Early recanalization and vasospasm after endovascular treatment in a case of ruptured vertebral artery dissecting aneurysm associated with COVID-19.

Background: The coronavirus disease 2019 (COVID-19) pandemic has caused significant structural changes in acute care hospitals. COVID-19-associated stroke has gained attention, with abnormal coagulation and vascular endothelial damage being recognized. While ischemic cases are commonly reported, hemorrhagic cases have also been reported. This report presents a case of ruptured vertebral artery dissection aneurysm associated with COVID-19, resulting in subarachnoid hemorrhage (SAH). The treatment course, challenges in managing cerebral vasospasm, and early recanalization achieved through endovascular therapy are described. Case Description: A 67-year-old male patient was brought to our hospital for emergency treatment of impaired consciousness that occurred while recovering from COVID-19. He underwent endovascular internal trapping using coils, and although the rupture did not recur, he required long-term tracheal management, which resulted in a cerebral infarction caused by cerebral vasospasm. In addition, early recanalization was seen, which required retreatment. Conclusion: This case highlights the challenges in managing COVID-19-associated SAH and emphasizes the need for infection control measures and proper postoperative care. Establishing protocols for detecting and managing cerebral vasospasm is essential.

Bold-S Signs on Computed Tomography Angiography Are Sensitive Markers for Diagnosing Subcortical Hemorrhage Due to Dural Arteriovenous Fistulae on Emergent Admission.

An optimal treatment strategy for subcortical hematomas caused by dural arteriovenous fistulae (dAVF) is important because of the high rebleeding rate. However, it is very difficult to diagnose that on admission. Therefore, an early sensitive predictive marker for subcortical hemorrhage caused by dAVF is necessary, especially during the first contact on admission. S-shaped dilated vessels around the hematoma (bold-S sign) on computed tomography angiography (CTA) performed during admission could be one such marker. Herein, we evaluated the characteristics of these vessels. Among 273 patients with intracerebral hemorrhage between April 2012 and March 2020, 67 patients with subcortical hematomas who underwent CTA on admission without arteriovenous malformations were included. The patients in the dAVF group (n = 7) showed fewer disturbances in consciousness, milder neurological deficits, and more frequent seizures than patients without dAVF (without dAVF group, n = 60). All patients in the dAVF group had dilated S-shaped vessels (2.59 ± 0.27 mm) around the hematomas, and only 20% of the patients in the without dAVF group had these vessels (1.69 ± 0.22 mm). The ratio of the ipsilateral S-shaped/contralateral largest vessels was 1.80 ± 0.29 in the dAVF group and 1.07 ± 0.16 in the group without dAVF. We called the dilated S-shaped vessels the "bold-S sign," with a cutoff ratio of 1.5. Bold-S sign findings are novel and help in diagnosing subcortical hematomas caused by dAVF on admission.

Increased plasma glutamate by antipsychotic medication and its relationship to glutaminase 1 and 2 genotypes in schizophrenia -- Juntendo University Schizophrenia Projects (JUSP).

Disturbed glutamatergic neurotransmission has become recognized as a key component in the pathophysiology of schizophrenia. The change in serum/plasma glutamate with the use of antipsychotic medication has been studied and may be a possible clinical marker. In the present study, we examined plasma glutamate concentration, including a comprehensive investigation of its involvement with clinical course of schizophrenia and a genomic analysis. We performed a case-control genetic association analysis of the glutaminase 1 (GLS) and 2 (GLS2) genes. In addition, the difference in plasma glutamate concentration between the "acute stage" and "remission stage", and the effect of genotypes of SNPs within the two genes were assessed. The genetic association analysis of the GLS and GLS2 genes showed no association with schizophrenia. Plasma glutamate was increased with antipsychotic medication at "remission stage". Although GLS and GLS2 are not likely genetic risk factors for schizophrenia, changes in plasma glutamate concentration might be connected with clinical course of schizophrenia.

