In the United States, major depressive disorder, or clinical depression, occurs in 16.2% of patients. It is associated with an increased risk of suicide, mortality from comorbid diseases, and reduced life expectancy (Kaplan & Beech, 2015). It should be noted that there are still difficulties with the diagnosis and treatment of depression. The negative effects of pain on the course of depressive disorder are discussed in the literature. In addition, information is provided on the recognition of depression in individuals with somatic symptoms, on the neurological communality of depression and pain syndromes, and effective pharmacological treatment regimens for pain and depression have been proposed (Li & Peng, 2017). Pain is one of the most common concomitant symptoms of depression.
According to meta-analysis, pain symptoms are present in 65% of patients with depressive disorder (Sheng et al., 2017). Persons suffering from various types of pain are at increased risk of developing clinical depression ‑ the more complaints, the higher the risk (Hoffelt & Zwack, 2014). In fact, the presence of major depressive syndrome is predicted not by the severity or duration of pain, but by the number of pain symptoms. Obviously, with episodes of depression, pain has a cumulative effect, aggravates the course of the disease and increases its duration. This is clearly confirmed by the clinical case under consideration.
It has now been established that the pathogenesis of pain and depression affects in many respects the same structures of the nervous system and develops in a similar way, involving the same receptor-mediator interactions. So, the main common links in the pathogenesis of depression and pain are the following: hyperactivity of the hypothalamic-pituitary-adrenal and limbic-reticular systems, increased activity of glutamate, GABA deficiency, disruption of the relationship of glutamatergic and monoaminergic pathways, impaired metabolism of substance P and neurokinins, monoamine deficiency.
It is also known that dysregulation of 5-HT receptors in the brain is directly related to the development of depression and the regulation of the effects of substance P, glutamate, GABA and other pain mediators (Li & Peng, 2017). Anxiety-depressive conditions lead to a decrease in pain thresholds associated with overexpression of the substance P, a change in the metabolism of serotonin, etc., to an increase in muscle tension, which also increases the severity of the pain syndrome.
In turn, dysfunction of the descending neuroendocrine and 5-HT systems, characteristic of depression, can lead the body to interpret the usual stimuli as discomfort or even pain (Li & Peng, 2017). Indeed, in the case under consideration, it appears that the patient is constantly in pain. His voice appeared that he gets anxious and irritated very easily. The patient himself noted that he has panic attacks almost every day and his pain is worse because of that. In accordance with PHQ-9, the patient manifests mild depression. However, overall examination allowed concluding the following as a diagnosis: Anxiety disorder Unspecified; Panic attacks; Major Depressive Disorder.
Today it is understood that somatic symptoms and depression have a common pathophysiology, similar causes, mechanisms of action, neurotransmitters, and, therefore, require general treatment. So, there is a need for the simultaneous treatment of depression and pain. Given the fact that chronic pain with a neuropathic component is a fairly frequent combination, the appointment of anticonvulsants will be justified.
Among this group of drugs, Pregabalin and Gabapentin are the most recognized (Kaplan & Beech, 2015). The main mechanism of their action is associated with an effect on central sensitization, improvement of the neurotransmitter balance in the direction of enhancing the anti-pain GABAergic effects and reducing the effects of glutamate, the main pain neurotransmitter (Kaplan & Beech, 2015).
If necessary, additional painkillers ‑ NSAIDs ‑ should be prescribed for pain relief, and the effectiveness of Xanax increases when combined with high doses of NSAIDs (Hoffelt & Zwack, 2014). A necessary factor and fundamental moment is the adherence to the prescribed therapy, which should include not only drug therapy, but also non-drug correction methods aimed at the root cause of the formation of chronic pain syndrome.
References
Hoffelt, C., & Zwack, A. (2014). Assessment and management of chronic pain in patients with depression and anxiety. Mental Health Clinician, 4(3), 146-152.
Kaplan, G., & Beech, D. (2015). Total recovery: Breaking the cycle of chronic pain and depression. Rodale Books.
Li, A., & Peng, Y. B. (2017). Comorbidity of depression and pain: A review of shared contributing mechanisms. Journal of Neurology & Neuromedicine, 2(3), 4-11.
Sheng, J., Liu, S., Wang, Y., Cui, R., Zhang, X. (2017). The link between depression and chronic pain: Neural mechanisms in the brain. Neural Plasticity, 17, 1-10.