This issue of CNS Spectrums contains a series of articles that examine historical and current notions regarding the association between classical organic brain concepts such as those seen in encephalitis, Sydenham's chorea, Parkinson's disease, and obsessive-compulsive disorder (OCD). From Griesinger's unitary theory of mental illness and Watson's revolutionary approach of radical behavior therapy, to current neuropsychiatric advancements, our knowledge of OCD has been enriched considerably. Modern technologies have partially confirmed the biological mechanisms of OCD, providing a welcome addition to our earlier understanding of the psychosocial components of the disease. One such biological mechanism is the brain system, which hosts a plurality of biological parameters. Heterogeneous diseases such as OCD may cause widespread bodily disequilibrium represented by symptoms, signs, and laboratory abnormalities, indirectly reflecting pathology. The brain system is a theoretical outline that includes the organic brain paradigm represented by the putative anatomy of OCD, neural correlates, somatosensorial aspects, and a behavioral-neurochemical model directed to explain OCD mechanisms and employed as a therapeutic tool.
Hymas reviews the neurology of OCD, which manifests itself in a series of soft signs and neurologic symptoms imbricating within the main pathology of the disease. This approach brings into the headlines of OCD pathophysiology the importance of motor activity (eg, as seen in Gilles de la Tourette syndrome), slowness, catatonia, and attention-deficit/hyperactivity disorder.
Stevens and colleagues comment on OCD sensorimotor input and output, aspects seemingly associated with schizophrenic pathophysiology. Within this context we may infer, for instance, that obsessional images, sounds, and melodies are actually "reasoned" hallucinatory experiences. The authors maintain that, at a neuroanatomical level, OCD is a faulty information process that forces one to modify behavior. Overall, this process is a model of cognitive and metacognitive operations. This article also comments on doubting, a symptom currently disregarded as part of the main OCD cluster, despite the fact that the French judiciously called OCD "la folie du doute."
Rauch and colleagues explore the presence of clinical indices, including factor scores. Symptom clusters, such as religious, aggressive, and sexual obsessions, and checking compulsions, were positively correlated with regional cerebral blood flow in the striatum. This preliminary report shows the possibility of isolating OCD subtypes that may or may not be interdependent. These modules may then be inserted in comorbid nosology and may help to explicate clinical vagueness.
According to Goldar and colleagues, OCD brain anatomy encompasses the dorsal praxic brain, which regulates sensorial and motor activity, and the ventral pragmatic brain, which regulates preventive and inhibitory mechanisms. Lesions in these areas will cause a reduction or loss of perceptive and motor functions. Orbitofrontal lesions may cause a disinhibitory response, such as loss of moral precepts with regard to sexual behavior, or an overabundance of preventive mechanisms that may induce excessive morality.
Neziroglu and Hsia propose an innovative biobehavioral model targeted to OCD mechanisms rather than treatment. They partially reject social learning theory to fully explain OCD mechanisms and adhere to the serotonergic hypothesis of OCD. They theorize, based on animal and human empirical evidence, that behavior therapy and medication may utilize similar neurobiological mechanisms. Of note, the authors suggest that OCD may develop from preexisting conditions initially dormant, as we observe in prodromal nosologies. They posit that compulsions precede anxiety, and that obsessions are secondary to compulsions, or are simply a form of compulsion.
On page 54, I discuss the philosophy regarding OCD in an attempt to consolidate pathology under one umbrella and reconceptualize the historical and traditional beliefs associated with the disease. The pathology of OCD comprises a histochemical network intertwining large portions of the brain. This configuration awakens, or brings to the surface, dormant sets of symptoms, thus expressing a new vocabulary of mosaic characteristics that requires translation. The unified theory of OCD necessitates continuity, contiguity, extension, and perhaps teletransmission. It is my hope that this theory will help to make clear the concepts and findings of the other articles in this issue.
We should remember that our knowledge reflects limitations. This indisputable message commands modesty for our theories.
* Dr. Yaryura-Tobias is the medical director of the Institute of Bio-Behavioral Therapy and Research in Great Neck, NY, and associate professor of psychiatry at New York University in New York City.
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