Neafsey organizes his discussion from an anatomical/functional point of view while Henderson & Dittrich's commentary deals mainly with the problem of the mutual relationships between functions and structures. We address each of their critcisms individually.
1.0. The debate between psychiatrists interested in observing mental processes in their patients and cognitive psychologists interested in studying the physiology of mental processes is still in its infancy. We are hence particularly grateful to Neafsey (1993) and Henderson & Dittrich (1993), first, for their helpful critical comments on our target article, and second, for giving us the opportunity to interact in a very useful way with the field of cognitive psychology, which has addressed the problems of psychopathology little until now. The two commentaries look at our results (Abbruzzese et al. 1993) in a different way:
2.1 Neafsey organizes his discussion from an anatomical/functional point of view, providing a good deal of information regarding the projections of Dorso-Lateral-Prefrontal-Cortex (DLPC) and Orbito-Frontal-Cortex (OFC), respectively, to the Superior Colliculus (SC) and the Autonomic and Endocrine Systems (AS and ES). Because the animal and human models of the dysfunctions in these two neuroanatomical pathways show an important sensorimotor component, Neafsey stresses a unitary view of the body-mind dualism and minimizes functional interpretation of mental abnormal behavior.
2.2. This point of view is valid in lesional studies where it seems reasonable to infer a causal relation between a single, specific, well-documented lesion and a single, specific, well-described abnormal behaviour. In psychopathology we are far from this model, however. We have few reasonable neurofunctional hypotheses for psychopathological conditions such as obsessive-compulsive disorder, and even these are still only schematic (see Wise and Rapoport 1987). We have no valid animal models of complex human mental disorders (with the sole possible exception of generalized anxiety disorder): Hence this approach seems to be of limited value right now. Obviously, we can create an animal model with a single psychopathological symptom (hallucinations, fear, compulsive behaviour, insomnia, hopelessness, and so on), but we cannot yet formulate a model of the entire syndrome or disease.
2.3. In the near future, the metabolic investigation of the brain (PET [positron emission tomography] and NMR [nuclear magnetic resonance] spectroscopy studies) may elucidate some simple psychopathological phenomena: yet even then we would need some prior hypotheses about the possible neurofunctional mechanisms involved. The recent literature in these two fields is, in our opinion, discouraging.
2.4. We agree with Neafsey that the DLPC deficit in schizophrenia may not be reducible simply to an abnormal increase in perseverative behaviour and that the dysfunctions reported in the mechanisms of eye-movement control can improve our understanding of such a complex problem. Nevertheless, it must be kept in mind that schizophrenia is, from a clinical point of view, a heterogeneous and multifactorial syndrome (for a review, see Tsuang et al., 1990).
3.1. Henderson & Dittrich's commentary deals mainly with the problem of the mutual relationships between functions and structures. As we understand it, the following are their 6 main criticisms of our work:
3.1.1. The neuropsychological approach to any brain malfunctioning must be related to a well defined anatomical lesion or to a well defined and circumscribed anatomic-functional model, which must precede the experimental study. REPLY: We can use any neuropsychological instrument that is reasonably related to a relatively simple and well defined neurophysiological function. It is part of the nature of the clinical field of CNS functional disorders that we do not have any well defined anatomical lesion and that the models proposed are derived mainly from neuropsychological results. Anderson & Ditrich do not suggest any way to get out of the circle.
3.1.2. Schizophrenia is a heterogenous and poorly defined syndrome and schizophrenics perform poorly on almost every task involving the central as well as the peripheral nervous system. REPLY: From a clinical point of view this criticism is as old as the definition of the syndrome. We see two alternative strategies for getting around it: First, select patients that are as homogeneous as possible based on clinical variables taking into account the distribution (between and within subject groups) of the values of a series of variables. Second, select a series of biological variables on the basis of neurofunctional reasoning, looking at their discriminative power in a series of successive admissions (i.e., not only schizophrenic patients) to an inpatient unit.
3.1.3. Frontal lobes are untestable from a neuropsychological point of view and WCST (Wisconsin Card Sorting Test) is a nonspecific neuropsychological instrument. REPLY: Considerable experimental and clinical data support the hypothesis that frontal lobe patients show a characteristic neuropsychological profile. There is also a good deal of experimental evidence that perseveration is a clinical symptom specific to frontal lesions and that there exist at least two different types of perseverative behavior (Freedman 1990). WCST appears to be the best available clinical instrument for evaluating DLPC perseveration (see Milner 1963).
3.1.4. The choice of paranoid schizophrenics is inappropriate because "negative" symptomatology is supposed to be related to frontal malfunction. REPLY: One of the most recent neurofunctional models of schizophrenia hypothesizes a complex malfunctioning in the CNS areas which connect temporo-limbic regions with frontal regions (Gray et al. 1991). This appears to be particularly applicable to positive schizophrenics.
3.1.5. Our work lacks a control group of patients lesioned in CNS regions other than frontal ones. REPLY: We are not concerned directly with confirming a specific anatomical hypothesis about schizophrenia, but in studying the perseverative modalities in different CNS functional pathologies.
3.1.6. OAT [object alternation test] and WCST are neuropsychological instruments that evaluate perseveration; the fact that the two test sets are in opposition indicates that they are nonspecific. REPLY: If it is reasonable to accept the experimental evidence that DLFC and OFC control different neurofunctional pathways related to at least two different kind of perseveration, then the data from our experiment appear to be highly specific.
Abbruzzese, M., Ferri, S., Bellodi, L., and Scarone, S. (1993) Frontal lobe dysfunction in mental illness. PSYCOLOQUY 4(9) frontal-cortex.1.
Freedman, M. (1990). Object Alternation and Orbito-Frontal System dysfunction in Alzheimer's and Parkinson's disease. Brain and Cognition 14: 134-143.
Gray, J.A., Feldon, J., Rawlins, J.N.P., Hemsley, D.R. and Smith, D.R. (1991) The Neuropsychology of Schizophrenia. Behavioral and Brain Sciences 14: 1 - 84.
Henderson, L. & Dittrich, W. (1993) Decomposing the Corpus of Neuropsychological Tests. PSYCOLOQUY 4(32) frontal-cortex.3.
Milner, B. (1963) Effects of different brain lesions on card sorting. The role of the frontal lobes. Archives of Neurology 9: 90-100.
Neafsey, E.J. (1993) Frontal Cortex, the Mind, and the Body. PSYCOLOQUY 4(15) frontal-cortex.2.
Tsuang, M.T., Lyons, M.J. and Faraone, S.V. (1990) Heterogeneity of Schizophrenia: Conceptual Models and Analytic Strategies. British Journal of Psychiatry 156: 17-26.
Wise, S.P. and Rapoport, J.L. (1989) Obsessive-compulsive disorder: is it basal ganglia dysfunction? In: Rapoport, J.L. (ed.) Obsessive-Compulsive Disorder in Children and Adolescence. American Psychiatric Press. Bethesda, Maryland. Chapter 19: 327-344.