are likely to be made if these distinctions are acknowledged; for example, efforts to identify trait markers might better be served by distinguishing primary (i.e. idiopathic) and secondary (e.g. substance abuse, medication nonadherence) forms of relapse. Similarly, it has been suggested that relapse is 'neurotoxic', yet individuals do very well on clozapine after multiple relapses and the designation of treatment resistance. An alternative explanation holds that schizophrenia is characterized by different trajectories, at least to some extent biologically and/or structurally distinguishable from the outset, with differential patterns of response and relapse. Just as with schizophrenia, it seems naïve to conceptualize the neurobiology of relapse as a singular process. We propose that it is shaped by the form of illness and in place from the outset, modified by constitutional factors like resilience, as well as treatment, and confounded by secondary forms of relapse.

Original languageEnglish
Pages (from-to)381-390
Number of pages10
JournalSchizophrenia Research
Volume152
Issue number2-3
DOIs
Publication statusPublished - 2014 Feb
Externally publishedYes

Fingerprint

Neurobiology
Schizophrenia
Recurrence
Psychotic Disorders
Dopamine
Methylphenidate
Medication Adherence
Clozapine
Amphetamine
Substance-Related Disorders
Neurotransmitter Agents

Keywords

  • Neurobiology
  • Outcome
  • Psychosis
  • Relapse
  • Response
  • Schizophrenia

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Remington, G., Foussias, G., Agid, O., Fervaha, G., Takeuchi, H., & Hahn, M. (2014). The neurobiology of relapse in schizophrenia. Schizophrenia Research, 152(2-3), 381-390. https://doi.org/10.1016/j.schres.2013.10.009

The neurobiology of relapse in schizophrenia. / Remington, Gary; Foussias, George; Agid, Ofer; Fervaha, Gagan; Takeuchi, Hiroyoshi; Hahn, Margaret.

In: Schizophrenia Research, Vol. 152, No. 2-3, 02.2014, p. 381-390.

Research output: Contribution to journalArticle

Remington, G, Foussias, G, Agid, O, Fervaha, G, Takeuchi, H & Hahn, M 2014, 'The neurobiology of relapse in schizophrenia', Schizophrenia Research, vol. 152, no. 2-3, pp. 381-390. https://doi.org/10.1016/j.schres.2013.10.009
Remington G, Foussias G, Agid O, Fervaha G, Takeuchi H, Hahn M. The neurobiology of relapse in schizophrenia. Schizophrenia Research. 2014 Feb;152(2-3):381-390. https://doi.org/10.1016/j.schres.2013.10.009
Remington, Gary ; Foussias, George ; Agid, Ofer ; Fervaha, Gagan ; Takeuchi, Hiroyoshi ; Hahn, Margaret. / The neurobiology of relapse in schizophrenia. In: Schizophrenia Research. 2014 ; Vol. 152, No. 2-3. pp. 381-390.
@article{64be76da74874096b607b62acf7d7e9e,
title = "The neurobiology of relapse in schizophrenia",
abstract = "Dopamine's proposed role in psychosis proved a starting point in our understanding of the neurobiology of relapse, fitting given the central role positive symptoms play. This link is reflected in early work examining neurotransmitter metabolite and drug (e.g. amphetamine, methylphenidate) challenge studies as a means of better understanding relapse and predictors. Since, lines of investigation have expanded (e.g. electrophysiological, immunological, hormonal, stress), an important step forward if relapse per se is the question. Arguably, perturbations in dopamine represent the final common pathway in psychosis but it is evident that, like schizophrenia, relapse is heterogeneous and multidimensional. In understanding the neurobiology of relapse, greater gains are likely to be made if these distinctions are acknowledged; for example, efforts to identify trait markers might better be served by distinguishing primary (i.e. idiopathic) and secondary (e.g. substance abuse, medication nonadherence) forms of relapse. Similarly, it has been suggested that relapse is 'neurotoxic', yet individuals do very well on clozapine after multiple relapses and the designation of treatment resistance. An alternative explanation holds that schizophrenia is characterized by different trajectories, at least to some extent biologically and/or structurally distinguishable from the outset, with differential patterns of response and relapse. Just as with schizophrenia, it seems na{\"i}ve to conceptualize the neurobiology of relapse as a singular process. We propose that it is shaped by the form of illness and in place from the outset, modified by constitutional factors like resilience, as well as treatment, and confounded by secondary forms of relapse.",
keywords = "Neurobiology, Outcome, Psychosis, Relapse, Response, Schizophrenia",
author = "Gary Remington and George Foussias and Ofer Agid and Gagan Fervaha and Hiroyoshi Takeuchi and Margaret Hahn",
year = "2014",
month = "2",
doi = "10.1016/j.schres.2013.10.009",
language = "English",
volume = "152",
pages = "381--390",
journal = "Schizophrenia Research",
issn = "0920-9964",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - The neurobiology of relapse in schizophrenia

