Stenting for subclavian steal phenomenon to restore cerebral perfusion due to acute carotid occlusion following carotid endarterectomy: a case report.

BACKGROUND: Perioperative symptomatic carotid artery occlusion after carotid endarterectomy is a rare complication. In this study, we present a case of symptomatic acute carotid artery occlusion that occurred after carotid endarterectomy in a patient with coexistent subclavian artery steal phenomenon, which was successfully treated with subclavian artery stenting. CASE PRESENTATION: A 57-year-old East Asian female presented with stenosis in the left common carotid artery and left subclavian artery along with subclavian steal. The proximal segment of the left anterior cerebral artery was hypoplastic, and the posterior communicating arteries on both sides were well-developed. Left internal carotid artery stenosis progressed during the follow-up examination; therefore, left carotid endarterectomy was performed. On the following day, symptoms of cerebral perfusion deficiency appeared due to occlusion of the left carotid artery. The stenotic origin of the left common carotid artery and the suspected massive thrombus in the left carotid artery posed challenges to carotid revascularization. Therefore, left subclavian artery stenting for the subclavian steal phenomenon was determined to be the best option for restoring cerebral blood flow to the whole brain. Her symptoms improved after the procedure, and the postprocedural workup revealed improved cerebral blood flow. CONCLUSION: Subclavian artery stenting is safe and may be helpful in patients with cerebral perfusion deficiency caused by intractable acute carotid occlusion coexisting with the subclavian steal phenomenon. Revascularization of asymptomatic subclavian artery stenosis is generally not recommended. However, cerebral circulatory insufficiency as a comorbidity may be worth considering.

Spontaneous occlusion of ruptured microaneurysm formed on postoperative transosseous anastomosis after indirect revascularization in a patient with moyamoya disease.

A 40-year-old female with a history of ischemic moyamoya disease treated with indirect revascularization at ages 12 and 25 years presented with a sudden severe headache. Imaging studies revealed focal parenchymal hemorrhage and acute subdural hematoma, confirming a microaneurysm formed on the postoperative transosseous vascular network as the source of bleeding. Conservative management was performed, and no hemorrhage recurred during the 6-month follow-up period. Interestingly, follow-up imaging revealed spontaneous occlusion of the microaneurysm. However, due to the rarity of this presentation, the efficacy of conservative treatment remains unclear. Further research on similar cases is warranted.

Encephalo-Duro-Pericranio-Synangiosis for the Treatment of Moyamoya Disease with Posterior Cerebral Artery Lesions.

OBJECTIVE: We describe our experience performing encephalo-duro-pericranio synangiosis for the parieto-occipital region (EDPS-p) as a treatment for moyamoya disease (MMD) with hemodynamic disturbances caused by lesions of the posterior cerebral artery. METHODS: From 2004 to 2020, 60 hemispheres of 50 patients with MMD (38/50 females, age 1-55 years) underwent EDPS-p as a treatment for hemodynamic disturbances in the parieto-occipital region. A skin incision was made on the parieto-occipital area to avoid the major skin arteries, and the pedicle flap was created by attaching the pericranium to the dura mater under the craniotomy with multiple small incisions. The surgical outcome was assessed on the basis of the following points: perioperative complications, postoperative improvement of clinical symptoms, subsequent novel ischemic events, qualitative assessment of the development of collateral vessels by magnetic resonance arteriography, quantitative assessment of postoperative perfusion improvement based on the mean transit time, and cerebral blood volume on dynamic susceptibility contrast imaging. RESULTS: Perioperative infarction occurred in 7/60 hemispheres (11.7%). The transient ischemic symptoms observed preoperatively disappeared in 39/41 hemispheres (95.1%) during the follow-up period (12-187 months), and none of the patients experienced novel ischemic events. Collateral vessels supplied from the occipital arteries, middle meningeal arteries, and posterior auricular arteries developed postoperatively in 56/60 hemispheres (93.3%). Postoperative mean transit time and cerebral blood volume showed significant improvement in the occipital, parietal, and temporal areas (P < 0.001), as well as the frontal area (P = 0.01). CONCLUSIONS: EDPS-p seems to be an effective surgical treatment for patients with MMD who suffer hemodynamic disturbances caused by posterior cerebral artery lesions.

Nonconvulsive status epilepticus characteristics in glioma patients: a retrospective study.

PURPOSE: Epilepsy is a common complication of gliomas. The diagnosis of nonconvulsive status epilepticus (NCSE) is challenging because it causes impaired consciousness and mimics glioma progression. NCSE complication rate in the general brain tumor patient population is approximately 2%. However, there are no reports focusing on NCSE in glioma patient population. This study aimed to reveal the epidemiology and features of NCSE in glioma patients to enable appropriate diagnosis. METHODS: We enrolled 108 consecutive glioma patients (45 female, 63 male) who underwent their first surgery between April 2013 and May 2019 at our institution. We retrospectively investigated glioma patients diagnosed with tumor-related epilepsy (TRE) or NCSE to explore disease frequency of TRE/NCSE and patient background. NCSE treatment approaches and Karnofsky Performance Status Scale (KPS) changes following NCSE were surveyed. NCSE diagnosis was confirmed using the modified Salzburg Consensus Criteria (mSCC). RESULTS: Sixty-one out of 108 glioma patients experienced TRE (56%), and five (4.6%) were diagnosed with NCSE (2 female, 3 male; mean age, 57 years old; WHO grade II 1, grade III 2, grade IV 2). All NCSE cases were controlled by stage 2 status epilepticus treatment as recommended in the Clinical Practice Guidelines for Epilepsy by the Japan Epilepsy Society. The KPS score significantly decreased after NCSE. CONCLUSION: Higher prevalence of NCSE in glioma patients was observed. The KPS score significantly decreased after NCSE. Actively taking electroencephalograms analyzed by mSCC may facilitate accurate NCSE diagnosis and improve the activities of daily living in glioma patients.

