Mood disorders

2012 ◽  
pp. 205-253 ◽  
Author(s):  
Philip Cowen ◽  
Paul Harrison ◽  
Tom Burns
Keyword(s):  
Differential Diagnosis ◽  
Mood Disorders ◽  
Clinical Features ◽  
Acute Treatment ◽  
Depressive Disorders ◽  
Treatment Strategies ◽  
Term Treatment ◽  
Treatment Of Depression ◽  
Manic Patients

Chapter 10 discusses mood disorders, including clinical features, transcultural features, classification and differential diagnosis, epidemiology and aetiology, course and prognosis, acute treatment of depression and mania, longer-term treatment strategies, assessment and management of depressive disorders, assessment of mania, and management of manic patients.

Long-Term Treatment of Depression

1994 ◽  
Vol 165 (S26) ◽  
pp. 31-36 ◽  
Author(s):  
Stuart A. Montgomery
Keyword(s):  
Acute Treatment ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Term Treatment ◽  
Recurrent Depression ◽  
Recurrence Prevention ◽  
Treatment Of Depression ◽  
Long Term Treatment ◽  
Effective Doses ◽  
Therapeutic Doses

Long-term treatment of depression encompasses two separate phases: relapse and recurrence prevention. Relapse prevention aims to consolidate the response to acute treatment. Some tricyclic antidepressants (TCAs) have been shown to be effective, possibly in lower than standard acute treatment doses. The selective serotonin reuptake inhibitors (SSRIs) have been shown to be effective at the same minimum effective doses used to treat acute depression, or in a lower dose as with citalopram. Recurrence prevention aims to reduce the risk of onset of a new episode of depression in patients with recurrent depression. Imipramine has been thoroughly studied in unipolar depressed patients in full therapeutic doses for up to five years and is clearly effective. Other TCAs have not been adequately tested and may not all be equally effective. The SSRIs fluoxetine, paroxetine and sertraline have also been shown to be effective in reducing the risk of new episodes of depression.

scholarly journals The NMDA receptor and new possibilities in antidepressant therapy

2018 ◽  
Vol 72 ◽  
pp. 788-794
Author(s):  
Weronika Stasiuk ◽  
Monika Prendecka ◽  
Krzysztof Chara ◽  
Teresa Małecka-Massalska
Keyword(s):  
Nmda Receptor ◽  
Affective Disorders ◽  
Depressive Disorders ◽  
Treatment Strategies ◽  
Antidepressant Effect ◽  
Antidepressant Medications ◽  
Treatment Of Depression ◽  
Potential Alternative ◽  
Disorder Treatment

Due to the inadequate effectiveness of pharmacological methods currently being utilized in the treatment of depression, there is an ongoing need to find newer and safer treatment strategies. Studies undertaken to date aimed at finding more effective methods for the treatment of affective disorders have been widened to incorporate other neurotransmission systems. Experiments with compounds that modify the function of the glutamatergic system highlight a new direction in the study of affective disorder treatment methods. It has been shown that one of the key mechanisms in achieving an antidepressant effect is by weakening the function of the NMDA receptor. Pre-clinical as well as clinical trials have revealed that compounds that modulate the activity of the NMDA receptor are characterized by a significant antidepressant effect which identifies them as potential antidepressant medications. In this study an attempt was made at identifying the role of the NMDA receptor in the pathogenesis and therapy of depressive disorders as well as the influence of ligands (especially antagonist) of this receptor on the function of classical antidepressant medications. Results shown in the attached studies by numerous scientists will in the future potentially add to the development of more effective and safer therapies for patients with affective disorders as well as offering a potential alternative in the treatment of drug resistant forms of depression.

scholarly journals Animal Models of Depression: What Can They Teach Us about the Human Disease?

