Effect of Hospital Arrival Time on Functional Prognosis of Stroke Patients: Japan Stroke Data Bank Over 20 Years.

AIMS: The impact of weekend/holiday and nighttime hospitalization on functional outcomes and long-term trends in stroke patients is unclear. We examined functional and life outcomes and changes over time. METHODS: We analyzed the clinical data of 203,176patients for hospital arrival day of week and 76,442patients for arrival times using Japan Stroke Data Bank. The endpoints were favorable outcome (Modified Rankin Scale[mRS]0-2), unfavorable outcome(mRS 5-6), and in-hospital mortality. We calculated odds ratios(OR) and 95% confidence interval(CI) of weekends/holidays and off-hours versus weekdays and on-hours for 2000-2009 and 2010-2020 using a mixed-effect multivariate model adjusted for confounding factors and evaluated interactions. Thereafter, we performed to check for year trends. RESULTS: All endpoints were worse in weekend/holiday admissions for all stroke and in off-hours hospitalization for total stroke(TS), ischemic stroke(IS), and intracerebral hemorrhage(ICH). The adjusted ORs for favorable outcomes of weekend/holiday admissions were TS, 0.90(0.87-0.93); IS, 0.89(0.86-0.93); ICH, 0.91(0.84-0.98) and unfavorable outcome TS, 1.04(1.002-1.08) IS, 1.06(1.01-1.11). Off-hour hospitalization had adjusted ORs for favorable outcome(TS, 0.86 [95% CI: 0.82-0.91]; IS, 0.90 [0.84-0.95]; ICH, 0.85 [0.75-0.96]), unfavorable outcome(TS, 1.14 [1.07-1.22]; IS, 1.13 [1.04-1.23]; ICH, 1.15 [1.01-1.31]), and mortality (TS, 1.15 [1.05-1.26]; IS, 1.17 [1.04-1.32]). For IS, the incidence of unfavorable outcomes during off-hours was significantly lower in 2010-2020 than in 2000-2009; after adjusting for reperfusion therapy, it was no longer significant. CONCLUSION: Stroke patients admitted on weekends/holidays and off-hours had worse functional and life outcomes. Functional outcomes for off-hour admission for IS improved at 10-year intervals, possibly due to improvements in stroke care systems.

Transventricular Preforniceal Approach Combined with Endoscopic Transnasal Surgery for a Giant Pituitary Adenoma: A Case Report and Literature Review.

Giant pituitary adenomas carry significant surgical risks when treated with transsphenoidal approaches or the transcranial approach alone. Combined transsphenoidal and transcranial approaches have been reported; however, removing adenomas extending into the third ventricle may still be challenging. We report a case of giant pituitary adenoma expanding into the third ventricle, which was removed using a combined transventricular preforniceal approach and an endoscopic endonasal transsphenoidal surgery (ETSS). A 41-year-old man with headache, nausea, and a 1-week history of a visual field defect was transferred to our hospital. He had a disturbed left visual acuity, right homonymous hemianopia, and choked disc in both eyes. Preoperative magnetic resonance imaging revealed a giant pituitary adenoma with a maximum diameter of 55 mm extending from the intrasellar to the suprasellar region, thus occupying the entire third ventricle and causing hydrocephalus. The space between the anterior commissure and the fornix was expanded. The foramen of Monro was shifted backward due to compression by the tumor. He underwent maximum surgical resection using a combined transventricular preforniceal approach and ETSS. Considering technical demands and reliability, the intra- to suprasellar parts were removed by ETSS while the intraventricular part was removed through the preforniceal approach. The residual tumor in the right cavernous sinus and behind the anterior communicating artery was treated with stereotactic radiotherapy. One year after the operation, the patient leads an independent life. The combined technique of the preforniceal approach and ETSS provided a direct view of the entire third ventricle and hemostasis in the present case.

Angiography of Cervical Carotid Plaque Rupture Due to Percutaneus Transluminal Balloon Arterioplasty.

We describe the rare imaging of a plaque rupture at cervical internal carotid artery stenosis after balloon arterioplasty. The patient was an 82-year-old male who complained of left hemiparesis. Diffusion-weighted magnetic resonance imaging revealed multiple high-signal intensity in the right cerebral hemisphere. Magnetic resonance angiography showed severe stenosis at the cervical internal carotid artery. We considered the high risk of hyperperfusion syndrome after revascularization. We planned staged angioplasty. Angiography after arterioplasty revealed a meshlike appearance, like a net, in the arterial wall, which indicated the critical sign of ischemic complications.

