1 Hz rTMS enhances extrastriate cortex activity in migraine

Fierro, Brigida; Ricci, Raffaella; Piazza, Aurelio; Scalia, Simona; Giglia, Giuseppe; Vitello, G.; Brighina, Filippo

doi:10.1212/01.wnl.0000094823.74175.92

Cited by 54 publications

(44 citation statements)

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“…In visual cortex, the deficiency of the inhibitory tone was suggested to explain the lack of inhibitory effects to single pulse TMS [28] and the paradoxical facilitation to 1 Hz rTMS [13,29]. In motor cortex, more direct evidence on the activity of inhibitory circuits has been achieved by techniques like paired pulse stimulation [14] or cortical silent period [30][31][32] that allow exploration of GABA Aand GABA B -mediated circuits.…”

Section: Discussionmentioning

confidence: 99%

Reduced Cerebellar Inhibition in Migraine with Aura: A TMS Study

et al. 2009

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Subtle clinical cerebellar alterations have been found in migraine. Moreover, abnormalities in visual and motor cortex excitability consistent with a lack of inhibitory efficiency have been described in migraine, and it is known that cerebellum exerts an inhibitory control on cerebral cortex. Here, we investigated if impairment of cerebellar activity on motor cortex, i.e. reduced inhibitory control, can be found in migraine. Ten migraineurs with aura and seven healthy controls underwent a transcranial magnetic stimulation (TMS) protocol to investigate the cerebellar inhibitory drive on motor cortex: a conditioning pulse on right cerebellar cortex was delivered 5, 7, 10, 15 ms before a test stimulus (TS) on contralateral motor cortex. The cerebellar conditioning stimulus inhibits the size of the motor-evoked potential (MEP) produced by the TS alone by approximately 30-50%. Amplitude of MEP to TS alone showed no significant difference between patients and controls. Cerebellar conditioning TMS showed a significant deficit of cerebellar inhibition in migraine patients as compared to controls at all interstimulus intervals (5-15 ms) tested. Cerebellar inhibition is reduced in migraineurs. This could account, at least in part, for the reduced inhibitory efficiency previously showed in cerebral cortex of these patients.

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Section: Discussionmentioning

confidence: 99%

Reduced Cerebellar Inhibition in Migraine with Aura: A TMS Study

et al. 2009

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“…In another study with rTMS in MwA patients, a failure of inhibitory circuits also involving the extrastriate cortex was reported. 19 A study by Afra et al 5 showing occipital hypoexcitability rather than hyperexcitability in MwA patients was later criticized by Aurora and Welch 36 In their letter they suggested that this controversy might be explained by different methods used in different studies (i.e. type of stimulator, size of coil, intensity of the stimulus).…”

Section: Discussionmentioning

confidence: 99%

“…Motor symptoms in some migraine subtypes have also drawn attention to the hyperexcitability of motor cortex. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Transcranial magnetic stimulation (TMS) is a non-invasive tool to investigate physiology and excitability of both motor-and occipital cortices. 11,[21][22][23][24][25] The changes in motor threshold, latency and amplitude of motor evoked potential, central motor conduction time and cortical silent period after magnetic ABSTRACT: Objective: We evaluated motor and occipital cortex excitability in migraine patients using transcranial magnetic stimulation.…”

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confidence: 99%

Motor and Occipital Cortex Excitability in Migraine Patients

et al. 2006

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Recent studies have demonstrated that central neuronal hyperexcitability has an important role in migraine pathogenesis. Hyperexcitability of occipital cortex has been proposed to be responsible for the elaboration of migraine attacks and visual aura. Motor symptoms in some migraine subtypes have also drawn attention to the hyperexcitability of motor cortex. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Transcranial magnetic stimulation (TMS) is a non-invasive tool to investigate physiology and excitability of both motor-and occipital cortices. 11,[21][22][23][24][25] The changes in motor threshold, latency and amplitude of motor evoked potential, central motor conduction time and cortical silent period after magnetic ABSTRACT: Objective: We evaluated motor and occipital cortex excitability in migraine patients using transcranial magnetic stimulation. Methods: In this study, we included 15 migraine patients with aura (MwA), 15 patients without aura (MwoA) between attacks, and 31 normal healthy controls. Motor thresholds at rest, amplitudes of motor evoked potentials, central motor conduction time and cortical silent period were measured by stimulation of the motor cortex by using 13.5 cm circular coil and recording from abductor digiti minimi muscle. Additionally, phosphene production and the threshold of phosphene production was determined by stimulation of the visual cortex with the same coil. Results: No significant differences were observed between the groups with respect to the motor thresholds, Motor evoked potential max/compound muscle action potential max (MEPmax/Mmax) amplitudes, central motor conduction times and duration of cortical silent period. Although not statistically significant, the proportion of the migraineurs with phosphene generation (90%) was found to be higher than that of normal controls (71%). Phosphene threshold levels in migraine patients, however, were significantly lower than those of the controls with MwA patients having the lowest levels. Conclusion: Our findings indicate that the occipital cortex, but not the motor cortex, is hyperexcitable in migraine patients. RÉSUMÉ: Excitabilité du cortex moteur et du cortex occipital chez les patients migraineux.Objectif: Nous avons évalué par stimulation magnétique transcrânienne l'excitabilité du cortex moteur et du cortex occipital chez des patients migraineux. Méthodes: Nous avons étudié entre les crises 15 patients ayant une migraine avec aura (MaA), 15 patients migraineux sans aura (MsA) et 31 témoins en bonne santé. Les seuils moteurs au repos, les amplitudes des potentiels évoqués moteurs (PÉM), le temps de conduction moteur central et la période de silence cortical ont été mesurés par stimulation du cortex moteur au moyen d'une spirale circulaire de 13,5 cm et enregistrement au niveau du muscle abducteur du petit doigt. De plus, la production de phosphènes et le seuil de production de phosphènes ont été déterminés par stimulation du cortex visuel avec la même spirale. Résultats: Nous n'avons observé aucune...

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“…This theory is supported by a study in 2001, demonstrating that after Transcranial Magnetic Stimulation, MA patients were more susceptible to hyperexcibility in the visual cortex than controls, indicating that MA patients may have a lower level of inhibition in the cerebral cortex than control subjects (Mulleners et al, 2001). Other studies have suggested that this lack of inhibition may be due to defective gamma-aminobutyric acid (GABA) circuits (Palmer et al, 2000;Fierro et al, 2003) Decreased GABA A receptor activation and expression has been demonstrated in several studies to result in decreased inhibition within the brain (Storer et al, 2001(Storer et al, , 2004Schiene et al, 1996), suggesting that GABA receptor activation and expression may be decreased in individuals with migraine.…”

Section: Introductionmentioning

confidence: 89%