Diagnostics ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 123
Author(s):  
Maria Becker ◽  
Albert Pinhasov ◽  
Asher Ornoy
Keyword(s):  
Animal Models ◽  
Mood Disorders ◽  
Learned Helplessness ◽  
Acute Treatment ◽  
Brain Injuries ◽  
Adult Population ◽  
Psychiatric Disease ◽  
Human Situation ◽  
Animal Models Of Depression ◽  
Treatment Of Depression

Depression is apparently the most common psychiatric disease among the mood disorders affecting about 10% of the adult population. The etiology and pathogenesis of depression are still poorly understood. Hence, as for most human diseases, animal models can help us understand the pathogenesis of depression and, more importantly, may facilitate the search for therapy. In this review we first describe the more common tests used for the evaluation of depressive-like symptoms in rodents. Then we describe different models of depression and discuss their strengths and weaknesses. These models can be divided into several categories: genetic models, models induced by mental acute and chronic stressful situations caused by environmental manipulations (i.e., learned helplessness in rats/mice), models induced by changes in brain neuro-transmitters or by specific brain injuries and models induced by pharmacological tools. In spite of the fact that none of the models completely resembles human depression, most animal models are relevant since they mimic many of the features observed in the human situation and may serve as a powerful tool for the study of the etiology, pathogenesis and treatment of depression, especially since only few patients respond to acute treatment. Relevance increases by the fact that human depression also has different facets and many possible etiologies and therapies.

Reconsidering NMIHBA Core Features: Macrocephaly Is Not a So Unusual Sign in PRUNE1-Related Encephalopathy

2020 ◽  
Author(s):  
Roberta Battini ◽  
Enrico Bertini ◽  
Roberta Milone ◽  
Chiara Aiello ◽  
Rosa Pasquariello ◽  
...  
Keyword(s):  
Nervous System ◽  
Differential Diagnosis ◽  
Clinical Features ◽  
Neurodevelopmental Disorder ◽  
Recurrent Mutation ◽  
Clinical Suspicion ◽  
Alexander Disease ◽  
Brain Anomalies ◽  
Progressive Encephalopathy ◽  
Core Features

Abstract PRUNE1-related disorders manifest as severe neurodevelopmental conditions associated with neurodegeneration, implying a differential diagnosis at birth with static encephalopathies, and later with those manifesting progressive brain damage with the involvement of both the central and the peripheral nervous system.Here we report on another patient with PRUNE1 (p.Asp106Asn) recurrent mutation, whose leukodystrophy, inferior olives hyperintensity, and macrocephaly led to the misleading clinical suspicion of Alexander disease. Clinical features, together with other recent descriptions, suggest avoiding the term “microcephaly” in defining this disorder that could be renamed “neurodevelopmental disorder with progressive encephalopathy, hypotonia, and variable brain anomalies” (NPEHBA).

Depressive Disorders in Old Age: Clinical Features and Course

Psychiatry ◽  
2019 ◽  
Vol 17 (3) ◽  
pp. 87-97
Author(s):  
Tatyana P. Safarova ◽  
Keyword(s):  
Old Age ◽  
Clinical Features ◽  
Depressive Disorders

Ketamine Treatment in Depression: A Systematic Review of Clinical Characteristics Predicting Symptom Improvement

2020 ◽  
Vol 20 (15) ◽  
pp. 1398-1414 ◽  
Author(s):  
Darby J.E. Lowe ◽  
Daniel J. Müller ◽  
Tony P. George
Keyword(s):  
Clinical Features ◽  
Clinical Characteristics ◽  
Bipolar Depression ◽  
Antidepressant Effect ◽  
Future Research ◽  
Symptom Improvement ◽  
Randomized Controlled ◽  
Treatment Of Depression ◽  
Future Direction

Ketamine has been shown to be efficacious for the treatment of depression, specifically among individuals who do not respond to first-line treatments. There is still, however, a lack of clarity surrounding the clinical features and response periods across samples that respond to ketamine. This paper systematically reviews published randomized controlled trials that investigate ketamine as an antidepressant intervention in both unipolar and bipolar depression to determine the specific clinical features of the samples across different efficacy periods. Moreover, similarities and differences in clinical characteristics associated with acute versus longer-term drug response are discussed. Similarities across all samples suggest that the population that responds to ketamine’s antidepressant effect has experienced chronic, long-term depression, approaching ketamine treatment as a “last resort”. Moreover, differences between these groups suggest future research to investigate the potential of stronger efficacy towards depression in the context of bipolar disorder compared to major depression, and in participants who undergo antidepressant washout before ketamine administration. From these findings, suggestions for the future direction of ketamine research for depression are formed.

