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

In this article, we systematically reviewed the results of application of biological markers of depression to children and adolescents. Concerning sleep EEG, only three studies on a total of twelve among 267 depressed children and adolescents aged 6 to 19 years found the typical sleep abnormalities described in depressed adults (eg, shortened REM latency and decreased sleep efficiency). Most authors insisted on the age-related sleep changes as a major confounding factor. Two studies of the effect of antidepressant therapy on sleep showed a decrease in sleep efficiency but a discrepancy in the evolution of REM latency. Concerning the dexamethasone suppression test, twenty studies including 374 depressed children and adolescents (3-20 years) and 533 psychiatric controls yielded an overall sensitivity of 57% and an overall specificity of 78%. These results may be considered as interesting, despite the lack of agreement among authors on various methodological parameters (dose of dexamethasone, times of blood sampling, method of cortisol assay ...) and the composition of control groups which often comprise subjects presenting disorders very close to major depression (dysthymia, minor depression ...). Among the other tests, the TRH test, used in two studies, showed limited interest. In contrast, the study of growth hormone secretion, performed in one centre, could present diagnostical usefulness. In conclusion, biological markers of depression in children and adolescents should still be considered as research tools and be part of a multidisciplinary approach to depressive illness.
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PMID:[Value of sleep and neuroendocrine tests as biological markers of depression in children and adolescents]. 178 92

In order to assess the predictive value of somatic and biological factors in antidepressant trials, non specific parameters, i.e. natural course of illness, life events, placebo effect ... have to be controlled by means of studies vs placebo. Among somatic factors, retardation seems to predict a positive response to antidepressants. The predictive value of other endogenous signs--like insomnia or weight loss--is still questioned. Few biochemical parameters appear relevant when metabolites of central monoamines, their precursors and the enzymatic processes involved are considered. The serotoninergic system is the focus of many studies. Among the neuroendocrine indices, the DST proved too poorly specific of depression. Among the physiological parameters, some characteristics of sleep EEG, like a shortening of REM latency, seem promising. Pharmacological challenges, for instance response to stimulant drugs, gave inconsistent results and should be discussed on ethical grounds. Many studies have been undertaken but presently no routine reliable biological index is available to predict a response to antidepressants.
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PMID:[Somatic and biological factors predicting a response to antidepressive agents]. 180 63

Sleep EEG and neuroendocrine disturbances have been described in the acute phase of affective illness. The question arises as to whether these biological marker disturbances are state- or trait-related. This important issue can be addressed by evaluating changes in sleep EEG and neuroendocrine parameters from a chronobiological approach before and after antidepressant treatment. Among the circadian variables explored in affectively ill patients are REM sleep and slow wave sleep, as well as circadian secretion of plasma GH, cortisol, ACTH and prolactin. Our studies show that depressed patients mainly of the unipolar type secrete more GH and cortisol during the circadian period than control subjects do. GH hypersecretion appears mainly during wakefulness while cortisol hypersecretion is observed during the 24 h space. Temporal disorganization of hormonal secretion is also present since an advance of the quiescent period of the ACTH-cortisol rhythm as well as pre-sleep GH spikes were described in our depressed unipolar patients before treatment. After antidepressive treatment, these chronobiological anomalies tend to normalize, as state biological markers. These observations are giving support to the phase-advance hypothesis of depression.
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PMID:Sleep-related chronobiological markers of affective illness. 184 28

