ISSN: 2455-5460

Archives of Depression and Anxiety

Review Article       Open Access      Peer-Reviewed

Depressive disorders: Defi nitions, contexts, differential diagnosis, neural correlates and clinical strategies

Giulio Perrotta*

Psychologist sp.ing in psychotherapy with a strategic approach, Forensic Criminologist expert in sectarian cults, esoteric and security profiles, Director of the Department of Criminal and Investigative Psychology UNIFEDER, Jurist sp.ed SSPL, Lecturer, International Essayist, Italy

Author and article information

*Corresponding author: Dr. Giulio Perrotta, Psychologist sp.ing in psychotherapy with a strategic approach, Forensic Criminologist expert in sectarian cults, esoteric and security profiles, Director of the Department of Criminal and Investigative Psychology UNIFEDER, Jurist sp.ed SSPL, Lecturer, International Essayist, Italy, E-mail: [email protected]
doi : 10.17352/2455-5460.000038
Submited: 08 June, 2019 | Accepted: 26 July, 2019 | Published: 27 July, 2019
Keywords: Psychology; Neuroscience; Prefrontal cortex; Frontal lobe; Temporal lobe; Limbic system; Depressive disorder; Psychotherapy; Psychopharmacology; Benzodiazipines; Antidepressants; Mood stabilizers; Strategic approach

Cite this as

Perrotta G (2019) Depressive disorders: Defi nitions, contexts, differential diagnosis, neural correlates and clinical strategies. Arch Depress Anxiety. 2019; 5(2): 009-033. Available from: 10.17352/2455-5460.000038

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© 2019 Perrotta G. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Starting from the categorical defi nitions of “depressive disorders”, we proceeded to list the individual forms provided by the DSM-V, with a particular focus on historical, clinical, neurobiological and therapeutic profi les, concluding the analysis of the possible strategies to be used to fi nalize the resolutions to problems arising from the disorder in question.

the fi rst in 2030, resulting in a substantial loss of productivity per day of illness and increased mortality. In other words, depressed patients will have a higher work and social disability than diseases such as hypertension, diabetes, arthritis and low back pain (Murray CJL, Lopez AD, Lancet 1997; WHO, 2004) (...)>> [2].

Indexing and Abstracting

Conclusions

Depressive disorders are now widely known in the academic and clinical world, as the most widespread category of mental disorders. And despite the fact that the nature and presence of depressive symptoms is widely recognized in medicine, the diagnostic revisions of the last decades support the need for a process that aims to further identify clinical pictures in an increasingly valid and reliable way.

The best treatment to date is the one combined between psychotherapy and targeted drug therapy, supplemented by somatic and nutritional therapies.

The identifying profile of the pathology is also fundamental, to then find the most suitable targeted therapy; an identifying error would de facto annul the possibility of recovery and management of the disease, as in the case of an erroneous diagnosis of bipolar disorder or personality disorders, and vice versa.

In the neurobiological field, recent research shows the crucial role of reduced neuronal plasticity in the etiology of depressive pathology, and suggests that a drug therapy, especially if combined with a valid psychosocial or psychoeducational support, can guarantee a better adherence of the patient to the treatment. In fact, drug therapy can only benefit from the association with non-pharmacological practices capable of favoring mechanisms that modulate trophism and brain plasticity. The consolidated neurobiological evidences show that the depressed subject’s neurons present a loss of trophism and neuronal plasticity that limit their best adaptation to negative environmental stimuli. The same evidences show how antidepressants activate, although with non-specific mechanisms, the function of genes involved in the synthesis of trophic factors. The profile linked to pharmacogenetics and drug-resistance deserves great attention. Neurostimulation is still an expanding field aimed at improving the efficacy, safety and tolerability of DRT treatments.

Major Depressive Disorder (MDD) is one of the most common but also the most debilitating mental disorders; however, its etiology remains unclear, seeking it in both neurobiological and environmental factors [38]. In recent years, several genetic and genotypic components have been found that predispose to depression; predisposition which is not in itself triggering the pathology but which would be triggered in the presence of other elements, such as environmental stress-causing and physiopathological hormones. Genetic expression would therefore predispose but would not be a trigger. Other factors related to the triadial alterations of the serotonin-dopamine-norepinephrine transmitters, but in recent years the patient has not completely recovered; the neurotrophic and neuroplastic factors, and also the sudden changes of sex hormones, cortisone and catecholamine, and the immune aspects treated and cytokines. Still, other profiles concern the inflammatory profiles found in the presence of increased levels of histamine and interleukin-1 and -6 (related to the increase in hunger) and interleukin-4 (linked to the decrease in hunger) [39].

Future research perspectives must be clearly oriented in the hypothesis of correlating all these analysis profiles, reconstructing the psycho-bio-pathological path of a disorder still with an etiology that is not completely explained.

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