Conclusions

It should be evident from the above discussion that the past 20 years have produced an exponential growth in our understanding of the pathophysiology of schizophrenia. The availability of increasingly sophisticated brain imaging and molecular approaches have made it possible to investigate the structure and function of the human brain under both normal and abnormal conditions. So, what have we learned about schizophrenia? Although the genetic component of this disorder has remained elusive, brain imaging studies have demonstrated that schizophrenia probably involves multiple brain regions, including the prefrontal region, anterior cingulate cortex, hippocampus and amygdala. Post-mortem studies are suggesting that superficial layers of these cortical areas and sectors CA4, CA3 and CA2, but not CA1, show more prominent, though not exclusive, changes in schizophrenia. There is not as yet a consensus as to whether the metabolism in these various regions is over- or underactive, and there continues to be conflicting evidence as to whether the glutamate system is up- or down-regulated. There is, however, a growing consensus that GABAergic inter-neurons within the cortico-limbic system are probably unable to provide sufficient amounts of inhibitory modulation to excitatory projection neurons and possibly also to other GABA cells in the hippocampal formation.

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