The impact of hormonal dynamics and serum sodium fluctuations on symptomatic vasospasm after subarachnoid hemorrhage.

BACKGROUND: Symptomatic vasospasm (SVS) is a major cause of morbidity and mortality in aneurysmal subarachnoid hemorrhage (SAH), and serum sodium frequently decreases before SVS. Serum sodium changes might be regulated by sodium metabolism-related hormones. This multi-institutional prospective cohort study therefore investigated the measurement of sodium metabolism-related hormones to elucidate the pathophysiology of serum sodium changes in SAH. METHODS: SAH patients were treated with clipping or coiling from September 2017 to August 2020 at five hospitals. The laboratory data of 133 SAH patients were collected over 14 days and correlations between changes in serum sodium, sodium metabolism-related hormones (plasma adrenocorticotropic hormone (ACTH), serum cortisol, plasma arginine vasopressin (AVP)), and SVS were determined. Serum sodium concentrations were measured every day and serum sodium levels >135 mEq/L were maintained until day 14. RESULTS: Of the 133 patients, 18 developed SVS within 14 days of subarachnoid hemorrhage onset (SVS group) and 115 did not suffer from SVS (non-SVS group). Circulating AVP, ACTH, and cortisol concentrations were significantly higher on day 1 in the SVS group compared with the non-SVS group. Fluctuations in serum sodium in the SVS group were significantly higher than those in the non-SVS group. There were antiparallel fluctuations in serum sodium and potassium from days 2 to 14. CONCLUSIONS: Elevated levels of ACTH/cortisol and AVP on day 1 may be predictive markers for the occurrence of SVS. Multiple logistic regression analysis showed that serum sodium fluctuations were associated with SVS occurrence. Serum sodium fluctuations were associated with stress-related hormonal dynamics. (249 words).

Ruptured traumatic posterior inferior cerebellar artery pseudoaneurysm: A case report and literature review.

Background: Traumatic intracranial aneurysm (TICA) accounts for approximately 1% of cerebral aneurysms. There are few reports of TICA limited to the posterior inferior cerebellar artery (PICA-TICA). Case Description: A 69-year-old woman fell into a shallow river, bruising her head and chest, and was admitted to our emergency department with disorientation. Computed tomography (CT) showed subarachnoid hemorrhage (SAH), intraventricular hemorrhage (IVH), left temporal lobe contusion, and fractures of the right temporal bone. A cerebral CT angiogram revealed no vascular abnormalities or aneurysms. The patient was in a semi-comatose state 2 h later, and CT showed worsening SAH. A cerebral angiogram revealed an 11 mm aneurysm of the anterior medullary segment of the right PICA. We attempted intra-aneurysmal embolization intending to preserve the PICA, but the aneurysmal neck was thin, and the microcatheter could not be placed in a stable position. Therefore, n-butyl-2-cyanoacrylate (NBCA) was injected to embolize the aneurysm. When the microcatheter was removed, NBCA was scattered distally in the PICA, and the distal PICA was occluded. The aneurysm could be embolized, but there was an increase in hemorrhagic contusion in the left temporal lobe. Decompression craniectomy was performed, but she died due to hemorrhagic contusion and uncal herniation 6 days after surgery. Conclusion: PICA-TICA is often accompanied by IVH and SAH, and there are some reports of cases with a vascular anomaly of the posterior circulation. Since TICA is at risk of rapid growth and rupture, an early and appropriate diagnosis is important.

Potential of machine learning to predict early ischemic events after carotid endarterectomy or stenting: a comparison with surgeon predictions.

Carotid endarterectomy (CEA) and carotid artery stenting (CAS) are recommended for high stroke-risk patients with carotid artery stenosis to reduce ischemic events. However, we often face difficulty in determining the best treatment strategy. We aimed to develop an accurate post-CEA/CAS outcome prediction model using machine learning that will serve as a basis for a new decision support tool for patient-specific treatment planning. Retrospectively collected data from 165 consecutive patients with carotid stenosis underwent CEA or CAS and were divided into training and test samples. The following five machine learning algorithms were tuned, and their predictive performance was evaluated by comparison with surgeon predictions: an artificial neural network, logistic regression, support vector machine, random forest, and extreme gradient boosting (XGBoost). Seventeen clinical factors were introduced into the models. Outcome was defined as any ischemic stroke within 30 days after treatment including asymptomatic diffusion-weighted imaging abnormalities. The XGBoost model performed the best in the evaluation; its sensitivity, specificity, positive predictive value, and accuracy were 31.9%, 94.6%, 47.2%, and 86.2%, respectively. These statistical measures were comparable to those of surgeons. Internal carotid artery peak systolic velocity, low-density lipoprotein cholesterol, and procedure (CEA or CAS) were the most contributing factors according to the XGBoost algorithm. We were able to develop a post-procedural outcome prediction model comparable to surgeons in performance. The accurate outcome prediction model will make it possible to make a more appropriate patient-specific selection of CEA or CAS for the treatment of carotid artery stenosis.

Importance of source images of time-of-flight magnetic resonance angiography in the diagnosis of low-flow dural arteriovenous fistulae after traumatic brain injury.

