Reduced brain habituation to somatosensory stimulation in patients with fibromyalgia

Department of Psychology, University of the Balearic Islands, Palma, Balearic Islands, Spain
Arthritis & Rheumatology (Impact Factor: 7.76). 06/2006; 54(6):1995-2003. DOI: 10.1002/art.21910
Source: PubMed


To examine brain activity elicited by repetitive nonpainful stimulation in patients with fibromyalgia (FM) and to determine possible psychophysiologic abnormalities in their ability to inhibit irrelevant sensory information.
Fifteen female patients with a diagnosis of FM (ages 30-64 years) and 15 healthy women (ages 39-61 years) participated in 2 sessions, during which electrical activity elicited in the brain by presentation of either tactile or auditory paired stimuli was recorded using an electroencephalogram. Each trial consisted of 2 identical stimuli (S1 and S2) delivered with a randomized interstimulus interval of 550 msec (+/-50 msec), which was separated by a fixed intertrain interval of 12 seconds. Event-related potentials (ERPs) elicited by 40 trials were averaged separately for each sensory modality.
ERP amplitudes elicited by the somatosensory and auditory S2 stimuli were significantly reduced compared with those elicited by S1 stimuli in the healthy controls. Nevertheless, significant amplitude reductions from S1 stimuli to S2 stimuli were observed in FM patients for the auditory, but not the somatosensory, modality.
Our findings suggest that in FM patients, there is abnormal information processing, which may be characterized by a lack of inhibitory control to repetitive nonpainful somatosensory information during stimulus coding and cognitive evaluation.

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Available from: Pedro Montoya, Oct 04, 2015
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    • "Within the first 150-ms interval, SEPs elicited by non-painful tactile stimuli are usually characterized by a prominent positive peak around 50 ms (P50), followed by a second positive peak around 100 ms after stimulus onset (P100) [6,33,34]. Although both peaks were clearly observable after thumb stimulation in our grand averages, peak detection was difficult in CP individual SEP averages and, therefore, mean amplitudes were computed in two time-windows: 20–70 ms and 70–120 ms after stimulus onset. "
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    ABSTRACT: Although cerebral palsy (CP) is usually defined as a group of permanent motor disorders due to non-progressive disturbances in the developing fetal or infant brain, recent research has shown that CP individuals are also characterized by altered somatosensory perception, increased pain and abnormal activation of cortical somatosensory areas. The present study was aimed to examine hemispheric differences on somatosensory brain processing in individuals with bilateral CP and lateralized motor impairments compared with healthy controls. Nine CP individuals with left-dominant motor impairments (LMI) (age range 5-28 yrs), nine CP individuals with right-dominant motor impairments (RMI) (age range 7-29 yrs), and 12 healthy controls (age range 5-30 yrs) participated in the study. Proprioception, touch and pain thresholds, as well as somatosensory evoked potentials (SEP) elicited by tactile stimulation of right and left lips and thumbs were compared. Pain sensitivity was higher, and lip stimulation elicited greater beta power and more symmetrical SEP amplitudes in individuals with CP than in healthy controls. In addition, although there was no significant differences between individuals with RMI and LMI on pain or touch sensitivity, lip and thumb stimulation elicited smaller beta power and more symmetrical SEP amplitudes in individuals with LMI than with RMI. Our data revealed that brain processing of somatosensory stimulation was abnormal in CP individuals. Moreover, this processing was different depending if they presented right- or left-dominant motor impairments, suggesting that different mechanisms of sensorimotor reorganization should be involved in CP depending on dominant side of motor impairment.
    BMC Neuroscience 01/2014; 15(1):10. DOI:10.1186/1471-2202-15-10 · 2.67 Impact Factor
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    • "Differences in the temporal profile of central responses when patients and controls are subjected to the same amount of stimulation have also been reported. EEG components evoked by nociceptive stimuli have higher amplitude and longer duration (Lorenz et al., 1996) and habituation responses to nonpainful repetitive stimuli are delayed in FMS patients (Montoya et al., 2006). "
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    ABSTRACT: OBJECTIVE: The precise pathophysiology of fibromyalgia, a syndrome characterized by chronic widespread pain, remains to be clarified. When subjected to the same amount of stimulation, patients show enhanced brain responses as compared to controls, providing evidence of central pain augmentation in this syndrome. We aimed to characterize brain response differences when stimulation is adjusted to elicit similar subjective levels of pain in both groups. METHODS: Magnetoencephalography (MEG) was used to investigate the brain responses to pressure stimulation applied both above and below the pain threshold in nine patients and nine control subjects. A device was developed to deliver pressure pulses in a quantifiable and precise manner. The amount of pressure was adjusted to produce similar subjective pain in both groups. RESULTS: A between-group comparison of differences between responses evoked by stimulation above and below the pain threshold was performed using cluster-based permutation testing. Increases in signal amplitude in somatosensory, temporal and parietal areas at short latencies, and in prefrontal areas at both short and long latencies, were found to be larger for patients than for control subjects. CONCLUSION: Fibromyalgia patients show enhanced brain responses after reducing the amount of pressure to produce similar subjective levels of pain than to the control subjects. SIGNIFICANCE: The present results suggest that central pain augmentation is present in fibromyalgia, not only when the objective level of stimulation is kept the same as for control subjects, but also when stimulation is adjusted to produce similar levels of pain in patients and controls.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 10/2012; 124(4). DOI:10.1016/j.clinph.2012.09.015 · 3.10 Impact Factor
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    • "Since similar descending control systems, including attentional and emotional regulatory circuitry, affect multiple sensory modalities [113–119], a dysfunction (or saturation) in these systems could lead to the hypersensitivity in multiple sensory modalities. FM patients show reduced habituation to nonpainful tactile stimuli and increased cortical response to intense auditory stimuli, both of which have been linked to deficient inhibition of incoming sensory stimuli [120, 121]. Also in support of the idea of a central dysregulation or saturation of pain modulation are changes in the opioid and dopamine neurotransmitter systems, both known to be involved in hedonic regulation [122]. "
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    ABSTRACT: Fibromyalgia is characterized by chronic widespread pain, clinical symptoms that include cognitive and sleep disturbances, and other abnormalities such as increased sensitivity to painful stimuli, increased sensitivity to multiple sensory modalities, and altered pain modulatory mechanisms. Here we relate experimental findings of fibromyalgia symptoms to anatomical and functional brain changes. Neuroimaging studies show augmented sensory processing in pain-related areas, which, together with gray matter decreases and neurochemical abnormalities in areas related to pain modulation, supports the psychophysical evidence of altered pain perception and inhibition. Gray matter decreases in areas related to emotional decision making and working memory suggest that cognitive disturbances could be related to brain alterations. Altered levels of neurotransmitters involved in sleep regulation link disordered sleep to neurochemical abnormalities. Thus, current evidence supports the view that at least some fibromyalgia symptoms are associated with brain dysfunctions or alterations, giving the long-held "it is all in your head" view of the disorder a new meaning.
    Pain Research and Treatment 01/2012; 2012(2):585419. DOI:10.1155/2012/585419
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