Genetic association between Notch4 polymorphisms and Alzheimer's disease in the Japanese population.

It is shown that Notch 4 plays important roles in the pathogenesis of Alzheimer's disease (AD). To investigate whether three single nucleotide polymorphisms (SNPs) of the Notch4 gene are associated with AD, the three SNPs were genotyped by a polymerase chain reaction-restriction fragment length polymorphism method for 243 AD patients and 130 age-matched controls. We also confirmed the linkage disequilibrium among these three SNPs of the gene using the EH program. The three SNPs did not seem to alter risk for AD. Our study suggests that SNPs studied are not associated with AD. The linkage disequilibrium of this locus indicates that there is genetic heterogeneity in the Notch4 gene. We could not confirm the previous synergetic associations of the 5' untranslated region (rs367398) C/C genotype in apolipoprotein E epsilon4 bearers in AD patients. Potential markers nearby the 5' untranslated region polymorphism might affect risk for AD.

Genetic association between USF 1 and USF 2 gene polymorphisms and Japanese Alzheimer's disease.

To investigate the effect of single nucleotide polymorphisms (SNPs) of the upstream stimulatory factor (USF) 1 and 2 genes on the onset of Alzheimer's disease (AD), a case-control study was performed. The SNPs were genotyped by a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 236 AD patients and 120 age-matched controls of Japanese descent. We observed no significant association between the three SNPs of the USF 1 gene and AD in our Japanese participants. In addition, the SNPs studied did not affect plasma cholesterol levels in our AD cases. For the USF 2 gene, the two SNPs did not show significant association with onset of AD. Our study suggests that the three SNPs of the USF 1 gene and two SNPs of the USF 2 gene presented here are not associated with onset of AD.

Genetic association between Notch4 polymorphisms and Japanese schizophrenics.

The objective of this study was to investigate whether three single nucleotide polymorphisms of the Notch4 gene are associated with the onset of schizophrenia. To confirm the linkage disequilibrium among these three single nucleotide polymorphisms of the gene, the three single nucleotide polymorphisms were genotyped by a polymerase chain reaction-restriction-fragment length polymorphism method for all samples. The genotypic frequencies of each single nucleotide polymorphism in the schizophrenic were compared with respective controls using a chi method. To check linkage disequilibrium, the haplotype frequency program was utilized. No statistical association between the two single nucleotide polymorphisms of the Notch4 gene and schizophrenia was observed in our Japanese samples. Although one nonsynonymous single nucleotide polymorphism did show a weakly significant P-value, its allelic frequencies are not positive. Two of the single nucleotide polymorphisms showed strong linkage disequilibrium in our Japanese samples. The single nucleotide polymorphism between the other two single nucleotide polymorphisms showed a weaker linkage disequilibrium with the others. Our study suggests that the three single nucleotide polymorphisms are not associated with the onset of schizophrenia. The linkage disequilibrium of this locus indicates that there is genetic heterogeneity in the Notch4 gene. Linkage disequilibrium may differ among ethnic groups, and so a larger study should be performed in this region.

No genetic association between the myeloperoxidase gene -463 polymorphism and estrogen receptor-alpha gene polymorphisms and Japanese sporadic Alzheimer's disease.

Myeloperoxidase (MPO) presence has been demonstrated in microglia associated with senile plaques and contributes to Alzheimer's disease (AD) pathology through oxidation-induced damage. MPO activity is normally higher in women than in men. Additionally, a functional biallelic (G/A) polymorphism in the promoter region (-463) of the MPO gene has been associated with a gender-specific risk factor for AD, but reports of this association have been inconsistent. Furthermore, estrogen is known to enhance MPO activity in myeloid cells and increases the amount of MPO in plasma. Recently, estrogen replacement therapy has been reported to reduce the risk of developing AD and to help maintain cognitive function in patients with AD. In the current study, we analyzed the MPO -463 polymorphism and two estrogen receptor-alpha polymorphisms in 205 Japanese sporadic AD patients and 92 controls. The results suggest that there is no significant difference in the genotypic frequencies and allelic frequencies of the MPO -463 polymorphism and the estrogen receptor-alpha polymorphisms between the Japanese sporadic AD group and the control group.

