Objective To review the literature of organic OCD and establish what links can be made between brain injury and secondary OCD. Then to compare this with sample of patients from Lishman Unit.

Method The relevant articles were reviewed and findings compared with neuroradiological analysis of brain injury patients on unit with secondary OCD.

Results There was some consistency in noting that OCD developed after injury to the orbitofrontal region and basal ganglia. However several other areas have been implicated including mesial prefrontal cortex, temporal lobe, and thalamus, albeit on smaller scale. There are also contradictory reports of OCD development and imaging results- some report increase in caudate nucleus volume, others a decrease. The general lack of uniformity in areas of brain injury is reflected in the wide variety of brain diseases that are sometimes associated with secondary OCD such as Temporal Lobe Epilepsy, Huntington's Chorea, Parkinson's Disease. This variety of differing pathologies suggests that secondary OCD can not be easily localised and suggest a more diffuse pathology. Furthermore, differing results from the studies can be attributed to the different imaging used: CT, MRI, functional MRI and SPECT. Some of the studies include neuropsychological testing, but as with imaging, testing is not consistent in conclusions but does suggest that dysexecutive factors play a factor in aetiology of organic OCD. On some occasions, OCD developed despite no abnormalities noted on imaging, nor loss/change in consciousness at time of injury. Interestingly syndrome often develops many weeks or months after injury, which could be related to pathogenesis. Or perhaps other psychosocial factors in recovery may be impacting.

Conclusion The main focus of organic OCD seems to be from disruption to the OFC and basal ganglia but other areas have been implicated as has been reflected in the literature as well as the patients on the Lishman brain injury unit, Maudsley Hospital.