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Query: UMLS:C0011570 (depression)
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The increased risk of physical health problems in adult depressed patients has been shown in numerous studies. A recent study of the offspring of depressed parents found similar associations. The purpose of this study is to examine the strength and specificity of the association between depression and physical health problems in children and adolescents whose parents are dependent upon opiates. The sample consisted of offspring ages 6-17 (mean age 11 years) of opiate addicts who had a history of major depressive disorder (MDD; n = 28); other mood disorders (n = 31); no history of mood disorders but other psychiatric disorders (n = 92); or no history of psychiatric disorder (n = 127). Detailed psychiatric assessment and medical history of the offspring by direct interview with the offspring and an informant were obtained blind to parental diagnosis. After controlling for possible confounders, there was an increased risk of dermatological disorders, headache, other neurological/neuromuscular disorders, bronchitis, other respiratory disorders and hospitalizations for nonsurgical procedures in offspring with MDD, as compared to nonpsychiatrically ill controls. The offspring with other mood disorders had a slightly elevated risk. Major depression in children and adolescents whose parents are dependent on opiates is associated with increased risk of physical health problems. This finding is consistent with other reports and the timing of the physical health problems requires further study.
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PMID:Physical health problems in depressed and nondepressed children and adolescents of parents with opiate dependence. 1020 60

Overlap between depression scale item content and medical symptoms may exaggerate depression estimates for patients with multiple sclerosis (MS). We reconsider Mohr and co-workers' (1997) recommendation to omit Beck Depression Inventory (BDI) items assessing work ability (item 15), fatigue (17), and health concerns (20) for MS patients. Subjects were medical patients with either MS (n = 105) or a medical disorder for which the BDI is empirically supported [diabetes mellitus (DM), n = 71; chronic pain (CP), n = 80], psychiatric patients with depressive disorder (MDD; n = 37), and healthy controls (HC; n = 80). Relative scores for the eight "somatic" BDI items were analyzed by multivariate analysis of variance with demographic variables and BDI total as covariates. The only significant difference was MS > HC (item 15). On raw scores, MS patients exceeded HCs on items 15 and 21 (sexual disinterest), but this was attributable to the low HC item endorsement. There were no other differences on somatic items or item-total correlations. Scale consistency was good across groups, regardless of item omission. Somatic items were unassociated with major MS parameters. We thus encourage continued application of the full BDI for assessing depressive symptoms in patients with MS.
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PMID:Assessing depressive symptoms in multiple sclerosis: is it necessary to omit items from the original Beck Depression Inventory? 1037 39

Differential risk factors for the onset of depression were prospectively examined in a community-based sample of adolescents (N = 1,709), some of whom had a history of major depressive disorder (MDD; n = 286) and some of whom did not (n = 1,423). From the theories of J. Teasdale (1983, 1988) and R. Post (1992) concerning the etiology of initial versus recurrent episodes of depression, the authors hypothesized that (a) dysphoric mood and dysfunctional thinking styles would be correlated more highly among those with a previous history of MDD than among those without a history of MDD; (b) dysphoric mood or symptoms and dysfunctional thinking would be a stronger predictor of onset of recurrent episodes (n = 43) than of first onsets (n = 70); and (c) major life stress would be a stronger predictor of first onsets of MDD than of recurrent episodes. The results provide support for the 3 hypotheses and suggest that distinct processes are involved in the onset of first and recurrent episodes of MDD.
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PMID:First onset versus recurrence of depression: differential processes of psychosocial risk. 1046 72

