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Cortical Excitability in Migraine and Epilepsy: A Common Feature?

Badawy, Radwa A. B.*,†; Jackson, Graeme D.*,†,‡


In the article published on pages 244-249 in the June 2012 issue of the Journal of Clinical Neurophysiology, a typing error appears in the motor threshold of non-epilepsy controls.

In Table 1, line 1“Control subjects” appears as 55.2 ± 8.3. The correct data should read 55.4 ± 8.3.

This error has no bearing on the results or conclusions based on them. All result analyses performed in relation to this manuscript are correct.

The author apologizes for this error.

Journal of Clinical Neurophysiology. 33(6):572, December 2016.

Journal of Clinical Neurophysiology: June 2012 - Volume 29 - Issue 3 - p 244–249
doi: 10.1097/WNP.0b013e3182570fee
Original Research

Objective: There is evidence for comorbidity of migraine and epilepsy. We used transcranial magnetic stimulation (TMS) to assess cortical excitability in migraine compared with control subjects and patients with epilepsy.

Methods: Twenty-six patients drug-naive patients with newly diagnosed migraine were studied. These were compared with 19 healthy control subjects and 50 patients with new onset epilepsy. Motor threshold (MT) and responses to paired pulse stimulation at short (2, 5, 10, and 15 milliseconds) and long (50–400 milliseconds) interstimulus intervals (ISIs) were measured.

Results: Compared with control subjects, cortical excitability was higher in migraine only at 250 milliseconds (P < 0.05; effect size 0.7), while in epilepsy, it was higher at 2, 5, 250, and 300 milliseconds. Compared with epilepsy, cortical excitability was lower in migraine only at 250 milliseconds (P < 0.05; effect size 0.6 compared with focal epilepsy and 1.1 compared with idiopathic generalized epilepsy [IGE]).

Conclusions: Cortical excitability increases in migraine suggesting the involvement of intracortical inhibitory circuits. This may be a common feature underlying some of the similarities observed in migraine and epilepsy.

*Department of Neurology, Austin Health, Heidelberg, Australia

Department of Medicine, University of Melbourne, Victoria, Australia

Brain Research Institute, Florey Neuroscience Institutes Heidelberg West, Victoria, Australia.

Address correspondence and reprint requests to Dr. Radwa Badawy, MBBCh, MSc, PhD, Department of Medicine, The University of Melbourne, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia; e-mail:

Copyright © 2012 American Clinical Neurophysiology Society