Evidence for a Biological Hypothesis of Obsessive-Compulsive Disorder

Abstract

There is scant but provocative evidence to support the concept of a biological etiology in obsessive-compulsive disorder (OCD). This evidence includes the phenomenologic similarities and associations with other major psychiatric disorders for which there is evidence of biologic etiologies; the genetic studies that show an increased familial occurrence of psychiatric illness including OCD and concordance for this disorder in monozygotic twins; biologic evidence and the historical association of OCD and CNS damage; the treatment response of OCD to antidepressant medication and possibly those medications that selectively modify serotonin neuronal activity and to selective anterior limbic leukotomy. This evidence and the evidence linking OCD to depressive illness are specifically reviewed and discussed.

Animal Behavioural Studies in the Evaluation of Antidepressant Drugs

“…However, as there are numerous anatomical and functional relationships between noradrenergic and serotonergic neurons (Parent et al, 1981;Cowen et al, 1982;Geyer & Lee, 1984), it can be expected that both systems are directly or indirectly involved in the control of waiting capacity. This may account for the finding that drugs with preferential action on noradrenergic transmission were also active in the T-maze and the DRL procedures which agrees with the reported efficacy of compounds that interfere more specifically with noradrenergic transmission (imipramine-like drugs) in bulimia and OCD (Lieberman, 1984;Pope et al, 1985). However, their efficacy, at least in OCD, is probably weaker than that of selective 5-HT uptake inhibitors (Marks et ai, 1980;Turner et al, 1985;Fontaine & Chouinard, 1986).…”

“…reversal of escape failures or of immobility) is released. It is relevant that antidepressants ameliorate conditions such as bulimia and OCD which are characterised by a severe impairment of impulse control, and it may be that such amelioration can be subsumed into a global antidepressant action (Lieberman, 1984;Pope et al, 1985;Turner et al, 1985).…”

Brain Regional α-[11C]Methyl-L-Tryptophan Trapping in Medication-Free Patients With Obsessive-Compulsive Disorder

“…Largely on the basis of the clinical efficacy of 5-HT reuptake inhibitors, it was proposed, more than 20 years ago, that perturbed serotonergic neurotransmission may contribute to the development and expression of OCD. 11,25,76 Our study provides some evidence that these putative disturbances may include regionally specific alterations in brain 5-HT synthesis capacity, with medication-free patients with OCD exhibiting, relative to age-and sex-matched controls, significantly elevated normalized ␣-[ 11 C]MTrp trapping in the right hippocampus and left inferior temporal gyrus (Brodmann area 20). These observations were more robust when the analysis was restricted to male patients with OCD (n = 15), who also demonstrated increased ␣-[ 11 C]MTrp trapping bilaterally in the caudate nucleus.…”

Meta‐analysis of the association between the catecholamine‐O‐methyl‐transferase gene and obsessive‐compulsive disorder

“…The essential features of OCD are recurrent obsessions or compulsions that are severe enough to be time‐consuming or cause marked distress or significant impairment [APA, 2000]. As with many other psychiatric syndromes, there is clearly a genetic component to the etiology, as indicated by the higher concordance between monozygotic twins compared with that of dizygotic twins [Lieberman, 1984; Rosario‐Campos et al, 2001]. The clinical features of the disorder can be quite heterogeneous, even among affected individuals in the same family.…”