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Objective: This study aimed to explore and evaluate the efficacy of non-invasive brain stimulation (NIBS) as a standalone or coupled intervention and understand its mechanisms to produce positive alterations in neuroplasticity and behavioral outcomes after acquired brain injury (ABI). Data sources: Cochrane Library, Web of Science, PubMed, and Google Scholar databases were searched from January 2013 to January 2024. Study selection: Using the PICO framework, transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) randomized controlled trials (RCTs), retrospective, pilot, open-label, and observational large group and single-participant case studies were included. Two authors reviewed articles according to pre-established inclusion criteria. Data extraction: Data related to participant and intervention characteristics, mechanisms of change, methods, and outcomes were extracted by two authors. The two authors performed quality assessments using SORT. Results: Twenty-two studies involving 657 participants diagnosed with ABIs were included. Two studies reported that NIBS was ineffective in producing positive alterations or behavioral outcomes. Twenty studies reported at least one, or a combination of, positively altered neuroplasticity and improved neuropsychological, neuropsychiatric, motor, or somatic symptoms. Twentyeight current articles between 2020 and 2024 have been studied to elucidate potential mechanisms of change related to NIBS and other mediating or confounding variables. Discussion: tDCS and TMS may be efficacious as standalone interventions or coupled with neurorehabilitation therapies to positively alter maladaptive brain physiology and improve behavioral symptomology resulting from ABI. Based on postintervention and follow-up results, evidence suggests NIBS may offer a direct or mediatory contribution to improving behavioral outcomes post-ABI. Conclusion: More research is needed to better understand the extent of rTMS and tDCS application in affecting changes in symptoms after ABI. [ABSTRACT FROM AUTHOR]

Background: Cerebral air embolism (CAE) is an uncommon medical emergency with a potentially fatal course. We have retrospectively analyzed a set of patients treated with CAE at our comprehensive stroke center and a hyperbaric medicine center. An overview of the pathophysiology, causes, diagnosis, and treatment of CAE is provided. Results: We retrospectively identified 11 patients with cerebral venous and arterial air emboli that highlight the diversity in etiologies, manifestations, and disease courses encountered clinically. Acute-onset stroke syndrome and a progressive impairment of consciousness were the two most common presentations in four patients each (36%). Two patients (18%) suffered from an acute-onset coma, and one (9%) was asymptomatic. Four patients (36%) were treated with hyperbaric oxygen therapy (HBTO), high-flow oxygen therapy without HBOT was started in two patients (18%), two patients (18%) were in critical care at the time of diagnosis and three (27%) received no additional treatment. CAE was fatal in five cases (46%), caused severe disability in two (18%), mild disability in three (27%), and a single patient had no lasting deficit (9%). Conclusion: Cerebral air embolism is a dangerous condition that necessitates high clinical vigilance. Due to its diverse presentation, the diagnosis can be missed or delayed in critically ill patients and result in long-lasting or fatal neurological complications. Preventative measures and a proper diagnostic and treatment approach reduce CAE's incidence and impact. [ABSTRACT FROM AUTHOR]

ObjectiveThis study aimed to explore and evaluate the efficacy of non-invasive brain stimulation (NIBS) as a standalone or coupled intervention and understand its mechanisms to produce positive alterations in neuroplasticity and behavioral outcomes after acquired brain injury (ABI).Data sourcesCochrane Library, Web of Science, PubMed, and Google Scholar databases were searched from January 2013 to January 2024.Study selectionUsing the PICO framework, transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) randomized controlled trials (RCTs), retrospective, pilot, open-label, and observational large group and single-participant case studies were included. Two authors reviewed articles according to pre-established inclusion criteria.Data extractionData related to participant and intervention characteristics, mechanisms of change, methods, and outcomes were extracted by two authors. The two authors performed quality assessments using SORT.ResultsTwenty-two studies involving 657 participants diagnosed with ABIs were included. Two studies reported that NIBS was ineffective in producing positive alterations or behavioral outcomes. Twenty studies reported at least one, or a combination of, positively altered neuroplasticity and improved neuropsychological, neuropsychiatric, motor, or somatic symptoms. Twenty-eight current articles between 2020 and 2024 have been studied to elucidate potential mechanisms of change related to NIBS and other mediating or confounding variables.DiscussiontDCS and TMS may be efficacious as standalone interventions or coupled with neurorehabilitation therapies to positively alter maladaptive brain physiology and improve behavioral symptomology resulting from ABI. Based on postintervention and follow-up results, evidence suggests NIBS may offer a direct or mediatory contribution to improving behavioral outcomes post-ABI.ConclusionMore research is needed to better understand the extent of rTMS and tDCS application in affecting changes in symptoms after ABI.

