Reduced Presynaptic Dopamine Activity in Fibromyalgia Syndrome Demonstrated With Positron Emission Tomography: A Pilot Study

Wood, Patrick B.; Patterson, James C.; Sunderland, John; Tainter, Kerrie H.; Glabus, Michael F.; Lilien, David L.

doi:10.1016/j.jpain.2006.05.014

Cited by 215 publications

(141 citation statements)

References 55 publications

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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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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

View full text Add to dashboard Cite

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“…Although the disorder has been dismissed by many physicians as purely psychological, recent neuroimaging studies show alterations in sensory processing (Gracely et al, 2002) and neurochemical abnormalities (Wood et al, 2006), indicating that fibromyalgia is associated with alterations in the brain's neural functioning.…”

Section: Introductionmentioning

confidence: 99%

Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain?

Kuchinad

Schweinhardt²,

Seminowicz³

et al. 2007

J. Neurosci.

530

361

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Fibromyalgia is an intractable widespread pain disorder that is most frequently diagnosed in women. It has traditionally been classified as either a musculoskeletal disease or a psychological disorder. Accumulating evidence now suggests that fibromyalgia may be associated with CNS dysfunction. In this study, we investigate anatomical changes in the brain associated with fibromyalgia. Using voxel-based morphometric analysis of magnetic resonance brain images, we examined the brains of 10 female fibromyalgia patients and 10 healthy controls. We found that fibromyalgia patients had significantly less total gray matter volume and showed a 3.3 times greater ageassociated decrease in gray matter than healthy controls. The longer the individuals had had fibromyalgia, the greater the gray matter loss, with each year of fibromyalgia being equivalent to 9.5 times the loss in normal aging. In addition, fibromyalgia patients demonstrated significantly less gray matter density than healthy controls in several brain regions, including the cingulate, insular and medial frontal cortices, and parahippocampal gyri. The neuroanatomical changes that we see in fibromyalgia patients contribute additional evidence of CNS involvement in fibromyalgia. In particular, fibromyalgia appears to be associated with an acceleration of age-related changes in the very substance of the brain. Moreover, the regions in which we demonstrate objective changes may be functionally linked to core features of the disorder including affective disturbances and chronic widespread pain.

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“…Interestingly, it has been shown in both animal and human chronic pain syndromes that there is a decrease in the tonic levels of dopamine in brain areas such as the prefrontal cortex, striatum, and hippocampus (Wood et al, 2007a;Wood et al, 2007b;Pais-Vieira et al, 2009), whereas there is some evidence of a correlation between a decrease in reduced dopamine activity and a decrease in hippocampal gray matter in chronic pain patients (Wood et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Activation of Dopaminergic D2/D3 Receptors Modulates Dorsoventral Connectivity in the Hippocampus and Reverses the Impairment of Working Memory after Nerve Injury

et al. 2014

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Dopamine plays an important role in several forms of synaptic plasticity in the hippocampus, a crucial brain structure for working memory (WM) functioning. In this study, we evaluated whether the working-memory impairment characteristic of animal models of chronic pain is dependent on hippocampal dopaminergic signaling. To address this issue, we implanted multichannel arrays of electrodes in the dorsal and ventral hippocampal CA1 region of rats and recorded the neuronal activity during a food-reinforced spatial WM task of trajectory alternation. Within-subject behavioral performance and patterns of dorsoventral neuronal activity were assessed before and after the onset of persistent neuropathic pain using the Spared Nerve Injury (SNI) model of neuropathic pain. Our results show that the peripheral nerve lesion caused a disruption in WM and in hippocampus spike activity and that this disruption was reversed by the systemic administration of the dopamine D2/D3 receptor agonist quinpirole (0.05 mg/kg). In SNI animals, the administration of quinpirole restored both the performance-related and the task-related spike activity to the normal range characteristic of naive animals, whereas quinpirole in sham animals caused the opposite effect. Quinpirole also reversed the abnormally low levels of hippocampus dorsoventral connectivity and phase coherence. Together with our finding of changes in gene expression of dopamine receptors and modulators after the onset of the nerve injury model, these results suggest that disruption of the dopaminergic balance in the hippocampus may be crucial for the clinical neurological and cognitive deficits observed in patients with painful syndromes.

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Reduced Presynaptic Dopamine Activity in Fibromyalgia Syndrome Demonstrated With Positron Emission Tomography: A Pilot Study

Cited by 215 publications

References 55 publications

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

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

Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain?

Activation of Dopaminergic D2/D3 Receptors Modulates Dorsoventral Connectivity in the Hippocampus and Reverses the Impairment of Working Memory after Nerve Injury

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