The construct of main depressive disorder makes no etiological assumptions about
May 17, 2017
The construct of main depressive disorder makes no etiological assumptions about populations with diverse symptom clusters. from the Hamilton Depression Rating Size as sensitive and prevalent to improve with existing remedies. A major restriction of the antidepressant therapies can be their narrow spectral Fadrozole range of action. While the core “mood and interest” symptoms have been the main focus of attention the associated symptoms listed above are often unaffected or exacerbated by current treatments. Careful clinical evaluation should address all of these dimensions recognizing that improvement may occur sooner in some symptoms (eg mood) compared with others (eg sleep disturbance). 4 ed. When these two “core symptoms” were used to screen for MDD using a 2-item version of the Patient Health Questionnaire (PHQ-2) they displayed a sensitivity of 83% and a specificity of Rabbit polyclonal to AGAP9. 92% Fadrozole for “caseness” based on a Structured Clinical Interview for (SCTD)3 and comparable results were obtained in a subsequent. .European replication.4 Confirmatory diagnosis of an MDE according to requires a minimum of five symptoms (at least one being mood or anhedonia) for a minimum of 2 weeks (see for It is easy to see how the multiple permutations and combinations of these symptoms contribute to substantial intraclass heterogeneity. Table I criteria for Major Depressive Episode. Main depressive episode subtypes Specifiers may be put into imply higher homogeneity within a subpopulation. For instance “with melancholic features” needs at least three of the next Fadrozole symptoms: complete lack of pleasure insufficient reactivity psychomotor retardation significant pounds loss extreme guilt or distinct quality of stressed out mood. Some writers have emphasized the current presence of Fadrozole psychomotor retardation like a primary feature of melancholic melancholy.5 The current presence of “atypical features” needs several of the next symptoms: overeating/weight gain hypersomnia leaden paralysis preservation of mood reactivity or interpersonal rejection sensitivity. These second option two symptoms (preservation of feeling reactivity and social rejection level of sensitivity) have already been criticized based on poor reliability plus some writers have suggested that just the invert vegetative symptoms hypersomnia and overeating aswell as leaden paralysis type the primary of atypical melancholy.6 There were attempts to dichotomize both of these melancholy subtypes on both treatment psychobiology and responsiveness. Historically tricyclic antidepressants and electroconvulsive therapy had been suggested for the melancholic individual 7 while individuals with atypical features seemed to respond easier to traditional monoamine oxidase inhibitors8 9 than to tricyclic antidepressants. These distinctions have already been less obvious with the existing era of selective serotonin reuptake inhibitor (SSRI) and serotonin-norepinephrine reuptake inhibitors (SNRI) antidepressants no available antidepressant posesses specific indicator for either melancholic or atypical symptoms. Actually Parker’s group lately acknowledged that symptom profiles within the “melancholia” population may vary with age. Hypersomnia was noted to be more common Fadrozole in the younger age group while late insomnia became the dominant sleep disturbance of older patients.10 Evidence of core symptoms from rating scales It is common to evaluate the severity of a depressive episode using classic rating scales particularly the Hamilton Rating Scale for Depression (HAMD-17)11 or the Montgomery Asberg Depression Rating Scale (MADRS).12 Differences in medication type and in the symptom profiles of the population being evaluated may influence outcomes on a rating scale. Among individual items the core “depressed mood” item on either the HAMD-17 or the MADRS was more sensitive to drug-placebo separation and to establishing optimal dosing compared with the full scales in several controlled trials.13 14 The sensitivity of some items to differentiate between active drug and placebo can be compromised when a drug has an unfavorable effect on certain items. For example increased anxiety may occur during the early weeks of SSRI therapy and activating antidepressants may disrupt some aspects of sleep.15 The net result is that prevalent items may not. emerge on rating scales that are designed to detect improvements during antidepressant.