Abstract:Cortical habituation in episodic migraine patients without medication overuse headache (MOH), recorded by contingent negative variation (CNV), is often reduced compared with healthy controls. There is evidence that with longer duration of migraine disease (DOD) amplitudes and habituation of CNV become progressively abnormal. The aim of the study was to examine habituation characteristics of contingent negative variation in episodic migraine patients suffering from short- and long-lasting migraine compared to m… Show more
“…A recent study reported a similar habituation pattern for the N1 orienting and N2b components to deviant tones in patients and matched controls . Habituation deficits have also been reported for the contingent negative variation CNV; in particular the initial (or early) CNV, which reflects the orienting properties of a warning stimulus in an active paradigm, was found increased in migraine . P300 (P3a and/or P3b) responses elicited by various paradigms also showed a deficit of habituation but not systematically .…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 65%
“…74,75 Habituation deficits have also been reported for the contingent negative variation CNV; in particular the initial (or early) CNV, which reflects the orienting properties of a warning stimulus in an active paradigm, was found increased in migraine. [76][77][78][79] P300 (P3a and/or P3b) responses elicited by various paradigms also showed a deficit of habituation 73,80-82 but not systematically. 74 Mismatch negativity (MMN) habituation has been reported as deficient in a first study, 104 but not in a more recent one.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 95%
“…Enhanced 65,[68][69][70][71] or normal 64 IDAP in migraineurs Deficit 68,69 or normal 64 in long-term habituation through IDAP paradigms Deficit of short-term habituation in migraineurs 72,73 Normal habituation for N1 orienting and N2b component 74,75 Habituation deficit of CNV in migraineurs [76][77][78][79] Deficit 73,80-82 or normal 74 habituation of P300 component in migraineurs Before a migraine attack Normalization of the lack of habituation of CNV 77 Somatosensory and painful stimuli Between migraine attacks Habituation deficit of N20 component [83][84][85] Habituation deficit of the N2-P2 amplitude in response to trigeminal and extra-trigeminal stimulation 86,87 without aura and controls, suggesting an alteration of neuronal inhibition within the visual system of patients with migraine with aura. 88 Auditory Evoked Potentials (AEPs).-Most studies showed normal short-latency (brainstem evoked potential) 64,89,90 and cortical auditory evoked potentials N100 and P200 in migraineurs during the headache-free period.…”
Section: Auditory Stimuli Between Migraine Attacksmentioning
confidence: 99%
“…Migraine patients also show increased CNV, which has been the first cognitive ERP investigated in migraineurs. 77,79,109 The CNV amplitude increase observed in migraineurs concerns mostly the early component (iCNV) and is associated with a decrease, or even a lack, of habituation over successive trials (see above). These CNV abnormalities suggest an increased orienting process and have been considered as a possible vulnerability marker for migraine.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 99%
“…Moreover, adult patients with a long disease history (>120 months) have higher CNV amplitudes than patients with a short history (<120 months) of migraine. 79 A few longitudinal studies investigated changes of CNV in children with migraine and age-matched control. 111,112 Over an 8-year period CNV amplitude tended to decrease and habituation of iCNV to increase in both groups, but this effect of brain maturation was less in migraineurs with persisting headaches than in healthy subjects and migraineurs in remission.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
Whereas considerable data have been generated about the pathophysiology of pain processing during migraine attacks, relatively little is known about the neural basis of sensory hypersensitivity. In migraine, the term "hypersensitivity" encompasses different and probably distinct pathophysiological aspects of sensory sensitivity. During attacks, many patients have enhanced sensitivity to visual, auditory and/or olfactory stimuli, which can enhance headache while interictally, migraineurs often report abnormal sensitivity to environmental stimuli that can cause nonpainful discomfort. In addition, sensorial stimuli can influence and trigger the onset of migraine attacks. The pathophysiological mechanisms and the origin of such sensitivity (individual predisposition to develop migraine disease or consequence of repeated migraine attacks) are ill understood. Functional neuroimaging and electrophysiological studies allow for noninvasive measures of neuronal responses to external stimuli and have contributed to our understanding of mechanisms underlying sensory hypersensitivity in migraine. The purpose of this review is to present pivotal neuroimaging and neurophysiological studies that explored the basal state of brain responsiveness to sensory stimuli in migraineurs, the alterations in habituation and attention to sensory inputs, the fluctuations of responsiveness to sensory stimuli before and during migraine attacks, and the relations between sensory hypersensitivity and clinical sensory complaints.
