In an attempt to determine the specific causes of depression or, at least to gain a better understanding of the biological structure of the disease, MRI imagining techniques have been employed, usually as studies of those with depression and a control group of non-depressed subjects. “Structural imaging studies of bipolar affective disorder and major depression have shown a spectrum of abnormal findings. However, a characteristic pattern of abnormality for either disease has not yet emerged” (Supprian 2004).
Despite this lack of consensus on the parts of the brain that may be most responsible for depression, there are several revealing findings based on theories that repeatedly implicate problems with the hippocampus and the amygdala specifically, and several studies have “concluded that the hippocampus and amygdala within limbic-cortical networks may play a crucial role in the pathogenesis of major depression” (Xia 2004). In general, several studies using MRI techniques have examined the relative sizes of these portions of the brain and, using controls, have determined that there appear to be connections between the size and balance in sizes of these two critical elements of the human brain.
The hippocampus plays an important role in particular brain functions that regulation one’s inhibitions as well as the function of memory and memory development as well as the relationship of external spatial awareness. The amygdala, which is also part of the limbic system, also processes memory and plays an important role in the process of learning as well as emotional responses to memories that produce a learning experience, among other important functions.
While it is not clear how these two parts of the brain function with respect to depression (how their functions in the brain relate to depression) in a universally-accepted way, it is clear that imbalances in the size and structures of both the hippocampus and amygdala play an important role in depression. One of the only ways to discover possible inconsistencies between healthy versus depressed individuals is to use internal imaging techniques such as MRI. One frequently cited study based on MRI scans revealed that “the weighted average [of participants with depression] showed a reduction of hippocampal volume” and also indicated that the volume of the hippocampus is “reduced in patients with unipolar depression, maybe as a consequence of repeated periods of major depressive disorder” (Videbech 2004) although it should be noted that the study found that bipolar disorder did not demonstrate the same results.
In addition to revealing important connections between the hippocampus and amygdala, anomalies in other parts of the brain have also been attributed to depression. These irregularities can be detected using MRI and the results can be compared with the MRI of healthy subjects versus those suffering from depressive disorders. Several studies have examined individual aspects of brain function including the the basal ganglia. One study for example cited that “Patients with abnormal MRI findings may be at higher risk for mood disorders and suicide attempts because of critical neuroanatomic pathways. Gray matter hyperintensities in the basal ganglia may be especially associated with risk for suicide attempts“ (Ahearn 2001).
While this study examined one critical part of the brain, it is suggested yet again that MRI studies are revealing problems with certain parts of the brain, thus further research into the parts of the brain cited in this and other studies will begin to yield results that can be considered more conclusive. Again, however, the important issue that emerges is that in this case, there are imbalances in the relative sizes of certain brain elements, thus again, just as in the case with certain chemicals such as serotonin and cortisol as discussed previously, there are imbalances. What emerges in the research-based study of depression from the standpoint of MRI scans, is that there are marked differences between the scans of healthy versus depressed subjects. As a result, further research will show more scans that offer these clear-cut differences, thus hopefully leading to a more conclusive body of research regarding the biological basis of depression from the standpoint of imagining of the human brain.
From this examination of some of the topics related to the biological foundations of depression and how these elements can be further reduced to component brain functions as revealed by MRI scans, a few facts emerge. First of all, this is certainly a process of ongoing research because, although certain brain chemicals (serotonin or cortisol, for instance) and brain parts such as the hippocampus, amygdala, and neurotransmitters in other parts of the brain such as the basal ganglia, are often studied in connection to depression, no fully conclusive finding has been researched that absolutely connects depression to the hypothetical cause that is agreed upon by all researchers. Secondly, and perhaps more generally, it is clear that there is a biological basis to depression, just as there is with other diseases, many of which can also be tied to genetics, including issues of inheritance and general mutation of particular genes. With the continued use of MRI imaging techniques to isolate brain parts, determine proper and improper function, size, or other relative discrepancies, more will be learned about what causes depression. It seems that each case might have different factors as well, which demonstrates that depression is a complicated disease that could have multiple biological influences.
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References
Ahearn EP, ., Jamison KR, ., Steffens DC, ., Cassidy F, ., Provenzale JM, ., Lehman A, . et al. (2001). MRI correlates of suicide attempt history in unipolar depression.Biological Psychiatry, 50(4), 266.
Caetano, S. C. (2004). Anatomical MRI study of hippocampus and amygdala in patients with current and remitted major depression. Psychiatry Research Neuroimaging,132(2), 141-147.
Haghighi. (2008). Genetic architecture of the human tryptophan hydroxylase 2 Gene: existence of neural isoforms and relevance for major depression. Molecular Psychiatry,13(8), 813-820.
Supprian, T. (2004). MRI of the brainstem in patients with major depression, bipolar affective disorder and normal controls. Psychiatry Research Neuroimaging, 131(3), 269-276.
Videbech, P., & Ravnkilde, B. (2004). Hippocampal Volume and Depression: A Meta-Analysis of MRI Studies. American Journal of Psychiatry, 161(11), 1957-1966.
Xia J. (2004). Volumetric MRI analysis of the amygdala and hippocampus in subjects with major depression. Journal Of Huazhong University Of Science And Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban, 24(5).