AU - Remington, Gary

AU - Foussias, George

AU - Agid, Ofer

AU - Fervaha, Gagan

AU - Takeuchi, Hiroyoshi

AU - Hahn, Margaret

PY - 2014/2

Y1 - 2014/2

N2 - Dopamine's proposed role in psychosis proved a starting point in our understanding of the neurobiology of relapse, fitting given the central role positive symptoms play. This link is reflected in early work examining neurotransmitter metabolite and drug (e.g. amphetamine, methylphenidate) challenge studies as a means of better understanding relapse and predictors. Since, lines of investigation have expanded (e.g. electrophysiological, immunological, hormonal, stress), an important step forward if relapse per se is the question. Arguably, perturbations in dopamine represent the final common pathway in psychosis but it is evident that, like schizophrenia, relapse is heterogeneous and multidimensional. In understanding the neurobiology of relapse, greater gains are likely to be made if these distinctions are acknowledged; for example, efforts to identify trait markers might better be served by distinguishing primary (i.e. idiopathic) and secondary (e.g. substance abuse, medication nonadherence) forms of relapse. Similarly, it has been suggested that relapse is 'neurotoxic', yet individuals do very well on clozapine after multiple relapses and the designation of treatment resistance. An alternative explanation holds that schizophrenia is characterized by different trajectories, at least to some extent biologically and/or structurally distinguishable from the outset, with differential patterns of response and relapse. Just as with schizophrenia, it seems naïve to conceptualize the neurobiology of relapse as a singular process. We propose that it is shaped by the form of illness and in place from the outset, modified by constitutional factors like resilience, as well as treatment, and confounded by secondary forms of relapse.

AB - Dopamine's proposed role in psychosis proved a starting point in our understanding of the neurobiology of relapse, fitting given the central role positive symptoms play. This link is reflected in early work examining neurotransmitter metabolite and drug (e.g. amphetamine, methylphenidate) challenge studies as a means of better understanding relapse and predictors. Since, lines of investigation have expanded (e.g. electrophysiological, immunological, hormonal, stress), an important step forward if relapse per se is the question. Arguably, perturbations in dopamine represent the final common pathway in psychosis but it is evident that, like schizophrenia, relapse is heterogeneous and multidimensional. In understanding the neurobiology of relapse, greater gains are likely to be made if these distinctions are acknowledged; for example, efforts to identify trait markers might better be served by distinguishing primary (i.e. idiopathic) and secondary (e.g. substance abuse, medication nonadherence) forms of relapse. Similarly, it has been suggested that relapse is 'neurotoxic', yet individuals do very well on clozapine after multiple relapses and the designation of treatment resistance. An alternative explanation holds that schizophrenia is characterized by different trajectories, at least to some extent biologically and/or structurally distinguishable from the outset, with differential patterns of response and relapse. Just as with schizophrenia, it seems naïve to conceptualize the neurobiology of relapse as a singular process. We propose that it is shaped by the form of illness and in place from the outset, modified by constitutional factors like resilience, as well as treatment, and confounded by secondary forms of relapse.

KW - Neurobiology

KW - Outcome

KW - Psychosis

KW - Relapse

KW - Response

KW - Schizophrenia

UR - http://www.scopus.com/inward/record.url?scp=84892852653&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84892852653&partnerID=8YFLogxK

U2 - 10.1016/j.schres.2013.10.009

DO - 10.1016/j.schres.2013.10.009

M3 - Article

C2 - 24206930

AN - SCOPUS:84892852653

VL - 152

SP - 381

EP - 390

JO - Schizophrenia Research

JF - Schizophrenia Research

SN - 0920-9964

IS - 2-3

ER -