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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amplitude and time course of slow-wave activity (SWA) during NREM sleep were compared in 76 outpatients with depression and 55 healthy control subjects. Lower SWA amplitude was evident in the depressed group, especially among depressed men. For the most part, significant differences between patients and control subjects were restricted to the first NREM period and only in those 20-30 years of age. Significant age-related declines in SWA amplitude were evident in control subjects but not in depressed patients. In addition, sex differences in the depressed group were twice as large as those seen in control subjects. The time course of SWA amplitude, presumed to reflect homeostatic sleep regulation of SWA, was only abnormal in depressed men with lower accumulation and slower dissipation over NREM sleep. Depressed women showed no evidence of an abnormal SWA time course. Furthermore, no sex differences in the time course of SWA were evident in control subjects, and age-related changes in this aspect of regulation were not striking in any group. Thus, the amplitude of SWA showed strong age effects in healthy individuals but not in those with MDD whereas the time course showed very subtle age effects. It was suggested that men, but not women, with MDD show impaired SWA regulation that is evident from 20 to 40 years of age. These findings provide further support that the pathophysiology of depression differs for men and women and suggest that maturational effects on SWA in depression differ from those observed in healthy individuals.
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PMID:Slow-wave activity in NREM sleep: sex and age effects in depressed outpatients and healthy controls. 1097 59

The study objective was to examine the prevalence and course of depressive disorders (DDs) in teenage-onset anorexia nervosa (AN) over a period of 10 years. Fifty-one adolescents with AN and a sex- and age-matched control group (n = 51) were assessed at ages 16, 21, and 24 years. Probands and controls were examined in depth using semistructured and structured interviews. Their parents were interviewed on the occasion of the first examination. DDs were assessed using DSM-III-R criteria. Subjects with AN had a greatly increased rate of DDs (85%) of all kinds and at all ages as compared with control subjects. The risk of DD during the follow-up period from 21 up to and including 24 years could be predicted by diagnostic group status and the presence of DD during the period from 16 to 21 years, while the risk of DD during the follow-up period from 16 up to and including 21 years was solely predicted by the presence of AN at age 16 years. Long-term resolution of the eating disorder (ED) was associated with the absence of mood disorder or vice versa. Bipolar disorder (BP) occurred at roughly the expected rate (11%) among subjects (probands and controls) with major depression (MDD). In conclusion, depression is a very common comorbid problem in AN: more than four of five individuals with teenage-onset AN had at least one episode of DSM-III-R depression (MD or dysthymia [DT]) within 10 years after onset of the ED. AN appears to trigger the first episode of depression, but once it is manifest, depression predicts further depressive episodes.
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PMID:Depressive disorders in teenage-onset anorexia nervosa: a controlled longitudinal, partly community-based study. 1101 38

This article reviews data on the prevalence of panic, social phobia, generalized anxiety, and posttraumatic stress disorder, and research documenting the comorbidity of these disorders with major depression (MDD). These anxiety disorders are frequently comorbid with MDD, and 50-60% of individuals with MDD report a lifetime history of one or more of these anxiety disorders. The anxiety disorders are also highly correlated with one another, and approximately one-quarter to one-half of individuals with each of the anxiety disorders report a lifetime history of an alcohol or substance use disorder. Anxiety disorders rarely exist in isolation, with several studies reporting that over 90% of individuals with anxiety disorders have a lifetime history of other psychiatric problems. Implications for research are discussed, including the potential benefit of using combined categorical and dimensional rating scale approaches in future genetic, biochemical, neuroimaging, and treatment studies. The clinical implications of the findings are also discussed, and the results of recent clinical trials summarized. Available data suggests selective serotonin reuptake inhibitors are the first-line pharmacological treatment for these disorders, and that newer serotonin and norepinephrine reuptake inhibitors show significant promise, especially for comorbid cases. Comorbidity among depression and anxiety disorders is associated with greater symptom severity, and a considerably higher incidence of suicidality. Increased public awareness about these disorders and the availability of effective treatments is sorely needed.
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PMID:Comorbidity of mood and anxiety disorders. 1109 17