“…A recent study reported a similar habituation pattern for the N1 orienting and N2b components to deviant tones in patients and matched controls . Habituation deficits have also been reported for the contingent negative variation CNV; in particular the initial (or early) CNV, which reflects the orienting properties of a warning stimulus in an active paradigm, was found increased in migraine . P300 (P3a and/or P3b) responses elicited by various paradigms also showed a deficit of habituation but not systematically .…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 65%
“…74,75 Habituation deficits have also been reported for the contingent negative variation CNV; in particular the initial (or early) CNV, which reflects the orienting properties of a warning stimulus in an active paradigm, was found increased in migraine. [76][77][78][79] P300 (P3a and/or P3b) responses elicited by various paradigms also showed a deficit of habituation 73,80-82 but not systematically. 74 Mismatch negativity (MMN) habituation has been reported as deficient in a first study, 104 but not in a more recent one.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 95%
“…Enhanced 65,[68][69][70][71] or normal 64 IDAP in migraineurs Deficit 68,69 or normal 64 in long-term habituation through IDAP paradigms Deficit of short-term habituation in migraineurs 72,73 Normal habituation for N1 orienting and N2b component 74,75 Habituation deficit of CNV in migraineurs [76][77][78][79] Deficit 73,80-82 or normal 74 habituation of P300 component in migraineurs Before a migraine attack Normalization of the lack of habituation of CNV 77 Somatosensory and painful stimuli Between migraine attacks Habituation deficit of N20 component [83][84][85] Habituation deficit of the N2-P2 amplitude in response to trigeminal and extra-trigeminal stimulation 86,87 without aura and controls, suggesting an alteration of neuronal inhibition within the visual system of patients with migraine with aura. 88 Auditory Evoked Potentials (AEPs).-Most studies showed normal short-latency (brainstem evoked potential) 64,89,90 and cortical auditory evoked potentials N100 and P200 in migraineurs during the headache-free period.…”
Section: Auditory Stimuli Between Migraine Attacksmentioning
confidence: 99%
“…Migraine patients also show increased CNV, which has been the first cognitive ERP investigated in migraineurs. 77,79,109 The CNV amplitude increase observed in migraineurs concerns mostly the early component (iCNV) and is associated with a decrease, or even a lack, of habituation over successive trials (see above). These CNV abnormalities suggest an increased orienting process and have been considered as a possible vulnerability marker for migraine.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
confidence: 99%
“…Moreover, adult patients with a long disease history (>120 months) have higher CNV amplitudes than patients with a short history (<120 months) of migraine. 79 A few longitudinal studies investigated changes of CNV in children with migraine and age-matched control. 111,112 Over an 8-year period CNV amplitude tended to decrease and habituation of iCNV to increase in both groups, but this effect of brain maturation was less in migraineurs with persisting headaches than in healthy subjects and migraineurs in remission.…”
Section: Alteration Of Habituation and Attention To Sensory Inputs Inmentioning
Whereas considerable data have been generated about the pathophysiology of pain processing during migraine attacks, relatively little is known about the neural basis of sensory hypersensitivity. In migraine, the term "hypersensitivity" encompasses different and probably distinct pathophysiological aspects of sensory sensitivity. During attacks, many patients have enhanced sensitivity to visual, auditory and/or olfactory stimuli, which can enhance headache while interictally, migraineurs often report abnormal sensitivity to environmental stimuli that can cause nonpainful discomfort. In addition, sensorial stimuli can influence and trigger the onset of migraine attacks. The pathophysiological mechanisms and the origin of such sensitivity (individual predisposition to develop migraine disease or consequence of repeated migraine attacks) are ill understood. Functional neuroimaging and electrophysiological studies allow for noninvasive measures of neuronal responses to external stimuli and have contributed to our understanding of mechanisms underlying sensory hypersensitivity in migraine. The purpose of this review is to present pivotal neuroimaging and neurophysiological studies that explored the basal state of brain responsiveness to sensory stimuli in migraineurs, the alterations in habituation and attention to sensory inputs, the fluctuations of responsiveness to sensory stimuli before and during migraine attacks, and the relations between sensory hypersensitivity and clinical sensory complaints.
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