Psychiatric co‐morbidities in patients with chronic peripheral neuropathic pain: A multicentre cohort study

Abstract

Background: Psychiatric co-morbidities are common in patients with chronic pain, but no data are available about their prevalence in patients with neuropathic pain. Methods: A multicentre study involving neurology practices (n = 30) and pain departments (n = 8) was conducted to assess the prevalence of lifetime and current anxiety and mood disorders on the basis of DSM-IV criteria in patients with peripheral neuropathic pain. Factors independently associated with such co-morbidity were also studied. A total of 182 consecutive patients (age 59.5 ± 13.8 years, 48% men) were recruited. Assessments included lifetime and current anxiety and mood disorders (Mini International Neuropsychiatric Interview), sleep (Medical Outcome Study sleep scale), pain interference (Brief Pain Inventory) and catastrophizing (Pain Catastrophizing Scale). Results: Lifetime and current prevalence of psychiatric co-morbidity were 39% and 20.3%, respectively, for any anxiety disorder, and 47.2% and 29.7%, respectively, for any mood disorder. The two most common psychiatric disorders were generalized anxiety (current prevalence 12.1%) and major depressive episode (current prevalence: 16.5%). Logistic regression analyses showed that high catastrophizing was the most significant variable independently associated with both current anxiety ; p = 0.04) and mood disorders (OR = 6.9[2.2-21]; p < 0.001). Conclusions: Lifetime and current anxiety and mood disorders are highly prevalent in patients with peripheral neuropathic pain, and are associated with high levels of catastrophizing. Early management of catastrophizing may contribute to reducing the risk of psychiatric co-morbidities in these patients.

Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury

“…In this study, the hierarchical cluster analysis divided SNI rats into two clusters: one group (approximately 40%, 'anhedonia-like phenotype') with reduced sucrose preference in the SPT, the other group (approximately 60%, 'without anhedonia-like phenotype') with similar sucrose preference compared with sham-operated rats. The previous clinical studies demonstrated that the incidence of comorbid chronic pain and depression is around 30-50% [1,4,5], which is in line with the present study. In this study, we found that rats with or without anhedonia-like phenotypes showed similar mechanical withdrawal thresholds, suggesting that the alterations in mood-related behaviors were independent of the degree of nociceptive damage, consistent with the previous studies [8,31,[38][39][40].…”

“…Epidemiological studies have shown that the prevalence of depression in patients with pain is higher compared with that when these two conditions are separately evaluated [1][2][3]. Approximately 30% of patients in pain experience depression [4,5]. A recent longitudinal analysis demonstrated that chronic pain strongly predicts the development of more depressive symptoms in patients with pain compared with those without pain [6].…”

Pain, depression and sleep disorders in patients with diabetic and nondiabetic carpal tunnel syndrome: a vicious cycle

“…In the current study, depression was determined to be the most significant factor affecting sleep quality in patients with chronic neuropathic pain. Similar to the current study, several studies have been conducted on the relationship between depression and chronic pain 21,22 . Pain is likely to lead to depression, which lowers the pain threshold and can make the pain more intolerable.…”

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

“…Depression and chronic pain are widely recognised clinical co-morbidities, with up to 50% of chronic pain patients exhibiting depression (Radat et al, 2013), while almost 60% of depressed patients experience painful physical symptoms (Aguera-Ortiz et al, 2011). Recent data from animal studies support this clinical relationship and indicate that inflammatory and neuropathic pain-related responding is enhanced in various animal models of depression including olfactory bulbectomy (OB) (Burke et al, 2013a, Burke et al, 2010, early life stress (Uhelski andFuchs, 2010, Burke et al, 2013b) and the Wistar-Kyoto rat (Burke et al, 2010, Zeng et al, 2008, Rea et al, 2014.…”