Comparison of the Effect of Tanacethum Parthenium, 5-Hydroxy Tryptophan, and Magnesium (Aurastop) versus Magnesium Alone on Aura Phenomenon and Its Evolution.

None of the clinical trials on migraine conducted thus far have focused on the possibility to modulate the phenomenon of aura. Furthermore, whether proper management of aura results in a better control of the headache phase has been poorly investigated. In the setting of a single-center, pilot, clinical trial, we aimed at comparing the effects of Aurastop (a combination of tanacetum parthenium (150 mg extracted at 0.8% = 1.2 mg di of active parthenolide), griffonia simplicifoila (20 mg of 5-hydroxy tryptophan), and magnesium (185 mg of magnesium pidolatum)) with those of magnesium alone (2.25 grams/tablet, corresponding to 184 mg of Mg++) in the treatment of acute attacks of migraine with aura. Between June 2017 and June 2018, 50 consecutive patients (27/23 male/female; mean age, 31 [18-57] years) with at least 3 episodes of aura per year were included (t 0). Participants were instructed to keep track of the following 4 episodes of migraine with aura (t 1) and invited to assume (1) a tablet of Aurastop at the beginning of the following 2 episodes of aura and (2) a magnesium tablet alone at the occurrence of the third and fourth aura attacks. Forty-eight patients (96.0%) had >50% reduction in aura duration when treated with Aurastop vs. 7 patients (14.0%) when treated with magnesium alone (p < 0.001); 48 patients (96.0%) had >50% reduction of aura-related disability when receiving Aurastop vs. 5 patients (10.0%) when treated with magnesium alone (p < 0.001); however, patients receiving Aurastop did not need to take pain killers in 35% of aura attacks vs. 3% when assuming magnesium (p < 0.001). These results support the hypothesis that Aurastop might be effective in interfering with the phenomenon of aura and provide evidence that the clinical benefit attributable to this combination of molecules might be greater than that obtained with single compounds of proven effect on the biology of migraine.

Hematoma location and morphology of anticoagulation-associated intracerebral hemorrhage.

OBJECTIVE: To study hematoma location and morphology of intracerebral hemorrhage (ICH) associated with oral anticoagulants (OAC) and delineate causes and mechanism. METHODS: We performed a systematic literature research and meta-analysis of studies comparing neuroimaging findings in patients with OAC-ICH compared to those with ICH not associated with OAC (non-OAC ICH). We calculated pooled risk ratios (RRs) for ICH location using the Mantel-Haenszel random-effects method and corresponding 95% confidence intervals (95% CI). RESULTS: We identified 8 studies including 6,259 patients (OAC-ICH n = 1,107, pooled OAC-ICH population 17.7%). There was some evidence for deep ICH location (defined as ICH in the thalamus, basal ganglia, internal capsule, or brainstem) being less frequent in patients with OAC-ICH (OAC-ICH: 450 of 1,102/40.8% vs non-OAC ICH: 2,656 of 4,819/55.1%; RR 0.94, 95% CI 0.88-1.00, p = 0.05, I 2 = 0%) while cerebellar ICH location was significantly more common in OAC-ICH (OAC-ICH: 111 of 1,069/10.4% vs non-OAC ICH: 326 of 4,787/6.8%; RR 1.45, 95% CI 1.12-1.89, p = 0.005, I 2 = 21%) compared to non-OAC ICH. There was no statistically significant relationship to OAC use for lobar (OAC-ICH: 423 of 1,107/38.2% vs non-OAC ICH: 1,884 of 5,152/36.6%; RR 1.02, 95% CI 0.89-1.17, p = 0.75, I 2 = 53%, p for heterogeneity = 0.04) or brainstem ICH (OAC-ICH: 36 of 546/6.6% vs non-OAC ICH: 172 of 2,626/6.5%; RR 1.04, 95% CI 0.58-1.87, p = 0.89, I 2 = 59%, p for heterogeneity = 0.04). The risk for intraventricular extension (OAC-ICH: 436 of 840/51.9% vs non-OAC ICH: 1,429 of 3,508/40.7%; RR 1.26, 95% CI 1.16-1.36, p < 0.001, I 2 = 0%) was significantly increased in patients with OAC-ICH. We found few data on ICH morphology in OAC-ICH vs non-OAC ICH. CONCLUSION: The overrepresentation of cerebellar ICH location and intraventricular extension in OAC-ICH might have mechanistic relevance for the underlying arteriopathy, pathophysiology, or bleeding pattern of OAC-ICH, and should be investigated further.