Vonoprazan versus conventional proton pump inhibitor-based triple therapy as first-line treatment against Helicobacter pylori: A multicenter retrospective study in clinical practice.

OBJECTIVE: Vonoprazan is a potassium-competitive acid blocker, a new type of acid-suppressing drug, and has recently become available for peptic ulcers, gastroesophageal reflux disease, and Helicobacter pylori (H. pylori) eradication. Its efficacy for H. pylori eradication has been reported. However, the evidence for its efficacy and feasibility remains limited. We aimed to compare the feasibility, effectiveness and safety of vonoprazan-based triple therapy with conventional proton pump inhibitor (PPI)-based triple therapy in multicenter clinical practice. METHODS: We performed a multicenter retrospective study on patients receiving first-line H. pylori eradication therapy between March 2013 and November 2015 with either vonoprazan-based triple therapy or conventional PPI-based triple therapy. RESULTS: A total of 2715 patients aged 63.0 ± 12.1 years (1412 [52.0%] males) were analyzed. Eradication rates were 87.2% (368/422) for vonoprazan-based therapy and 72.4% (1661/2293) for conventional PPI-based therapy (P < 0.01). Among the former group, there were 10 cases of diarrhea, six of nausea/vomiting, and five of rash, but the rates of these adverse events were similar to those in the conventional PPI group. CONCLUSION: Vonoprazan-based triple therapy is feasible, and has a higher rate for H. pylori eradication than conventional PPI as a first-line regimen.

Negative pressure pulmonary edema following foramen magnum decompression for Chiari malformation type I.

A 57-year-old obese female presented with vagal and hypoglossal nerve pareses, and magnetic resonance imaging revealed Chiari malformation type I. Standard surgical treatment for Chiari malformation type I was successfully performed. However, immediately after the patient was extubated, she developed signs of upper airway obstruction and chest radiography revealed pulmonary edema. Her ventilation was assisted by maintaining positive end-expiratory pressure at 8 cmH2O. Intravenous furosemide and hydrocortisone were administered. Her respiratory status improved 12 hours later, and she was extubated 3 days after the operation. Postextubational course was uneventful, and the patient was discharged 2 weeks after extubation. The initial neurological deficits had mostly disappeared by 10 months after the operation. This unusual case of negative pressure pulmonary edema indicates that obesity and lower cranial nerve paresis are further risk factors for pulmonary edema as a postextubational complication of surgical treatment.

Direct correlation between ischemic injury and extracellular glycine concentration in mice with genetically altered activities of the glycine cleavage multienzyme system.

BACKGROUND AND PURPOSE: Ischemia elicits the rapid release of various amino acid neurotransmitters. A glutamate surge activates N-methyl-d-aspartate (NMDA) glutamate receptors, triggering deleterious processes in neurons. Although glycine is a coagonist of the NMDA receptor, the effect of extracellular glycine concentration on ischemic injury remains controversial. To approach this issue, we examined ischemic injury in mice with genetically altered activities of the glycine cleavage multienzyme system (GCS), which plays a fundamental role in maintaining extracellular glycine concentration. METHODS: A mouse line with increased GCS activity (340% of C57BL/6 control mice) was generated by transgenic expression of glycine decarboxylase, a key GCS component (high-GCS mice). Another mouse line with reduced GCS activity (29% of controls) was established by transgenic expression of a dominant-negative mutant of glycine decarboxylase (low-GCS mice). We examined neuronal injury after transient occlusion of the middle cerebral artery in these mice by measuring extracellular amino acid concentrations in microdialysates. RESULTS: High-GCS and low-GCS mice had significantly lower and higher basal concentrations of extracellular glycine than did controls, respectively. In low-GCS mice, the extracellular glycine concentration reached 2-fold of control levels during ischemia, and infarct volume was significantly increased by 69% with respect to controls. In contrast, high-GCS mice had a significantly smaller infarct volume (by 21%). No significant difference was observed in extracellular glutamate concentrations throughout the experiments. An antagonist for the NMDA glycine site, SM-31900, attenuated infarct size, suggesting that glycine operated via the NMDA receptor. CONCLUSIONS: There is a direct correlation between ischemic injury and extracellular glycine concentration maintained by the GCS.

Candesartan reduces superoxide production after global cerebral ischemia.

