Neurobiology plays a very important path in the causation of OCD. Recently there have been a lot of developments in the understanding we have developed in matters regarding OCD. The basis for this development includes improved imaging techniques of the brain (to obtain images of the involved regions such as anterior cingulate area, orbitofrontal cortex, etc), use of newer pharmacological agents, etc. There has also been a greater understanding of the mechanisms in which neurotransmitters work and hence, better ability to identify how drugs would be acting to treat the symptoms of OCD.
The serotonin system (5-HT) plays a very vital role in the development and the progression of OCD. Other studies demonstrate that Dopamine disorders are required to develop OCD. When OCD develops in association with Tourette’s syndrome, the chances of dopamine problems is higher (PAULS, 2006). One of the first drugs that were useful in the treatment of OCD was clomipramine (a TCA agent) that help reduce the intensity and severity of the obsessions. Today several of the selective serotonin reuptake agents seem to be effective in the treatment of OCD.
Studies have clearly demonstrated that in people with OCD, the 5-HT transmission seems to be defective. Several medications that encourage the release of 5-HT at the presynaptic and the postsynaptic regions seem to be effective in reducing the symptoms of OCD. However, some patients are also responsive to the administration of 5-HT antagonist metergoline. Some patients also developed worsening of symptoms following administration of 5-HT compounds.
This included those who were acutely challenged. This may be due to the 5-HT nerves having basal hyperactivity (arising from hypersensitivity of the postsynaptic receptors or hypoactivity of the presynaptic receptors). Hence individual who are administered 5-HT compounds tend to have an exacerbation of acute symptoms, but in the long run the symptoms tends to reduce. Serotonin reuptake inhibitor agents seem to be effective would enhance the release of 5-HT (PAULS, 2006).
As OCD is related Gilles de la Tourette syndrome (GTS), but the understanding of how the dopamine system would affect the development of OCD is still not understood clearly. GTS is significantly related to the dopamine system, as whenever dopamine antagonists are administered, the symptoms tend to worsen. Patients suffering from OCD and GTS and administered serotonin enhancing agents are usually resistant to treatment. Studies have shown that administration of dopamine to such patients can be beneficial (Pauls, 2006).
One of the areas where both the serotonin system and the dopamine system would interact would be the basal ganglia, and in patients suffering from OCD, this tends to be a vital location. Through various functional radiographic imaging techniques, it has been found that several other locations including the orbitofrontal cortex, striatum and the basal ganglia are involved in the development of OCD. Several studies performed using oxytocin, vasopressin and somatostatin have demonstrated that complex neuroendocrime mechanisms are involved (Pauls, 2006).
Experts have previously suggested the involvement of the immune system in the development of OCD symptoms. In some children, following infection with the beta-hemolytic streptococcus bacteria, the symptoms of OCD initiate. Besides, several viruses are also known to be involved. One observation found that the symptom Sydenham’s chorea to be associated with streptococcal infection and OCD. Besides, links between the streptococcal infection and GTS also seem to exist (Pauls, 2006). Several studies even point out to the genetic implications of OCD.
Earlier studies have demonstrated that in monozygotic twins, the chances of one twin developing OCD when the other was already affected were about 63%. This figure was very much the same as that occurred in anxiety and affective disorders. With regards to dizygotic twins, a greater amount of research is required. Earlier studies have found that in twins, when obsessive symptoms develop in one twin, there was a 47 % of the other developing it in dizygotic twins (and 87 % in case of monozygotic twins).
The chances of identical twins (monozygotic twins) suffering from obsessive and compulsive symptoms was higher than in non-identical twins (dizygotic twins) (Pauls, 2006). Family studies have shown that frequently OCD runs in families. The earlier study models were not appropriate to provide realistic results. Pauls et al (2006) have mentioned that in one of the previous studies it was found that out of the 46 children, who were affected with the disease, about 25 % had affected fathers and 9 % had affected mothers with OCD.
In another study mentioned by Pauls et al (2006), it was found that in about 15 % of the affected patients had relatives who had suffered from the disorder. When relatives affected with the disorder are present, the chances of getting affected with the disorder earlier are higher than later (tends to occur more often when the individual is below the age of 14 years). Other study models demonstrate that although the rate of OCD may not be high in relatives, the chances of developing the symptoms present in OCD or the subclinical features are higher (Pauls, 2006).
Paul Et al conducted a study to determine the relationship between OCD and GTS. He found that actually there was no close relationship between OCD and GTS. GTS was not found in the familial, genetic or person history amongst those who suffered from OCD. In such patients suffering from OCD, a positive family history of OCD itself was found (Pauls, 2006). In another study conducted by Nestadt et al (2000), about 11. 5 % of the patients with OCD had close family relative suffering from OCD (Nestadt, 2000).