Although there are several reports of MRI signal alteration of BR in depression, a characteristic neuroimaging pattern of BR abnormality has not yet been found [21]. Ultrasound investigations have been supplemented by T2-weighted MRI studies in order to investigate pathomorphological pattern of the BR Selleckchem Saracatinib in depression. Increased intensity of the midline has been reported for unipolar depressed patients when compared to bipolar patients and controls in a retrospective study using T2-weighted MRI [22]. A difference between patients with major depression and control subjects for T2-relaxation times was found in a region
of interest located along the midline of the pons. No difference was found between patients with bipolar disorder and control subjects. Alterations of
T2-relaxation times might indicate subtle tissue changes [23]. These findings are in line with the results of pathoanatomic and PET studies demonstrating morphological and functional alteration of the dorsal raphe nucleus in major depression, with decreased serotonin type 1A receptor binding and fewer neurons expressing serotonin transporter mRNA compared with findings in controls [24]. The relationship of BR echogenicity and SSRI responsivity which was found in the study of Walter [19] further supports the idea that reduced BR echogenicity reflects an alteration of the serotonergic system. In contrast with previous CH5424802 research buy reports,
no difference in echogenicity of the BR of unipolar depressed patients was found in the study of Steele, the only one which investigated possible structural changes of the BR in unipolar depression using diffusion tensor imaging, did not confirm structural changes of the BR in unipolar depressive patients using this method [25]. One of the important advantages of TCS is that it could also detect a subgroup of patients with depression characterized by mild clinical Mannose-binding protein-associated serine protease signs of parkinsonism who are possibly at an elevated risk of developing definite PD. TCS data in a recent study showed that the finding of SN hyperechogenicity, which is characteristic for idiopathic PD, was related to motor asymmetry and reduced verbal fluency in patients with depressive disorders. This relationship was even stronger in younger patients (<50 years) and independent from age, in patients who had reduced BR echogenicity [21]. Since, both liability for developing PD and frequency of PD-like TCS findings were found to be increased in depression, patients with depressive disorders might be an important population to screen for sonographic and clinical signs of early PD. Major depressive disorder (MDD) and adjustment disorder with depressed mood (ADDM) are currently regarded as distinct disease entities [26]. Especially, DSM axis-II comorbidity and suicidal behavior have been reported to differ between MDD and ADDM.