1. To distinguish GAD from panic disorder is not difficult if a patient has frequent, spontaneous panic attacks and agoraphobic symptoms, but many patients with GAD have occasional anxiety attacks or panic attacks. Such patients should be considered as having GAD. An even closer overlap probably exists between GAD and social phobia. Patients with clear-cut phobic avoidant behavior may be distinguished easily from patients with GAD, but patients with social anxiety without clear-cut phobic avoidant behavior may overlap with patients with GAD and possibly should be diagnosed as having GAD and not social phobia. The cardinal symptoms of GAD commonly overlap with those of social phobia, particularly if the social phobia is more general and not focused on a phobic situation. For example, free-floating anxiety may cause the hands to perspire and may cause a person to be shy in dealing with people in public, and thus many patients with subthreshold social phobic symptoms have, in the authors' opinion, GAD and not generalized social phobia. The distinction between GAD and obsessive-compulsive disorder, acute stress disorder, and posttraumatic stress disorder should not be difficult by definition. At times, however, it may be difficult to distinguish between adjustment disorder with anxious mood from GAD or anxiety not otherwise specified, particularly if the adjustment disorder occurs in a patient with a high level of neuroticism or trait anxiety or type C personality disorder. Table 2 presents features distinguishing GAD from other psychiatric disorders. 2. Lifetime comorbid diagnoses of other anxiety or depression disorders, not active for 1 year or more and not necessitating treatment during that time period, should not effect a diagnosis of current GAD. On the other hand, if concomitant depressive symptoms are present and if these are subthreshold, a diagnosis of GAD should be made, and if these are full threshold, a diagnosis of MDD should be made. 3. If GAD is primary and if no such current comorbid diagnosis, such as other anxiety disorders or MDD, is present, except for minor depression and dysthymia, or if only subthreshold symptoms of other anxiety disorders are present, GAD should be considered primary and treated as GAD; however, patients with concurrent threshold anxiety or mood disorders should be diagnosed according to the definitions of these disorders in the DSM-IV and ICD-10 and treated as such. 4. Somatization disorders are now classified separately from anxiety disorders. Some of these, particularly undifferentiated somatization disorder, may overlap with GAD and be diagnostically difficult to distinguish. The authors believe that, as long as psychic symptoms of anxiety are present and predominant, patients should be given a primary diagnosis of GAD. 5. Two major shifts in the DSM diagnostic criteria for GAD have markedly redefined the definition of this disorder. One shift involves the duration criterion from 1 to 6 months, and the other, the increased emphasis on worry and secondary psychic [table: see text] symptoms accompanied by the elimination of most somatic symptoms. This decision has had the consequence of orphaning a large population of patients suffering from GAD that is more transient and somatic in its focus and who typically present not to psychiatrists but to primary care physicians. Therefore, clinicians should consider using the ICD-10 qualification of illness duration of "several months" to replace the more rigid DSM-IV criterion of 6 months and to move away from the DSM-IV focus on excessive worry as the cardinal symptom of anxiety and demote it to only another important anxiety symptom, similar to free-floating anxiety. One also might consider supplementing this ICD-10 criterion with an increased symptom severity criterion as, for example, a Hamilton Anxiety Scale of 18. Finally, the adjective excessive, not used in the definition of other primary diagnostic criteria, such as depressed mood for MDD, should be omitted (Table 3). 6. One may want to consider the distinction of trait (chronic) from state (acute) anxiety, but whether the presence of some personality characteristics, particularly anxious personality or Cluster C personality and increased neuroticism, as an indicator of trait [table: see text] anxiety is a prerequisite for anxiety disorders; occurs independently of anxiety disorders; or is a vulnerability factor that, in some patients, leads to anxiety symptoms and, in others, does not, is unknown. 7. Symptoms that some clinicians consider cardinal for a diagnosis of GAD, such as extreme worry, obsessive rumination, and somatization, also are present in other disorders, such as MDD. (ABSTRACT TRUNCATED)
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PMID:Overview and clinical presentation of generalized anxiety disorder. 1122 2

