Journal of the neurological sciences · 2011
The effect of propranolol on cerebrovascular reactivity to visual stimulation in migraine.
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Min Ju-Hong, Kwon Hyung-Min, Nam Hyunwoo
Аннотация
BACKGROUND: Propranolol is effective for migraine prophylaxis. However, its exact mechanism is not known. We postulated that the protective effect is due to the lowering of cerebrovascular reactivity (CVR). To verify this, we applied photic stimuli to migraineurs and analyzed the results.
METHODS: We checked the mean flow velocity (MFV) of the posterior cerebral artery by transcranial Doppler in 22 migraineurs during a headache-free period and in 14 normal controls. During the photic stimulation, MFV was remeasured and the CVR was estimated in both groups. Migraineurs received prophylactic propranolol for 2 months, and they were then reevaluated for the above-mentioned parameters and assessed for a headache index (HI).
RESULTS: There were no baseline differences in MFV between migraineurs and controls before treatment. Both groups showed a similar degree of increase in MFV with the photic stimulation, thus CVR was not significantly different between them. After the treatment period, CVR decreased significantly in migraineurs compared to baseline (p<0.01), although MFV remained unchanged. The prophylactic effect of propranolol treatment on symptomatic migraine was demonstrated on the HI, which significantly improved (p<0.05).
CONCLUSIONS: Considering that CVR was decreased but the baseline MFV was not changed in the posterior cerebral artery prior to the visual stimulation in migraineurs after propranolol treatment, we assume that the protective effect of propranolol was not due to the direct effect on the cerebral vessels but due to the modulation of the CVR to sensory stimulation through its action on central centers associated with autonomic vascular tone.
METHODS: We checked the mean flow velocity (MFV) of the posterior cerebral artery by transcranial Doppler in 22 migraineurs during a headache-free period and in 14 normal controls. During the photic stimulation, MFV was remeasured and the CVR was estimated in both groups. Migraineurs received prophylactic propranolol for 2 months, and they were then reevaluated for the above-mentioned parameters and assessed for a headache index (HI).
RESULTS: There were no baseline differences in MFV between migraineurs and controls before treatment. Both groups showed a similar degree of increase in MFV with the photic stimulation, thus CVR was not significantly different between them. After the treatment period, CVR decreased significantly in migraineurs compared to baseline (p<0.01), although MFV remained unchanged. The prophylactic effect of propranolol treatment on symptomatic migraine was demonstrated on the HI, which significantly improved (p<0.05).
CONCLUSIONS: Considering that CVR was decreased but the baseline MFV was not changed in the posterior cerebral artery prior to the visual stimulation in migraineurs after propranolol treatment, we assume that the protective effect of propranolol was not due to the direct effect on the cerebral vessels but due to the modulation of the CVR to sensory stimulation through its action on central centers associated with autonomic vascular tone.