Guest Editorial
Neuropsychiatry: Grasping the Body–Mind and Mind–Body Problems
Trevor A Hurwitz, MD1
If the brain is the most complicated material object in the known universe, the mind is its most wondrous product (1). Precisely how the brain generates mental events is an unsolved mystery. The field of neuropsychiatry concerns itself with psychopathology caused by structural brain disease, brain electrical malfunction, and extrinsic toxic metabolic disturbances. As such, neuropsychiatry is ideally placed to study brain–behaviour correlations wherein the underlying biological disturbance can be identified and often localized to specific brain regions. The advent of increasingly sophisticated structural and functional imaging, permitting visualization of the brain in vivo, has given new life to this undertaking.
In this issue, Dr Anthony Feinstein reviews the neuropsychiatry of multiple sclerosis, which causes both localized and diffuse brain injury (2). The full spectrum of psychiatric syndromes occurs in association with this disease; however, studies to date have failed to make convincing correlations between specific lesion locations and the syndromes of depression, mania, psychosis, and cognitive-intellectual disturbance.
Progress in the neurodegenerative diseases has now moved beyond histopathology to molecular pathology. The data suggest that neurodegenerative diseases can be classified according to a signature molecular abnormality that allows them to be broadly divided into tauopathies and alpha- synucleinopathies, based upon the accumulation of abnormal intracellular tau or alpha-synuclein proteins. These abnormal protein accumulations result in, or are associated with, cellular death. Dr Craig Hou, Dr Danielle Carlin, and Dr Bruce Miller take this approach to classification in their review of the non-Alzheimer’s disease dementias (3).
While the molecular pathology helps us better understand the causes of cell death, brain–behaviour correlations are still best understood in terms of injury to an aggregate of neurons with similar functions operating within large-scale networks (4). The non-Alzheimer’s disease dementias provide rich models for these brain–behaviour correlations. Frontotemporal dementia is associated with disinhibition, apathy, and repetitive behaviours; primary progressive aphasia and semantic dementia are associated with speech and language disturbances. In all 3 conditions, cognitive-intellectual failure is a late-occurring event.
Dr Feinstein and Dr Hou and colleagues, respectively, review the available and emerging treatments in the neuropsychiatry of multiple sclerosis and the non-Alzheimer’s disease dementias. Treatment of the non-Alzheimer’s disease dementias is in its infancy, with no treatments that stop progressive neurodegeneration. Treatment of the associated behavioural disturbances in frontotemporal dementia is currently based upon augmenting serotonergic, rather than cholinergic, function.
In multiple sclerosis, the psychiatric syndromes of depression, mania, and psychosis are treated according to general psychiatric principles. These syndromes respond to the same therapies that are effective in primary psychiatric disorders. These therapies remain the state-of-the-art treatment approach, not only for the psychiatric syndromes associated with demyelination but also for the psychiatric syndromes associated with diverse organic pathologies such as trauma, degeneration, and inflammation. The efficacy of these general psychiatric principles, as seen in daily neuropsychiatric practice, suggests that there are final common neurobiological pathways into psychopathology—an observation that strengthens the belief that better understanding of neuropsychiatric disorders will shed light upon the patho- physiology of primary psychiatric disorders where there is no visible pathology.
How the brain generates mental events (the body–mind problem) is only one part of the equation. An equally challenging question is how a disordered mind generates physical symptoms (the mind–body problem). These are the somatoform disorders. Patients with somatoform disorders form a sizable proportion of the population seen and treated in contemporary neuropsychiatric practice. In the somatoform disorders, the ostensible physical symptoms and signs are products of aberrant mental forces and events. This problem is best studied in conversion disorders, where symptom formation is externalized in examinable neurological deficits. Interventions such as narcoanalysis can reverse these externalized, incarnated mental forces and events, revealing in the process the operative psychological mechanisms.
Increasing data from studies over the past 2 decades indicate that conversion symptoms are based upon beliefs of illness developed unconsciously but applied consciously. The symptoms are fixed because the beliefs are fixed and, as such, behave as somatic delusions. This is not a novel concept: it was first proposed in 1869 by JR Reynolds, who described paralysis and other disorders of motion and sensation based upon an “idea which should take possession of the mind and lead to its own fulfillment” (5). In this issue, I review somatization and conversion disorder (6).
Much work is needed to address the body–mind and mind–body problems and determine how to best treat the associated psychopathology. As pointed out by Dr Feinstein, the field of neuropsychiatry needs more evidenced-based data to inform clinical practice. Hopefully, more doctors will decide to enter this emerging and exciting subspecialty wherein daily clinical encounters confront clinicians with fundamental questions and challenges about the brain, its functioning in health and disease, and how it works to create the mind.
References
1. Edelman GM. Bright air, brilliant fire on the matter of mind. New York: Basic Books; 1992.
2. Feinstein A. The neuropsychiatry of multiple sclerosis. Can J Psychiatry 2004;49:157–63.
3. Hou C, Carlin D, Miller B. Non-Alzheimer’s disease dementias: anatomic, clinical, and molecular correlates. Can J Psychiatry 2004;49:164–71.
4. Mesulam MM. Principles of behavioral and cognitive neurology. 2nd ed. New York: Oxford University Press; 2000.
5. Reynolds JR. Paralysis, and other disorders of motion and sensation dependent on idea. BMJ 1869;2:483–5.
6. Hurwitz T. Somatization and conversion disorder. Can J Psychiatry 2004;49:172–8.
Author(s)
1. Clinical Professor, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia.
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