By means of a review of genetic, biological and neurophysiological studies, we attempted to validate the DSM III-R depressive disorder categories. Genetic studies support the distinction between bipolar and recurrent major (unipolar) depression although genetic heterogeneity and variable phenotypic expressivity have been suggested in bipolar depression. Biological and neuroendocrine abnormalities in depression seem to relate more to a particular symptomatological profile than to a specific depressive subtype including the bipolar-unipolar dichotomy. For example, catecholamines and serotonin metabolism seem to reflect respectively psychomotor status and aggressiveness in depression. Using genetic and biological criteria, major depression with psychotic features is the best validated category of the four main DSM-R major depressive subclasses or specifications (psychotic, chronic, melancholic, seasonal). Psychotic depression seems to constitute the most coherent subgroup and biological abnormalities such as dexamethasone non suppression and shortened REM latency are very often observed. An important confounding variable in these biological validation studies is the severity of the depressive state. Psychotic depression is considered to be a more severe depressive subtype and also shows marked biological disturbances. Conversely, in seasonal depression, a less severe depressive subtype, CSF monoamine metabolism abnormalities, dexamethasone non suppression and shortened REM latency could not clearly be demonstrated. Genetic studies show that early onset dysthymia and cyclothymia could be part of the affective spectrum and some maintain that these two clinical entities are attenued forms of bipolar or recurrent major depression.
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PMID:[Biological psychiatry and current classifications of depressive disorders]. 186 51

The EEG sleep of 75 subjects aged 16-25 years was studied. Thirty-eight were in an episode of RDC major depression, and 37 were normal controls. Only one sleep continuity measure differed between the two groups: sleep latency was significantly longer in the depressive group. REM period latencies and other sleep variables did not differ between the groups. Subgroup analyses, within the depressed group with respect to inpatient status, revealed significantly higher REM density (P less than 0.03) and a marginally shortened REM period latency (P less than 0.07) among the inpatient depressives. Subgroup analysis across suicidal ratings revealed a significantly higher REM density (P less than 0.04) among suicidal depressives. Severity estimates of depression did not correlate with sleep findings. These results parallel another recent report on adolescent depressed subjects, suggesting that inpatient and/or suicidal status is an important variable in the expression of EEG sleep abnormalities in the adolescent/young adult age group.
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PMID:EEG sleep of young adults with major depression: a controlled study. 188 Mar 13

It is not in the best interest of persons with epilepsy to deny the possibility that seizures could cause enduring behavioral disturbances. Rather, it is essential to pursue clinical and animal investigations in order to identify any such changes that might occur and to elucidate their mechanisms. Many testable hypotheses can be developed from existing evidence. Antiepileptic medication may produce interictal behavioral disturbances in patients with epilepsy by indirect mechanisms. Some aberrant behaviors could be due to medication-induced systemic disorders, neuroendocrine dysfunction, or REM deficit, whereas depression following successful treatment with drugs, as well as with surgery, may be related more specifically to cessation of seizures. The underlying neuropathological process also induces neurological and mental deficits, but it is not always possible to differentiate those behavioral disturbances due to destructive effects of the lesion from those due to recurrent epileptic seizures. Behavioral disturbances are associated more frequently with epileptogenic lesions in limbic structures than with those elsewhere in the brain, but a relationship between hemispheric lateralization of the epileptogenic lesion and specific interictal behavioral symptoms remains controversial. When considering the effects of seizures per se on interictal behavior, it is important to realize that some "interictal" behavioral disturbances may actually be ictal events. Prolonged affective, autonomic, and psychic disturbances can occur in clear consciousness with unilateral limbic seizures that are not associated with scalp EEG changes. When epilepsy is acquired as a result of cerebral damage, the epileptogenic process takes time to develop before spontaneous seizures appear. It is more reasonable to assume that this progressive process continues than to postulate that it stops completely at the time the first seizure occurs. Epilepsy-induced protective homeostatic mechanisms that act to terminate ictal events, prevent ictal spread, and maintain the interictal state may also disrupt interictal function. Furthermore, seizures could indirectly influence interictal behavior as a result of their effects on neuroendocrine function and sleep. Because of confounding biological factors, it is difficult to document the association of any epilepsy disorder, by itself, with progressive behavioral disturbances in humans. Secondary epileptogenesis, protective homeostatic mechanisms, and epilepsy-induced disturbances in development can be readily demonstrated, however, in experimental animal models. In experimental animals, endogenous opoids are released during seizures and mediate some postictal behaviors. A physiological dependency on high levels of endogenous opioids released during seizures could produce depression as a withdrawal symptom interictally or when seizures no longer occur as a result of successful therapy. Experimental animal models of depression exist to test hypotheses concerning pro- and antidepressant effects of epileptogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurobiological evidence for epilepsy-induced interictal disturbances. 200 26

