Delayed-maturation theory of obsessive–compulsive disorder
Medical hypothesis / From Wikipedia, the free encyclopedia
Dear Wikiwand AI, let's keep it short by simply answering these key questions:
Can you list the top facts and stats about Delayed-maturation theory of obsessive–compulsive disorder?
Summarize this article for a 10 year old
The delayed-maturation theory of obsessive–compulsive disorder suggests that obsessive–compulsive disorder (OCD) can be caused by delayed maturation of the frontal striatal circuitry or parts of the brain that make up the frontal cortex, striatum, or integrating circuits.[1] Some researchers suspect that variations in the volume of specific brain structures can be observed in children that have OCD (Lambert, K.G; Kinsley, C.H., 2011).[1] It has not been determined if delayed-maturation of this frontal circuitry contributes to the development of OCD or if OCD is the ailment that inhibits normal growth of structures in the frontal striatal, frontal cortex, or striatum. However, the use of neuroimaging has equipped researchers with evidence of some brain structures that are consistently less adequate and less matured in patients diagnosed with OCD in comparison to brains without OCD. More specifically, structures such as the caudate nucleus, volumes of gray matter, white matter, and the cingulate have been identified as being less developed in people with OCD in comparison to individuals that do not have OCD (Lambert, K.G.; Kinsley, C.H.).[1] However, the cortex volume of the operculum (brain) is larger and OCD patients are also reported to have larger temporal lobe volumes; which has been identified in some women patients with OCD (Jenike, M.; Breiter, H.; at el, 1996).[2] Further research is needed to determine the effect of these structural size differences on the onset and degree of OCD and the maturation of specific brain structures.
This article needs additional citations for verification. (October 2013) |