Depression Pain Syndrome Research Articles

Neuroinflammation, Pain and Depression: An Overview of the Main Findings.

Chronic pain is a serious public health problem with a strong affective-motivational component that makes it difficult to treat. Most patients with chronic pain suffer from severe depression; hence, both conditions coexist and exacerbate one another. Brain inflammatory mediators are critical for maintaining depression-pain syndrome and could be substrates for it. The goal of our paper was to review clinical and preclinical findings to identify the neuroinflammatory profile associated with the cooccurrence of pain and depression. In addition, we aimed to explore the regulatory effect of neuronal reorganization on the inflammatory response in pain and depression. We conducted a quantitative review supplemented by manual screening. Our results revealed inflammatory signatures in different preclinical models and clinical articles regarding depression-pain syndrome. We also identified that improvements in depressive symptoms and amelioration of pain can be modulated through direct targeting of inflammatory mediators, such as cytokines and molecular inhibitors of the inflammatory cascade. Additionally, therapeutic targets that improve and regulate the synaptic environment and its neurotransmitters may act as anti-inflammatory compounds, reducing local damage-associated molecular patterns and inhibiting the activation of immune and glial cells. Taken together, our data will help to better elucidate the neuroinflammatory profile in pain and depression and may help to identify pharmacological targets for effective management of depression-pain syndrome.

A novel pyrazole-containing selenium compound modulates the oxidative and nitrergic pathways to reverse the depression-pain syndrome in mice

Bearing in mind that pain and major depressive disorder (MDD) often share biological pathways, this condition is classified as depression-pain syndrome. Mounting evidence suggests that oxidative stress is implicated in the pathophysiology of this syndrome. The development of effective pharmacological interventions for the depression-pain syndrome is of particular importance as clinical treatments for this comorbidity have shown limited efficacy. Therefore, the present study aimed to evaluate whether the 3,5-dimethyl-1-phenyl-4-(phenylselanyl)-1H-pyrazole (SePy) was able to reverse the depression-pain syndrome induced by intracerebroventricular (i.c.v) streptozotocin (STZ) in mice and the possible modulation of oxidative and nitrergic pathways in its effect. The treatment with SePy (1 and 10 mg/kg) administered intragastrically (i.g.) reversed the increased immobility time in the tail suspension test, decreased grooming time in the splash test, latency time to nociceptive response in the hot plate test, and the response frequency of Von Frey hair (VFH) stimulation induced by STZ (0.2 mg/4 μl/per mouse). Additionally, SePy (10 mg/kg, i.g.) reversed STZ-induced alterations in the levels of reactive oxygen species, nitric oxide, and lipid peroxidation and the superoxide dismutase and catalase activities in the prefrontal cortices (PFC) and hippocampi (HC) of mice. Treatment with SePy (10 mg/kg, i.g.) also reversed the STZ-induced increased expression of inducible nitric oxide synthase (iNOS) and glycogen synthase kinase 3 beta (GSK3β) in the PFC and HC. An additional molecular docking investigation found that SePy binds to the active site of iNOS and GSK3β. Altogether, these results indicate that the antidepressant-like effect of SePy is accompanied by decreased hyperalgesia and mechanical allodynia, which were associated with its antioxidant effect.

Management of the Depression-Pain Syndrome

Patients often visit their primary care provider hoping to find relief from physical pain. When a physiological origin cannot be identified, one hypothesis suggests depression is responsible for the pain. Depression screening is recommended for those experiencing unexplained pain because the diagnosis may be depression-pain syndrome. A treatment plan using both pharmacologic agents and psychotherapy is suggested; however, these may not fully resolve all symptoms. Providers should be knowledgeable about complementary/alternative therapies. A balanced combination of conventional and complementary/alternative medical services can enhance treatment and provide practical tools to improve the quality of life for a patient with depression-pain syndrome.

The depression-pain syndrome and its response to antidepressants

Abstract In an attempt to elucidate the relationship between depression and pain, the authors studied 300 pain center patients; 261 (87%) of these patients referred for diagnosis and treatment of their pain syndromes were depressed. In another study of 196 private patients with depression, 116 (59%) also had recurring benign pain. When treated with antidepressant medications, 96 of these 116 (83%) obtained significant relief of their pain syndromes. The frequency with which antidepressants can significantly alleviate pain associated with depression highlights the importance of the link between pain and depression, which may be partially explained by the close relationship of enkephalins and biogenic amines

The depression-pain syndrome and its response to antidepressants

In an attempt to elucidate the relationship between depression and pain, the authors studied 300 pain center patients; 261 (87%) of these patients referred for diagnosis and treatment of their pain syndromes were depressed. In another study of 196 private patients with depression, 116 (59%) also had recurring benign pain. When treated with antidepressant medications, 96 of these 116 (83%) obtained significant relief of their pain syndromes. The frequency with which antidepressants can significantly alleviate pain associated with depression highlights the importance of the link between pain and depression, which may be partially explained by the close relationship of enkephalins and biogenic amines