In the not‐so‐distant past, individuals who experienced chronic pain without an identifiable “organic” cause of their pain were often characterized as being psychopathological [1]. Historically it was thought that the mental illness was the underlying etiology for the pain that these individuals were experiencing. We now know that there are many underlying neurobiological aetiologies that lead to the development and maintenance of chronic pain and that chronic pain can exist in the presence or absence of a psychiatric disorder [2, 3]. Of note, pain is rarely the primary symptom of any psychiatric disorder [4]. That being said, individuals can experience physical manifestations of underlying emotional distress and occasionally this sensation can be pain. This has been termed “somatization” [5]. However, pain is rarely the dominant symptom and is usually accompanied by a number of other physical sensations. In the past, somatization was a term that was often used in a pejorative manner. However, more recently the term somatization has been reclaimed to more effectively and positively describe these physical sensations while facilitating the conceptualization of a mind‐body connection [6]. With this in mind, we can begin to see how psychiatric symptoms overlap with symptoms associated with chronic pain such as fatigue, sleep disturbance and cognitive disruption with the hope that concurrent treatment of these symptoms in a holistic, patient‐centered approach will improve patient outcomes.

In this chapter, high rates of comorbidity, overlapping symptom profiles and neurobiological aetiologies will be discussed to highlight the importance of detection and treatment of psychiatric disorders in individuals with pain since comorbidity of psychiatric illness and chronic pain negatively affects prognosis and treatment success [7].

Mood Disorders

Depressive disorders are one of the most common psychiatric disorders in individuals that suffer from chronic pain. Chronic pain is most commonly comorbid with major depressive disorder (MDD), with prevalence rates of comorbidity being 27% in primary care clinics [7]. Interestingly, studies have shown that in general pain clinics the prevalence of MDD is approximately 52% and in some subspecialty pain clinics such as dental pain clinics, prevalence rates can be as high as 85%⁷; highlighting the profound association between chronic pain and mood disorders. Persistent depressive disorder on the other hand is not as strongly associated with chronic pain with a prevalence of between 1 to 9% [8]. The combined prevalence of bipolar I and bipolar II disorder with chronic pain ranges between 1 to 21%⁸. Of note, in patients with bipolar I or bipolar II disorder, the prevalence of migraine is almost twice the prevalence rate of the general population with some studies showing a prevalence rate of 24% [9, 10]. The focus of the rest of this section will primarily be on the comorbidity between MDD and chronic pain.

Not only is MDD a common comorbidity of chronic pain but it also increases the risk of the development of chronic pain. It has been shown that there is a positive correlation between MDD symptom severity and pain severity over time [11]. Further, some clinical features of pain disorders including severity of pain, duration of pain and pain location may be indicative of the presence of a depressive disorder. Individuals with pain lasting greater than 6 months are at four‐fold increased the risk of developing MDD and individuals with three or more sites of pain are at an eight‐fold increased risk [7, 12]. Finally, individuals with back pain, fibromyalgia, temporomandibular joint disorder and chronic abdominal pain have the highest probability of developing a depressive disorder [13–16].

The importance of identifying MDD in individuals with chronic pain cannot be emphasized enough. The presence of a MDD is a better predictor of disability than pain severity or duration and leads to higher treatment resistance for both pain and depression [7]. One of the most important reasons for identifying individuals with comorbid MDD and chronic pain is that this population is more likely to have thoughts of suicide than individuals with MDD alone and the risk of completing suicide is two to three times higher [17]. Therefore, it is of utmost importance for any health care professional treating individuals with pain to be able to properly identify the presence of a depressive disorder in their patient population.

Given the consistent findings of highly prevalent comorbidity and synchronicity between depressive symptoms and pain, there has been a significant amount of research focused on identifying shared pathways and common mechanisms between pain and depression. We know that the pathophysiology of both chronic pain and depression can involve dysfunctional serotonergic and noradrenergic signaling [8, 18]. The abnormal ascending serotonergic and noradrenergic signalling to the brain leads to the signs we see and symptoms of depression whereas the abnormal descending signalling can impact pain perception [19]. Additionally, there are a number of different brain regions that are known to function abnormally in both depressive and pain disorders including the anterior cingulate cortex, dorsolateral prefrontal cortex and insula [8, 18].

With this shared mechanism of overlapping neurotransmitter systems in mind, it is not surprising that serotonin‐norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively treat both depressive symptoms and pain. Duloxetine has been the most studied medication for the treatment of concurrent MDD and chronic pain with significant positive response rates for both pain and depression, though in some studies the improvements in pain are independent of changes in depressive symptom severity [11]. Interestingly, ketamine (NMDA receptor antagonist) has been shown to be an effective treatment for treatment‐resistant depression and is used for management of treatment‐resistant neuropathic pain, again suggesting shared mechanistic pathways [20, 21].

In addition to pharmacological interventions, psychotherapeutic treatments such as cognitive behavioral therapy and mindfulness‐based therapies have been demonstrated to lead to sustained improvements in a number of functional domains in both depressive and pain disorders with very few side effects. Therefore, these treatments should be considered first line treatments in individuals with this comorbidity [8, 11].

Anxiety Disorders

Anxiety disorders are also some of the most common comorbid psychiatric disorders in individuals living with chronic pain [22]. Anxiety disorders are defined as disorders of excessive fear and anxiety and related behavioral disturbances. Individuals with anxiety disorders often overestimate the danger in the situations they fear or avoid. This is of particular importance in individuals with chronic pain who can experience pain‐related fear and subsequent avoidance of physical activity. This avoidance can further perpetuate pain‐related disability and the maintenance of the pain symptoms [23].

Epidemiological studies show an increased prevalence of anxiety disorders in various pain disorders including osteoarthritis, chronic back pain and migraine. Individuals with back pain are two to three times more likely to have a panic disorder, agoraphobia or social anxiety disorder; and three times more likely to have a diagnosis of generalized anxiety disorder or post‐traumatic stress disorder [22, 24].

A direct correlation has been shown between the severity of the anxiety symptoms and the severity of pain and pain‐associated disability [25, 26]. Interestingly, having a past history of an anxiety disorder without any active symptoms also increases the odds ratio of having a more severe pain with a high level of disability [25]. Conversely, a high level of pain that interferes with daily activities is associated with more severe anxiety symptoms and a decreased chance of responding to treatment for certain anxiety disorders [27].

Like in depressive disorders, there are common neurobiological circuits and altered areas of activity in certain brain regions in anxiety and chronic pain disorders. Dysfunction of the regulation of the noradrenergic system is commonly seen in both chronic pain and anxiety disorders leading to impaired descending pain inhibition and increased arousal and sympathetic overdrive, respectively [19, 28]. Anxiety disorders are thought to result in part from disruption of balance of neural activity between higher cognitive regions and emotional regions in the brain. One of the regions that is commonly observed to have altered activity in anxiety disorders is the limbic cortex, which includes the insular cortex and cingulate cortex. These regions integrate the sensory, affective and cognitive components of pain and functional abnormally in individuals with chronic pain [29].

Treatment options for anxiety disorders and pain disorders are often overlapping and complementary. Some of the most effective treatments for anxiety disorders and chronic pain disorders are psychotherapeutic treatments such as cognitive behavioral therapy [30, 31

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