Interictal Motor Cortex Excitability in Migraine and Chronic Tension Type Headache using Transcranial Magnetic Stimulation

Song, Eun Hyang; Lee, Chung Seok; Choi, Yong Seok; Kim, Jung Mee; Kim, Woo Jung; Kim, Doo Eung; Han, Jeong Ho

Abstract

BACKGROUND: The pathophysiology of migraine is only partly understood. Transcranial magnetic stimulation has been developed to study cortical physiology noninvasively. Chronic tension-type headache has not been studied with transcranial magnetic stimulation. Among other hypotheses, it has been proposed that interictal hypoexcitability could be partly responsible for the migraine.
METHODS
Patients were divided into three groups: normal subjects(n=30), migraine with(n=11) or without aura(n=19) and chronic tension-type headache(n=30) according to the International Headache Society criteria. We studied cortical excitability between normal subjects and patients with migraine with or without aura and between normal and patients with chronic tension-type headache.
RESULTS
The mean amplitude of cortex and spinal cord for normal subjects was 3.76 +/-1.74 mV, 2.03 +/-1.54 mV(abductor digiti minimi muscles, respec-tively) and 2.99 +/-2.04 mV, 3.88 +/-3.89 mV(abductor hallucis muscles, respectively). The mean amplitude of cortex and spinal cord for migraine with aura or without aura was 2.16 +/-1.21 mV, 0.90+0.80 mV(abductor digiti minimi muscles, respectively) and 1.88 +/-1.23 mV, 2.31 +/-2.25 mV(abductor hallucis muscles, respectively). The mean amplitude of cor-tex and spinal cord for chronic tension-type headache was 1.61 +/-0.50 mV, 0.72 +/-0.32 mV(abductor digiti minimi mus-cles, respectively) and 1.54 +/-0.55 mV, 1.51 +/-0.59 mV(abductor hallucis muscles, respectively). The amplitude of motor evoked potentials of cortex and spinal cord in migraine and chronic tension-type headache showed significant decreases compared to normal subjects( p < 0.001).
CONCLUSIONS
These results are explained by cortical and spinal hypoexcitability in migraine and chronic tension-type headache. We suggest that enhanced serotonergic activity could be some rule for cortical hypoexcitability.