Biological causes of Obsessive Compulsive Disorder
In the past 15 years there has been an explosion of researches investigating the possible biological cause for obsessive compulsive disorder. Some studies have sought to discover whether there is a genetic contribution to this disorder. Others have explored whether there are structural brain abnormalities associated with obsessive compulsive disorder (OCD) and yet others studies whether there are abnormalities in specific neurotransmitter systems associated with Obsessive compulsive disorder (OCD). The accumulating evidence from all three kinds of studies is that biological casual factors are probably more clearly implicated in the causes of Obsessive Compulsive Disorder(OCD) than in any of the other anxiety disorders.
Genetic studies have involved both twin studies are family studies. Evidence from twin studies reveals a moderately high concordance rate for monozygotic twins (about 65% averaged across the studies reviewed by Rasmussen & Tsuang 1986), but these results are somewhat difficult to interpret given the failure to include dizygotic twins (Pauls, Raymond & Robertson 1991). One small study by Carey & Gottesman (1981) did include dizygotic twins and found that concordance rates were smaller, although not significantly, perhaps because of the small sample sizes. Most family studies have also found substantially higher rates of Obsessive Compulsive Disorder (OCD) in first degree relatives of OCD patients.
The search for structural abnormalities in the brains of OCD patients has also been intense in the past decade as major advances have been made in techniques used to study the functioning of brain structures in living patients. Findings from studies using Positron Emission Tomography (PET) scans have shown that patients with OCD have abnormally active metabolic levels, in the orbital prefrontal cortex and caudate nucleus (Baxter, Schwartz & Guze 1991). Other studies have shown some normalization of some of these abnormalities with successful treatment (Baxter etal 1992). Rapoport & Wise (1988) in their study found abnormalities in the functioning of basal ganglia.
There is also evidence suggesting biochemical abnormalities as casual factor in OCD. Most contemporary findings suggest that increased serotonin activity and increased sensitivity of some brain structures to serotonin may be involved in OCD symptoms.
Pharmacological studies of OCD also suggest that drugs that are effective in treatment of OCD are those that effect neurotransmitter serotonin.