A subgroup of bipolar affective psychoses is characterized as rapid cycling affective disorder with at least four affective episodes resp. two bipolar cycles per year, including cycles of 48 hours ("ultra-rapid-cycling"). We show that rapid cycling-syndromes but not ultra rapid cycling-syndromes are comparable to traditional cyclothymic psychoses with respect to psychopathology, sex distribution, age of onset, REM sleep parameters and neuroendocrinological findings. Rapid cycling-syndromes exhibit acute switches, a peculiar coherence of course and intensity and a atypical combination of depression and hypersomnia. Ultra rapid cycling-syndromes are psychopathologically closely linked to some hypo- und hyperphases of endogenous psychoses. Like seen through a window they represent phenomena of syndromal shifting and can be related to organic dienzephaloses. They verify experiences of the sleep deprivation therapy that show the most sensitive night time for shifting being that between 1 and 3 o'clock a.m. The meaning of the drug induced rapid cycling may be overrated. The differential diagnosis includes various symptomatic affective psychoses as well as catatonic schizophrenic syndromes. Pathogenetic ideas discuss disorders of the pituitary dienzephalic regulation.
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PMID:[Biological findings in rapid cycling syndromes]. 200 6

Although the clinical interview retains a central role in psychiatric diagnosis, recent research has suggested that "biological markers" may ultimately increase the precision of clinicians' nosologic and therapeutic decisions. Evaluating and operationalizing diagnostic tests require mathematical techniques that reflect the tests' essential features and limitations, and that guide clinicians in particular clinical situations. In this article we describe a technique that combines signal detection theory and utility-based decision theory, and apply the technique to published data in which sleep architecture was used as a biological marker for depression. We show how outcome utilities influence the optimum REM latency cut-off and show how this relationship is influenced by the prevalence of depression in the population being tested. We also make specific calculations of the practical limits that must be imposed on uncertainties in utilities to operationalize a diagnostic test for a specific clinical situation.
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PMID:"Biological markers" and psychiatric diagnosis: risk-benefit balancing using ROC analysis. 205 54

Fluoxetine (60 mg), a selective inhibitor of the reuptake of 5-HT, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 34 patients fitting the Research Diagnostic Criteria for a major depressive disorder. Patients were studied after a drug washout period of 10 days and an active treatment period of 42 days. Sleep polygraphic recordings were performed before and at the end of the study. As indicated by the significant decrease in the Hamilton Depression scale and the Montgomery Asberg Depression scale, fluoxetine showed similar antidepressant effects to amitriptyline with significantly fewer adverse effects. Fluoxetine and amitriptyline decreased the amount of REM sleep, a well known effect of classical antidepressants. Fluoxetine showed some specific effects on sleep continuity (potentially dose related) as indicated by the significant increase in the number of awakenings and in stage shifts, without interfering with the therapeutic response.
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PMID:Fluoxetine in major depression: efficacy, safety and effects on sleep polygraphic variables. 208 96

This study was designed to compare the antidepressant effects of alprazolam and amitriptyline in a group of 30 inpatients suffering from a severe major endogenous depression, diagnosed by Research Diagnostic Criteria and the Newcastle Rating scale, and to examine the effects of alprazolam and amitriptyline on two biological markers of depression, the dexamethasone suppression test and sleep EEG parameters. The 6-week study was double-blind with a random allocation of treatment. Patients were treated with flexible doses of 4-9 mg of alprazolam and 100-225 mg of amitriptyline. After 4 weeks of treatment the antidepressant effects of amitriptyline significantly exceeded those of alprazolam, as measured on the Hamilton Rating Scale for Depression. There was a high drop-out rate in the alprazolam group because of ineffectiveness of treatment. Alprazolam showed similar effects on sleep parameters as amitriptyline: lengthening of the REM latency and a tendency to shorten stages 3 and 4 and stage REM. These negative clinical results should be interpreted with caution, because of the severity of our selection criteria, and should not be extended to all depressive disorders.
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PMID:Alprazolam and amitriptyline in the treatment of major depressive disorder: a double-blind clinical and sleep EEG study. 213 71


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