UNASSIGNED: 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.
UNASSIGNED: 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%).
UNASSIGNED: 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.

Transient receptor potential vanilloid subfamily member 1 (TRPV1) has been strongly implicated in the pathophysiology of cerebral stroke. However, the exact role and mechanism remain elusive. TPRV1 channels are exclusively present in the neurovascular system and involve many neuronal processes. Numerous experimental investigations have demonstrated that TRPV1 channel blockers or the lack of TRPV1 channels may prevent harmful inflammatory responses during ischemia-reperfusion injury, hence conferring neuroprotection. However, TRPV1 agonists such as capsaicin and some other non-specific TRPV1 activators may induce transient/slight degree of TRPV1 channel activation to confer neuroprotection through a variety of mechanisms, including hypothermia induction, improving vascular functions, inducing autophagy, preventing neuronal death, improving memory deficits, and inhibiting inflammation. Another factor in capsaicin-mediated neuroprotection could be the desensitization of TRPV1 channels. Based on the summarized evidence, it may be plausible to suggest that TPRV1 channels have a dual role in ischemia-reperfusion-induced cerebral injury, and thus, both agonists and antagonists may produce neuroprotection depending upon the dose and duration. The current review summarizes the dual function of TRPV1 in ischemia-reperfusion-induced cerebral injury models, explains its mechanism, and predicts the future.

Molecular pathways involved in cerebral stroke are diverse. The major pathophysiological events that are observed in stroke comprises of excitotoxicity, oxidative stress, mitochondrial damage, endoplasmic reticulum stress, cellular acidosis, blood-brain barrier disruption, neuronal swelling and neuronal network mutilation. Various biomolecules are involved in these pathways and several major proteins are upregulated and/or suppressed following stroke. Different types of receptors, ion channels and transporters are activated. Fluctuations in levels of various ions and neurotransmitters have been observed. Cells involved in immune responses and various mediators involved in neuro-inflammation get upregulated progressing the pathogenesis of the disease. Despite of enormity of the problem, there is not a single therapy that can limit infarction and neurological disability due to stroke. This is because of poor understanding of the complex interplay between these pathophysiological processes. This review focuses upon the past to present research on pathophysiological events that are involved in stroke and various factors that are leading to neuronal death following cerebral stroke. This will pave a way to researchers for developing new potent therapeutics that can aid in the treatment of cerebral stroke.

Similar reports in the past pay less attention to the anesthetic management of these patients. We reported a 46-year-old man who suffered from hypertensive cerebral apoplexy 5 months ago and accepted C7 nerve transfer to improve the central spastic paralysis in the right upper limb. After careful evaluation and anesthesia management before anesthesia, the operation was successfully completed under general anesthesia. The patient was cured and discharged without complications. The anesthesia management of C7 nerve transfer should choose appropriate operation opportunities for patients according to the type of stroke, improve the preoperative preparation, and form a multidisciplinary diagnosis and treatment.

UNASSIGNED: Description of the behavioural therapy of a patient after a subarachnoid haemorrhage from a ruptured aneurysm of the anterior communicating artery with an intracerebral haemorrhage, after aneurysm embolisation and left craniotomy, and after an ischemic cerebral stroke.
UNASSIGNED: The author presents behavioural therapy techniques used in patient rehabilitation in all areas requiring improvement in the daily functioning of a disabled person. The course of selected therapeutic interventions is analysed and the effects of the interventions are assessed. The presented case is an example of successful behavioural therapeutic intervention that led to changes compared to the initial functional state of the organism. Thanks to the use of behavioural techniques, independent multi- profile patient functioning was achieved. Given the limited availability of health services, the focus on the therapy on evidence-based teaching makes them intrinsic to the patient\'s success.
UNASSIGNED: The presented phases of therapy fully reflect the effective modification of behaviour patterns in a person after a subarachnoid haemorrhage from a ruptured aneurysm in the anterior communicating artery with an intracerebral haemorrhage, after aneurysm embolisation and left craniotomy, and after an ischemic cerebral stroke. The outcome of the applied behaviour approach seems to be significant enough to encourage the further development of the therapy for stroke patients regardless of the type of neurological disorders, functional difficulties, and age.