Electroconvulsive therapy improves severe pain associated with fibromyalgia.

The pathophysiology of fibromyalgia remains unknown. Several reports have recently suggested the novel concept that fibromyalgia is due to the central nervous system becoming hyper-responsive to a peripheral stimulus. The effect of electroconvulsive therapy (ECT) as pain remedication in cases of fibromyalgia without major depressive disorder was studied in a prospective trial lasting three months. All of the patients taking part in the study fulfilled the American College of Rheumatology diagnostic criteria for fibromyalgia. Technetium-99m ethyl cysteinate dimer single photon emission computed tomography was used to assess regional cerebral blood flow (rCBF) before and after a course of ECT. Pain assessment in the patients was undertaken by use of the visual analog scale (VAS) and by evaluation of tender points (TPs). Beck's depression inventory (BDI) was further used to assess depressive mood change in the patients. Our study clearly demonstrated that pain was significantly less severe after ECT, as indicated by the VAS scale for pain and the evaluation of TPs. A further notable observation was that thalamic blood flow was also improved. We conclude that a course of ECT produced notable improvements in both intractable severe pain associated with fibromyalgia and also in terms of thalamic blood flow.

No genetic association between ATP binding cassette proteins and Japanese sporadic Alzheimer's disease.

The identification of the epsilon4 variant of apolipoprotein E as a genetic risk factor for late-onset Alzheimer's disease (AD) suggests that cholesterol may play a direct role in the pathogenesis of the disease. Recent studies have suggested that the ATP-binding cassette (ABC) protein G5 (ABCG5) may be involved in the regulation of intestinal cholesterol absorption. Furthermore, genetic variation of this locus may affect blood cholesterol concentrations. We therefore studied whether the ABCG5 C1950G (Gln640Glu) polymorphism affects the risk of AD. In addition, there was no difference in mean baseline cholesterol concentrations between individuals with the C/C genotype and carriers of the G allele. Recent studies have shown that genetic regions including the ABCA12 gene might also be associated with the risk of AD. The ABCA12 gene, located <1 Mb from the peak marker on chromosome 2q34, is also a member of the ABC transporter superfamily. In the current study, two common polymorphisms of the ABCA12 gene, rs952718 (T/G) and rs956133 (A/G), were analyzed in our subjects. These polymorphisms showed no association with the risk of AD. Furthermore, we observed weak linkage disequilibrium between these two single nucleotide polymorphisms. These results indicate that the common polymorphisms of the ABCG5 and ABCA12 genes investigated here are not associated with AD.

Genetic association between matrix metalloproteinase MMP-9 and MMP-3 polymorphisms and Japanese sporadic Alzheimer's disease.

Recent studies suggested that matrix metalloproteinases (MMPs) might play an important role in the pathophysiology of Alzheimer's disease (AD). MMP-9 and MMP-3 are reported to degrade amyloid beta and have several functional polymorphisms associated with other common diseases. Four common polymorphisms in each of MMP-9 and MMP-3 were examined in AD cases and normal control individuals. Common polymorphisms of MMP-9, rs3918248, rs2664538, rs2250889 and rs2274756 showed no association with risk for AD. We observed strong linkage disequilibrium (LD) between rs2664538 and rs2250889 in our Japanese samples. The polymorphisms of MMP-3; 5A/6A insertion polymorphism in the promoter, rs3025079, rs520540 and rs679620 also did not influence risk for AD. LD of the 5A/6A polymorphism with rs679620 was relatively strong. These results suggest that the common polymorphisms of MMP-9 and MMP-3 investigated here are not associated with AD.