Neurobiological Reward-Related Abnormalities Across Mood Disorders

2019 ◽  
pp. 222-238
Author(s):  
Alexis E. Whitton ◽  
Michael T. Treadway ◽  
Manon L. Ironside ◽  
Diego A. Pizzagalli
Keyword(s):  
Decision Making ◽  
Mood Disorders ◽  
Treatment Strategies ◽  
Reward Processing ◽  
Reward Learning ◽  
Symptom Presentation ◽  
Psychiatric Symptomatology ◽  
Symptom Dimensions ◽  
Psychotherapeutic Interventions ◽  
Primary Focus

This chapter provides a critical review of recent behavioral and neuroimaging evidence of reward processing abnormalities in mood disorders. The primary focus is on the neural mechanisms underlying disruption in approach motivation, reward learning, and reward-based decision-making in major depression and bipolar disorder. Efforts focused on understanding how reward-related impairments contribute to psychiatric symptomatology have grown substantially in recent years. This has been driven by significant advances in the understanding of the neurobiology of reward processing and a growing recognition that disturbances in motivation and hedonic capacity are poorly targeted by current pharmacological and psychotherapeutic interventions. As a result, numerous studies have sought to test the presence of reward circuit dysfunction in psychiatric disorders that are marked by anhedonia, amotivation, mania, and impulsivity. Moreover, as the field has increasingly eschewed categorical diagnostic boundaries in favor of symptom dimensions, there has been a parallel rise in studies seeking to identify transdiagnostic neural markers of reward processing dysfunction that may transcend disorders. The thesis of this chapter is twofold: First, evidence indicates that specific subcomponents of reward processing map onto partially distinct neurobiological pathways. Second, specific subcomponents of reward processing, including reward learning and effort-based decision-making, are impaired across different mood disorder diagnoses and may point to dimensions in symptom presentation that possess more reliable behavioral and neural correlates. The potential for these findings to inform the development of prevention and treatment strategies is discussed.

scholarly journals Astroglial Connexin43 as a Potential Target for a Mood Stabiliser

2020 ◽  
Vol 22 (1) ◽  
pp. 339
Author(s):  
Motohiro Okada ◽  
Tomoka Oka ◽  
Misaki Nakamoto ◽  
Kouji Fukuyama ◽  
Takashi Shiroyama
Keyword(s):  
Gap Junction ◽  
Mood Disorders ◽  
Depressive Disorders ◽  
Bipolar Disorders ◽  
Depressive Mood ◽  
The Other ◽  
Health Concern ◽  
Monoamine Transporter ◽  
Other Hand ◽  
Novel Strategy

Mood disorders remain a major public health concern worldwide. Monoaminergic hypotheses of pathophysiology of bipolar and major depressive disorders have led to the development of monoamine transporter-inhibiting antidepressants for the treatment of major depression and have contributed to the expanded indications of atypical antipsychotics for the treatment of bipolar disorders. In spite of psychopharmacological progress, current pharmacotherapy according to the monoaminergic hypothesis alone is insufficient to improve or prevent mood disorders. Recent approval of esketamine for treatment of treatment-resistant depression has attracted attention in psychopharmacology as a glutamatergic hypothesis of the pathophysiology of mood disorders. On the other hand, in the last decade, accumulated findings regarding the pathomechanisms of mood disorders emphasised that functional abnormalities of tripartite synaptic transmission play important roles in the pathophysiology of mood disorders. At first glance, the enhancement of astroglial connexin seems to contribute to antidepressant and mood-stabilising effects, but in reality, antidepressive and mood-stabilising actions are mediated by more complicated interactions associated with the astroglial gap junction and hemichannel. Indeed, several depressive mood-inducing stress stimulations suppress connexin43 expression and astroglial gap junction function, but enhance astroglial hemichannel activity. On the other hand, monoamine transporter-inhibiting antidepressants suppress astroglial hemichannel activity and enhance astroglial gap junction function, whereas several non-antidepressant mood stabilisers activate astroglial hemichannel activity. Based on preclinical findings, in this review, we summarise the effects of antidepressants, mood-stabilising antipsychotics, and anticonvulsants on astroglial connexin, and then, to establish a novel strategy for treatment of mood disorders, we reveal the current progress in psychopharmacology, changing the question from “what has been revealed?” to “what should be clarified?”.

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