BACKGROUND: Systemic infections are a common complication of cerebral stroke, while the development of a cerebral abscess on the background of infarcted brain tissue is an extremely rare occurrence. Here, we present a new case alongside a literature review.
METHODS: A previously healthy 37-year-old man presented with sudden right-sided weakness and speech difficulties, progressing to complete aphasia. Initial tests showed no abnormalities, but subsequent CT scans revealed left basal ganglia infarction. Despite treatment and improvement, three months later, his condition worsened, leading to surgical intervention to excision of a cerebral abscess caused by Staphylococcus aureus. Following successful surgery and treatment, the patient showed improvement and was discharged for regular follow-up care.
CONCLUSIONS: The convergence of stroke and brain abscess poses serious clinical challenges, requiring prompt diagnosis and treatment to mitigate catastrophic consequences. Brain abscess, stemming from cerebral infection, may arise from various sources, including contiguous spread, hematogenous dissemination, or traumatic injury. Diagnosis is complicated by nonspecific radiological findings, which often lead to misdiagnosis. Risk factors include age, immunocompromised states, and certain medical conditions. Despite challenges, early detection and appropriate management, involving surgical drainage and antimicrobial therapy, are crucial for favorable outcomes.
CONCLUSIONS: Cerebral abscess following cerebral infarction is rare but should be suspected in patients with prior stroke or hemorrhage, experiencing worsening focal deficits and consciousness. Advanced age and comorbidities increase clinical suspicion.

Inflammatory responses and oxidative stress contribute to the pathogenesis of brain ischemia/reperfusion (IR) injury. Naturally occurring bioflavonoids possess antioxidant and anti-inflammatory properties. The phytochemicals of Juniperus sabina L., known as \"Abhal\" in Saudi Arabia, have been studied and cupressuflavone (CUP) has been isolated as the major bioflavonoid. This study aimed to investigate the neuroprotective potential of CUP in reducing brain IR damage in rats and to understand probable mechanisms. After 60 min of inducing cerebral ischemia by closing the left common carotid artery (CCA), blood flow was restored to allow reperfusion. The same surgical procedure was performed on sham-operated control rats, excluding cerebral IR. CUP or vehicle was given orally to rats for 3 days prior to ischemia induction and for a further 3 days following reperfusion. Based on the findings of this study, compared to the IR control group, CUP-administered group demonstrated reduced neurological deficits, improved motor coordination, balance, and locomotor activity. Additionally, brain homogenates of IR rats showed a decrease in malondialdehyde (MDA) level, an increase in reduced glutathione (GSH) content, and an increase in catalase (CAT) enzyme activity following CUP treatment. CUP suppressed neuro-inflammation via reducing serum inflammatory cytokine levels, particularly those of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) and enhancing the inflammatory cytokine levels, such as Nuclear factor kappa- B (NF-κB), TANK-binding kinase-1 (TBK1), and interferon beta (IFN-β) in brain tissues. Furthermore, CUP ameliorated the histological alterations in the brain tissues of IR rats. CUP significantly suppressed caspase-3 expression and downregulated the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway as a result of suppressing High mobility group box 1 (HMGB1). To our knowledge, this is the first study to document the neuroprotective properties of CUP. Thus, the study findings revealed that CUP ameliorates IR-induced cerebral injury possibly by enhancing brain antioxidant contents, reducing serum inflammatory cytokine levels, potentiating the brain contents of TBK1 and IFN-β and suppressing the HMGB1/TLR-4 signaling pathway. Hence, CUP may serve as a potential preventive and therapeutic alternative for cerebral stroke.

BACKGROUND: Cerebral stroke is a leading cause of death and disability worldwide. Ligusticum Chuanxiong Hort. (LCH), a well-known Chinese herb, is widely used for the treatment of cerebral stroke. This study aimed to investigate the underlying mechanisms of LCH in cerebral stroke and develop a diagnostic model.
METHODS: We employed network pharmacology analyses to identify the active compounds, targets, and underlying mechanisms of LCH for treating cerebral stroke. Molecular docking was performed to visualize the binding site between the core active compounds and hub targets. Furthermore, a diagnostic model for cerebral stroke was constructed based on transcriptomic analysis.
RESULTS: Our findings revealed that LCH contains multiple active ingredients, including oleic acid and caffeic acid. Protein-protein interaction network analysis identified IL1B, CCL2, MAPK3, PTGS2, JUN, MMP9, TLR4, HIF1A, PPARA, FOS, PTEN, NFE2L2, TLR2, TIMP1, and SOD2 as the top 15 hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted the enrichment of TNF and IL-17 signaling pathways. Molecular docking analysis demonstrated binding sites between oleic acid, caffeic acid, and MMP9, PPARP, PTEN, and TIMP1. The diagnostic model indicated that FOS, MMP9, PPARA, PTEN, TIMP1, and TLR2 serve as blood biomarkers for cerebral stroke.
CONCLUSIONS: This study demonstrates that LCH alleviates the symptoms following cerebral stroke through interactions with the TNF and IL-17 signaling pathways. The findings contribute to a better understanding of the therapeutic mechanisms of LCH and offer insights into the development of a diagnostic model for cerebral stroke.

