Objective: Carotid artery stenosis (CAS) is a major pathological substrate of ischemic cerebrovascular disease and has been increasingly recognized as an important contributor to the development and progression of vascular cognitive impairment. Through multiple interacting mechanisms, including chronic cerebral hypoperfusion, increased microembolic burden, inflammatory responses, and blood-brain barrier disruption, CAS may initiate or accelerate progressive cognitive decline, thereby adversely affecting long-term clinical outcomes and quality of life. Conventional cognitive assessment scales are limited by their inherent subjectivity and insufficient sensitivity to subtle early changes, highlighting the need for objective and quantifiable biomarkers for early risk identification, longitudinal disease monitoring, and therapeutic evaluation.

Methods: This review summarizes recent advances in biological biomarkers, including markers of inflammation and immune activation, lipid metabolism abnormalities, and vascular or neuronal injury, as well as multimodal imaging biomarkers encompassing brain structural alterations, white matter integrity, cerebral perfusion and metabolism, and functional connectivity networks.

Results: We highlight the potential applications of these biomarkers in risk stratification, personalized intervention strategies, and clinical decision-making for CAS-related cognitive decline, and outline future directions for research in this field.

Conclusion: This review provides a comprehensive reference for both clinical practice and future investigations into cognitive impairment associated with CAS.

Objective: Postoperative delirium is a common complication following deep brain stimulation (DBS) surgery, which can prolong hospital stays and potentially impair cognitive function, exacerbating the progression of the disease. The clinical understanding of risk factors, pathophysiology, pathogenesis, prevention, and management of postoperative delirium after DBS is often inadequate, leading to delayed treatment.

Methods: This systematic review aims to summarize key aspects, including definition and incidence, clinical presentation and classification, pathophysiology, risk factors, assessment and prediction, and clinical management, to provide a scientifically rigorous basis for the early identification and intervention of postoperative delirium in DBS surgery patients.

Results: DBS-related delirium typically occurs within 72 hours, with > 50% cases missed. Pathogenesis involves neurotransmitter imbalance, neuroinflammation, mechanical damage to target nuclei, and default mode network dysfunction. Risk factors include advanced age, comorbidities, cognitive impairment, and brain atrophy. Diagnosis relies on Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Confusion Assessment Method, and 4 A’s Test. Prophylactic antipsychotics show no benefit; quetiapine is preferred when pharmacotherapy is needed, while haloperidol is contraindicated in Parkinson’s disease (PD).

Discussion: Postoperative delirium following DBS surgery in PD patients is a complex neuropsychiatric complication with multifactorial etiology. The overlapping symptoms between PD and delirium pose significant challenges to accurate identification. Future research should focus on elucidating the specific pathophysiological mechanisms of DBS-related delirium, developing optimized assessment tools tailored for PD populations, and validating the effectiveness of prevention and treatment strategies through large-scale prospective studies. Given the current lack of evidence supporting prophylactic antipsychotic use, emphasis should be placed on non-pharmacological preventive measures and individualized risk stratification to reduce the burden on healthcare providers and caregivers while improving patient outcomes.

Objective: Cerebrovascular diseases remain a leading cause of mortality and disability worldwide. Despite significant advances in acute interventions such as thrombolysis, endovascular therapy, and neurocritical care, effective neuroprotective strategies remain limited. Molecular hydrogen has recently attracted increasing attention due to its antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective properties. This review aims to summarize the mechanisms, experimental evidence, therapeutic effects, and future perspectives of hydrogen in cerebrovascular diseases.

Methods: A comprehensive review of studies investigating hydrogen therapy in cerebrovascular diseases was conducted, including hydrogen gas inhalation, hydrogen-rich saline, and hydrogen-rich water. We focused on delivery methods, biological mechanisms, effects on vascular risk factors, and therapeutic outcomes in experimental models such as carotid artery occlusion, ischemic brain injury, subarachnoid hemorrhage, and related conditions.

Results: Current evidence suggests that hydrogen exerts neuroprotective effects by selectively scavenging reactive oxygen species, suppressing neuroinflammation, regulating microglial polarization, inhibiting apoptosis-related signaling pathways, protecting the blood-brain barrier, and improving cerebral blood flow. In addition, hydrogen may improve major cerebrovascular risk factors, including hyperglycemia, hypertension, and hyperlipidemia. Experimental studies have demonstrated that hydrogen reduces oxidative stress, brain edema, neuronal apoptosis, infarct volume, and neurological deficits in various disease models.

Discussion: Hydrogen appears to be a promising adjunctive therapy for cerebrovascular diseases. However, current evidence is limited by inconsistent administration protocols, unclear optimal dosage and timing, and a lack of large-scale clinical trials with long-term follow-up. Future research should focus on standardized treatment strategies and rigorous clinical validation.

Objective: This study primarily aimed to evaluate the impact of minimally invasive surgery and other contributing factors on the clinical prognosis of severe primary brainstem hemorrhage (PBSH).

Methods: A retrospective analysis was conducted on the clinical data of 152 severe PBSH patients admitted to the neurological intensive care unit of Linyi People’s Hospital from 2020 to 2023.

Results: Univariate Cox regression analysis identified significant correlations between prognosis and factors including surgery (modified-frameless stereotactic minimally invasive drainage for intracerebral hemorrhage [ICH]), smoking history, homocysteine levels, cardiac arrest, mechanical ventilation, brainstem hemorrhage volume, and spontaneous breathing at discharge (all p < 0.05).Surgery (HR = 0.583, 95% CI: 0.345–0.986) and spontaneous breathing at discharge (HR = 0.355, 95% CI: 0.196–0.645) were identified as independent protective factors, while brainstem hemorrhage volume (HR = 1.049, 95% CI: 1.012–1.088) and cardiac arrest (HR = 1.882, 95% CI: 1.135–3.12) were independent risk factors (all p < 0.05). Kaplan-Meier indicated the surgical group had a significantly higher 180-day survival rate than the non-surgical group (p < 0.05).

Conclusion: Surgery (modified-frameless stereotactic minimally invasive drainage for ICH) and spontaneous breathing at discharge have been identified as independent protective factors for the survival of patients with severe PBSH. The brainstem hemorrhage volume and cardiac arrest serve as independent risk factors.