BackgroundCerebral air embolism (CAE) is an uncommon medical emergency with a potentially fatal course. We have retrospectively analyzed a set of patients treated with CAE at our comprehensive stroke center and a hyperbaric medicine center. An overview of the pathophysiology, causes, diagnosis, and treatment of CAE is provided.ResultsWe retrospectively identified 11 patients with cerebral venous and arterial air emboli that highlight the diversity in etiologies, manifestations, and disease courses encountered clinically. Acute-onset stroke syndrome and a progressive impairment of consciousness were the two most common presentations in four patients each (36%). Two patients (18%) suffered from an acute-onset coma, and one (9%) was asymptomatic. Four patients (36%) were treated with hyperbaric oxygen therapy (HBTO), high-flow oxygen therapy without HBOT was started in two patients (18%), two patients (18%) were in critical care at the time of diagnosis and three (27%) received no additional treatment. CAE was fatal in five cases (46%), caused severe disability in two (18%), mild disability in three (27%), and a single patient had no lasting deficit (9%).ConclusionCerebral air embolism is a dangerous condition that necessitates high clinical vigilance. Due to its diverse presentation, the diagnosis can be missed or delayed in critically ill patients and result in long-lasting or fatal neurological complications. Preventative measures and a proper diagnostic and treatment approach reduce CAE’s incidence and impact.

P53 protein is the product of P53 gene, which is a well acknowledged tumor suppressor gene. The function of P53 and the relevant mechanisms of anti-neoplasm have raised the interest of researchers since many years ago. It is demonstrated that P53 is a basic cell cycle regulator and a strong inhibitor for versatile cancers in humans. However, most research focuses on other organs and systems instead of the central nervous system (CNS). In fact, in recent years, more and more studies have been suggesting that P53 plays a significant role in multiple CNS tumors and other diseases and disorders such as cerebral stroke and neurodegenerative diseases. In this work, we mainly reviewed the P53’s relationship with CNS tumors, cerebral stroke and neurodegenerative diseases, together with the relevant mechanisms, aiming to summarize the research achievements and providing new insight to the future study on diseases in CNS.

Cerebral stroke is one of the highest-ranking causes of death and the leading cause of disability globally, particularly with an increasing incidence and prevalence in developing countries. Steadily more evidence has indicated that micro ribonucleic acids (miRNAs) have important regulatory functions in gene transcription and translation in the course of cerebral stroke. It is beyond arduous to understand the pathophysiology of cerebral stroke, due in part to the perplexity of influencing the network of the inflammatory response, brain edema, autophagy and neuronal apoptosis. The recent research shows miRNA plays a key role in regulating aquaporin 4 (AQP4), and many essential pathological processes after cerebral stroke. This article reviews the recent knowledge on how miRNA influences the inflammatory response, brain edema, infarction size, and neuronal injury after cerebral stroke. In addition, some miRNAs may serve as potential biomarkers in stroke diagnosis and therapy since the expression of some miRNAs in the blood is stable after cerebral stroke. [ABSTRACT FROM AUTHOR]

Cerebral stroke is one of the highest-ranking causes of death and the leading cause of disability globally, particularly with an increasing incidence and prevalence in developing countries. Steadily more evidence has indicated that micro ribonucleic acids (miRNAs) have important regulatory functions in gene transcription and translation in the course of cerebral stroke. It is beyond arduous to understand the pathophysiology of cerebral stroke, due in part to the perplexity of influencing the network of the inflammatory response, brain edema, autophagy and neuronal apoptosis. The recent research shows miRNA plays a key role in regulating aquaporin 4 (AQP4), and many essential pathological processes after cerebral stroke. This article reviews the recent knowledge on how miRNA influences the inflammatory response, brain edema, infarction size, and neuronal injury after cerebral stroke. In addition, some miRNAs may serve as potential biomarkers in stroke diagnosis and therapy since the expression of some miRNAs in the blood is stable after cerebral stroke.

Stroke is a common and devastating disease with an escalating prevalence worldwide. The known secondary injuries after stroke include cell death, neuroinflammation, blood-brain barrier disruption, oxidative stress, iron dysregulation, and neurovascular unit dysfunction. Lipocalin-2 (LCN-2) is a neutrophil gelatinase-associated protein that influences diverse cellular processes during a stroke. The role of LCN-2 has been widely recognized in the peripheral system; however, recent findings have revealed that there are links between LCN-2 and secondary injury and diseases in the central nervous system. Novel roles of LCN-2 in neurons, microglia, astrocytes, and endothelial cells have also been demonstrated. Here, we review the evidence on the regulatory roles of LCN-2 in secondary injuries following a stroke from various perspectives and the pathological mechanisms involved in the modulation of stroke. Overall, our review suggests that LCN-2 is a promising target to promote a better understanding of the neuropathology of stroke. [ABSTRACT FROM AUTHOR]