Initial Management of Patients with Suspected Stroke in the SARS-CoV-2 Era: Effects on the Door-to-Picture Time.

Objective: To examine the effectiveness of a newly developed emergency room (ER) protocol to treat patients with stroke and control the spread of SARS-CoV-2 by evaluating the door-to-picture time. Methods: We retrospectively enrolled 126 patients who were transported to our ER by ambulance with suspected stroke between April 15 and October 31, 2020 (study group). A risk judgment system named the COVID level was introduced to classify the risk of infection as follows: level 0, no infection; I, infection unlikely; II, possible; III, probable; and IV, definite. Patients with COVID levels 0, I, or II and a Glasgow Coma Scale (GCS) score >10 were placed in a normal ER (nER) without atmospheric pressure control; the medical staff wore standard personal protective equipment (PPE) in such cases. Patients with COVID level II, III, or IV, and a GCS score of ≤10 were assigned to the negative pressure ER (NPER); the medical staff wore enhanced PPE for these cases. The validity of the protocol was assessed. The door-to-picture time of the study group was compared with that of 114 control patients who were transported with suspected stroke during the same period in 2019 (control group). The difference in the time for CT and MRI between the two groups was also compared. In the study group, the time spent in the nER and NPER was evaluated. Results: In all, 118 patients (93.7%) were classified as level I, 6 (4.8%) as level II, and 2 (1.6%) as level III. Only five patients (4.0%) were treated with NPER. Polymerase chain reaction tests were performed on 118 out of 126 patients (93.7%) and were negative. No significant differences were observed in age, sex, neurological severity, modalities of diagnostic imaging, and diagnosis compared with the control group. The median door-to-picture time was 18 (11-27.8) min in the study group and 15 (10-25) min in the control group (p = 0.08). No delay was found on CT (15 [10-21] vs. 14 [9-21] min, p = 0.24). In contrast, there was an 8-min delay for MRI (30 [21.8-50] vs. 22 [14-30] min, p = 0.01). The median door-to-picture time was 29 min longer in patients treated with NPER than in those treated with nER, although the difference was not significant due to the small number of patients (47 [27-57] vs. 18 [11-26] min, p = 0.07). Conclusion: Our protocol could optimize the use of medical resources with only a 3-min delay in the door-to-picture time in an area without explosive outbreak. Unfortunately, the effectiveness of the protocol in preventing infection could not be verified because of the low incidence of COVID-19. When developing and modifying an institutional protocol, recognizing the outbreak status surrounding each institution is important.

The Role of Cysteine String Protein α Phosphorylation at Serine 10 and 34 by Protein Kinase Cγ for Presynaptic Maintenance.

Protein kinase Cγ (PKCγ) knock-out (KO) animals exhibit symptoms of Parkinson's disease (PD), including dopaminergic neuronal loss in the substantia nigra. However, the PKCγ substrates responsible for the survival of dopaminergic neurons in vivo have not yet been elucidated. Previously, we found 10 potent substrates in the striatum of PKCγ-KO mice. Here, we focused on cysteine string protein α (CSPα), a protein from the heat shock protein (HSP) 40 cochaperone families localized on synaptic vesicles. We found that in cultured cells, PKCγ phosphorylates CSPα at serine (Ser) 10 and Ser34. Additionally, apoptosis was found to have been enhanced by the overexpression of a phosphorylation-null mutant of CSPα, CSPα(S10A/S34A). Compared with wild-type (WT) CSPα, the CSPα(S10A/S34A) mutant had a weaker interaction with HSP70. However, in sharp contrast, a phosphomimetic CSPα(S10D/S34D) mutant, compared with WT CSPα, had a stronger interaction with HSP70. In addition, total levels of synaptosomal-associated protein (SNAP) 25, a main downstream target of the HSC70/HSP70 chaperone complex, were found to have decreased by the CSPα(S10A/S34A) mutant through increased ubiquitination of SNAP25 in PC12 cells. In the striatum of 2-year-old male PKCγ-KO mice, decreased phosphorylation levels of CSPα and decreased SNAP25 protein levels were observed. These findings indicate the phosphorylation of CSPα by PKCγ may protect the presynaptic terminal from neurodegeneration. The PKCγ-CSPα-HSC70/HSP70-SNAP25 axis, because of its role in protecting the presynaptic terminal, may provide a new therapeutic target for the treatment of PD.SIGNIFICANCE STATEMENT Cysteine string protein α (CSPα) is a protein belonging to the heat shock protein (HSP) 40 cochaperone families localized on synaptic vesicles, which maintain the presynaptic terminal. However, the function of CSPα phosphorylation by protein kinase C (PKC) for neuronal cell survival remains unclear. The experiments presented here demonstrate that PKCγ phosphorylates CSPα at serine (Ser) 10 and Ser34. CSPα phosphorylation at Ser10 and Ser34 by PKCγ protects the presynaptic terminal by promoting HSP70 chaperone activity. This report suggests that CSPα phosphorylation, because of its role in modulating HSP70 chaperone activity, may be a target for the treatment of neurodegeneration.