The relationship between white mattter hyperintensities and retinal nerve fiber layer, ganglion cell layer and choroid layer thickness in migraine patients

Migraine constitutes an important part of primary headaches. White matter hyperintensities are more commonly seen among migraineurs compared to normal population. The pathophysiology of these lesions are unknown. One theory suggests that these lesions are an indirect indicator of cerebral hypoperfusion induced by repeating migraine attacks. In this study our aim was to evaluate the relationship between white matter hyperintensities shown in brain magnetic resonance imaging and retinal nerve fiber layer,choroid and ganglion cell layer thicknesses and to compare the thicknesses of migraine patients with healthy individuals. With this study it was expected to evaluate whether the cerebral hypoperfusion plays a role in the formation of these lesions. Thirty five migraine patients without white matter hyperintensities, 37 migraine patients with white matter hyperintensities and 37 healthy control subjects who were examined in the Baskent University Medical Faculty Hospital Neurology outpatient clinic among May 2015- December 2015 were enrolled in our study. Retinal nerve fiber layer, choroid and ganglion cell layer thicknesses were measured by the optic coherence technique and the differences among the groups were studied. No significant differences in the retinal nerve fiber layer, choroid and ganglion cell layer thicknesses were found between migraine patients with and without white matter hyperintensities (p>0.05). Compared with control group, retinal nerve fiber layer and ganglion cell layer thicknesses showed no significant difference in migraine patients (p>0.05). Choroid thicknesses were significantly lower in migraine pateints than control group (p<0.05). In conclusion; in our study given the fact that no difference was found in retinal nerve fiber layer, choroid and ganglion cell layer thicknesses between migraine patients with and without white matter hyperintensities, it was thought that only cerebral hypoperfusion theory was insufficient to explain the pathophysiology of these lesions and the formation of these might be multifactoriel. In addition the thinning of the choroid thicknesses detected in migraineurs defends that cerebral hypodinamic changes might cause a decrease in the perfusion pressure of choroid layer.