Stroke is a common and devastating disease with an escalating prevalence worldwide. The known secondary injuries after stroke include cell death, neuroinflammation, blood-brain barrier disruption, oxidative stress, iron dysregulation, and neurovascular unit dysfunction. Lipocalin-2 (LCN-2) is a neutrophil gelatinase-associated protein that influences diverse cellular processes during a stroke. The role of LCN-2 has been widely recognized in the peripheral system; however, recent findings have revealed that there are links between LCN-2 and secondary injury and diseases in the central nervous system. Novel roles of LCN-2 in neurons, microglia, astrocytes, and endothelial cells have also been demonstrated. Here, we review the evidence on the regulatory roles of LCN-2 in secondary injuries following a stroke from various perspectives and the pathological mechanisms involved in the modulation of stroke. Overall, our review suggests that LCN-2 is a promising target to promote a better understanding of the neuropathology of stroke.

Mitochondrial autophagy is an early defense and protection process that selectively clears dysfunctional or excessive mitochondria through a distinctive mechanism to maintain intracellular homeostasis. Mitochondrial dysfunction during cerebral stroke involves metabolic disbalance, oxidative stress, apoptosis, endoplasmic reticulum stress, and abnormal mitochondrial autophagy. This article reviews the research progress on the mechanism of mitochondrial autophagy in ischemic stroke to provide a theoretical basis for further research on mitochondrial autophagy and the treatment of ischemic stroke.

Stroke is a multiphasic process, and the initial ischemic phase of neuronal damage is followed by secondary innate and adaptive responses that unfold over days after stroke, offer a longer time frame of intervention, and represent a novel therapeutic target. Therefore, revealing the distinct functions of immune cells in both brain and periphery is important for identification of immunotherapeutic targets for stroke to extend the treatment time window. In this paper an examination of the cellular dynamics of the immune response in the central nervous system (CNS) and periphery provoked by cerebral ischemia is provided. New data is presented for the number of immune cells in brain and spleen of mice during the 7 days following middle cerebral artery occlusion (MCAO). A novel analysis of the correlation among various cell types in the brain and spleen following stroke is presented. It is found that the infiltrated macrophages in the ischemic hemisphere positively correlate with neutrophils which implies their synergic effect in migrating into the brain after stroke onset. It is noted that during infiltration of adaptive immune cells, the number of neutrophils correlate positively with T cells, which suggests neutrophils contribute to T cell infiltration in the stroked brain. Furthermore, the correlation among neurological deficit and various immune cells suggests that microglia and splenic adaptive immune cells (T and B cells) are protective while infiltrating peripheral myeloid cells (macrophage and neutrophils) worsen stroke outcome. Comprehension of such immune responses post cerebral ischemia is crucial for differentiating the drivers of outcomes and also predicting the stroke outcome.

Mitochondrial autophagy is an early defense and protection process that selectively clears dysfunctional or excessive mitochondria through a distinctive mechanism to maintain intracellular homeostasis. Mitochondrial dysfunction during cerebral stroke involves metabolic disbalance, oxidative stress, apoptosis, endoplasmic reticulum stress, and abnormal mitochondrial autophagy. This article reviews the research progress on the mechanism of mitochondrial autophagy in ischemic stroke to provide a theoretical basis for further research on mitochondrial autophagy and the treatment of ischemic stroke. [ABSTRACT FROM AUTHOR]

Stroke is a multiphasic process, and the initial ischemic phase of neuronal damage is followed by secondary innate and adaptive responses that unfold over days after stroke, offer a longer time frame of intervention, and represent a novel therapeutic target. Therefore, revealing the distinct functions of immune cells in both brain and periphery is important for identification of immunotherapeutic targets for stroke to extend the treatment time window. In this paper an examination of the cellular dynamics of the immune response in the central nervous system (CNS) and periphery provoked by cerebral ischemia is provided. New data is presented for the number of immune cells in brain and spleen of mice during the 7 days following middle cerebral artery occlusion (MCAO). A novel analysis of the correlation among various cell types in the brain and spleen following stroke is presented. It is found that the infiltrated macrophages in the ischemic hemisphere positively correlate with neutrophils which implies their synergic effect in migrating into the brain after stroke onset. It is noted that during infiltration of adaptive immune cells, the number of neutrophils correlate positively with T cells, which suggests neutrophils contribute to T cell infiltration in the stroked brain. Furthermore, the correlation among neurological deficit and various immune cells suggests that microglia and splenic adaptive immune cells (T and B cells) are protective while infiltrating peripheral myeloid cells (macrophage and neutrophils) worsen stroke outcome. Comprehension of such immune responses post cerebral ischemia is crucial for differentiating the drivers of outcomes and also predicting the stroke outcome. [ABSTRACT FROM AUTHOR]