Depression and Pain: use of antidepressant

2021 ◽  
Vol 19 ◽  
Author(s):  
José Armando Sánchez-Salcedo ◽  
Maribel Maetizi Estevez Cabrera ◽  
Tania Molina-Jiménez ◽  
José Luis Cortes-Altamirano ◽  
Alfonso Alfaro-Rodríguez ◽  
...  

Background: Emotional disorders are common comorbid affectations that exacerbate the severity and persistence of chronic pain. Specifically, depressive symptoms can lead to an excessive duration and intensity of pain. The use of antidepressant drugs is associated with pain reduction. The recent development of animal models has accelerated studies focusing on the underlying mechanisms of chronic pain and depression comorbidity. Aim: This review provides an overview of the comorbid relationship of chronic pain and depression, the clinical and pre-clinical studies performed on the neurobiological aspects of pain and depression, and the use of antidepressants as analgesics. Method: A systematic search of literature databases was conducted according to the pre-defined criteria. The authors independently conducted a focused analysis of the full-text articles. Results: Studies suggest that pain and depression are highly-intertwined and may co-exacerbate physical and psychological symptoms. One important biochemical basis for pain and depression focuses on the serotonergic and norepinephrine system, which have been shown to play an important role in this comorbidity. Brain structures that codify pain are also involved in mood. It is evident that using serotonergic and norepinephrine antidepressants are strategies commonly employed to mitigate pain. Conclusion: Literature indicates that pain and depression impact each other and play a prominent role in the development and maintenance of other chronic symptoms. Antidepressants continue to be a major therapeutic tool for managing chronic pain. Tricyclic antidepressants (TCAs) are more effective in reducing pain than selective serotonin reuptake inhibitors (SSRIs) and serotonin-noradrenaline reuptake inhibitors (SNRIs).

1999 ◽  
Vol 5 (2) ◽  
pp. 104-111 ◽  
Author(s):  
Allan I. F. Scott

The January 1997 issue of this journal contained four reviews that compared tricyclic antidepressants with selective serotonin reuptake inhibitors (SSRIs) and other newer antidepressants in terms of their pharmacology (Palazidou, 1997), adverse effects, potential drug interactions and toxicity (Henry, 1997), efficacy in the prevention of relapse and recurrence (Edwards, 1997), and findings from meta-analyses (Anderson, 1997). In July 1997 reboxetine was promoted as the first selective noradrenaline reuptake inhibitor (NARI), and in October of the same year mirtazapine was promoted as the first noradrenergic and specific serotonergic antidepressant (NaSSA). Milnacipran is presently being registered by the manufacturers, after which it will be the second antidepressant drug promoted as a specific serotonin and noradrenaline reuptake inhibitor (SNRI).


Ból ◽  
2021 ◽  
Vol 22 (2) ◽  
pp. 33-41
Author(s):  
Krzysztof Wojtasik-Bakalarz ◽  
Jarosław Woroń ◽  
Marcin Siwek ◽  
Anna Krupa

Depression and pain are often coexisting phenomena, and the relationship between both phenomena is two-way – the occurrence of depression increases the risk of pain, and both acute and chronic pain increase the risk of depression. Pain may be part of the clinical picture of depression, be a result of comorbid psychiatric disorders, be associated with comorbidities, be a chronic pain syndrome, or be a complication of pharmacotherapy. The comorbidity of pain and depression is associated with a worse prognosis, lower therapeutic response, lower quality of life, impaired functioning, and a greater risk of relapse and suicide. There are indications that the same structures and neurotransmitters are involved in the pathophysiology of pain and depression, which may explain the coanalgesic effect of some antidepressants. The drugs with the best proven effectiveness are serotonin and noradrenaline reuptake inhibitors (especially duloxetine) and amitriptyline. Other drugs that may be of use in the treatment of pain are mirtazapine, mianserin, trazodone, agolemelatine, bupropion, and moclobemide. Selective serotonin reuptake inhibitors are used primarily in the treatment of depression symptomatic pain, but there is little evidence that they are effective in other types of pain. The use of certain psychotropic drugs, incl. SSRIs, clomipramine, benzodiazepines, Z drugs, and anticholinergics may be associated with increased pain. Caution is required when using polypharmacy in the form of a combination of an antidepressant and an analgesic because of the risk of worsening side effects or loss of treatment effectiveness. In the case of opioid drugs, in particular tramadol, the combination with drugs with a serotonergic effect may be associated with the risk of serotonin syndrome.


