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1.
BMC Neurol ; 24(1): 25, 2024 Jan 12.
Article in English | MEDLINE | ID: mdl-38216859

ABSTRACT

OBJECTIVE: This study aimed to investigate the efficacy of rTMS in the treatment of poststroke epilepsy and the effect of rTMS on patients' cognitive function and depressive status. METHODS: One hundred and twenty-one poststroke epilepsy patients with mild cognitive impairment and depressive status admitted to the Department of Neurology of the Second People's Hospital of Nanning from January 1, 2017, to April 31, 2023, were selected and divided into the rTMS treatment group (treated group) and the control group. MMSE scores and HAMD scores were recorded before and after treatment. The frequency of EEG spiky waves recorded before and after treatment within 24 h and the frequency of any clinical seizure form (the number of clinical seizures within 1 month after treatment) and changes in observed indices before and after treatment were calculated. The differences between the data of the two groups were analyzed, to further assess the efficacy of rTMS in the treatment of poststroke epilepsy and the rTMS' effects on cognition and depression. RESULTS: Compared with drug treatment alone, rTMS significantly decreased clinical seizures and epileptiform discharges after stroke, especially in patients with lesions in the frontal, temporal, and parietal lobes. Compared with drug treatment alone, rTMS treatment can effectively reduce cognitive impairment and mood disorders, such as depression, especially for patients with lesions in the frontal and temporal lobes. The results of this experiment suggest that rTMS treatment does not increase adverse effects. CONCLUSION: rTMS reduces clinical seizures while improving cognitive impairment and depression in patients with epilepsy. Therefore, we suggest that low-frequency rTMS can be used as an adjunctive treatment for patients with epilepsy and provide some ideas and references for the treatment of epilepsy with cognitive impairment and depression.


Subject(s)
Epilepsy , Humans , Treatment Outcome , Epilepsy/therapy , Epilepsy/etiology , Seizures/etiology , Transcranial Magnetic Stimulation/methods , Cognition
2.
Exp Brain Res ; 241(11-12): 2751-2763, 2023 Dec.
Article in English | MEDLINE | ID: mdl-37847304

ABSTRACT

Ischemic stroke followed by cerebral artery occlusion is a main cause of chronic disability worldwide. Recombinant human brain natriuretic peptide (rhBNP) has been reported to alleviate sepsis-induced cognitive dysfunction and brain I/R injury. However, the function and molecular mechanisms of rhBNP in ischemic brain injury have not been clarified. For establishment of an animal model of ischemic brain injury, C57BL/6 mice were treated with middle cerebral artery occlusion (MCAO) surgery for 1 h and reperfusion for 24 h. After subcutaneous injection of rhBNP into model mice, neurologic deficits were assessed by evaluating behavior of mice according to Longa scoring system, and TTC staining was utilized to determine the brain infarct size of mice. The levels of oxidative stress markers, superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA), were detected in hippocampal tissues of mice by corresponding kits. Cell apoptosis in hippocampus tissues was examined by TUNEL staining. Protein levels of antioxidant enzymes (HO-1 and NQO1) in cerebral cortex, apoptotic markers (Bax, Bcl-2, and cleaved caspase), and PI3K/AKT pathway-associated factors in hippocampus were tested by western blot analysis. The results revealed that injection of rhBNP decreased neurologic deficit scores, the percent of brain water content, and infarct volume. Additionally, rhBNP downregulated MDA level, upregulated the levels of SOD, CAT, and GSH in hippocampus of mice, and increased protein levels of HO-1 and NQO1 in the cortex. Cell apoptosis in hippocampus tissues of model mice was inhibited by rhBNP which was shown as the reduced TUNEL-positive cells, the decreased Bax, cleaved caspase-3, and cleaved caspase-9 protein levels, and the enhanced Bcl-2 protein level. In addition, rhBNP treatment activated the PI3K/AKT signaling pathway and upregulated the protein levels of HO-1 and NRF2. Overall, rhBNP activates the PI3K/AKT/HO-1/NRF2 pathway to attenuate ischemic brain injury in mice after MCAO by suppression of cell apoptosis and oxidative stress.


Subject(s)
Brain Injuries , Brain Ischemia , Reperfusion Injury , Mice , Humans , Animals , Natriuretic Peptide, Brain/pharmacology , Natriuretic Peptide, Brain/therapeutic use , Natriuretic Peptide, Brain/metabolism , Proto-Oncogene Proteins c-akt/metabolism , NF-E2-Related Factor 2/metabolism , Phosphatidylinositol 3-Kinases/metabolism , bcl-2-Associated X Protein/metabolism , Mice, Inbred C57BL , Oxidative Stress , Infarction, Middle Cerebral Artery/complications , Infarction, Middle Cerebral Artery/drug therapy , Brain Ischemia/complications , Brain Ischemia/drug therapy , Proto-Oncogene Proteins c-bcl-2/metabolism , Apoptosis , Superoxide Dismutase/metabolism
3.
Neurotherapeutics ; 19(6): 1932-1941, 2022 10.
Article in English | MEDLINE | ID: mdl-36151441

ABSTRACT

Hyperglycemia is associated with decreased recanalization probability and increased risk of hemorrhagic complications for stroke patients treated with intravenous alteplase. However, whether hyperglycemia modifies alteplase treatment effect on clinical outcome in patients with large vessel occlusion stroke undergoing endovascular thrombectomy is uncertain. We conducted this study to determine a possible interaction effect between admission hyperglycemia and intravenous alteplase prior to thrombectomy in patients with large vessel occlusion stroke. In this post-hoc analysis of a randomized trial (DIRECT-MT) comparing intravenous alteplase before endovascular treatment vs. endovascular treatment only, 649 with available baseline glucose measurements were included. The treatment-by-admission hyperglycemia (defined as plasma glucose levels ≥ 7.8 mmol/L [140 mg/dL]) interaction was assessed using logistic regression models. As a result, among 649 patients included, 224 (34.5%) were hyperglycemic at admission. There was evidence of alteplase treatment effect modification by hyperglycemia (Pinteraction = 0.025). In patients without hyperglycemia, combination therapy was associated with better outcomes compared to mechanical thrombectomy alone (adjusted common odd ratio [acOR] 1.46, 95% CI [1.04-2.07]), but not in hyperglycemic patients (acOR 0.74, 95% CI [0.46-1.20]). Combination therapy led to an absolute increase of 6% excellent outcome (mRS 0-1) in non-hyperglycemic patients (aOR 1.71, 95% CI [1.05-2.79]), but resulted in a 12.3% absolute decrease (aOR 0.42 [95% CI, 0.19-0.95] in hyperglycemic patients (Pinteraction = 0.003). In conclusion, for large vessel occlusion patients directly presenting to a thrombectomy-capable hospital, hyperglycemia modified combination treatment effect on clinical outcome. Combination therapy was beneficial in patients without hyperglycemia, while thrombectomy alone may be preferred in hyperglycemic patients. Further studies are needed to confirm this result.Trial Registration Information: clinicaltrials.gov Identifier: NCT03469206.


Subject(s)
Brain Ischemia , Hyperglycemia , Ischemic Stroke , Stroke , Humans , Brain Ischemia/complications , Brain Ischemia/drug therapy , Fibrinolytic Agents/therapeutic use , Hyperglycemia/complications , Hyperglycemia/drug therapy , Stroke/drug therapy , Thrombectomy/adverse effects , Thrombectomy/methods , Tissue Plasminogen Activator/therapeutic use , Treatment Outcome
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