Table 6 Neural imaging in fibromyalgia (FM)

Giesecke and colleagues [37]

QST evoked rCBF association to depression

Pressure pain MRS

Clinical pain intensity – associated with increased rCBF of insula bilaterally, contralateral ACC, prefrontal cortex. Symptoms of depression – not associated with increased rCBF of SI, SII; associated amygdala and contralateral anterior insula

Gracely and colleagues [40]

QST evoked rCBF association to catastrophizing

Pressure pain MRS

Both low and high with increased rCBF in contralateral insula, SI, SII, inferior parietal lobule and thalamus, ipsilateral S1, cerebellum, posterior cingulated gyrus, and superior and inferior frontal gyrus. High catastrophizers with unique activation in contralateral anterior ACC, contralateral ipsilateral lentiform

Giesecke and colleagues [124]

QST evoked rCBF

Pressure pain MRS

In CLBP and FM patients, QST (equal pressure) increased rCBF of contralateral SI and SII, inferior parietal lobule, cerebellum, and ipsilateral SII. In HC, QST (equal pressure) activation of contralateral SII. Equal evoked equal pain associated with similar activation

Koeppe and colleagues [39]

Injection of 5-HT-3 receptor antagonist (topisetron) rCBF

n/a

In FM patients, topisetron treatment reduced rCBF of SI, contralateral posterior insula, ACC

Cook and colleagues [38]

QST evoked activation of rCBF

Nonpainful and painful heat, 47°C

In FM, nonpainful heat increased rCBF in prefrontal, supplemental motor, insular, and ACC as compared with HC. In FM patients, painful heat increased activity in contralateral insular cortex as compared with HC

Gracely and colleagues [126]

QST evoked activation of rCBF

Pressure pain MRS, neutral site

Common areas of evoked equal pain increased rCBF including contralateral SI, inferior parietal lobule, SII, superior temporal gyrus (STG), insula, putamen, and ipsilateral cerebellum. Decreased rCBF in ipsilateral SI. In HC, QST (equal pressure) activated ipsilateral STG and precentral gyrus

Yunus and colleagues [130]

Resting rCBF

n/a

No difference

Chang and colleagues [131]

QST evoked activation of rCBF

Noxious visceral and somatic pressure

In IBS patients, noxious visceral stimuli evoked increased rCBF increase in middle subregion of the ACC. In IBS + FM patients, somatic stimuli evoked greater rCBF in middle subregion of the ACC extending to ACC and the thalamus

Wik and colleagues [132]

QST evoked activation of rCBF

Acute pain

In FM patients, frontal and parietal cortical activation during acute pain compared with rest (as expected). Reduced rCBF in retrosplenial cortex (evaluative processing)

Wood and colleagues [41]

QST evoked binding of D2/D3 ligand

Nonpainful and painful saline injection

In FM patients, lack of dopamine release in basal ganglia compared with HC during painful stimuli. In HC, amount of dopamine release correlated with amount of perceived pain; in FM patients, no such correlation observed

Adiguzel and colleagues [42]

Amitriptyline (3 months) resting rCBF

n/a

Increased rCBF in bilateral hemithalami after amitriptyline. No correlation between symptoms and findings

Gur and colleagues [45]

Resting rCBF

n/a

Increased rCBF in caudate nucleus. FM patients with less depression had increased uptake in pons

Kwiatek and colleagues [43]

Resting rCBF

n/a

Reduced rCBF in right thalamus and potine tegmentum, no reduction in left thalamus, or caudate nucleus. No correlation between symptoms and findings

Mountz and colleagues [44]

Resting rCBF

n/a

Reduced rCBF in bilateral hemithalami and caudate nucleus correlated with low pain threshold No correlation between symptoms and findings