An Elephant Among Us: The Role of Dopamine in the Pathophysiology of Fibromyalgia

Wood, Patrick B.; Holman, Andrew J.

doi:10.3899/jrheum.080583

Cited by 27 publications

(16 citation statements)

References 28 publications

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“…Still others have suggested that the ventral striatum functions more generally in motivated behavior (Horvitz, 2000; Zink et al, 2003, 2004; Delgado et al, 2004; Nicola et al, 2004; Leknes and Tracey, 2008). Our results showed increased ventral striatal activity in anticipation of fewer shocks, which suggests that the striatum is not simply functioning to prime the system to avoid pain – i.e., an analgesic effect (Scott et al, 2006, 2007; Wood and Holman, 2009). If that were the case, we would expect to see increased striatal activity to more potential shocks.…”

Section: Discussionmentioning

confidence: 63%

From Bad to Worse: Striatal Coding of the Relative Value of Painful Decisions

Brooks¹,

Pammi²,

Noussair³

et al. 2010

Front. Neurosci.

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The majority of decision-related research has focused on how the brain computes decisions over outcomes that are positive in expectation. However, much less is known about how the brain integrates information when all possible outcomes in a decision are negative. To study decision-making over negative outcomes, we used fMRI along with a task in which participants had to accept or reject 50/50 lotteries that could result in more or fewer electric shocks compared to a reference amount. We hypothesized that behaviorally, participants would treat fewer shocks from the reference amount as a gain, and more shocks from the reference amount as a loss. Furthermore, we hypothesized that this would be reflected by a greater BOLD response to the prospect of fewer shocks in regions typically associated with gain, including the ventral striatum and orbitofrontal cortex. The behavioral data suggest that participants in our study viewed all outcomes as losses, despite our attempt to induce a status quo. We find that the ventral striatum showed an increase in BOLD response to better potential gambles (i.e., fewer expected shocks). This lends evidence to the idea that the ventral striatum is not solely responsible for reward processing but that it might also signal the relative value of an expected outcome or action, regardless of whether the outcome is entirely appetitive or aversive. We also find a greater response to worse gambles in regions previously associated with aversive valuation, suggesting an opposing but simultaneous valuation signal to that conveyed by the striatum.

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Section: Discussionmentioning

confidence: 63%

From Bad to Worse: Striatal Coding of the Relative Value of Painful Decisions

Brooks¹,

Pammi²,

Noussair³

et al. 2010

Front. Neurosci.

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“…The monoaminergic system plays a key role in expression of pain (Kayser et al, 2007;Mansikka et al, 2005;Millan, 2002;Papaleo et al, 2008;Plaznik et al, 1985), and pain has been shown to be associated with alterations in monoamine signalling in cognitive-associated brain regions (Finn et al, 2006;Omote et al, 1998;Wood, 2008;Wood and Holman, 2009;Wood et al, 2007a;Wood et al, 2007b). In addition, tricyclic antidepressants (TCAs) which block reuptake of noradrenaline and serotonin are efficacious in the treatment of chronic pain (McClene, 2003).…”

Section: Neurotransmitters and Receptors In Pain And Cognitionmentioning

confidence: 99%

The effect of pain on cognitive function: A review of clinical and preclinical research

Moriarty

McGuire

Finn

2011

Progress in Neurobiology

872

710

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Cognitive impairment is commonly associated with the pain experience. This impairment represents a major obstacle to daily activities and rehabilitation, especially in the chronic pain population. Here we review clinical and preclinical studies that have investigated pain-related alterations in cognition. These include impaired attentional, executive and general cognitive functioning. We describe the anatomical, neurochemical and molecular substrates common to both cognitive processing and supraspinal pain processing, and present the evidence for their involvement in pain-related cognitive impairment. We also examine the added complexity of cognitive impairment caused by analgesic medications and how this can further impact on morbidity in chronic pain patients. The need for a better understanding of the mechanisms of both pain-induced and treatment-related cognitive impairment is highlighted. Further research in this area will aid our understanding of patient symptoms and their underlying pathophysiology, ultimately leading to increased provision of guided therapy.

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“…Similar to serotonin and noradrenalin, dopamine activity has been demonstrated to be attenuated in fibromyalgia (see [41] for review): CSF levels of dopamine [28] and presynaptic dopamine function are reduced (examined with positron emission tomography (PET)) [42], and dopamine responses to acute pain are diminished in fibromyalgia patients [43]. Since inactivation of D2 receptors has been shown to lead to hyperalgesia [44], these findings may suggest that dysfunctional dopaminergic neurotransmission contribute to patients' pain symptomatology.…”

Section: Dysfunctional Transmitter Systems In Fibromyalgiamentioning

confidence: 99%

Dysfunctional Neurotransmitter Systems in Fibromyalgia, Their Role in Central Stress Circuitry and Pharmacological Actions on These Systems

Becker

Schweinhardt

2012

Pain Research and Treatment

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Fibromyalgia is considered a stress-related disorder, and hypo- as well as hyperactive stress systems (sympathetic nervous system and hypothalamic-pituitary-adrenal axis) have been found. Some observations raise doubts on the view that alterations in these stress systems are solely responsible for fibromyalgia symptoms. Cumulative evidence points at dysfunctional transmitter systems that may underlie the major symptoms of the condition. In addition, all transmitter systems found to be altered in fibromyalgia influence the body's stress systems. Since both transmitter and stress systems change during chronic stress, it is conceivable that both systems change in parallel, interact, and contribute to the phenotype of fibromyalgia. As we outline in this paper, subgroups of patients might exhibit varying degrees and types of transmitter dysfunction, explaining differences in symptomatoloy and contributing to the heterogeneity of fibromyalgia. The finding that not all fibromyalgia patients respond to the same medications, targeting dysfunctional transmitter systems, further supports this hypothesis.

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An Elephant Among Us: The Role of Dopamine in the Pathophysiology of Fibromyalgia

Cited by 27 publications

References 28 publications

From Bad to Worse: Striatal Coding of the Relative Value of Painful Decisions

From Bad to Worse: Striatal Coding of the Relative Value of Painful Decisions

The effect of pain on cognitive function: A review of clinical and preclinical research

Dysfunctional Neurotransmitter Systems in Fibromyalgia, Their Role in Central Stress Circuitry and Pharmacological Actions on These Systems

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