RESUMO
Background: There are very few studies on transcranial magnetic stimulation (TMS) therapy for facial paralysis and no studies comparing the efficacy of central and peripheral TMS in the treatment of peripheral facial paralysis (PFP). Purpose: To observe the therapeutic effect and security of central and peripheral repetitive transcranial magnetic stimulation (rTMS) on PFP. Methods: Patients with unilateral onset of peripheral facial paralysis within 1 month were prospectively recruited, 97 patients with PFP were divided into the peripheral group, central group, and control group. The control group was given common treatment (drug therapy and acupuncture), and the peripheral and central groups received rTMS in addition to conventional treatment. After 2 weeks of treatment, the House-Brackmann (HB) grading scale, Sunnybrook facial grading system (SFGS), and modified Portmann scale (MPS) were used to evaluate the facial muscle function of patients in the three groups. Result: After 2 weeks of rTMS treatment, the HBGS/SFGS/MPS scores of the three groups were significantly better than before (p < 0.05), and the mean change values of HBGS, SFGS, and MPS scores were significantly higher in participants in Peripheral Group (p < 0.001; p < 0.001; p = 0.003; respectively) and Central Group (p = 0.004; p = 0.003; p = 0.009; respectively) than in Control Group. But the mean change values of HBGS, SFGS, and MPS scores showed no significant differences in participants in the Peripheral Group than in the Central Group (p = 0.254; p = 0.139; p = 0.736; respectively) after 2 weeks of treatment (p > 0.05). Conclusion: Our study shows that rTMS can be a safe and effective adjuvant therapy for patients with PFP. Preliminary studies have shown that both peripheral and central stimulation can effectively improve facial nerve function, but there is no significant difference in the efficacy of the two sites.
RESUMO
Subarachnoid hemorrhage (SAH) is a neurological emergency characterized by dysfunctional inflammatory response. However, no effective therapeutic options have been reported so far. Microglia polarization has been proposed to exert an essential role in modulating inflammatory response after SAH. Sestrin2 is a stress response protein. Growing evidence has reported that sestrin2 could inhibit M1 microglia and promote M2 microglia polarization. The current study investigated the effects of sestrin2 on microglia phenotype switching and the subsequent brain injury and sought to elucidate the underlying mechanism. We conducted an endovascular perforation SAH model in mice. It was found that sestrin2 was significantly increased after SAH and was mainly distributed in neurons and microglia. Exogenous recombinant human sestrin2 (rh-sestrin2) evidently alleviated inflammatory insults and oxidative stress, and improved neurofunction after SAH. Moreover, rh-sestrin2 increased M2-like microglia polarization and suppressed the number of M1-like microglia after SAH. The protection by rh-sestrin2 was correlated with the activation of Nrf2 signaling. Nrf2 inhibition by ML385 abated the cerebroprotective effects of rh-sestrin2 against SAH and further manifested M1 microglia polarization. In conclusion, promoting microglia polarization from the M1 to M2 phenotype and inducing Nrf2 signaling might be the major mechanism by which sestrin2 protects against SAH insults. Sestrin2 might be a new molecular target for treating SAH.
