Proton MR Spectroscopy in the Evaluation of Cerebral Metabolism in Patients with Fibromyalgia: Comparison with Healthy Controls and Correlation with Symptom Severity

Petrou, M.D. Ilya; Harris, Richard E.; Foerster, Bradley R.; McLean, Samuel A.; Sen, Ananda; Clauw, Daniel J.; Sundgren, Pia C.

doi:10.3174/ajnr.a0959

Cited by 56 publications

(40 citation statements)

References 35 publications

(33 reference statements)

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“…Although the results of these studies are not homogeneous, [21][22][23][24][25][26][27] because of the different MRS protocols, magnetic fields used, and areas of study, in 4 of these, alterations of the glutamatergic system were detected.…”

Section: Discussionmentioning

confidence: 99%

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Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study

Feraco¹,

Bacci²,

Pedrabissi³

et al. 2011

AJNR Am J Neuroradiol

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Section: Discussionmentioning

confidence: 99%

“…Recently, some MRS studies [21][22][23][24][25][26][27] have demonstrated alteration of cerebral metabolites in patients with FM, and though the results are not homogeneous, they strengthen the hypothesis of a neural dysfunction secondary to the pain processing.…”

mentioning

confidence: 94%

Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study

Feraco¹,

Bacci²,

Pedrabissi³

et al. 2011

AJNR Am J Neuroradiol

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“…Recent studies have shown that specific stimuli such as pain or anxiety may markedly influence spectroscopic conditions in the brain metabolically [25,26]. Furthermore, MRS is successfully used in various addictive disorders to elucidate their pathophysiology and withdrawal [27,28,29].…”

Section: Discussionmentioning

confidence: 99%

Insula-Specific 1H Magnetic Resonance Spectroscopy Reactions in Heavy Smokers under Acute Nicotine Withdrawal and after Oral Nicotine Substitution

et al. 2012

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The aim of this study was to clarify whether addiction-specific neurometabolic reaction patterns occur in the insular cortex during acute nicotine withdrawal in tobacco smokers in comparison to nonsmokers. Fourteen male smokers and 10 male nonsmokers were included. Neurometabolites of the right and the left insular cortices were quantified by magnetic resonance spectroscopy (MRS) on a 3-Tesla scanner. Three separate MRS measurements were performed in each subject: among the smokers, the first measurement was done during normal smoking behavior, the second measurement during acute withdrawal (after 24 h of smoking abstinence), and the third shortly after administration of an oral nicotine substitute. Simultaneously, craving, withdrawal symptoms, and CO levels in exhaled air were determined during the three phases. The participants in the control group underwent the same MR protocol. In the smokers, during withdrawal, the insular cortex showed a significant increase in glutamine (Gln; p = 0.023) as well as a slight increase not reaching significance for glutamine/glutamate (Glx; p = 0.085) and a nonsignificant drop in myoinositol (mI; p = 0.381). These values tended to normalize after oral nicotine substitution treatment, even though differences were not significant: Gln (p = 0.225), Glx (p = 0.107) and mI (p = 0.810). Overall, the nonsmokers (control group) did not show any metabolic changes over all three phases (p > 0.05). In smokers, acute nicotine withdrawal produces a neurometabolic reaction pattern that is partly reversed by the administration of an oral nicotine substitute. The results are consistent with the expression of an addiction-specific neurometabolic shift in the brain and confirm the fact that the insular cortex seems to play a possible role in nicotine dependence.

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“…These modifications seem to be caused by what has come to be called "sensitisation": i.e. a permanent state of neuronal hyperexcitability involving all of the peripheral and central structures of the nociceptive system (18)(19)(20)(21)(22)(23). It has only recently been postulated by some researchers that sensitisation of the nociceptive system plays a major role in determining the intensity and chronicisation of the pain accompanying other rheumatic diseases such as OA and rheumatoid arthritis (24)(25)(26).…”

mentioning

confidence: 99%

Physiopathology of pain in rheumatology

et al. 2014

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summary Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.

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Proton MR Spectroscopy in the Evaluation of Cerebral Metabolism in Patients with Fibromyalgia: Comparison with Healthy Controls and Correlation with Symptom Severity

Cited by 56 publications

References 35 publications

Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study

Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study

Insula-Specific 1H Magnetic Resonance Spectroscopy Reactions in Heavy Smokers under Acute Nicotine Withdrawal and after Oral Nicotine Substitution

Physiopathology of pain in rheumatology

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