2020 ◽  
Vol 2020 ◽  
pp. 1-22 ◽  
Author(s):  
Yi Zheng ◽  
Meimei Wu ◽  
Ting Gao ◽  
Li Meng ◽  
Xiaowei Ding ◽  
...  

Ample evidence suggests that estrogens have strong influences on the occurrence of stress-related mood disorders, but the underlying mechanisms remain poorly understood. Through multiple approaches, we demonstrate that the G protein-coupled estrogen receptor (GPER) is widely distributed along the HPA axis and in brain structures critically involved in mood control. Genetic ablation of GPER in the rat resulted in significantly lower basal serum corticosterone level but enhanced ACTH release in response to acute restraint stress, especially in the female. GPER-/- rats of either sex displayed increased anxiety-like behaviors and deficits in learning and memory. Additionally, GPER deficiency led to aggravation of anxiety-like behaviors following single-prolonged stress (SPS). SPS caused significant decreases in serum corticosterone in WT but not in GPER-deficient rats. The results highlight an important role of GPER at multiple sites in regulation of the HPA axis and mood.


2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii86-ii86
Author(s):  
Dorothee Gramatzki ◽  
James Rogers ◽  
Marian Neidert ◽  
Caroline Hertler ◽  
Emilie Le Rhun ◽  
...  

Abstract PURPOSE Antidepressant drugs have shown anti-tumor activity in preclinical glioblastoma studies. Antidepressant drug use, as well as its association with survival, in glioblastoma patients has not been well characterized on a population level. METHODS Patient characteristics, including the frequency of antidepressant drug use, were assessed in a glioblastoma cohort diagnosed in a 10-year time-frame between 2005 and 2014 in the Canton of Zurich, Switzerland. Cox proportional hazards regression models were applied for multivariate analysis. Kaplan-Meier survival curves were used to estimate overall survival data and the log-rank test was performed for comparisons. RESULTS Four hundred four patients with isocitrate dehydrogenase (IDH) wildtype glioblastoma were included in this study. Sixty-five patients (16.1%) took antidepressant drugs at some point during the disease course. Patients were most commonly prescribed selective serotonin reuptake inhibitors at any time (N=46, 70.8%). Nineteen patients (29.2%) were on antidepressant drugs at the time of their tumor diagnosis. No differences were observed in overall survival between those patients who had taken antidepressants at some point in their disease course and those who had not (p=0.356). These data were confirmed in a multivariate analysis including age, Karnofsky performance status, gender, extent of resection, O6-methylguanine DNA methyltransferase (MGMT) promoter methylation status, and first-line treatment as cofounders (p=0.315). Also, there was no association of use of drugs modulating voltage-dependent potassium channels (citalopram; escitalopram) with survival (p=0.639). CONCLUSIONS This signal-seeking study does not support the hypothesis that antidepressants have antitumor efficacy in glioblastoma on a population level.


2012 ◽  
Vol 27 (6) ◽  
pp. 519-523 ◽  
Author(s):  
Kim Usher ◽  
Lawrence H. Brown ◽  
Petra Buettner ◽  
Beverley Glass ◽  
Helen Boon ◽  
...  

