Primary visual cortex excitability in migraine: a systematic review with meta-analysis

Abstract

The objective is to update and extend previous results of a systematic review of the literature with meta-analysis performed to determine the prevalence of phosphenes and the phosphene threshold (PT) values obtained during single-pulse transcranial magnetic stimulation (TMS) in adults with migraine. Both published and unpublished controlled studies measuring PT by single-pulse TMS in adults with migraine with or without aura (MA, MwA) were systematically reviewed. Prevalence of phosphenes and PT values were assessed calculating mean difference (MD) and odds ratio (OR) with 95 % confidence intervals (CI). Fifteen trials (369 migraine patients and 269 controls), were included. Patients with MA had a statistically significant lower PT compared with controls when a circular coil was used (MD: -22.27, 95 % CI -33.44 to -11.10); with a figure-of-eight coil the difference was not statistically significant. There was a significant higher phosphene prevalence in MA compared with controls (OR: 3.57, 95 % CI 1.16-10.94). No significant differences were found either in phosphene reporting between patients with MwA and controls, or in PT values obtained by figure-of-eight coil in subjects with MwA versus controls. In general, these results slightly support the hypothesis of a primary visual cortex hyper-excitability in MA, providing not enough evidence for MwA. A significant heterogeneity across studies probably reflects relevant clinical and methodological heterogeneity.

Transcranial direct current stimulation in the prophylactic treatment of migraine based on interictal visual cortex excitability abnormalities: A pilot randomized controlled trial

“…Main findings of our electrophysiological study confirm the metaanalysis results on lower PT values obtained by circular coil TMS in migraineurs with and without aura than control subjects [20] and support the concept of an interictal visual cortical hyperexcitability in migraine patients. The pathophysiologic mechanism responsible for increased visual cortex excitability in migraine is still controversial and may be multifactorial.…”

“…A 10 cm circular coil connected to stimulator (Neurosoft, Russia; peak magnetic field = 2.2 T) was placed in a vertical position (its handle pointing upward) on the inion-nasion line, with its inferior limit 1 cm above the inion, as described before [19]. The circular coil may induce a larger electric field increasing chances of evoking phosphenes [20]. After each TMS single-pulse over visual cortex, the volunteers were encouraged to relate any sensory experiences (e.g.…”

Evaluation of Electroencephalogram Using Exact Low-Resolution Electromagnetic Tomography During Photic Driving Response in Patients with Migraine

“…Visual cortex hyperexcitability in migraine in response to sound-induced flash illusions, especially MWA, has been described [24]. A systematic review on transcranial magnetic stimulation studies of migraine patients supported a hyperexcitability in the primary visual cortex in MWA, but not MWOA [25]. In contrast, a recent study suggested that CSD can cause the destruction of the blood–brain barrier by activation of matrix metalloproteinase-9 [26].…”

Impaired visual inhibition in migraine with aura

“…According to our results, such habituation abnormalities might be interpreted -at least for MA patients -as the result of a defective visual system inhibition (possibly, hypofunction of intracortical inhibitory circuits), rather than ''reduced preactivation'' of the visual cortex (Coppola et al, 2013). Similar considerations may extend to the occipital cortex hyperexcitability revealed by TMS studies (Brigo et al, 2013).…”

“…When considered both together, the most consistent finding was a defective habituation of pattern reversal-visual evoked potentials (PR-VEPs) (Schoenen, 2006). In turn, transcranial magnetic stimulation (TMS) provided sufficient evidence of a primary visual cortex hyperexcitability in MA (Brigo et al, 2013) whether hyperexcitability is the result of excessive excitation or defective inhibition (Coppola et al, 2007(Coppola et al, , 2013 and whether these abnormalities are exclusively attributed to MA or, conversely, to migraine in general.…”