For many years, a number of psychodynamic conceptualizations held sway of obsessional states as the product of intrapsychic conflicts. Only relatively recently has a more reasonable neurobiologic model been advanced. These are largely derived from the findings of functional imaging, which have been quite consistent in demonstrating increased metabolic activity in the orbitofrontal cortex, cingulate, and, to a lesser extent, striatum. The orbitofrontal cortex and amygdala were reported to be shrunken in other cases. In a study of 13 patients who developed elements of obsessiveness and compulsive disorder after incurring focal brain lesions, Berthier and colleagues found lesions in diverse loci, including the cingulate, frontal, and temporal cortices, as well as the basal ganglia. Two of the most accurately localized lesions in their series were a hamartoma of the right parahippocampal gyrus and an infarction in the posterior putamen. The presence of brain injuries and seizure disorders in other of their patients made precise localization less certain.
Additional insight into obsessive-compulsive disorder may be obtained from the many cases in which acquired striatal damage may be linked to obsessional behavior. One such entity is a poststreptococcal tic disorder termed PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), discussed in Chap. 4. This disorder is presumably related to another extrapyramidal condition, Sydenham chorea, in which tics and similar movement disorders, as well as obsessive behavioral abnormalities, have long been known to coexist. Functional imaging studies in patients with
PANDAS have yielded variable findings but generally there has been increased activity in the caudate nucleus and orbitofrontal cortex in association with the patient’s compulsive thoughts.
The Gilles de la Tourette syndrome of multiple tics, including vocal ones, beginning in childhood or adolescence and lasting more than a year, has a strong component of obsessive-compulsive disorder in more than half of patients. Both disorders occur in a pattern of inheritance that is close to an autosomal dominant trait with incomplete penetrance (Kurlan). Because dopamine antagonists (Haldol was the first of these to be tried systematically, by Shapiro) have been beneficial in the management of the Tourette syndrome, a number of etiologic hypotheses revolve around serotonergic and dopaminergic neurotransmitter systems (Baxter). The neurochemical alterations in obsessive-compulsive disorder have been based in part on the responses to medications, notably to the serotonin reuptake inhibitors, as noted further on. These agents are found to be of therapeutic benefit, as are stereotactic neurosurgical lesions in the cingulate gyri (see further on). More extensive comments on the Gilles de la Tourette syndrome are found in Chap. 4.
This is best left to the experienced psychiatrist. At the least there should be a trial of therapy using behavioral modification techniques. In the case of phobic neurosis, the aim is to reduce the patient’s fear to the extent that exposure to the phobic situation can be tolerated. A popular form of therapy is systematic desensitization, which consists of increasing and graded exposure of the patient to the object or situation that arouses the fear. Psychotherapy, if undertaken, need not be intensive, consisting instead of repeated explanation, reassurance, and guidance in dealing with symptoms. As with phobic neurosis, several reports have indicated that compulsive rituals can often be abolished by the techniques of behavior therapy. Much in vogue is cognitive-behavioral psychotherapy discussed in Chap. 48.
Certain medications, particularly the SSRI types such as fluoxetine, are considered to be effective in reducing obsessions and compulsions in more than half of patients. The less selective agent, clomipramine, is also highly effective, as were the commonly used tricyclic antidepressants in the past, but clomipramine is not nearly as well tolerated as are the conventional SSRI drugs (see review by Stein).