Recent neuroimaging studies have focused on the neurobiological differences between healthy controls and abnormalities associated with MDD, such as dysfunctional or structural differences in cerebral regions, including the prefrontal cortex, amygdala, anterior cingulate cortex ACC , and hippocampus. Previous structural magnetic resonance imaging MRI studies using region-of-interest ROI analyses have shown a variety of inconsistent findings.
Because depression is heterogeneous, subtyping the disease will be helpful for understanding imaging results. However, there are few imaging studies which were done according to depression subtype.
There is no VBM study. One chimeric faces study measured of perceptual asymmetry and showed that those with atypical depression differed from those with typical depression and controls in showing abnormally large right hemisphere bias. A chimeric face consists of fusion of a neutral right half-face with a smiling left half-face. Its mirror image creating a neutral left half-face fused with a smiling right half-face is randomly placed above or below.
The task is to quickly determine which of the two faces is happier. Preference for choosing one side as happier relative to the other has been interpreted as reflecting increased activation of the contralateral parietal lobe,[ ] although inhibitory mechanisms could also be hypothesized. This was present in patients having either MDD or dysthymia and was not related to anxiety, physical anhedonia, or vegetative symptoms.
In contrast, patients with melancholic depression showed essentially no right hemisphere bias. The authors suggest that this is further evidence that atypical depression is a biologically-distinct subtype and underscores the importance of this diagnostic distinction for neurophysiologic studies. Single photon emission computerized tomography SPECT in 50 depressed patients with MDD, including subtype assessment indicated differential brain activity in patients with atypical depression compared with typical depression.
In two brain regions, patients with atypical depression differed from both controls and at least one of the other depressed groups Table 1. Conclusively, those with atypical depression had increased frontal, temporal, and parietal perfusion coupled with decreased occipital perfusion, relative to the other two depressed groups. Patients with atypical depression also had increased right frontal perfusion, whereas those with melancholia and undifferentiated depression had decreased perfusion in the majority of nonoccipital regions, relative to controls.
Thus, all three depressed groups showed abnormal perfusion, but the patterns differed. Melancholia and undifferentiated depression had similar patterns of abnormal perfusion that differed from those with atypical depression.
Perfusion findings of depressed patients and controls [], adapted from [ ]. A, atypical depression. C, control. M, melancholic depression. U, undifferentiated depression. These imaging studies are consistent, suggesting that atypical depression does not have the biological features of melancholia. Currently, researchers have determined that MDD results from the interaction of multiple genetic factors and various environmental factors, such as childhood adversity and many stressful life events.
Although the development of antidepressant drugs has skyrocketed in recent decades, the neurobiological effects underlying the therapeutic actions of these agents remain poorly understood.
For example, melancholic depression is associated with hyperactivity of the HPA axis while atypical depression is associated with hypoactivity of the HPA axis. Researchers have searched for biological mechanisms according to depression subtypes in an effort tto understand the pathogenesis of depression subtypes.
Concerning pharmacological treatment, it was reported that the group of patients with atypical depression showed a significantly higher cortisol response to desipramine, a relatively selective noradrenaline reuptake inhibitor, than a group with no atypical symptoms and a group with mood reactivity as the only atypical symptom, indicating that atypical depression may be associated with a smaller impairment of the noradrenaline neurotransmitter system. Similarly, hypersecretion of corticotropin-releasing hormone CRH and the resulting hypercortisolism were not found in patients with atypical depression.
Imaging studies are consistent with that finding, suggesting that atypical depression does not have the biological features of melancholia. The results are summarized in Table 2. Different clinical symptoms and biological mechanisms between melancholic and atypical depression based on the DSM Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications.
Edited by Yong-Ku Kim. Edited by Michael Fitzgerald. We are IntechOpen, the world's leading publisher of Open Access books. Built by scientists, for scientists. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Hormonal axis MDD generally features the hyperactivity of the hypothalamic-pituitaryadrenal HPA , a neuroendocrine abnormality[ 7 ] In particular, the majority of depressed patients exhibit hypersecretion of cortisol in their plasma, urine, and cerebrospinal fluid CSF , and a hyperactive cortisol response to adrenocorticotrophic hormone ACTH.
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Do You Have Psychotic Depression? In modern times, depression has been treated with a diverse range of methods, including rest, talk therapy, amphetamines s , meprobamate s , and benzodiazepines s. Melancholia has primarily been treated with somatic therapy, such as electroconvulsive therapy, and tricyclic antidepressants.
In the first edition of RDC, Spitzer adopted most of the Feighner criteria, including essential criteria A "dysphoric mood" and eight optional criteria B1-B8. However, he reduced the minimal morbid duration for diagnosis. Moreover, for the purpose of excluding neurosis from the diagnostic criteria, Spitzer eliminated the distinction between primary and secondary depression, which had been used to differentiate melancholia from depression.
In the revised RDC, Spitzer upgraded optional criteria B5 "loss of pleasure or interest" to one of the essential criteria A with "dysphoric mood.
In exploring the possibility of melancholia, the clinician can ask general questions and then move to closed questions. Observe the patient. In severe melancholia, he or she may be monosyllabic and slow to move.
In assessing a new patient, seek information from a corroborative witness-a relative or friend. Those with severe melancholia may report total mood non-reactivity, but most patients will acknowledge some level of reactivity-such as when they see their grandchildren. DSM-5 symptom criteria for melancholic features-anhedonia, non-reactive mood, early morning wakening, depression worse in the morning, psychomotor disturbance, loss of appetite and weight-capture most of the historically favored endogeneity symptoms.
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