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. Key Words: Bottom-up modulation; catatonia; horizontal modulation; Parkinson's disease; top-down modulation; vertical modulation. (shrink)

Catatonia is a psychomotor disorder that has gone through numerous descriptions since 1874, reflecting the many changes in psychiatric disease conceptualization that have occurred within that time frame. Catatonia has been variously described as a distinct disease entity, as a part of schizophrenia, and as a nonspecific manifestation of many disorders. Because of its association with schizophrenia, the description of catatonia was particularly affected by the psychopharmacological era, beginning in the 1950s, and by the development of the (...) Diagnostic and Statistical Manual of Mental Disorders (DSM). Changing trends in psychiatric research—especially the brain-based disease model, research methods favoured by the evidence-based medicine movement, and the codes and categories of the DSM—also profoundly influenced the evolving concept of catatonia. This paper discusses these important factors that affected recognition, treatment, and study of catatonia in order to reveal the biases and assumptions made when constructing a disease concept. (shrink)

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). (shrink)

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.

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. (shrink)

Recurrent complex visual hallucinations (RCVH) represent a form of psychosis. It may be useful to compare RCVH to another form of psychosis, catatonia. Both include a long list of medical illnesses and have been examined using several different hypotheses. Catatonia has a variety of hypotheses, including neurocircuitry, neurochemistry, and an integrated neuropsychiatric hypothesis. This hypothesis for catatonia supports Collerton et al.'s Perception and Attention Deficit model (PAD) for RCVH.

The text traces the development of the notion of catatonia in the work of Gilles Deleuze across three spheres – the individual, social and literary. The need for an analysis is based on the author’s perception that Deleuze thought on catatonia and slowness has been undervalued in many interpretations ; the recognition, in works of sociologists such as Hartmut Rosa, of the adverse effects of social acceleration. In the individual sphere, catatonia is the effect of a radical (...) withdrawal into anti-production or the body without organs. In the social sphere, catatonia is also linked to anti-production, but since in capitalism most anti-production is included in the sphere of production, catatonia represents a special case of resistance to this tendency. Deleuze shows how these two spheres intertwine in his analyses of Herman Melville’s works, especially Billy Budd and Bartleby; the title characters of these two texts are interpreted as embodiments of the catatonic as a political-revolutionary figure. (shrink)

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.

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.

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.

K L Kahlbaum published in 1874 the first recorded description of catatonia. Akinetic catatonia is now defined as a neuropsychiatric syndrome principally characterised by akinesia, mutism, stupor, and catalepsy. 1 Even if some advances have been made in the recognition of catatonia, in particular by the development of different rating scales, 1 the pathophysiology of this syndrome is not clearly established. A right handed 14 year old girl presented with akinetic catatonia during an episode of depression (...) in the context of a bipolar type I disorder. Her catatonic status was characterised by akinesia with brief episodic spontaneous stereotyped movements, mutism, no spontaneous oral intake, catalepsy, waxy flexibility, and stupor with brief occasional eye contacts. This corresponded to a total score of 19 on the Northoff Catatonia Scale.1 Electroencephalogram performed one day after onset of symptoms showed diffuse theta activity with sporadic diffuse delta activity. Cerebral magnetic resonance imaging was normal. Brain positron emission tomographies (PET) were obtained on a CTI-Siemens HR+ tomograph. A first PET (PET1) using (18F(- fluorodeoxyglucose (FDG) was performed on day 2 in a drug free state. Thereafter, intramuscular injection of 2 mg of lorazepam induced rapid clinical remission of the akinetic phase. Oral lorazepam was then given (3.75 mg/day) during five days. On day 8, a second PET with FDG was performed while the patient was treated by olanzapine (15 mg/day) and presented hyperactivity, logorrhoea, and disinhibition characterised by uncontrolled social interactions and physical contacts. Neuropsychological testing performed some days after remission revealed no apraxia or language disturbances but dysfunction of executive tasks manifested in the revised Wisconsin card sorting, the Tower of London, Stroop, and Trailmaking tests. Voxel based analyses comparing patient’s cerebral glucose metabolism with that of 29 right handed healthy controls (16 women and 13 men, mean age 32) were performed using Statistical Parametric Mapping (SPM99) (Wellcome Department of Cognitive Neurology, London, UK).. (shrink)

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.

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.

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.

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.

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.”.

Long-standing psychiatric practice confirms the pervasive use of pharmacological therapies for treating severe mental disorders. In many circumstances, drugs constitute the best allies of psychotherapeutic interventions. A robust scientific literature is oriented on finding the best strategies to improve therapeutic efficacy through different modes and timing of combined interventions. Nevertheless, we are far from triumphal therapeutic success. Despite the advances made by neuropsychiatry, this medical discipline remains lacking in terms of diagnostic and prognostic capabilities when compared to other branches of (...) medicine. An ethical principle remains as the guidance of therapeutic interventions: improving the quality of life for patients. Unfortunately, psychotropic drugs and psychotherapies do not always result in an efficient remission of symptoms. In this paper I corroborate the idea that therapists should provide drug-resistant patients with every effective and available treatment, even if some of such interventions could be invasive, like Electroconvulsive Therapy (ECT). ECT carries upon its shoulders a long and dramatic history that should be better investigated to provide new insights. In fact, ECT has attracted renewed interest in recent years. This is due to the fact that antidepressant drugs in younger patients show often scarce effectiveness and unpleasant side-effects. Moreover, I show that, thanks to modern advances, ECT may work as a successful form of treatment for specific and rare cases, such as severe depression (with suicide attempts) and catatonia. (shrink)

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.

An evolutionary theory of schizophrenia needs to address all symptoms associated with the condition. Burns' framework could be extended in a way embracing behavioural signs such as catatonia. Burns' theory is, however, not specific to schizophrenia. Since no one single symptom exists that is pathognomonic for “schizophrenia,” an evolutionary proposal of psychiatric disorders raises the question whether our anachronistic psychiatric nosology warrants revision.