e found in the locus caeruleus of bipolar patients, compared to unipolar depression. Both unipolar and bipolar patients showed structural deficits in the dorsal raphe and there was a regional reduction in the synthesis of noradrenalin and serotonin, which may be compensated with antidepressants. Thus it was concluded that there may be structural abnormalities in the brain that contribute to mood disorder pathogenesis.
Strakowski, DelBello, Sax, Zimmerman, Shear, Hawkins, and Larson (1999) used brain magnetic resonance imaging to determine structural abnormalities in bipolar disorder, noting that neuropathogenesis of this disorder is inconclusive. However, it has been hypothesized that there are neural pathway abnormalities that modulate human mood states in patients. In a study of 24 patients and 22 healthy controls, findings showed that patients had an enlarged amygdala and possibly an enlarged thalamus and globus pallidus. It was concluded that the hypothesis was supported.
Deicken, Pegues, Anzalone, Feiwell, and Soher (2003) pointed out that previous studies have resulted in inconclusive evidence regarding the identification of neuropathological alterations in the hippocampus in bipolar patients. This study used proton magnetic resonance spectroscopy and measured N-acetylaspartate, choline, and creatine in the hippocampus of familial bipolar I disorder and healthy controls. Findings showed that significantly lower concentrations of N-acetylaspartate and creatine were found in patients but choline was normal. There was also a significant negative correlation between N-acetylaspartate in the
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