Three-dimensional time-of-flight (TOF) magnetic resonance angiography (MRA) can reliably detect dural arteriovenous fistula (dAVF); however, TOF source images should be checked in cases with low-flow dAVFs. A 69-year-old woman reported intractable pulsatile tinnitus after head trauma. It was difficult to diagnose dAVF using conventional MRA, but it was confirmed using a TOF source image. Cerebral angiography revealed a dAVF with a small shunted pouch draining into the sigmoid sinus, accompanying the arterial jet flow. Transarterial embolisation of the shunted pouch completely obliterated the dAVF. The patient's tinnitus immediately disappeared after embolisation. This case suggests that a low-flow Borden type I dAVF is undetectable using conventional MRA, and we emphasise the importance of evaluating TOF source images. Transarterial embolisation of the shunted pouch while preserving the normal sinus flow was safe and effective.

A Novel Rac1-GSPT1 Signaling Pathway Controls Astrogliosis Following Central Nervous System Injury.

Astrogliosis (i.e. glial scar), which is comprised primarily of proliferated astrocytes at the lesion site and migrated astrocytes from neighboring regions, is one of the key reactions in determining outcomes after CNS injury. In an effort to identify potential molecules/pathways that regulate astrogliosis, we sought to determine whether Rac/Rac-mediated signaling in astrocytes represents a novel candidate for therapeutic intervention following CNS injury. For these studies, we generated mice with Rac1 deletion under the control of the GFAP (glial fibrillary acidic protein) promoter (GFAP-Cre;Rac1flox/flox). GFAP-Cre;Rac1flox/flox (Rac1-KO) mice exhibited better recovery after spinal cord injury and exhibited reduced astrogliosis at the lesion site relative to control. Reduced astrogliosis was also observed in Rac1-KO mice following microbeam irradiation-induced injury. Moreover, knockdown (KD) or KO of Rac1 in astrocytes (LN229 cells, primary astrocytes, or primary astrocytes from Rac1-KO mice) led to delayed cell cycle progression and reduced cell migration. Rac1-KD or Rac1-KO astrocytes additionally had decreased levels of GSPT1 (G1 to S phase transition 1) expression and reduced responses of IL-1ß and GSPT1 to LPS treatment, indicating that IL-1ß and GSPT1 are downstream molecules of Rac1 associated with inflammatory condition. Furthermore, GSPT1-KD astrocytes had cell cycle delay, with no effect on cell migration. The cell cycle delay induced by Rac1-KD was rescued by overexpression of GSPT1. Based on these results, we propose that Rac1-GSPT1 represents a novel signaling axis in astrocytes that accelerates proliferation in response to inflammation, which is one important factor in the development of astrogliosis/glial scar following CNS injury.

Cilostazol administration with combination enteral and parenteral nutrition therapy remarkably improves outcome after subarachnoid hemorrhage.

OBJECTIVE: In order to prevent cerebral vasospasm (VS) following aneurysmal subarachnoid hemorrhage (SAH), we introduced combined enteral nutrition (EN) and parenteral nutrition (PN) with oral cilostazol administration to the postoperative patient after SAH and investigated the effect on VS. METHODS: After aneurysmal SAH, 130 postoperative patients were enrolled in this study between April 2008 and March 2012. The patients enrolled before April 2010 were treated by conventional therapy (control group). The patients enrolled after April 2010 were administrated cilostazol 200 mg/day and received EN and PN simultaneously (combined group). RESULTS: The combined group consisted of 62 patients and the control group of 68 patients. Angiographic VS occurred in 33.9 % (n = 21) of the combined group and in 51.5 % (n = 35) of the control group (p = 0.051, Fisher exact test). The incidence of symptomatic VS was significantly lower in the combined group (p = 0.001). The incidence of new cerebral infarctions was also significantly lower in the combined group (p = 0.0006). Clinical outcome at discharge was also significantly better in the combined group than in control group (p = 0.031). CONCLUSIONS: Cilostazol administration with combination EN and PN is remarkably effective in preventing cerebral VS after aneurysmal SAH.

Immunohistochemical and molecular genetics study of a granular cell astrocytoma: a case report of malignant transformation to a glioblastoma.

We treated a 56-year-old woman who had a right temporal lobe tumor found by chance after a traffic accident. MRI confirmed a heterogeneously enhanced tumor in the temporal lobe with large peritumoral edema extending to the superior parietal lobe. The patient underwent tumor resection. The tumor consisted largely of distinct cells with discrete borders and granular cytoplasm. In granular cells, the accumulation of PAS-positive granules was observed. Immunohistochemical analysis demonstrated positive staining for GFAP, S-100, and oligodendrocyte transcription factor 2 and negative staining for synaptophysin. CD68 was negative in granular cells, but positive in stromal cells. Ki-67 labeling index was quite low. The tumor was diagnosed as a granular cell astrocytoma (GCA). Postoperative radiotherapy combined with temozolomide was administered. One month after chemoradiotherapy, the tumor occurred in the parietal lobe, and a tumorectomy was performed. The tumor was composed of poorly differentiated astrocytic tumor cells with prominent microvascular proliferation and necrosis. A small number of granular cells were locally observed and the tumor was diagnosed as a glioblastoma. O6-methylguanine-DNA methyltransferase promoter methylation was detected in the GCA but not in the glioblastoma. Isocitrate dehydrogenase mutations were not detected in either tumor. Comparative genomic hybridization analysis demonstrated that no chromosomal abnormality was found in the GCA; however, a gain of chromosomes 7 and 19 and a loss of chromosomes 10 and 9p21 (CDKN2A) were found in the glioblastoma. p53 was strongly expressed in both the GCA and glioblastoma. The tumor progressed despite extensive chemotherapy, and the patient died 1 year after the initial treatment. Our immunohistochemical, genetic and chromosomal analyses indicate that the glioblastoma was transformed from the GCA.