Prediction of migraine attacks using a slow cortical potential, the contingent negative variation

Kropp, Peter; Gerber, Wolf‐Dieter

doi:10.1016/s0304-3940(98)00811-8

Cited by 138 publications

(169 citation statements)

References 15 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…In this way, we avoided possible preictal~Kropp & Gerber, 1995! or postictal Kropp & Gerber, 1998! effects on CNV amplitudes in headachefree migraineurs.…”

Section: Methodsmentioning

confidence: 99%

Reduced sensory anticipation in migraine

2002

View full text Add to dashboard Cite

We examined differences between migraine patients and matched healthy controls in anticipatory processes preceding a warning stimulus and preceding a response stimulus during a forewarned choice reaction time task. We manipulated stimulus preceding negativity~SPN! by inserting full response information either at the instant of the warning stimulus cue! or at the instant of the response stimulus. In contrast to control subjects, migraineurs with aura show low anticipation towards an informative cue and high anticipation towards a noninformative cue. Migraineurs without aura showed a cortical hypoactivation during motor preparation prior to the response stimulus. We propose a functional deficiency within frontal structures or the anterior cingulate cortex in migraine. This might explain the reduced anticipation, as well as the slow responses during selective attention that we previously reported in these patients.

show abstract

“…In this way, we avoided possible preictal~Kropp & Gerber, 1995! or postictal Kropp & Gerber, 1998! effects on CNV amplitudes in headachefree migraineurs.…”

Section: Methodsmentioning

confidence: 99%

Reduced sensory anticipation in migraine

2002

View full text Add to dashboard Cite

show abstract

“…During the days preceding an attack, CNV and P300 habituation is minimal, and the ampli tude of these responses is maximal. 70,71 Within the 12-24 h immediately preceding an attack, and during the attack, habituation of evoked potentials normalizes. This pattern has been shown for CNV, 36,70,71 VEP, 57,72 and SSEP 61 amplitudes, and for visual P300 latency.…”

Section: Episodic Migrainementioning

confidence: 99%

“…70,71 Within the 12-24 h immediately preceding an attack, and during the attack, habituation of evoked potentials normalizes. This pattern has been shown for CNV, 36,70,71 VEP, 57,72 and SSEP 61 amplitudes, and for visual P300 latency. 73 The R2 component recorded during blink reflexes-evoked by an electrical stimulus delivered with a classic non nociceptive surface electrode-showed a habituation deficit in patients before a migraine attack, 76 although in another study only slight habituation abnormalities were found interictally.…”

Section: Episodic Migrainementioning

confidence: 99%

“…Interestingly, the habituation deficit reappears when patients evolve from chronic to episodic migraine. 83 Since the response pattern in chronic migraine is indistinguishable from that observed during migraine attacks, 43,[51][52][53][54][55][56][57][58][59][60][61][62][70][71][72] our research group has suggested that patients with chronic migraine are locked in an ictal like state. 84 The most prevalent factor associated with the tran sition from episodic to chronic migraine is acute medication overuse.…”

Section: Chronic Migrainementioning

confidence: 99%

See 1 more Smart Citation

Altered processing of sensory stimuli in patients with migraine

et al. 2014

View full text Add to dashboard Cite

| Migraine is a cyclic disorder, in which functional and morphological brain changes fluctuate over time, culminating periodically in an attack. In the migrainous brain, temporal processing of external stimuli and sequential recruitment of neuronal networks are often dysfunctional. These changes reflect complex CNS dysfunction patterns. Assessment of multimodal evoked potentials and nociceptive reflex responses can reveal altered patterns of the brain's electrophysiological activity, thereby aiding our understanding of the pathophysiology of migraine. In this Review, we summarize the most important findings on temporal processing of evoked and reflex responses in migraine. Considering these data, we propose that thalamocortical dysrhythmia may be responsible for the altered synchronicity in migraine. To test this hypothesis in future research, electrophysiological recordings should be combined with neuroimaging studies so that the temporal patterns of sensory processing in patients with migraine can be correlated with the accompanying anatomical and functional changes.

show abstract

“…In addition, VEP and IDAP as well as CNV were found to undergo marked changes in temporal relation to the attack. Amplitudes tended to normalize during the attack [62], but they increased 2 days before the attack and returned to interictal levels during the days following the attack [69,73,74]. In most previous studies of evoked-or event-related potentials, the delay between the recordings and the next attack was not determined, which may in part account for the variability of findings.…”

Section: Psychophysical Studies Of the Visual Pathwaysmentioning

confidence: 99%

Cortical excitability in migraine

Áfra¹

2000

J Headache Pain

View full text Add to dashboard Cite

Cortical hyperexcitability in migraine has been suggested to play a pivotal role in triggering migraine attacks, possibly via generation of spreading depression. Low levels of plasma, intracellular and brain magnesium as well as increased amplitudes of visual evoked potentials support this theory. More recent data on evoked and event related potentials, i.e. lack of habituation and low initial amplitudes during repetitive stimulation, however, may indicate reduced levels of cortical excitability. Transcranial magnetic stimulation of motor and visual cortices, a direct method to assess cortical excitability, yielded contradictory results. Lower or elevated motor thresholds, amplitudes and/or phosphene prevalence or even no significant differences at all were demonstrated suggesting also cortical hypo-rather than hyperexcitability in migraine. Methodological differences, selection of subjects, and timing of investigations might partly explain these marked differences. Clinical and genetic heterogeneity of migraine, for instance via opposite influence on neuronal excitability caused by recently described ionchannel mutations, might provide further explanation.

show abstract

Prediction of migraine attacks using a slow cortical potential, the contingent negative variation

Cited by 138 publications

References 15 publications

Reduced sensory anticipation in migraine

Reduced sensory anticipation in migraine

Altered processing of sensory stimuli in patients with migraine

Cortical excitability in migraine

Contact Info

Product

Resources

About