Antithrombotic medications and the etiology of intracerebral hemorrhage: MUCH-Italy.

OBJECTIVE: To test the hypothesis that the effect of antithrombotic medications on the risk of intracerebral hemorrhage (ICH) varies according to the location of the hematoma. METHODS: Consecutive patients with ICH were enrolled as part of the Multicenter Study on Cerebral Hemorrhage in Italy (MUCH-Italy). Multivariable logistic regression models served to examine whether risk factors for ICH and location of the hematoma (deep vs lobar) predict treatment-specific ICH subgroups (antiplatelets-related ICH and oral anticoagulants [OACs]-related ICH). RESULTS: A total of 870 (313 lobar ICH, 557 deep ICH) subjects were included. Of these, 223 (25.6%) were taking antiplatelets and 77 (8.8%) OACs at the time of stroke. The odds of antiplatelet-related ICH increased with aging (odds ratio [OR] 1.05; 95% confidence interval [CI] 1.03-1.07) and hypertension (OR 1.86; 95% CI 1.22-2.85) but had no relation with the anatomical location of ICH. Conversely, lobar location of the hematoma was associated with the subgroup of OAC-related ICH (OR 1.70; 95% CI 1.03-2.81) when compared to the subgroup of patients taking no antithrombotic medications. Within the subgroup of patients taking OACs, international normalized ratio (INR) values were higher in those with lobar ICH as compared to those with deep ICH (2.8 ± 1.1 vs 2.2 ± 0.8; p = 0.011). The proportion of patients with lobar hematoma increased with increasing intensity of anticoagulation, with a ~2-fold increased odds of lobar compared to deep ICH (odds 2.17; p = 0.03) in those exposed to overanticoagulation (INR values >3.0). CONCLUSIONS: OACs, as opposed to antiplatelets, predispose to lobar location of brain hematomas according to a dose-response relationship.

Folic acid and vitamin E supplementation effects on homocysteinemia, endothelial function and plasma antioxidant capacity in young myocardial-infarction patients.

We examined the effects of folate (either alone or co-supplemented with Vitamin E) on endothelial function in hyperhomocysteinimic patients and correlated results with serum antioxidant capacity. A randomized trial was carried out in 30 young patients with recent acute myocardial infarction (AMI) and high plasma homocysteine concentrations. Intervention consisted of high doses of folate, either alone (group A) or in combination with Vitamin E (group B), for three months. Main outcome measures were endothelial function, serum antioxidant capacity, and homocysteinemia. Folic acid treatment reduced plasma homocysteine concentrations in both groups by 41% and, as compared with baseline values, was associated with a significant (P<0.001) improvement of endothelial function (from 0.322 (0.03) to 0.450 (0.02)mm in group A and from 0.338 (0.03) to 0.584 (0.04)mm in group B). However, there was no difference in endothelial function improvement between folic acid and folic acid plus Vitamin E group. Plasma antioxidant capacity significantly (P<0.001) increased in both groups. In conclusion, beneficial effects of folic acid on vasomotion appear to be independent of antioxidant action but, rather, seem to be strongly associated with reduction of homocysteinemia. Confirming previous reports, the effects of Vitamin E are still equivocal.

Hyperhomocysteinemia: a potential risk factor for cervical artery dissection following chiropractic manipulation of the cervical spine.

Despite the increasing incidence of cervical artery dissection (CAD) due to chiropractic manipulation of the cervical spine, risk factors predisposing to vascular damage are still unknown. In the present study we measured fasting total plasma homocysteine (tHcy) concentration in 4 subjects with manipulation-related CAD selected from a larger series of patients with spontaneous dissection of the neck arteries (sCAD) and in a group of 36 control subjects. C677T MTHFR genotypes and 844ins68bp CBS genotypes were also determined. Median tHcy levels were significantly (P = 0.002) higher in patients with manipulation-related CAD (18.2 micromol/l, range 14.3 to 30.0) compared with controls (8.9 micromol/l, range 5 to 17.3) and not significantly different (P = 0.129) from those observed in patients with sCAD (13.9 micromol/l, range 7 to 32.8). No significant difference in the distribution of genotypes was observed in the three groups. Hyperhomocysteinemia may represent a potential risk factor for manipulation-related CAD, leading to structural abnormalities of the arterial wall and increasing the susceptibility to mechanical stress.