Effects of Topiramate on Migraine Frequency and Cortical Excitability in Patients with Frequent Migraine

Артеменко, А. Р.; Al, Kurenkov; Filatova, E G; Nikitin, S S; Kaube, Holger; Katsarava, Zaza

doi:10.1111/j.1468-2982.2007.01491.x

Cited by 30 publications

(26 citation statements)

References 26 publications

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“…This is consistent with a previous study showing that the anticonvulsant drug topiramate may reduce migraine headaches. 24 However, the drug did cause a headache in one of our patients, a result consistent with the findings of Piovesan et al 25 There are several potential limitations of this study. Firstly, this paper is only a descriptive case series and not a randomised controlled trial.…”

Section: Discussionsupporting

confidence: 85%

Oxcarbazepine for the treatment of binge eating disorder: a case series

et al. 2008

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We present a case series of nine obese outpatients with a diagnosis of binge eating disorder who were treated with a flexible dose of the anticonvulsant oxcarbazepine. The drug has not previously been used to treat this disorder. Five patients dropped out at various points of the study, giving only fragmented data. Where data were available, all patients reported side effects (n=7) and some showed a reduction (n=4) or no change (n=3) in binge episode frequency. Some patients lost weight over the study period (n=3; range, 3-5 kg); others showed no change (n=2) or an increase in weight (n=3; range, 1.8-2.9 kg). Our results were inconsistent, but the drug was effective for some patients who showed marked impulsivity in eating behaviours and depressive symptoms.

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Section: Discussionsupporting

confidence: 85%

Oxcarbazepine for the treatment of binge eating disorder: a case series

et al. 2008

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“…In an open label trial with levetiracetam change of headache frequency and change of PT were negatively correlated at the 10% but not at the 5% significance level [25]. Mean PT were also increased following preventive treatment with topiramate in patients with migraine without aura [24]. Surprisingly, an inverse correlation was reported between decrease of migraine frequency and increase of mean PT.…”

Section: Discussionmentioning

confidence: 99%

“…Findings of previous studies and the present data suggest that migraine prophylaxis with different centrally acting substances may be more complex and cannot only be explained by modification of cortical excitability. A non-linear relation between migraine activity and PT in patients with frequent migraine has also been discussed [24]. …”

Section: Discussionmentioning

confidence: 99%

“…Most studies reported decreased PT suggesting a higher excitability of the visual cortex between attacks [17–22], but opposite findings (increased PT, reduced excitability) have been reported by some authors [11, 23]. Using TMS an increase of mean PT in migraine patients was found in few uncontrolled trials following treatment with valproate [19], topiramate [24] and levetiracetam [25]. …”

Section: Introductionmentioning

confidence: 99%

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Beta-blocker migraine prophylaxis affects the excitability of the visual cortex as revealed by transcranial magnetic stimulation

et al. 2011

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The objective of this study is to assess effects of beta-blocker migraine prophylaxis on cortical excitability determined by transcranial magnetic stimulation (TMS). Phosphene and motor thresholds (PT, MT) were investigated in 29 patients with migraine, in 15 of them prior to and following preventive medication with metoprolol and in 14 patients without prophylaxis. Following prophylaxis headache frequency significantly decreased (p = 0.005) and mean PT were significantly increased (51.5 ± 7.5 vs. 63.6 ± 8.4%) compared to patients without preventive treatment (53.7 ± 5.3 vs. 52.3 ± 6.3%; p = 0.040). Mean MT did not significantly differ either between groups or due to treatment. In the group of all patients, a significant inverse correlation between headache frequency and the level of PT was found (R = −0.629; p < 0.01). There was, however, no significant correlation in the subgroups of patients. We conclude that (a) clinical efficacy of beta-blocker treatment in migraine could be (at least partly) linked to its ability to modulate the excitability of the visual cortex and (b) the PT determined by TMS appears suitable to assess the effects of prophylaxis on cortical excitability in the individual patient. This may be useful in clinical trials investigating migraine preventive drugs.

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“…Preventive treatment for migraine which is essentially the same for patients with or without aura, has modulatory role on excitability of the cerebral cortex. Neurophysiological studies demonstrated that the cortical hyper-responsivity in migraine patients seemed to be normalized during preventive medication, in parallel to clinical improvement (Artemenko et al 2008;Mulleners et al 2002;Schoenen et al 1986). The application of cathodal stimulation over the occipital cortex could play a role with regard to pain control in migraine (Antal et al 2011).…”

Section: Effective Preventive Medications Modulate Cortical Excitabilitymentioning

confidence: 96%

The first phase of a migraine attack resides in the cortex

Bolay

2012

J Neural Transm

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Migraine headache is generated by the complex interaction of various players such as genetic predisposition, environmental triggers and intrinsic factors. The initial mechanism of a migraine attack has long been a controversial topic and exploring its origin is a challenging task. The scientific evidences so far indicate neuronal dysfunction in the cerebral cortex and particularly cortical spreading depression waves, as upstream to cascade of events leading to a migraine attack. Neocortex, evolutionary valuable part of the brain, is surrounded by pain sensing system that is finely tuned for detecting noxious signals. Abnormal functioning of more than one cortical area in migraineurs may suggest that hyperexcitable neocortex could be more easily challenged, overreacts and depolarize to repetitive sensorial stimuli and could switch to extreme excitability state where spreading depression waves occur. In this paper, I will review the data supporting the notion that migraine is a neuronal disorder where cortex has prime importance. Despite clear demonstration of cortical participation in migraine, the contribution of brain structures other than cortex to the development of migraine remains unclear.

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Effects of Topiramate on Migraine Frequency and Cortical Excitability in Patients with Frequent Migraine

Cited by 30 publications

References 26 publications

Oxcarbazepine for the treatment of binge eating disorder: a case series

Oxcarbazepine for the treatment of binge eating disorder: a case series

Beta-blocker migraine prophylaxis affects the excitability of the visual cortex as revealed by transcranial magnetic stimulation

The first phase of a migraine attack resides in the cortex

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