Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called “conflict of paradigms.” Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting “horizontal modulation” of cortico-cortical relation. Furthermore, alteration in “top-down modulation” reflecting “vertical modulation” of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered “bottom-up modulation” between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation – “vertical” and “horizontal” modulation, respectively.

We argue that the pivotal role assigned by Northoff to the principle of top-down modulation in catatonia might successfully be applied to other symptoms of schizophrenia, for example, hallucinations. Second, we propose that Northoff's account would benefit from a more comprehensive analysis of the cognitive level of explanation. Finally, contrary to Northoff, we hypothesize that “top-down modulation” might play as important a role as “horizontal modulation” in affective-behavioral alterations.

A composite cognitive model of a neuropsychiatric condition should integrate clinical symptoms with the impairments of cognitive information processing. A model of catatonia, for example, should emphasize deficits of nonconscious information processing that impair a patient's ability to use implicit motor feedback for execution and termination of a voluntary motor activity.

Northoff's target article presents a unifying theory of the pathophysiology of catatonia, as compared to Parkinson's disease. We address two arguments in particular that do not appear justified by available evidence: (1) The physiological basis of catatonia is the breakdown of right hemisphere prefrontal-parietal cortical connectivity, and (2) Dysfunction in this system results in specific deficits in termination of action.

Dr. Northoff's comprehensive comparison of clinical symptoms and neurobiological findings in catatonia with that of Parkinson's disease through integration of various levels of investigation, from neurochemistry up to the subjective experience, is a good example of the new strategies we need to improve our understanding of psychiatric disorders. His multimodal approach, leading to the hypothesis that different pathophysiologies of transcortical “horizontal modulation” and “bottom-up/top-down” – orbitofrontal/basal ganglia – “vertical modulations,” may explain many clinical aspects of catatonia and Parkinson's disease, and thereby fills an important gap in current theories of psychomotor syndromes. However, to analyze more specifically the pathophysiology of catatonia, comparison not only with Parkinson's disease, but also with schizophrenia and anxiety disorders would be helpful. As long as the pathohistological and molecular basis of catatonic syndromes is unknown, theories based mainly on functional considerations remain preliminary.

Catatonia resulting from a general medical condition (as defined in the DSM-IV) seems to account for a large percentage of patients presenting with catatonia in psychiatric settings. In view of Dr. Northoff's hypothesis, it is important to emphasize that medical catatonias provide additional information to support his neuropsychiatric hypothesis of the anatomical and biochemical mechanisms of catatonia.

The will is one of the three pillars of the trilogy of mind that has pervaded Western thought for millennia, the other two being affectivity and cognition (Hilgard 1980). In the past century, the concept of will was imperceptibly replaced by the cognitive-oriented behavioral qualifiers “voluntary,” “goal-directed,” “purposive,” and “executive” (Tranel et al. 1994), and has lost much of its heuristic merits, which are related to the notion of “human autonomy” (Lhermitte 1986). We view catatonia as the clinical expression of impairment of the brain mechanisms that promote human will. Catatonia is to the brain systems engaged in will, as coma is to the reticular ascending systems that promote sleep and wakefulness (Plum 1991).

Georg Northoff employs a comparison with Parkinson's disease in an effort to tease apart the underlying pathophysiology of psychogenic catatonia. Northoff's extensive treatment of the subject is abetted by his own research as well as the research of others. Nevertheless, a number of points concerning basal ganglia/thalamocortical processing need to be raised, some adding support to his hypothesis and others detracting from it.

Disruptions in dopamine transmission within the basal ganglia (BG) produce deficits in voluntary actions, that is, in the interface between cortically-generated goal representation and BG-mediated response selection. Under conditions of dopamine loss in humans and other animals, responses are impaired when they require internal generation, but are relatively intact when elicited by external stimuli.

While there may be interesting theoretical differences between cortical and subcortical malfunctions, it is not a difference that is going to separate the psychological from the biological. For, the distinctions we draw between the “psychological” and “biological” turn on our assessments of others' conscious experiences, and not on anything deeper or more profound.

