Activation of the somatosensory cortex during Aβ-fiber mediated hyperalgesia

Baron, Ralf; Baron, Yvonne; Disbrow, Elizabeth A.; Roberts, Timothy P. L.

doi:10.1016/s0006-8993(00)02444-6

Cited by 31 publications

(6 citation statements)

References 32 publications

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“…From a physiological point of view, demonstrative of central sensitization are the plastic changes in neural networks devoted to the processing of pain information [27] that results in abnormal neural excitability with decreased nociceptive thresholds and increased responsiveness to noxious and usually innocuous peripheral stimuli, such as, in our case, somatosensory ones [28]. Experimental studies in animals [29] and humans [30] show that SSEP amplitudes increase when transient intense activation of nociceptive afferents induces central sensitization, as happens in clinical pain conditions including chronic headache. Our study shows that sensitization, as reflected by increased initial SSEP amplitudes, is equally present in CM and MOi, although we managed not to record CM patients during a full-blown migraine attack.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological correlates of episodic migraine chronification: evidence for thalamic involvement

et al. 2013

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BackgroundEpisodic migraine is characterized by decreased high-frequency somatosensory oscillations (HFOs), reflecting thalamo-cortical activity, and deficient habituation of low-frequency (LF-) somatosensory evoked potentials (SSEPs) to repetitive sensory stimulation between attacks. Here, we study conventional LF-SSEPs and HFOs in episodic migraineurs who developed chronic migraine (CM).MethodsThirty-four episodic (15 interictally [MOii], 19 ictally [MOi]) and 19 CM patients underwent right median nerve SSEPs. The patient groups were compared to a group of 20 healthy volunteers (HV) of comparable age and gender distribution. We measured the N20-P25 LF-SSEP 1st amplitude block and habituation, and, after applying a band-pass filter (450–750 Hz), maximal peak-to-peak latency and the amplitudes of the early and late HFOs.ResultsReduced early HFOs, lower 1st block LF-SSEPs and deficient habituation characterize MOii. Initially higher SSEP amplitudes and late normal habituation characterize both CM and MOi patients. After the digital filtration, both patient groups showed shortened latency peaks and normalization of early HFO amplitudes with increased late HFOs. When data of MO and CM patients were combined, the monthly number of days with headache negatively correlated with the LF-SSEP slope (r = −0.385, p = 0.006), which in turn negatively correlated with the 1st amplitude block (r = 0.568, p < 0.001).ConclusionsOur results show abnormalities in chronic migraine that are also reported during attacks in episodic migraineurs, namely early response sensitization and late habituation. The HFO analysis suggests that this sensory sensitization may be explained by an increase in the strength of the connections between the thalamus and cortex compared to episodic migraine between attacks. Whether this electro-functional behaviour is primary or secondary to daily headache, thus reflecting an electrophysiological fingerprint of the somatosensory system central sensitization process, remains to be determined.

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Section: Discussionmentioning

confidence: 99%

Electrophysiological correlates of episodic migraine chronification: evidence for thalamic involvement

et al. 2013

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“…Illustrative of central sensitization are the plastic changes in neural structures belonging to the "pain matrix" [19] that result in decreased nociceptive thresholds and increased responsiveness to noxious and innocuous peripheral stimuli [20]. Studies in animals [21] and humans [22] show that SEP amplitudes increase when transient intense activation of nociceptive afferents induces central sensitization, as happens in clinical pain conditions including chronic headache. Our study shows that sensitization, as reflected by increased initial SEP amplitudes, is common to MOH and migraine attacks, although we did not record MOH patients during an attack.…”

Section: Discussionmentioning

confidence: 99%

Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

et al. 2010

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BackgroundMedication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura (MOA) characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli (habituation deficit), despite a normal initial amplitude (lack of sensitization). Whether central sensitization alters this electrophysiological profile is unknown. We therefore sought differences in somatosensory evoked potential (SEP) sensitization and habituation in patients with MOH and episodic MOA.MethodsWe recorded median-nerve SEPs (3 blocks of 100 sweeps) in 29 patients with MOH, 64 with MOA and 42 controls. Episodic migraineurs were studied during and between attacks. We measured N20-P25 amplitudes from 3 blocks of 100 sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks.ResultsIn episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally. Patients with MOH had larger-amplitude block 1 SEPs than controls, and also lacked SEP habituation. SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs (NSAIDs) or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification.Conclusions In patients with MOH, especially those overusing NSAIDs, the somatosensory cortex becomes increasingly sensitized. Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission.

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“…Additionally, a study of capsaicin-induced CS observing somatosensory evoked potentials showed increased excitability in the somatosensory cortex. 27 In patients with fibromyalgia, region-specific changes in the gray matter volume of the prefrontal cortex, anterior cingulate cortex, insula, thalamus, pons and left precuneus, altered functional connectivity in the descending pain-modulating system, and increased activity in the pain matrix related to CS, such as the dorsolateral prefrontal cortex, periaqueductal gray and anterior cingulate cortex, have been reported. 28 In patients with chronic fatigue syndrome, the white matter volume in the midbrain 29 and left inferior fronto-occipital fasciculus are decreased 30 and this volume correlated with disease duration.…”

Section: Methodsmentioning

confidence: 99%

Central Sensitization in Migraine: A Narrative Review

Suzuki¹,

Suzuki²,

Shiina³

et al. 2022

JPR

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Central sensitization (CS) is an increase in the responsiveness of nociceptive neurons in the central nervous system to their normal afferent input. As a result, even minor irritation can induce severe pain, leading to the chronicity and severity of various diseases, such as neurological disorders. CS is associated with migraine, which is a major neurological disorder that inflicts a high disability in daily life. Specifically, CS is thought to be involved in the pathogenesis of cutaneous allodynia as well as chronification of migraine. In this article, we reviewed the association between CS and migraine, including pathophysiological aspects and evidence from clinical studies. We suggest that appropriate screening and management of CS in migraine could further improve the quality of life of migraine patients.

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Activation of the somatosensory cortex during Aβ-fiber mediated hyperalgesia

Cited by 31 publications

References 32 publications

Electrophysiological correlates of episodic migraine chronification: evidence for thalamic involvement

Electrophysiological correlates of episodic migraine chronification: evidence for thalamic involvement

Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

Central Sensitization in Migraine: A Narrative Review

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