Although an increased recognition of depressive disorders in youth represents a positive conceptual change over the past decades, there still is a very limited amount of research on useful treatment interventions. The paucity of data is particularly keen for the use of psychotropic drugs. For example, by applying the criteria suggested by the International Psychopharmacology Algorithm Project, there barely are enough first-grade ("Level A," meaning at least two RCTs) data supporting the short-term efficacy of antidepressants (the SSRIs) in the treatment of juvenile depression. And yet, limited data have not translated into limited use in routine clinical practice. In fact, the use of antidepressant medications has increased exponentially over the last decade, a change that is especially conspicuous for individuals less than 18 years of age. The perceived safety of the SSRIs and other novel antidepressants is partly at the root of their increased popularity. Data regarding their safety are likewise quite limited, however, and essentially are nonexistent for longer-term use. Based on the reviewed data, a medication algorithm for the treatment of early-onset depression can be suggested (Fig. 1). The algorithm underscores the need for adequate evaluation and diagnostic assessment, with particular attention to comorbid conditions (such as a bipolar diathesis) that may dictate alternative treatment strategies. In general, psychotherapy is the initial approach to juvenile MDD, with medication use reserved for more severe cases or those not responding to psychotherapy alone. Given that only two types of psychotherapy and two SSRIs have adequate controlled short-term efficacy data, all but the initial steps must be undertaken guided by clinical judgment and an individualized risk-benefit analysis. An algorithm such as this one, based on the very limited efficacy and safety data available, may be viewed as setting priorities for a comprehensive research agenda, more than dictating rigid treatment guidelines. In closing, it can be suggested that future research on the pharmacotherapy of early-onset depressive disorder pay particular attention to the following three aspects: 1. Too many drugs, too few data: Rapid advances in drug development have led to a plethora of available antidepressant agents. It is clear that there are many more agents available than can be adequately studied at present. Because many such agents are mechanistically similar, if not identical, it may be wise to focus research efforts on truly novel agents, particularly those (such as the CRH receptor antagonists, or those affecting neurosteroidogenesis) whose action is based on preclinical and clinical pathophysiologic disease paradigms. 2. Longitudinal follow-up and maintenance studies: Essentially all reviewed treatment studies have been short-term trials. There is a marked paucity of longer-term follow-up data, or of naturalistic and "real-world" effectiveness studies. For example, one of the few studies addressing maintenance pharmacotherapy for early-onset depression has demonstrated surprisingly high recurrence rates, even for those subjects actively on maintenance medication. 3. Long-term safety: Clinicians and parents alike often face difficult decisions regarding the long-term exposure of antidepressant drugs on the developing brain. Although no definitive long-term safety data are likely to become available anytime soon, real risks, such as suicide, and potential sequelae of long-term exposure to the underlying illness itself need all to be part of any decision-making process. Preclinical studies have shown that brain-derived neurotrophic factor (BDNF) levels can be upregulated by antidepressants, and low BDNF factors have been associated with atrophic brain changes in recurrent forms of adult MDD. Although these observations require specific application to juvenile forms of the disorder, they raise the exciting prospect that the natural course of the illne
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PMID:Pharmacotherapy of early-onset depression. Update and new directions. 1067 94

Recent studies have found high rates of familial aggregation of major depression (MDD) in relatives of depressed children coming for treatment, leading investigators to suggest that probands for genetic studies of MDD should be selected from samples of depressed children being brought for treatment. Implicit in this recommendation is the assumption that childhood and adult depression are similar disorders. This assumption in turn implies that children with prepubertal or adolescent onset depression are at high risk for having recurrent episodes of MDD that continue into adulthood. The data supporting this latter hypothesis, however, is limited and contradictory. In this article we report results from a high-risk longitudinal family study in which we explored the recurrence and continuity into adulthood of prepubertal or adolescent onset MDD in offspring who were at high or low risk for MDD, by virtue of their parental depression status. One hundred eighteen offspring from 55 families in which one or more parents had MDD and 50 offspring from 21 families in which neither parent had MDD were followed for more than 10 years (all offspring were 20 years or older at the end of follow-up time) and blindly reassessed using a semistructured diagnostic instrument. Offspring with childhood/adolescent onset MDD were at significantly greater risk for recurrence in adulthood (after age 25) as compared with offspring without an onset of childhood/adolescent MDD, if they had a history of parental MDD. In contrast, among offspring without a history of parental MDD, those with childhood/adolescent onset MDD were at no greater risk for continuing to have MDD in adulthood (after age 25) than those without childhood/adolescent onset MDD. Moreover, there was a trend for offspring with childhood/adolescent onset MDD to be at greater risk for recurrence after age 25 if they had a history of parental MDD, as compared with offspring without a history of parental MDD (60 vs. 18%). We conclude that childhood/adolescent onset MDD is a heterogeneous disorder, with family history of MDD appearing to define a subtype of childhood/adolescent onset MDD that is recurrent and continues into adulthood. Our findings suggest that caution should be exercised in selecting depressed children and adolescents brought for treatment as probands in genetic studies of early onset MDD. A conservative strategy would be to select only those depressed children and adolescents with a family history of MDD and reassess the treated sample as they mature, ensuring that they go on to have MDD in adulthood. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:93-101, 2000
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PMID:Selecting early onset MDD probands for genetic studies: results from a longitudinal high-risk study. 1068 60

Major depression (MDD) following traumatic brain injury (TBI) is a common phenomenon. There are no adequate studies in the literature defining optimum treatments for this condition following TBI. The opportunity arose to analyse a group of patients who were included in a larger study of an antidepressant (moclobemide). As the treatment, but not the delivery, was known, this has the status of an open study. Twenty-six patients with major depression of late onset (mean 4.67 years post-TBI) were identified (18 male, 8 female), with a mean age at injury 28.49 years. The group was moderately depressed with Hamilton Depression score (HAM-D) of 23.385 and moderately anxious with Hamilton Anxiety score (HAM-A) of 21.231. Mean HAM-D reduction was 81% and HAM-A reduction 81%. Of the 26 subjects 23 were defined as responders. Onset of action was rapid, with 17 responding by day 3. Irritability scores showed a mean reduction of 57% and pain scores a reduction of 39%. It is concluded that moclobemide may be an effective treatment for MDD following TBI, but properly controlled studies must be carried out to confirm this.
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PMID:Moclobemide in the treatment of major depressive disorder (DSM-3) following traumatic brain injury. 1090 91

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


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