الفهرس 
MIGRAINEOnly 14 pages are availabe for public view
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Abstract
M
igraine is one of the most disabling neurological diseases and often requires preventive therapy to reduce attack frequency. Recently, migraine-specific prophylactic agents targeting the calcitonin gene-related peptide (CGRP) pathway have been introduced into the field.
Migraine underlying pathophysiology is incompletely understood, but may be explained by several factors; some of them are activation of trigeminal sensory pathways which may be responsible for pain or may be related to CGRP activity in CNS in form of release of CGRP into cranial venous outflow and increased expression of its receptors in trigeminal neurons that form C-fibers and A-fibers, respectively during migraine attack or may be due to vasodilatation of meningeal blood vessels or may be due to cortical spreading depression through glutamate and other ion channels So, targeting these options may be beneficial in relieving migraine pain.
Topiramate is an anti-epileptic drug and was found to be effective in migraine prevention.propranolol which is a non-selective beta-blocker with lipophilic properties that enable it to cross the blood-brain barrier (BBB), however it does not act directly on the cerebral vessels; instead, it can centrally modulate the sensitivity of the autonomic tone of the vessels to sensory stimuli during the migraine attack.
The aim of the study was to assess the effect of topiramate and propranolol on serum CGRP on migraine patients and to assess their clinical response regarding headache days, headache severity, HIT-6 score, MIDAS score.
Fifty patients was diagnosed with migraine were recruited in this study.
At the beginning, blood sampling were be obtained from all patients for estimation of CGRP in peripheral blood before receiving any medication. Patients were randomly divided in two groups; Topiramate (50 mg) given in one group for 2 months and the second group received propranolol (80mg) for 2 months,then blood sample were obtained from all patients after 2 months.
Evaluation of Efficacy was evaluated using:
• Diaries completed by patients before medication,one months and two months after medication.
• Visual analogue scale by patients to evaluate headache severity before medication, one month and two months after medication.
• Migraine disability assessment scale (MIDAS)before and 3 months after medication.
• Headache impact test (HIT-6) before medication,one month and two months after medication.
This study revealed that there was no statistically significant difference found between the two studied groups regarding CGRP before treatment. While there was statistically significant decrease in CGRP score at 2 months in topiramate group than propranolol group. Also, there was statistically significant decrease in the CGRP score after 2 months than before treatment in both groups with superiority of topiramate over propranolol.
This study revealed that there was no statistically significant difference found between the two studied groups regarding headache days before treatment, after 1 month and after 2 months. While there was statistically significant decrease in the days of headache at 1 month and 2 months than before treatment in both groups for propranolol 80 mg and topiramate 50 mg respectively with no superiority for one group over another.
This study revealed that there was no statistically significant difference found between the two studied groups regarding severity of headache before treatment. There was statistically significant decrease in the severity of headache at 1 month and 2 months than before treatment in both groups. While there was statistically significant decrease in severity of headache at 1 month and 2 months in topiramate 50 mg group than propranolol 80 mg group.
This study revealed that there was no statistically significant difference found between the two studied groups regarding MIDAS score before treatment and after 3 months. Also, there was statistically significant decrease in the MIDAS score after 3 months than before treatment in both groups with no superiority for one group over another.
This study revealed that there was no statistically significant difference found between the two studied groups regarding HIT-6 score before treatment, after 1 month and after 2 months follow up. While there was statistically significant decrease in the HIT-6 score at 1 month and 2 months than before treatment in both groups with no superiority for one group over another.
This study revealed that there was positive correlation between percentage of CGRP change and percentage of headache days change in Propranolol group but it was non significant. Also, there was positive correlation between percentage of CGRP change and percentage of headache days change in topiramate group but it was not significant.
This study revealed that there was negative correlation between percentage of CGRP change and percentage of headache severity change in propranolol group but it was non significant. Also there was positive correlation between percentage of CGRP change and percentage of headache severity change in topiramate group but it was non significant.
This study revealed that there was positive correlation between percentage of CGRP change and percentage of MIDAS score change in Propranolol group but it was non significant. Also, there was positive correlation between percentage of CGRP change and MIDAS score percentage of change in topiramate group but it was not significant.
This study revealed that there was positive correlation between percentage of CGRP change and HIT-6 score percentage of change in Propranolol group but it was non significant. Also, there was significant positive correlation between percentage of CGRP change and HIT-6 score percentage of change in topiramate group.
RECOMMENDATIONS
• Further studied enrolling larger sample size with control group for comparison.
• Increase duration of prophylactic oral medical treatment and to assess CGRP level for longer period and follow up patients clinically
• More studies to assess correlation between CGRP changes in response to treatment and to correlate CGRP levels and other migraine biomarkers as VIP
• Studies to assess other prophylactic medication and effect on CGRP levels