Human evidence of a supra‐spinal modulating role of dopamine on pain perception

Potvin, Stéphane; Grignon, Sylvain; Marchand, Serge

doi:10.1002/syn.20616

Cited by 118 publications

(77 citation statements)

References 101 publications

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“…Human studies confirm that patients with fibromyalgia have lowered levels of monoamines (12) in their cerebrospinal fluid and higher levels of substance P (13) and nerve growth factor (14). Serotonin and norepinephrine are thought to be the key neurotransmitters in the descending pain inhibitory system, and dopamine also appears to be involved in pain control in the central nervous system (15,16). Altered serotonin metabolism associated with reduced transcription activity of the short allele of the serotonin transporter gene promoter occurs more frequently in patients with fibromyalgia than in healthy control subjects and has been linked to higher levels of depression and psychological distress (17).…”

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confidence: 99%

Quetiapine Fumarate Extended‐Release for the Treatment of Major Depression With Comorbid Fibromyalgia Syndrome: A Double‐Blind, Randomized, Placebo‐Controlled Study

McIntyre

Paisley

Kouassi

et al. 2014

Arthritis & Rheumatology

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Objective. Fibromyalgia and major depressive disorder (MDD) frequently co-occur. Quetiapine fumarate extended-release (quetiapine XR) has demonstrated efficacy in the treatment of MDD and has been shown to have analgesic properties in patients with depression. The primary objectives of this study were to evaluate the effects of quetiapine XR on depressive and pain symptoms in patients with MDD and comorbid fibromyalgia, and to assess its safety and tolerability. Results. The mean change in the HAM-D score from baseline to week 8 was significantly greater in the quetiapine XR group compared with the placebo group (؊10.0 versus ؊5.8; P ‫؍‬ 0.001). Improvements in most secondary outcomes were also significantly greater in the quetiapine XR group. Quetiapine XR was generally well tolerated.Conclusion. This study is the first to demonstrate that measures of depression, pain, and quality of life are significantly improved with quetiapine XR compared with placebo in patients with a dual diagnosis of MDD and fibromyalgia.Fibromyalgia is a syndrome characterized by widespread musculoskeletal pain that lasts at least 3 months, with a reduced pain threshold. Widespread pain is the defining feature of fibromyalgia. Associated symptoms include fatigue, sleep disturbance, stiffness, cognitive symptoms, and mood abnormalities including depression and anxiety (1,2). Pain, fatigue, and sleep disturbance are present in at least 75% of patients (3). The condition is estimated to occur in ϳ2-4% of the general adult population (4,5), and the prevalence is higher among women (4.9%) than men (1.6%) (6).Patients with fibromyalgia are at increased risk of mood disorders. Studies suggest that the prevalence of current depression among patients with fibromyalgia is as high as 22-40% (7), and that lifetime prevalence rates reach 58-86% (8,9). This high degree of co-occurrence is thought to be related in part to pathophysiologic abnormalities that are shared between fibroClinicalTrials.gov identifier: NCT00675896.

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mentioning

confidence: 99%

Quetiapine Fumarate Extended‐Release for the Treatment of Major Depression With Comorbid Fibromyalgia Syndrome: A Double‐Blind, Randomized, Placebo‐Controlled Study

McIntyre

Paisley

Kouassi

et al. 2014

Arthritis & Rheumatology

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“…Although highly speculative, we consider dopamine signaling as a potential candidate able to preserve hedonic processing in the absence of opioid mediation. Along this line of reasoning, a recent review of the literature has shown a key role of dopamine on pain perception in humans, suggesting its involvement in endogenous pain modulation systems (Potvin et al, 2009). In addition, pleasure and reward expectation have been associated with increased phasic dopamine signaling (Schultz, 2010).…”

Section: Discussionmentioning

confidence: 99%

Pleasure-Related Analgesia Activates Opioid-Insensitive Circuits

Kut

Candia²,

Overbeck³

et al. 2011

J. Neurosci.

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Recent findings suggest that pain and pleasure share common neurochemical circuits, and studies in animals and humans show that opioid-mediated descending pathways can inhibit or facilitate pain. We explored the role of endogenous opioid neurotransmission in pleasure-related analgesia. -Opioidergic activity was blocked with 0.2 mg/kg naloxone to assess its effects on hedonic responses to pleasant emotional pictures (International Affective Picture System) and its modulating effects on heat pain tolerance. Naloxone did not alter subjective and autonomous reactions to pleasure induction or overall mood of participants. In addition, pleasure-related increases in pain tolerance persisted after reversal of endogenous -opioidergic neurotransmission. Subjective pain intensity and unpleasantness ratings increased after naloxone administration. These findings suggest that, in addition to opioid-sensitive circuits, mainly opioidinsensitive pain-modulating circuits are activated during pleasure-related analgesia.

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“…However, some experimental studies have shown the opposite effect, where there appears to be a higher pain threshold and tolerance level in individuals with anxiety disorders or chronic pain [ 33 ]. This may be related to malfunctioning of the endogenous opioid system [ 114 ]. It has been suggested that this is related to the symptoms of emotional numbing present in PTSD, although the relationship between PTSD and chronic pain still remains unclear [ 48 ].…”

Section: Shared Vulnerability Modelmentioning

confidence: 96%

Chronic Pain and the Anxiety Disorders: Epidemiology, Mechanisms and Models of Comorbidity, and Treatment

Katz

Pagé

Fashler

et al. 2014

Mental Health and Pain

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Chronic pain was traditionally defi ned by the length of time that pain persists [ 54 ] but more recent conceptualizations have introduced a more nuanced approach [ 85 ]. The International Association for the Study of Pain (IASP) currently defi nes chronic pain variously as " pain without apparent biological value ", " that has persisted beyond the normal tissue healing time … as determined by common medical experience ", and/or as " a persistent pain that is not amenable, as a rule, to treatments based upon specifi c remedies " [ 85 ]. Moreover, some chronic pain syndromes, such as rheumatoid arthritis, will likely never heal and others, such as migraine headaches, remit (i.e., heal) and then recur [ 85 ]. Notwithstanding the challenges associated with defi ning chronic pain and the problems with a solely, time-based defi nition, for research purposes, chronic non-malignant pain is typically defi ned as pain that persists for longer than 3 or 6 months [ 58 , 59 , 74 , 126 ].Recent epidemiologic studies reveal considerable variability in prevalence estimates for chronic pain (using a liberal time frame of 3 months or longer). These studies show that between 11.5 and 55 % of the population worldwide report chronic

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Human evidence of a supra‐spinal modulating role of dopamine on pain perception

Cited by 118 publications

References 101 publications

Quetiapine Fumarate Extended‐Release for the Treatment of Major Depression With Comorbid Fibromyalgia Syndrome: A Double‐Blind, Randomized, Placebo‐Controlled Study

Quetiapine Fumarate Extended‐Release for the Treatment of Major Depression With Comorbid Fibromyalgia Syndrome: A Double‐Blind, Randomized, Placebo‐Controlled Study

Pleasure-Related Analgesia Activates Opioid-Insensitive Circuits

Chronic Pain and the Anxiety Disorders: Epidemiology, Mechanisms and Models of Comorbidity, and Treatment

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