Although they are likely to add their effects, physical and psychic traumata (or traumas) can provoke in different ways the appearance of depressive symptoms sometimes common. Post-traumatic depression, reactional depression, major depressive disorder and post-traumatic stress disorder represent different clinical and nosographic disorders in despite of their occasionally common symptomatic core. Historically, it is interesting to note during the XXth century the true semantic change of the terms of trauma from the somatic field to the psychic sphere. Physical traumatism is often represented by a material shock for the subject and by its organic consequences. It is defined as an event that leaves its mark which itself inflicts and handicaps the vital trajectory of the subject. It primarily comprises brain and rachis injuries, whose evolution is frequently characterized by the occurrence/appearance of a depressive disorder, whose genesis rests on psychological but also neurobiologic and physical arguments. Thus major depressive disorders are often present in the course of various physical traumatisms mainly related to nervous system. In accordance with several studies, the prevalence of major depressive disorders ranges from 25% to 50%. These mood disorders occur in the year which follows the accidental event. Their average time of revelation is estimated at four months and their average duration lies between three and six months. Lastly, although these depressive illnesses present clinical symptoms comparable with those observed in other contexts, some nuances can be raised. Nonetheless, they confine sometimes with true clinical forms depending on the intensity, the form, the circumstances or the consequences of the trauma. Psychic traumatism doesn't have the same profile and rests for much dedicated with the reexperiencing. Thus for some authors, depression illness represents a disorder that occurs after a traumatic event whereas others see a differential diagnosis which exludes or which represents a comorbidity with post-traumatic stress disorder. The review of the literature allows us to emphasize the complexity of the links as well as the clinical and epidemiologic differences between stress disorder and major depressive disorder. From the clinical point of view, the major features of PTSD are articulated around a triad of symptoms. They include the reexperiencing symptoms of the traumatic event such as intrusive memories and recurrent nightmares, the protective reactions such as avoidance of the stimuli associated with the trauma and emotional numbing, and the arousal symptoms such as the startled response and hypervigilance. The complexity of this syndrom is due to the frequent combination of these symptoms with other nonspecific ones. As far as the mood is concerned (the mood symptoms are concerned), the regrouping of some of these symptoms allows the clinician to sometimes releave a depressive symptomatology without being able to assess the DSM diagnosis of major depressive disorder. Epidemiologic studies dealing with the risk of installation of a PTSD after a traumatic event reveal differences in the prevalence depending on the nature of the traumatic events: ranging from 1% in general population to 80% following some situations of extreme and durable psychic suffering. Between both poles, one finds a prevalence ranging between 20 and 50% following other events such as serious accidents, natural disasters or criminal assaults. The clinical features of depressive episodes comorbid or associated with PTSD have some characteristics making it possible to individualize various clinical forms as a function of traumatic event type: asthenic, characterial or with somatic symptoms. According to the majority of authors, the co-occurrence of post-traumatic stress disorder and major depressive disorder is high although differential diagnosis is sometimes difficult. However, conceptual differences remain and two conceptions are distinguished. For some authors, like Bleich and Shalev, there would not be true chronological evolution from PTSD to MDD. Moreover the presence of symptoms considered as pertaining to the mood register within the criteria of PTSD would be clearly predictive of the occurrence and the severity of the diagnosis but not of the chronicity. For others, there would be a continuity between post-traumatic stress disorder and major depressive disorder. It is the case in many studies of veterans but also for civilian traumatic events. It is also the case for the American national study of comorbidity in which Kessler concludes that for 78% of the subjects who present a comorbidity PTSD/MDD (comorbidity raised for 48% of the 5,877 subjects included), the mood disorder is secondary to PTSD. (ABSTRACT TRUNCATED)
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PMID:[Post-traumatic stress, post-traumatic depression and major depressive episode: literature]. 1140 68

This 6-month open-label study evaluated the efficacy, tolerability, and safety of sertraline in 21 adolescent psychiatric outpatients, ages 12 to 18 years, diagnosed with major depressive disorder (MDD, n = 13) or dysthymic disorder (DD, n = 8). Both groups showed clinically significant improvements on the Hamilton Depression Scale (HAM-D), Hamilton Anxiety Scale, and the Clinical Global Impression Scale-Severity (CGI-S). The MDD group showed maximal clinical response (based on the method of last observation carried forward) on the HAM-D and CGI at weeks 12 (76.9%) and 20 (76.9%), respectively. Response rates were maintained at week 24 with all six MDD study completers (100%) responding to treatment. The DD group achieved maximal response on the HAM-D (100%) and the CGI (75%) at week 6. Response rates in this group did not remain as elevated over time with two out of three (66.7%) DD study completers responding to treatment at week 24. Generally, sertraline was safe and well tolerated. Most adverse events were mild to moderate in severity and resolved with no action taken. Results suggest that sertraline may be efficacious in acute and continuation treatment of MDD in adolescents. DD patients showed evidence of clinical response and improvement, particularly in the acute treatment phase. Incorporating a longer evaluation period in the study of antidepressant therapy for adolescents with MDD and/or DD is emphasized.
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PMID:Sertraline effects in adolescent major depression and dysthymia: a six-month open trial. 1143 52

