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  • Does a “Philosophy of the Brain” Tell Us Anything New about Psychomotor Disorders?
  • Sean A. Spence (bio)
Keywords

catatonia, Parkinson’s disease, action, attention, dorsolateral prefrontal cortex

In his paper on psychomotor phenomena, Northoff provides a detailed account of the different conceptual approaches that may be applied to disorders of the cerebral motor system. He attributes pathological (structural), physiological (functional), psychological (cognitive), and phenomenological (psychopathological) components to these disorders. There is little in his account to provoke strong disagreement. It seems entirely reasonable that localization of a static lesion is insufficient to provide a full explication of a disorder such as Parkinson’s disease and that the latter may be only fully characterized by a functional account (one that invokes cortico-subcortical “loops” and neurotransmitter disturbance). Indeed, in the case of Parkinson’s disease (PD), the neuroanatomical and pathophysiological mechanisms are now sufficiently well understood for physicians to prescribe rational treatments, using pharmacological and neurosurgical interventions.

That the interventions used to treat catatonia are as specific and well characterized (as those used in PD) is unlikely: the basic pathophysiology of catatonia awaits elucidation. Catatonia is now uncommon in industrialized societies and its relationship to schizophrenic psychosis is problematic, not least since Kahlbaum’s original case material probably comprised patients with psychotic depression and delirium (the latter in greater numbers, Berrios 1996, 382–83). When a factor analysis is performed using Kahlbaum’s original (1874) data, it reveals two factors accounting for 51 percent of the variance (“neurological,” 29 percent, and “psychotic depression,” 22 percent), but “posturing, flexibilitas cerea and verbigeration [behave] orthogonally, suggesting that no ‘catatonic’ factor seems to be present in Kahlbaum’s orginal cases” (Berrios 1996, 383). Hence, catatonia (as originally described) does not appear to be a coherent syndrome analogous to PD, a finding that may undermine any theoretical comparison between them. Northoff contrasts a well-understood disease (PD) with a poorly understood syndrome that may lack internal validity (catatonia). [End Page 227]

That “catatonia” may be related to affective disturbance is also apparent in Kahlbaum’s acknowledgment of the “anticipation” of “his” disease by older reports of “melancholia attonita” or melancholic stupor (Berrios 1996, 382). In describing a contemporary functional anatomy of catatonia, Northoff relies heavily on his own work, and throughout, the emphasis on the motor similarities between PD and catatonia is undermined by the acknowledgement that they are “similar” yet different. In this regard, it is important to emphasize that these diagnoses are syndromal and do not rely on single symptoms. Whereas the symptom of akinesia (lack of movement) may be common to PD and catatonia, they differ in other respects. Northoff outlines some of the bizarre motor behaviors that may be performed by catatonic patients and posits that there are phenomenological differences between these states (in terms of subjective experience). A similar point was made by Marsden and colleagues (1975):

The akinetic features of [catatonia] often closely resemble akinetic disorders of the extrapyramidal system. Lack of spontaneity, expressionless faces, fixed postures, transient bursts of activity in akinetic patients, sudden blocking, and frequent hypertonia all have their counterparts in Parkinson’s syndrome. The similarities that have been emphasized, however, appear to be limited to external appearances, while the disordered thought processes and extreme degree of negativism characterizing catatonic patients almost never have a counterpart in Parkinson’s disease

(223–24).

Hence, these motor disorders may resemble each other in certain respects, but their accompanying symptoms in other domains are rather different. However, it must be recognized that PD also has cognitive and psychopathological concomitants; patients exhibit executive deficits on formal cognitive assessment and experience increased rates of depression. So there is not the clear distinction between “psychiatric” and “neurological” disease that some might read into Northoff’s account of catatonia and PD (respectively). In fact, it is striking how often “movement disorders” and “psychiatric symptoms” are associated, suggesting to some authors that the basal ganglia play a major role in both syndromes: motoric and psychiatric.

Disorders that affect the basal ganglia (such as PD, Huntington’s, and Wilson’s diseases) may exert effects on specific cortical regions (to which specific thalamic nuclei project). Disturbance with-in these “loops” at any level may produce functional...

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