RESUMO
BACKGROUND AND PURPOSE: Migraine suffering is more than the onset of head pain. The broad non-painful clinical symptoms associated with migraine are not well recognized. Recent researches support that migraineurs suffer attention deficits, but these findings are not conclusive. The purpose of our study was to assess whether patients with migraine without aura (MwoA) during the interictal period have attention impairment and to identify the migraine characteristics related to attention deficits. METHODS: We enrolled subjects with MwoA during the interictal period and healthy controls matched for age, gender, and education level in this cross-sectional study. The attention network test (ANT) and a battery of neuropsychological tests, including the trail-making test (TMT), the digit span test (DST), and the Stroop test, were administered to the participants during the headache-free period. RESULTS: Forty-four subjects with MwoA (4 males, 40 females) and 20 controls matched for age, gender, and literacy education were included. Patients in MwoA were more anxious (P = 0.007) and depressed (P = 0.001) than healthy subjects. Significant differences between the two groups were detected in the executive network (P = 0.006) but not in the alerting and orienting networks of ANT. Mean reaction time of ANT in the MwoA group was significantly longer than that in the control group (P = 0.028). Patients showed worse performance on DST-forward (P < 0.001), DST-backward (P < 0.001), DS Total (P < 0.001), TMT-A (P < 0.001), TMT-B (P < 0.001) and TMT-d (P = 0.002). Differences found in executive functions between the two groups were unrelated to gender, age, literacy, anxiety, and depression. Multiple regression analysis revealed no relation between clinical characteristics of headache and scores on the executive function with MwoA. CONCLUSION: Our study suggested that patients in MwoA present worse performances on the executive control of attention networks during the headache-free period, which appear not be associated with measures of migraine severity. Although more studies are needed in this area, our results could be useful to find specific neuropsychological biomarker for migraine pathophysiology.
RESUMO
Trimethyltin chloride (TMT) is a by-product in the synthesis of organotin, a plastic stabilizer. With the rapid development of industry, the occupational hazards caused by TMT cannot be ignored. TMT is a typical neurotoxicant, which mainly damages the limbic system and brainstem of the nervous system. Previous studies have demonstrated that the neurotoxicity induced by TMT is linked to the inhibition of energy metabolism, but the underlying mechanism remains elusive. In order to investigate the mechanism of TMT-induced inhibition of energy metabolism, C57BL/6 male mice were administered by IP injection in different TMT doses (0 mg/kg, 1.00 mg/kg, 2.15 mg/kg and 4.64 mg/kg) and times (1d, 3d and 6d), and then the changes of superoxide dismutase (SOD) activity, malondialdehyde (MDA) level and Na+-K+-ATPase activity in cerebral cortex, cerebellum, hippocampus, pons, medulla oblongata of mice, the expressions of Na+-K+-ATPase protein, AMP-activated protein kinase (AMPK), phosphorylated AMP-activated protein kinase(p-AMPK)and peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α) in hippocampus and medulla oblongata were measured; the effects of TMT on the viability, the activity of SOD, glutathione (GSH) and Na+-K+-ATPase, MDA level, and the expression of PGC-1α and Na+-K+-ATPase protein in N2a cells were measured by different TMT doses and times, in order to verify the experiments in vivo. Our results found that most of the mice showed depression, tremor, epilepsy, spasm and other symptoms after TMT exposure. Moreover, with the increase of TMT dose, the activity of Na+-K+-ATPase and the expressions of AMPK protein in the hippocampus and medulla oblongata of mice decreased, and the expressions of p-AMPK protein increased. Peroxidative damage was evident in hippocampus, medulla oblongata of mice and N2a cells, and the expression of PGC-1α and Na+-K+-ATPase protein was significantly down-regulated. Therefore, it is reasonable to believe that TMT-induced neurotoxic symptoms and inhibition of energy metabolism may be related to p-AMPK and down-regulation of PGC-1α in the hippocampus and medulla oblongata.
