The Core of Classical Schizophrenia

Carpenter provides an incisive account of the evolution of the concept of schizophrenia in his commentary¹ on my article² about the core deficit of classical schizophrenia. He describes the way in which the Diagnostic and Statistical Manual of Mental Disorders, Third Edition consolidated the cardinal role of delusions and hallucinations at the cost of neglecting Kraepelin’s focus on persisting deficits. My article attempted to redress that neglect in order to provide a basis for investigating the mechanism(s) of persisting disability.

I discussed the evidence that impoverishment and disorganization of mental activity predict persisting disability and proposed that these “Bleulerian” symptoms might reasonably be described as the core of classical schizophrenia. I also proposed that this putative core reflected abnormal coordination of activity within a distributed brain network. Carpenter points out that this proposal should lead to formulation of a hypothesis regarding neural network pathology suitable for strong inference testing. He proposes that the test would entail testing difference between “classical” schizophrenia and “nonclassical” schizophrenia, characterized by reality distortion without the Bleulerian features. I strongly agree.

Carpenter implies that my proposal regarding the core does not accommodate the Extended Psychosis Phenotype and that I am conceptually opposed to schizophrenia as a reality distortion disorder. The concept of the Extended Psychosis Phenotype postulates a continuum of severity of reality distortion extending from the nonclinical population to cases with overt psychotic illness.³

It is necessary to clarify the relationship between the classical core and reality distortion before formulating a clear hypothesis regarding the neural network pathology associated with the core. While reality distortion can occur in the absence of core features, the frequent occurrence of reality distortion in classical schizophrenia indicates that the classical core is associated with predisposition to reality distortion. In the absence of marked core features, reality distortion is more likely to be transient and/or benign. In a 10-year longitudinal study, Dominguez and colleagues⁴ found that severity of Bleulerian symptoms predicts the likelihood of subsequent overt psychotic illness and the severity of disability. This indicates that classical core modulates the severity (and perhaps persistence) of reality distortion.

If the classical core modulates the severity of reality distortion, there must be a link between these phenomena. In psychological terms, aberrant salience is a plausible link. In neuronal terms, the insula, a key component of the Salience Network,⁵ is a candidate. Typically, lesions of the insula result in apathy and in many subtle disturbances of perception and action. The anterior insula is involved in distinguishing self-generated from externally generated information. In schizophrenia, diminished insula volume is associated with severity of hallucinations,⁶ in addition to psychomotor poverty and disorganization.

A strong test of the neural network pathology associated with the classical core should address the relationship between the postulated distributed network pathology associated with the core and the neural mechanism of reality distortion. The insula might play a potentially crucial role. Demonstrating that reality distortion can occur in the absence of the core network pathology, across a wide range of severity, would also be important.

Peter F. Liddle, BMBCh, PhD, MRCPsych
Division of Psychiatry and Applied Psychology, Institute of Mental Health, University of Nottingham, United Kingdom
peter.liddle@nottingham.ac.uk