Cerebral stroke (CS) is the leading cause of death in China, and a complex disease caused by both alterable risk factors and genetic factors. This study intended to investigate the association of MMP3, MMP14, and MMP25 single nucleotide polymorphisms (SNPs) with CS risk in a Chinese Han population.
A total of 1,348 Han Chinese were recruited in this case-control study. Four candidate loci including rs520540 A/G and rs679620 T/C of MMP3, rs2236302 G/C of MMP14, and rs10431961 T/C of MMP25 were successfully screened. The correlation between the four SNPs and CS risk was assessed by logistic regression analysis. The results were analyzed by false-positive report probability (FPRP) for chance or significance. The interactions between four SNPs associated with CS risk were assessed by multifactor dimensionality reduction (MDR).
rs520540 A/G and rs679620 C/T SNP in MMP3 were associated with risk of CS in allele, codominant, dominant and log-additive models. Ischemic stroke risk were significantly lower in carriers with rs520540-A allele and rs679620-T allele than those with G/G or C/C genotypes. However, rs520540-A allele and rs679620-T allele were associated with higher risk of hemorrhagic stroke. Stratified analysis showed that these two SNPs were associated with reduced risk of CS in aged < 55 years, non-smoking and non-drinking participants, and rs679620 SNP also reduced CS risk in male participants. The levels of uric acid, high-density lipoprotein cholesterol, and eosinophil were different among patients with different genotypes of rs520540 and rs679620. No statistically significant association was found between MMP14 rs2236302 G/C or MMP25 rs10431961 T/C with CS even after stratification by stroke subtypes, age, gender as well as smoking and drinking conditions in all the genetic models.
MMP3 rs520540 A/G and rs679620 C/T polymorphisms were associated with CS risk in the Chinese Han population, which provides useful information for the prevention and diagnosis of CS.

BACKGROUND: The appropriate choice of perioperative sedation during endovascular thrombectomy for ischemic stroke is unknown. Few studies have evaluated the role of nursing-administered conscious sedation supervised by a trained interventionalist.
OBJECTIVE: To compare the safety and efficacy of endovascular thrombectomy for ischemic stroke performed with nursing-administered conscious sedation supervised by a trained interventionalist with monitored anesthesia care supervised by an anesthesiologist.
METHODS: A retrospective review of a prospectively collected stroke registry was performed. The primary outcome was functional independence at 90 days, defined as a modified Rankin score of 0-2. Propensity score matching was performed to control for known confounders including patient comorbidities, access type, and direct-to-suite transfers.
RESULTS: A total of 355 patients underwent endovascular thrombectomy for large vessel occlusion between 2018 and 2022. Thirty five patients were excluded as they arrived at the endovascular suite intubated. Three hundred and twenty patients were included in our study, 155 who underwent endovascular thrombectomy with nursing-administered conscious sedation and 165 who underwent endovascular thrombectomy with monitored anesthesia care. After propensity score matching, there were 111 patients in each group. There was no difference in modified Rankin score 0-2 at 90 days (26.1% vs 35.1%, p = 0.190). Patients undergoing monitored anesthesia care received significantly more vasoactive medications (23.4% vs 49.5%, p < 0.001) and had a lower intraoperative minimum systolic blood pressure (134 vs 123 mmHg, p < 0.046). There was no difference in procedural efficacy, safety, intubation rates, and postoperative complications.
CONCLUSIONS: Perioperative sedation with nursing-administered conscious sedation may be safe and effective in patients undergoing endovascular thrombectomy for ischemic stroke.