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Atypical depression spectrum disorder – neurobiology and treatment
- Harald Murck
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- Journal:
- Acta Neuropsychiatrica / Volume 15 / Issue 4 / August 2003
- Published online by Cambridge University Press:
- 24 June 2014, pp. 227-241
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- Article
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Depressive syndromes are a group of heterogeneous disorders. Atypical depression (AD) with reversed vegetative signs, such as hyperphagia or hypersomnia, is traditionally neglected, demonstrated by the fact that in the most widely used depression scales, such as the Hamilton Depression Scale (HAMD), melancholic symptoms have a specific weight, while, by contrast, reversed vegetative signs are not included. However, epidemiologically and phenomenologically related disorders to AD do exist, such as somatoform disorders, neurasthenia (chronic fatigue syndrome) and fibromyalgia (FM). In this spectrum, here called the AD spectrum, instead a decrease in hypothalamus–pituitary–adrenocortical (HPA) axis activity seems to exist. This has similarities to Cushing's disease, where a suppression of central HPA system activity is accompanied by features of AD and somatization in a considerable number of patients. Opposite vegetative features might therefore be related to the opposite dysregulation of the HPA system. The psychopharmacological intervention in the AD spectrum should therefore differ from that used in typical major depression. MAO inhibitors, low-dose tricyclic antidepressants and 5-HT3 antagonists demonstrated therapeutic efficacy, but the existing studies focused on different aspects. Hypericum extracts might be an alternative pharmacological intervention, which demonstrated therapeutic efficacy in the symptom range of the spectrum.
38 - REM sleep in patients with depression
- from Section V - Functional significance
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- By Axel Steiger, Max Planck Institute of Psychiatry, Germany, Harald Murck, Philipps-University of Marburg, Germany
- Edited by Birendra N. Mallick, Jawaharlal Nehru University, S. R. Pandi-Perumal , Robert W. McCarley, Harvard University, Massachusetts, Adrian R. Morrison, University of Pennsylvania
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- Book:
- Rapid Eye Movement Sleep
- Published online:
- 07 September 2011
- Print publication:
- 14 July 2011, pp 383-394
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Summary
Summary
Disinhibition of REM sleep is a characteristic finding in patients with major depression. REM disinhibition includes shortened REM latency, prolonged first REM periods, and increased REM density (measure of the frequency of rapid eye movements). REM latency, but not REM density, is influenced by age. REM-sleep changes appear to be closely related to the development and the course of depression. A relationship between REM-sleep changes before treatment and treatment outcome is suggested by several studies. REM density is elevated in healthy subjects who have a high genetic load for affective disorders. Most antidepressants suppress REM sleep in patients, normal controls, and laboratory animals. REM-sleep suppression appears to be a distinct hint for the antidepressive properties of a substance, whereas it is not absolutely required. REM-sleep variables during treatment with antidepressants appear to predict the course of the illness. The noradrenergic locus coeruleus and the serotonergic dorsal raphe nuclei, the cholinergic nuclei, and the nucleus of the solitary tract (NTS) are involved in sleep and mood regulation. Hyperaldosteronism has been demonstrated in major depression. Subchronic aldosterone administration can induce anxiety-like behavior. Because of the unusual presence within the brain of both mineralocorticoid receptors and 11-β hydroxysteroid dehydrogenase (11-β HSD), the NTS can act as the gate of the influence of peripheral aldosterone into the brain. Importantly, aldosterone secretion is closely related to the REM/non-REM cycle and is sensitive to sleep manipulations. Hypersecretion of corticotropin-releasing hormone (CRH), the key hormone of the hypothalamo–pituitary–adrenocortical system appears to participate in the pathophysiology of REM-sleep disinhibition. This is supported by increased time spent in REM sleep in mice overexpressing corticotropin-releasing hormone (CRH) in the brain. Furthermore CRH-receptor-type 1 antagonism seems to induce normalization of the REM-sleep changes related to the depression.
Chapter 23 - Magnesium and major depression
- from Section 3 - Involvement of Magnesium in Psychiatric Diseases
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- By George A. Eby III, George Eby Research Institute, 14909-C 2109 Paramount Avenue, Austin, Texas 78704, USA.; george.eby “at” george-eby-research.com, Karen L. Eby, George Eby Research Institute, 14909-C 2109 Paramount Avenue, Austin, Texas 78704, USA, Harald Murck, Clinic of Psychiatry and Psychotherapy, University of Marburg, 35043 Marburg, Germany
- Edited by Robert Vink, University of Adelaide, Mihai Nechifor, University of Medicine and Pharmacy, Iasi, Romania
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- Book:
- Magnesium in the Central Nervous System
- Published by:
- The University of Adelaide Press
- Published online:
- 05 June 2012
- Print publication:
- 01 June 2011, pp 313-332
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Summary
Abstract
The treatment of major depression is still a major unmet medical need in the majority of patients. Sixty percent of cases of MD are treatment-resistant depression (TRD), showing that classical treatments for MD are poorly effective to non-effective. Magnesium has been largely removed from processed foods, especially refined grains, in the Western world harming the brain and causing mood disorders. Magnesium deficiency causes N-methyl-D-aspartate (NMDA) coupled calcium channels to be biased towards opening which causes neuronal injury and neurological dysfunction, which we believe results in MD. Oral administration of Mg to animals produced antidepressant-like effects that were comparable to those of antidepressant drugs. Cerebral spinal fluid (CSF) Mg has been found low in suicidal TRD. The first report of Mg treatment for agitated depression was published in 1921 showing success in 220 out of 250 cases. One 2008 randomized clinical trial showed that Mg was as effective as the tricyclic antidepressant imipramine in treating MD. Intravenous and oral Mg protocols have been reported to rapidly terminate MD safely and without side effects. Brain Mg deficiency reduces serotonin levels, and antidepressant drugs have been shown to have the action of raising brain Mg. Excessive calcium, glutamate and aspartate intake can greatly worsen MD. We believe that – when taken together – there is more than sufficient evidence to implicate inadequate dietary Mg as contributing to the cause of MD, and we suggest that physicians prescribe Mg for its prevention and treatment.