Excessive superoxide production after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor activation results in production of superoxide, but whether angiotensin II type 1 receptor blockade prevents production of superoxide and subsequent neuronal injury after ischemia remains unclear. Normotensive rats received the angiotensin II type 1 receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CA1 neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production was significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type 1 receptor may have an essential role in superoxide production and subsequent injury in vulnerable neurons after global cerebral ischemia.

[Supratentorial primitive neuroectodermal tumor: report of a surgical case].

We reported a rare case of supratentorial primitive neuroectodermal tumors (sPNET) and reviewed the literature. A 15-year-old girl presented with a one-month history of headache and vomiting. CT scans showed a huge, solid and cystic tumor with calcification, occupying the left anterior cranial fossa. The solid portion of the tumor was hypointense on T1-weighted images, slightly hyperintense on T2-weighted images, hyperintense on diffusion- weighted images, isointense on fluid-attenuated inversion recovery (FLAIR) images, and strongly enhanced after administration of contrast medium. The expansile tumor had a broad attachment to the dura matter of the anterior cranial fossa. The patient underwent an uneventful extirpation of the tumor. Microscopically, the solid tumor contained small, round poorly-differentiated cells with pleomorphic nuclei and brisk mitotic activity. The tumor cells were immunoreactive for synaptophysin and GFAP, whereas lack of MIC2 gene product expression was confirmed using the monoclonal antibody 12E7. The MIB-1-positive rate was 43%. The histological diagnosis was sPNET. Postoperatively, a dose of 30.6Gy was administrated to the whole brain and a boost of 19.6Gy to the T2-hyperintensity lesion. The patient successively received a dose of 30.4Gy to the whole spine and Linac stereotactic radiotherapy with a marginal dose of 16.8Gy at the tumor bed. Three months after radiotherapy the patient received chemotherapy using carboplatin and etoposide. Follow-up MR images showed no evidence of recurrent tumor 5 months after the radiochemotherapy. On the basis of MR findings on both diffusion-weighted and FLAIR images, preoperative diagnosis of sPNET may be important for choosing appropriate therapeutic strategies for this tumor.

[An outbreak of encephalopathy after eating autumn mushroom (Sugihiratake; Pleurocybella porrigens) in patients with renal failure: a clinical analysis of ten cases in Yamagata, Japan].

In September and October, 2004, an outbreak of encephalopathy of unknown etiology occurred in certain areas of Japan including Yamagata, Akita, and Niigata prefectures. These patients had a history of chronic renal failure, most of them had undergone hemodialysis, and also had a history of eating Sugihiratake (Pleurocybella porrigens), an autumn mushroom without known toxicity. Since clinical details of this type of encephalopathy remain unknown, we analyzed the clinical, radiological and electroencephalographic (EEG) features of ten cases of this encephalopathy in Yamagata prefecture. The summary of the present study is as follows: 1. Ten patients had chronic renal failure, and seven underwent hemodialysis. 2. Each patient had a history of eating Sugihiratake within 2-3 weeks of the onset of neurological symptoms. 3. The onset was subacute; the initial symptoms were tremor, dysarthria, and/or weakness of the extremities, which lasted an average of 4.5 days (ranging from 2 to 11 days), followed by severe consciousness disturbance and intractable seizures, resulting in status epilepticus in 5 patients. Myoclonus was also seen in 4 patients and Babinski reflex in 3. 4. Brain CT and MRI examinations were unremarkable in the early stages of the disease. Three to eight days after onset, however, conspicuous lesions appeared in the areas of the insula and basal ganglia in 6 patients. On MRI, these brain lesions were hyperintense on T2-weighted and FLAIR images, and hypointense on T1-weighted images. 5. EEG examination was performed in 6 patients, all of whom showed abnormal EEG findings. Periodic synchronous discharge (PSD) was seen in 2 patients, spike and wave complex in one patient, and non-specific slow waves in 3. 6. Prognosis was different from case to case. Three patients died at 13, 14, and 29 days after onset. Two patients still showed persistent disturbance of consciousness one month after onset. One patient showed parkinsonism after recovering from consciousness disturbance. Four patients recovered nearly completely around one month after onset In 3 of the 4 recovered patients, renal failure was not severe and they did not need to undergo hemodialysis. This suggests that the degree of renal failure is a key for the prognosis of this type of encephalopathy. The present study suggests that this endemic disease is a newly recognized clinical entity of encephalopathy.