We describe the successful treatment of five patients with treatment-resistant major depressive disorder (TR-MDD) with a combination pharmacotherapy of pindolol, tryptophan and nefazodone. Five TR-MDD outpatients who had previously not responded to at least four different antidepressant medication trials were initiated on 300 mg/day of nefazodone, 7.5 mg/day of pindolol and 1 g/day of tryptophan. Pindolol doses remained the same throughout the 20 weeks, while tryptophan and nefazodone dosages were gradually increased to 8 g/day and 450 mg/day, respectively. The Hamilton Depression Rating Scale (HAM-D) was used to evaluate outcome. By week 4, all cases demonstrated at least 50% decrease in HAM-D scores. At the end of the trial, the group mean HAM-D score had significantly decreased from 26.8 (+/- 1.9) to 1.8 (+/- 0.8) (p < 0.001). No significant adverse effects were reported. These results suggest that if serotonin availability and release is further enhanced by tryptophan in the presence of nefazodone and pindolol, an antidepressant effect may be produced in patients who are otherwise treatment-resistant. Due to limited sample size, an open design and an 'unusually' high successful efficacy rate of this preliminary study, controlled studies are required to confirm the efficacy of this treatment strategy.
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PMID:The 'dalhousie serotonin cocktail' for treatment-resistant major depressive disorder. 1144 87

Depersonalisation disorder may occur during severe anxiety or following a traumatic event, suggesting a possible role of stress hormones. This study investigated basal activity of the hypothalamic-pituitary-adrenal (HPA) axis in patients with depersonalisation disorder. Salivary cortisol levels were measured at four time points over 12 h in patients with depersonalisation disorder (N=13), major depressive disorder (MDD, N=14) and healthy controls (N=13). Beck Depression Inventory scores were significantly higher in depersonalised subjects than controls, while MDD subjects demonstrated higher scores than both groups. Basal cortisol levels of depersonalised subjects were significantly lower than those of MDD subjects but not healthy controls. These results point to reduced basal activity of the HPA axis in depersonalisation disorder. This pilot study supports the distinction between depersonalisation disorder and major depressive disorder which should be examined in a larger sample.
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PMID:Basal activity of the hypothalamic-pituitary-adrenal axis in patients with depersonalization disorder. 1160 Jan 92

The aim of this study was to measure the effectiveness of ECT in-patients who had failed to respond to a course of repetitive transcranial magnetic stimulation (rTMS) treatment. Seventeen patients with severe MDD who had not responded to a course of rTMS were switched to receive ECT treatments. All the patients were assessed with the Hamilton Rating Scale for Depression, the Global Assessment Functioning Scale, the Global Depression Scale, and the Pittsburgh Sleep Quality Index. Response to the treatment was defined as a 50% decrease in HDRS final score and a final GAS higher than 60. Seven out of 17 patients responded to ECT. Three out of 5 non-psychotics and 4 out of 12 psychotic patients responded. ECT seems to be an effective treatment for 40% of patients who failed to respond to rTMS treatment. Whether this is a result of reduced responsiveness to ECT in rTMS-resistant patients or a consequence of small sample size requires further study.
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PMID:Effect of electroconvulsive therapy in repetitive transcranial magnetic stimulation non-responder MDD patients: a preliminary study. 1160 32

The authors examined patterns of improvement in quality of life (QOL) in elderly patients with recurrent major depression (MDD) after acute treatment. One hundred elderly (age 60-88 years) patients with recurrent MDD were randomized to receive either bupropion sustained-release (100 mg-300 mg/day) or paroxetine (10 mg-40 mg/day) for 6 weeks. Treatment with both paroxetine and bupropion was associated with improvements in QOL. Lower perceived Physical- and Social-Functioning QOL ratings at baseline were associated with lower treatment response. Improvement in depression symptom ratings correlated significantly with improvement in QOL on many domains, but accounted for less than one-quarter of the total variance. Remitters showed significantly (P<0.001) greater improvement than both Partial Responders and Nonresponders on various measures. Findings support the importance of treating elderly depressed patients to full remission to maximize impact on both emotional and physical QOL domains.
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PMID:Quality of life in geriatric depression: a comparison of remitters, partial responders, and nonresponders. 1173 69


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