AbstractIntroductionThe need to manage psychological symptoms after disasters can result in an increase in the prescription of psychotropic drugs, including antidepressants and anxiolytics. Therefore, an increase in the prescription of antidepressants and anxiolytics could be an indicator of general psychological distress in the community.PurposeThe purpose of this study was to determine if there was a change in the rate of prescription of antidepressant and anxiolytic drugs following Cyclone Yasi.MethodsA quantitative evaluation of new prescriptions of antidepressants and anxiolytics was conducted. The total number of new prescriptions for these drugs was calculated for the period six months after the cyclone and compared with the same six month period in the preceding year. Two control drugs were also included to rule out changes in the general rate of drug prescription in the affected communities.ResultsAfter Cyclone Yasi, there was an increase in the prescription of antidepressant drugs across all age and gender groups in the affected communities except for males 14-54 years of age. The prescription of anxiolytic drugs decreased immediately after the cyclone, but increased by the end of the six-month post-cyclone period. Control drug prescription did not change.ConclusionThere was a quantifiable increase in the prescription of antidepressant drugs following Cyclone Yasi that may indicate an increase in psychosocial distress in the community.UsherK, BrownLH, BuettnerP, GlassB, BoonH, WestC, GrassoJ, Chamberlain-SalaunJ, WoodsC. Rate of prescription of antidepressant and anxiolytic drugs after Cyclone Yasi in North Queensland. Prehosp Disaster Med. 2012;27(6):1-5.


2015 ◽  
Vol 73 (7) ◽  
pp. 578-581 ◽  
Author(s):  
Francisco Moreira Mattos Júnior ◽  
Rafael Villanova Mattos ◽  
Manoel Jacobsen Teixeira ◽  
Silvia Regina Dowgan Tesseroli de Siqueira ◽  
Jose Tadeu Tesseroli de Siqueira

The objective was to investigate the effect of nitrous/oxygen in chronic pain. Seventy-seven chronic pain patients referred to dental treatment with conscious sedation with nitrous oxide/oxygen had their records included in this research. Data were collected regarding the location and intensity of pain by the visual analogue scale before and after the treatment. Statistical analysis was performed comparing pre- and post-treatment findings. It was observed a remarkable decrease in the prevalence of pain in this sample (only 18 patients still had chronic pain, p < 0.001) and in its intensity (p < 0.001). Patients that needed fewer sessions received higher proportions of nitrous oxide/oxygen. Nitrous oxide may be a tool to be used in the treatment of chronic pain, and future prospective studies are necessary to understand the underlying mechanisms and the effect of nitrous oxide/oxygen in patients according to the pain diagnosis and other characteristics.


2000 ◽  
Vol 176 (4) ◽  
pp. 363-368 ◽  
Author(s):  
David Michelson ◽  
Maurizio Fava ◽  
Jay Amsterdam ◽  
Jeffrey Apter ◽  
Peter Londborg ◽  
...  

BackgroundAbrupt interruption of therapy with selective serotonin reuptake inhibitors (SSRIs) has been associated with somatic and psychological symptoms.AimsSystematically to assess symptoms and effects on daily functioning related to interruption of SSRI therapy.MethodPatients treated with fluoxetine, setraline or paroxetine underwent identical five-day periods of treatment interruption and continued active treatment under double-blind, order-randomised conditions, with regular assessment of new symptoms.ResultsPlacebo substitution for paroxetine was associated with increases in the number and severity of adverse events following the second missed dose, and increases in functional impairment at five days. Placebo substitution for sertraline resulted in less pronounced changes, while interruption of fluoxetine was not associated with any significant increase in symptomatology.ConclusionsAbrupt interruption of SSRI treatment can result in a syndrome characterised by specific physical and psychological symptoms. Incidence, timing and severity of symptoms vary among SSRIs in a fashion that appears to be related to plasma elimination characteristics.


2020 ◽  
Vol 22 (3) ◽  
pp. 229-239

The endocannabinoid system is widely expressed in the limbic system, prefrontal cortical areas, and brain structures regulating neuroendocrine stress responses, which explains the key role of this system in the control of emotions. In this review, we update recent advances on the function of the endocannabinoid system in determining the value of fear-evoking stimuli and promoting appropriate behavioral responses for stress resilience. We also review the alterations in the activity of the endocannabinoid system during fear, stress, and anxiety, and the pathophysiological role of each component of this system in the control of these protective emotional responses that also trigger pathological emotional disorders. In spite of all the evidence, we have not yet taken advantage of the therapeutic implications of this important role of the endocannabinoid system, and possible future strategies to improve the treatment of these emotional disorders are discussed.


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