Northoff provides a compelling argument supporting a kind of “double dissociation” of Parkinson's disease and catatonia. We discuss a related form of akinetic mutism linked to mesodiencephalic injuries and suggest an alternative to the proposed “horizontal” versus “vertical” modulation distinction. Rather than a “directional” difference in patterned neuronal activity, we propose that both disorders reflect hypersynchrony within typically interdependent but segregated networks facilitated by a common thalamic gating mechanism.

We outline some ways in which motor neglect (the underutilization of a limb despite adequate strength) and hysterical paralysis (failure to move a limb despite no relevant structural damage or disease) may throw light on the pathophysiology of catatonia. We also comment on the manifold inadequacies of distinguishing too firmly between symptoms of “neurologic origin” and of “psychiatric origin.”

The intrinsic merit of Northoff's model lies primarily in the fact that it integrates data concerned with different levels of organization of the brain. This approach implicitly argues against reductionism, although, apparently, its rather simplistic assumption gives too many degrees of freedom. In considering that a symptom from two different syndromes indicates a common neural alteration, we grossly disregard neural plasticity.

Aspects of Northoff's argument lend themselves to the ongoing investigation of localizing the self in the brain. Recent data from the fields of neuropsychology and cognitive neuroscience provide evidence that the right hemisphere is a candidate for localization of self. The data on catatonia further that proposition and add insight into the continuing investigation of self in the brain across sensory and motor domains.

Georg Northoff encounters a problem regarding the logical status of “catatonia.” Whereas Parkinson's disease (PD) is a disease on the basis of Virchowian criteria, catatonia is not. PD is associated with pathognomonic neurological lesions. Catatonia does not require any such association. The diagnosis is rendered using social criteria rather than neuropathological ones. Therefore, Northoff is not comparing two disease states at all.

The target article suggests that the neurological disorders catatonia and Parkinson's disease share similar behavioral features that nevertheless reflect different forms of abnormal information processing. However, emerging research on Parkinson's disease and related age-dependent neurodegenerative disorders suggests that no simplistic notions about processing will be correct for all stages of the disease.

The excellent and highly interesting commentaries address the following concerns: (1) neuroanatomy and neurophysiology of catatonia; (2) cognitive-motor deficits in catatonia; (3) conceptual issues; (4) general methodology in neuropsychiatric research; and (5) neurophilosophical implications. The specific problems, issues, and aspects raised by the different commentators are grouped under these categories in Table R1 presented below. These five areas of concern are then discussed in the order listed in the five sections of the Response.

In recent years we have seen a dramatic shift, in several different areas of communication studies, from an information-theoretic to a dynamic systems paradigm. In an information processing system, communication, whether between cells, mammals, apes, or humans, is said to occur when one organism encodes information into a signal that is transmitted to another organism that decodes the signal. In a dynamic system, all of the elements are continuously interacting with and changing in respect to one another, and an aggregate pattern emerges from this mutual co-action. Whereas the information-processing paradigm looks at communication as a linear, binary sequence of events, the dynamic systems paradigm looks at the relation between behaviors and how the whole configuration changes over time.

One of the most dramatic examples of the significance of shifting from an information processing to a dynamic systems paradigm can be found in the debate over the interpretation of recent advances in ape language research (ALR). To some extent, many of the early ALR studies reinforced the stereotype that animal communication is functional and stimulus bound, precisely because they were based on an information-processing paradigm that promoted a static model of communicative development. But Savage-Rumbaugh's recent results with bonobos has introduced an entirely new dimension into this debate. Shifting the terms of the discussion from an information-processing to a dynamic systems paradigm not only highlights the striking differences between Savage-Rumbaugh's research and earlier ALR studies, but further, it sheds illuminating light on the factors that underpin the development of communication skills in great apes and humans, and the relationship between communicative development and the development of language.

This paper points to the need in ape language research to shift from experimentation to ethnography. We cannot determine what goes on inside the head of an ape when it communicates with a human being, but we can learn about the nature and content of the communication that occurs in such face-to-face interaction. This information is fundamental for establishing a baseline for the abilities of an ape-human common ancestor.

Shanker & King argue for a shift in the focus of ape language research from an emphasis on information processing to a dynamic systems approach. We differ from these authors in our understanding of how this “new paradigm” emerged and in our perceptions of its limitations. We see information processing and dynamic systems as complementary approaches in the study of communication.