Kaijun Zhao

To explore the role of ischemic cryptogenic vascular dissection (CVD) in a patient presenting with overlapping symptoms of amyotrophic lateral sclerosis (ALS) and spinocerebellar ataxia (SCA), and the impact of endovascular treatment on posterior circulation hypoperfusion, cerebellar atrophy, and clinical symptoms. A 22-year-old male patient with progressive neurological symptoms underwent MRI, CTA, and genetic testing, revealing cerebellar atrophy, a novel TGM6 gene variation associated with SCA type 35, and SETX gene deletions linked to ALS type 4. Ischemic CVD was diagnosed via dynamic contrast-enhanced CT (DCE-CT) and treated with endovascular stent repair followed by dual antiplatelet therapy. Following endovascular treatment, posterior circulation hypoperfusion and cerebellar atrophy were significantly improved. MRI follow-up showed increased cerebellar size and reduced interlobar spacing, with cerebellar dimensions expanding by up to 26.98% and interlobar spacing narrowing by up to 27.14%. Concurrently, the patient experienced marked improvement in clinical symptoms. At the 21-month follow-up, the patient’s Modified Rankin Scale (MRS) score was rated as favorable. Ischemic CVD may underlie overlapping ALS and SCA symptoms, suggesting a genetic-vascular link. Endovascular treatment of CVD led to improvements in posterior circulation hypoperfusion, cerebellar atrophy, and clinical symptoms, supporting further investigation into this potential pathogenic nexus.

This case explored the association among posterior circulation hypoperfusion, cryptogenic vertebral artery dissection (CVAD), and idiopathic intractable ot

Objective To evaluate the efficacy of treating cryptogenic vertebral artery dissections (CVADs) in patients with middle cerebral artery (MCA) stenosis/occlusion and posterior-circulation symptoms. Methods This retrospective study analyzed three patients who underwent endovascular stent reconstruction for CVADs between February 2024 and July 2025. All had symptomatic CVADs confirmed by dynamic contrast-enhanced computed tomography (DCE-CT), concurrent anterior-circulation lesions, and failed medical therapy. Results CVADs treatment alleviated posterior-circulation symptoms and improved hypoperfusion. Case 1 and 3 required staged treatments for recurring symptoms, while Case 2 improved after one treatment. Notably, parkinsonism-like symptoms in Case 3 improved post-treatment. Conclusions Targeting CVADs in complex cerebrovascular disease can improve clinical outcomes and reduce surgical risks. Further research on combined vascular-neurological therapies is warranted.

Objective: To evaluate the efficacy of flow diverter implantation for treating CTA-negative giant vertebral artery dissection aneurysm (VADA) and to address the challenges in lesion characterization using MRI. Methods: A 66-year-old male patient presented with a 3-month history of left facial numbness and dysarthria. Initial MRI-T1 revealed a mixed signal intensity lesion in the CPA region. However, both CTA and digital subtraction angiography (DSA) failed to identify any significant vascular abnormalities. Subsequently, CT-perfusion and dynamic contrast-enhanced computed tomography (DCE-CT) were performed to further characterize the lesion. Results: DCE-CT revealed a giant VADA, which was significantly larger than the lesion initially detected by MRI and was identified as the cause of hypoperfusion in the posterior circulation. Based on these findings, a flow diverter implantation procedure was performed successfully without complications. Angiographic follow-up at 8 months demonstrated no recurrence of the lesion. At the 14-month clinical follow-up, the patient exhibited complete resolution of symptoms, with a mRS score of 0, indicating an excellent functional outcome. Conclusion: Flow diverter implantation may be an effective treatment for CTA-negative giant VADAs. The limitations of MRI in accurately characterizing lesion size underscore the necessity of advanced imaging techniques, such as DCE-CT, for precise device selection and deployment.

Objective: The safety and effectiveness of thrombolysis in patients with intracranial artery dissection (IAD) are still controversial. This study aims to assess the safety and efficacy of intravenous thrombolysis (IVT) in patients with intracranial vertebrobasilar artery dissection (i-VBAD) related acute ischemic stroke (AIS).Methods: A retrospective review of 32 patients admitted to our Neurovascular Center between January 2016 and June 2021 with AIS due to i-VBAD was conducted. Patients were identified and divided into IVT group (n = 8) and non-IVT group (n = 24) receiving standard antithrombotic therapy.Results: The mean age of the 32 patients was 49.28 ± 15.6 years, with a male predominance (87.5%). All patients presented with clinical manifestations consistent with posterior circulation infarct. Patients in the IVT group were significantly older than those in non-IVT group (58.88 vs. 46.08 years, p = 0.043) and had a higher prevalence of diabetes mellitus (50.0% vs. 8.3%, p = 0.023). No intracranial hemorrhage was observed in of the eight patients in IVT group. An excellent functional outcome, defined as an modified Rankin Scale score of 0–1, was achieved in all eight patients in the IVT group (100%) compared to 15 of the 24 patients in the non-IVT group (62.5%, p = 0.070). Although the difference did not reach statistical significance, the trend suggested a potential benefit of IVT in this patient population.Conclusion: IVT appears safe with no hemorrhagic complications in i-VBAD patients. It may offer better functional outcomes compared to standard therapy. Larger, prospective, multicenter studies are needed for definitive validation.

