|Year : 2018 | Volume
| Issue : 1 | Page : 51-53
Chronic pain, substance abuse and depression: Unfolding the common linkage
Supriya Agarwal1, Kaveri Saxena2, Malvika Dahuja1, Sandeep Choudhary1
1 Department of Psychiatry, Subharti Medical College and Hospital, Meerut, Uttar Pradesh, India
2 Department of Psychiatry, Subharti Medical College and Hospital, Dehradun, Uttrakhand, India
|Date of Web Publication||30-Apr-2018|
Dr. Kaveri Saxena
28, Dev Nagar Mission Compound, Meerut, Uttar Pradesh 250001
Source of Support: None, Conflict of Interest: None
The population bears a huge psychological, social and financial burden due to chronic pain and with its comorbidities it further adds to this burden. There are high rates of co-occurrence of depression and substance abuse, which are often overlooked. Therefore, patients presenting with pain or depression or substance abuse or a combination of these need to be evaluated thoroughly for the presence of the others. We report a case of a patient with primary complaints of pain and depressive symptoms with opioid and benzodiazepine abuse for over 16-18 years and discuss the neurobiological linkage between the three comorbid conditions.
Keywords: Benzodiazepine abuse, chronic pain, depression, opioid abuse, reward pathway
|How to cite this article:|
Agarwal S, Saxena K, Dahuja M, Choudhary S. Chronic pain, substance abuse and depression: Unfolding the common linkage. Indian J Pain 2018;32:51-3
| Introduction|| |
Chronic inflammatory conditions, characterized by chronic widespread pain and heightened pain response to pressure such as small fiber neuropathies, reportedly have high rates of comorbidity with depression and drug dependence. Depression has a prevalence rate of 40%–60% in patients with chronic pain  and 27% with drug abuse/dependence. Comorbid substance abuse has also been frequently reported in patients with chronic pain. This could be due to shared neurobiology. Dysregulation of stress/inflammatory pathways promotes alterations in brain circuitry that modulates mood, pain, and stress response. Over time, the functional changes might disrupt the neurotrophic support. This correlates with the hypothesis of “kindling” in depression and central sensitization in pain disorders, suggestive of the continuing and self-perpetuating nature of these disorders. Chronic use of drugs, mainly opioids and benzodiazepines (BZDs), are therefore taken as self-medications. This may flare-up the symptoms of preexisting physical and mental disorder.
It is important, therefore, to understand the common neurobiological basis of these three disorders that share neural pathways, neural substrates, neural circuitry, and other physiological substrates. All three disorders need to be adequately managed to provide optimal and holistic care to the patient.
| Case Report|| |
A 58-year-old man presented with a history of chronic pain and paresthesia in the form of burning/tingling sensations and pins and needles in a glove-and-stocking pattern in all four extremities for the past 16–18 years. It was gradual in onset and progressively deteriorating. He was from a rural background, middle socioeconomic status, and unemployed for many years. He gave history of separation from his wife after a long conflictual relationship. Patient started consuming spasmo proxyvon capsules on advice of a local practitioner, which he gradually increased (1–2 to 15 capsules per day). Due to minimal relief, he stopped taking the capsules. He developed depressive symptoms such as low mood, loss of interest in work, nihilistic ideation, fatigue and sleep disturbances. The symptoms started gradually and became progressively worse and persistent. Further, patient started antihistaminic (pheniramine) and BZD (alprazolam 0.5 mg, gradually increasing from 40 to 60 tablets per day over 10 years). Patient felt no relief and started using injectable form of opioids. He quit cold turkey due to cost restraints. Over the course of 16 years, he did not seek medical help and continued to have persistent depressive symptoms with BZD abuse and ongoing family stressors. His mental status examination revealed depressive affect and cognition. His Montgomery–Asberg Depression Rating scale (MADRS) score was 45 (severe). His neurological assessment and review by a neurologist revealed motor sensory deficits in upper and lower limb with rigidity and hyporeflexia. Diagnosis of chronic pain syndrome due to small fiber polyneuropathy was made clinically as biopsy was refused by the patient. All routine blood investigations including the investigations for neuropathy panel were normal. Magnetic resonance imaging (MRI) of the brain was normal. MRI of the spine indicated desiccations at various cervical levels with cervical spinal canal stenosis. Patient was diagnosed as having severe depressive episode without psychotic symptoms with mental and behavioral disorders due to polysubstance use (opioids and BZDs), that is, F32.2 with F19.30. He was started on tab chlordiazepoxide (40 mg in divided doses), duloxetine (60 mg), oxcarbazepine (450 mg), pregabalin (150 mg) with methylcobalamin and prednisolone (4 mg). Patient's depressive and pain symptoms improved over 4 weeks (MADRS score 19). However, fatigue and rigidity persisted over 8 weeks with only partial improvement at 2-month follow-up.
| Discussion|| |
Pain is postulated to be a disorder of reward function. The brain reward circuitry also mediates the effects of drug abuse. Injury to sensory pain pathways has been shown to share the same brain regions involved in mood regulation, including the insular cortex, prefrontal cortex, anterior cingulate, thalamus, hippocampus and amygdala. These form a structural foundation for the coexistence of pain and depression.
Ventral tegmental area (VTA) with dopamine (DA) neurons and their projections into the nucleus accumbens (NAc) constitute the brain reward and reinforcement circuitry. DA increase in the NAc is associated with natural reward as well as reinforcing behavior in substance abuse. It can be said that both substance abuse and chronic pain share the same malfunctions in the circuitry.
Neurotransmitter systems contributing to aversive states include serotonin (raphe nucleus), norepinephrine (locus coeruleus) and acetylcholine (nucleus of Meynert). Deficiency of serotonin, norepinephrine and DA is known to lead to depression and substantiate further the coexistence of chronic pain and depression.
Reward function is inhibited by the β-aminobutyric acid (GABA) neurons (from the NAc back to the VTA), the glutamatergic neurons (from medial prefrontal cortex and stria terminalis to the VTA and from the hippocampus to the NAc) and the orexinergic pathways. This could explain the use of BZD by the patient as a self-medication in our case. The role of GABA has not been investigated extensively, but it has been hypothesized that decreased GABAergic neurotransmission leads to depression. Also, decreased catecholamine and opioid receptor activity can increase pain and depression whereas an increase in central substance P and cytokine activity increases pain and depression. In patients with chronic pain, pain relief is not the only desired treatment outcome, but it also includes mood improvement, sleep and quality of life. Aforementioned data support the self-medication hypothesis of drug abuse in patients with chronic pain and depression.
Multiple studies have found that the rate of drug abuse (opioid, BZD) among patients with pain (e.g., drug problems, drug seeking, psychological dependence, and craving) is slightly higher than in the general population.,
BZD abuse has not been widely investigated in patients with chronic pain but follows the similar pattern of self-medication hypothesis with some contrary evidence of worsening pain by influencing serotonin release. However, BZD abuse in patients with comorbid chronic pain might be secondary to the modulation of anxiodepressive symptoms as observed in our patient.
| Conclusion|| |
Chronic pain, substance abuse and depression undoubtedly share common neurobiological and neurophysiological mechanisms. Therefore, all three comorbid conditions need to be simultaneously addressed with liaison for holistic patient care.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
The authors thank Dr. Mani Gupta, Consultant Neurologist, Dayanand Hospital, Meerut, Uttar Pradesh, India, for his contributions in the management of the patient.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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