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  • Neuropsychiatry, Epistemology, and Ontology of the Brain: A Response to the Commentaries
  • Georg Northoff (bio)

Spence discusses four main issues with regard to my paper: (i) the syndrome character of catatonia; (ii) pathophysiological mechanisms of symptoms and syndromes in catatonia; (iii) role of attention in Parkinson’s disease and catatonia; and (iv) role of a “philosophy of the brain.”

(i) Even if in Kahlbaum’s original monograph the concept of catatonia is problematic, recent studies nevertheless have shown that catatonia as a syndrome has in fact a high internal validity. Peralta et al. (1997) showed that catatonia lies between schizophrenia and affective psychosis, so that it may either be regarded as a syndrome or an entity on its own. Starkstein et al. (1996) showed that depressive patients with and without catatonia can be clinically well distinguished from each other. Several studies in our own group showed that psychological and physiological alterations, as well as clinical symptoms, are specific for catatonia, compared to the underlying affective or schizophrenic psychosis (Northoff et al. 1997, 1999), which was demonstrated by grouping psychiatric patients either as catatonic and non-catatonic or as affective or schizophrenic psychotic. Hence these studies show that catatonia may be considered as a specific constellation of various symptoms subserved by specific psychological and physiological mechanisms independent of the underlying disease.

(ii) Of course I would fully agree with Spence that pathophysiological mechanisms of single symptoms should be investigated. For example, akinesia in Parkinson’s disease is probably due to a deficit in the “willed action system” subserved by the dorsolateral prefrontal cortex (DLPFC), the supplementary motor area (SMA), and the motor cortex (Jahanshahi and Frith 1998). In contrast ball experiments in catatonic patients (Northoff et al. 1995) showed that the “willed action system” by itself remains intact in catatonia. However, the “willed action system” seems to be blocked by the inability to “terminate” movements that may be related instead to dysfunction in right posterior parietal cortex, accounting for registration of the spatial position of movements as necessary for terminating movements (Northoff et al. 1999). Nevertheless, Spence is entirely right when he relates single symptoms not with single anatomical areas but rather with [End Page 231] cortico-subcortical loops. The difference between Parkinson’s disease and catatonia may be that distinct loops are altered. Whereas on the one hand in Parkinson’s disease, the dorsolateral prefrontal loop may be altered, in catatonia, on the other hand, the orbitofrontal loop may be altered (Northoff et al. 1999). In addition, the primary disturbance in Parkinson’s disease lies in the basal ganglia secondarily affecting the dorsolateral prefrontal cortex via the respective loop (Jahanshahi and Frith 1998). In catatonia, in contrast, there is evidence that the primary disturbance is cortical with secondary affection of the basal ganglia. Hence differences with regard to loops and primary disturbance may account for differences between Parkinson’s disease and catatonia, so that the latter may be regarded as “psycho-motor” and the former as “motor-psychological.”

(iii) Spence raises the question of the role of attention in Parkinson’s disease and catatonia. I would agree with him that attention plays a central role in catatonia. Catatonic patients probably suffer from “emotional hyperattention” (Northoff et al. 1998), so that a reduction of attention by lorazepam leads to symptomatic improvement, which is exactly inverse in Parkinson’s disease. These differences in attention may be reflected in differences with regard to neurotransmission. Parkinson’s disease can be characterized by dopaminergic deficiency (Jahanshahi and Frith 1998), whereas in catatonia alterations in GABA-ergic-mediated inhibition and desinhibition are of central importance (Northoff et al. 1999). Whether this difference in neurotransmission also accounts for differences in subjective experiences, i.e., awareness and unawareness of movements between Parkinsonian and catatonic patients (Northoff et al. 1998), remains uncertain, however. It is not clear whether Spence meant this when he spoke of “intentional differences” between both diseases.

(iv) Spence pursues an interesting approach to a “philosophy of the brain.” He argues that such a “philosophy of the brain” may only be worthwhile if it can contribute to the understanding of diseases. In contrast my intention was to suggest that a “philosophy of the brain” as derived...

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