Objective: To report a novel clinical entity, “Multi-regional Sequential Pain Syndrome” (MRSPS), and evaluate the relationship between hypoperfusion, cryptogenic vertebral artery dissection (CVAD), and MRSPS.Methods: A 59-year-old female patient, with a chronic MRSPS condition spanning 10–30 years, underwent a comprehensive diagnostic evaluation including cranial CTA, MRI, DSA, and CT perfusion, culminating in the identification of CVAD via dynamic contrast-enhanced computed tomography (DCE-CT). The treatment strategy integrated repairing CVADs with stent implantation to address the hypoperfusion and MRSPS.Results: Following intervention, hypoperfusion achieved complete improvement, and the patient achieved the complete resolution of pain and vertigo, with the modified Rankin Scale (mRS) score of 0 at the 1-year follow-up, signifying full neurological recovery.Conclusion: CVADs, a key cause of brain tissue hypoperfusion in MRSPS, can be effectively treated by repair to alleviate the syndrome.

Previous research have demonstrated that the stress hyperglycemia ratio (SHR) accurately reflects acute hyperglycemic states and correlates with adverse outcomes. This study aims to explore the relationship between SHR and the prognosis of patients with aneurysmal subarachnoid hemorrhage (aSAH). Patients with aSAH were categorized into four groups based on SHR tertiles. Functional outcomes were evaluated at 12 months using the modified Rankin Scale (mRS), with scores ranging from 0 to 2 indicating a good outcome and 3–6 indicating a poor outcome. The associations between SHR and functional outcomes were analyzed using logistic regression models and restricted cubic spline analysis. A total of 127 patients exhibited poor functional outcomes. Following comprehensive adjustments, those in the highest SHR tertile had a significantly increased risk of poor prognosis compared to those in the lowest tertile (odds ratio [OR], 4.12; 95% confidence interval [CI]: 1.87–9.06). Moreover, each unit increase in SHR was associated with a 7.51-fold increase in the risk of poor prognosis (OR, 7.51; 95% CI: 3.19–17.70). Further analysis using restricted cubic spline confirmed a linear correlation between SHR and poor prognosis (P for nonlinearity = 0.609). Similar patterns were observed across all studied subgroups. Elevated SHR significantly correlates with poor functional prognosis at one year in patients with aSAH, independent of their diabetes status.

IntroductionAutism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder with a multifaceted etiology. This case report explores the ischemic cryptogenic vascular dissection as a potential underlying cause of ASD.MethodsA 9-year-old child presented with symptoms of ASD, including social interaction difficulties, repetitive behaviors, and cognitive challenges. Despite conventional ASD treatments, significant improvement was only observed after addressing an underlying ischemic cryptogenic vascular dissection identified through DCE-CT.ResultsFollowing a reconstructive treatment approach to the vascular dissection, the patient showed marked improvement in cognitive functions, social abilities, and a reduction in ASD-related symptoms whether during the perioperative period or during approximately 5-month follow-up.ConclusionThis case suggests that ischemic cryptogenic vascular dissection may contribute to the symptoms of ASD. Identifying and treating underlying vascular anomalies may offer a new avenue for mitigating ASD symptoms, emphasizing the need for comprehensive diagnostic estimations in ASD management.

Purpose Glioma has been demonstrated as one of the most malignant intracranial tumors and currently there is no effective treatment. Based on our previous RNA-sequencing data for oxidative phosphorylation (OXPHOS)-inhibition resistant and OXPHOS-inhibition sensitive cancer cells, we found that vimentin (VIM) is highly expressed in the OXPHOS-inhibition resistant cancer cells, especially in glioma cancer cells. Further study of VIM in the literature indicates that it plays important roles in cancer progression, immunotherapy suppression, cancer stemness and drug resistance. However, its role in glioma remains elusive. This study aims to decipher the role of VIM in glioma, especially its role in OXPHOS-inhibition sensitivity, which may provide a promising therapeutic target for glioma treatment. Methods The expression of VIM in glioma and the normal tissue has been obtained from The Cancer Genome Atlas (TCGA) database, and further validated in Human Protein Atlas (HPA) and Chinese Glioma Genome Atlas (CGGA). And the single-cell sequencing data was obtained from TISCH2. The immune infiltration was calculated via Tumor Immune Estimation Resource (TIMER), Estimation of Stromal and Immune Cells in Malignant Tumors using Expression Data (ESTIMATE) and ssGSEA, and the Immunophenoscore (IPS) was calculated via R package. The differentiated expressed genes were analyzed including GO/KEGG and Gene Set Enrichment Analysis (GSEA) between the VIM-high and -low groups. The methylation of VIM was checked at the EWAS and Methsurv. The correlation between VIM expression and cancer stemness was obtained from SangerBox. We also employed DepMap data and verified the role of VIM by knocking down it in VIM-high glioma cell and over-expressing it in VIM-low glioma cells to check the cell viability. Results Vim is highly expressed in the glioma patients compared to normal samples and its high expression negatively correlates with patients’ survival. The DNA methylation in VIM promoters in glioma patients is lower than that in the normal samples. High VIM expression positively correlates with the immune infiltration and tumor progression. Furthermore, Vim is expressed high in the OXPHOS-inhibition glioma cancer cells and low in the OXPHOS-inhibition sensitive ones and its expression maintains the OXPHOS-inhibition resistance. Conclusions In conclusion, we comprehensively deciphered the role of VIM in the progression of glioma and its clinical outcomes. Thus provide new insights into targeting VIM in glioma cancer immunotherapy in combination with the current treatment. Graphical abstract