ABSTRACT
@#<p style="text-align: justify;"><strong>Introduction.</strong> Migraine is a common, debilitating primary headache. Memantine is a non-competitive N-methyl D-aspartate (NMDA) antagonist that lowers neuronal excitability that could prevent migraine attacks. This study aimed to determine the efficacy and safety of memantine in patients with episodic migraine attacks using a systematic review and meta-analysis.</p><p style="text-align: justify;"><strong>Methods.</strong> We searched CENTRAL, MEDLINE, Scopus, Cochrane, LILACS, ClinicalTrials.gov, HERDIN and Google Scholar for relevant studies until July 31, 2020. Prespecified screening and eligibility criteria for inclusion were applied. Included studies underwent methodological quality assessment. Study design, patient characteristics, interventions given, and relevant outcomes were extracted and synthesized.</p><p style="text-align: justify;"><strong>Results.</strong> This review included five relevant articles - two randomized controlled trials (RCT) and three non randomized studies (one retrospective records review and survey, two prospective open-label single-arm trials). There were 109 patients included in the RCTs and 197 patients reported in the non-randomized studies. Pooled data from the two RCTs showed that memantine at 10 mg/day significantly decreased the monthly number of migraine days at 12 weeks compared to placebo with a mean difference of -1.58 [95% confidence interval (CI) -1.84, -1.32]. Non-randomized studies also showed a decrease in migraine days per month with memantine (5 to 20 mg/day) after 12 weeks [95% CI]: -9.1 [-11, -7.23], -7.2 [-8.85, -5.55], and -4.9 [-6.29, -3.51]. Adverse drug events (ADE) did not differ significantly between patients treated with memantine compared to placebo.</p><p style="text-align: justify;"><strong>Conclusion.</strong> Memantine may be effective and well-tolerated as prophylaxis for episodic migraine.</p>
Subject(s)
Memantine , Systematic Review , Meta-AnalysisABSTRACT
@#Background and Objectives. Neuroprotection agents may help improve the outcomes of large vessel ischemic stroke. This study aims to explore the role of Virgin Coconut Oil (VCO), with its well-documented anti-oxidant properties, in neuroprotection after transient occlusion of the extracranial internal carotid artery in a rat model of stroke. Methods. Twenty-three Sprague-Dawley rats were randomized into two groups: 1) control group (n=11) given distilled water, and 2) treatment group (n=12) given virgin coconut oil at 5.15 ml/kg body weight for seven days. Subsequently, the rats underwent transient right extracranial internal carotid artery occlusion (EICAO) for 5 minutes using non-traumatic aneurysm clips. At 4 and 24 hours after EICAO, the animals were examined for neurologic deficits by an observer blinded to treatment groups, then sacrificed. Eight brain specimens (4 from each group) were subjected to histopathologic examination (H & E staining) while the rest of the specimens were processed using triphenyltetrazolium chloride (TTC) staining to determine infarct size and area of hemispheric edema. Results. VCO treatment significantly improved the severity of neurologic deficit (1.42 ± 2.31) compared to the control distilled water group (4.09 ± 2.59) 24 hours after EICAO. Whereas, infarct size and percent hemispheric edema did not significantly differ between the two groups. Conclusion. Prophylactic treatment of VCO is protective against EICAO-induced neurologic deficits in a rat model. VCO shows great potential as a neuroprotective agent for large vessel ischemic stroke. However, more studies are necessary to elucidate the neuroprotective mechanisms of VCO therapy in ischemic stroke.