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OBJECTIVE Preservation of neurological function is a priority when performing a resection of a vestibular schwannoma (VS). Few studies have examined the radiographic value of a fundal fluid cap—i.e., cerebrospinal fluid in the lateral end of a VS within the internal auditory canal—for prediction of postoperative neurological function. The aim of this study was to clarify whether the presence of a fundal fluid cap on preoperative magnetic resonance images has a clinical impact on facial nerve function after resection of VSs. METHODS The presence of a fundal fluid cap and its prognostic impact on long-term postoperative facial nerve function were analyzed. RESULTS A fundal fluid cap was present in 102 of 143 patients who underwent resection of sporadic VSs via the retrosigmoid approach. Facial nerve function was acceptable (House-Brackmann grade I–II) immediately after surgery in 82 (80.4%) patients with a fundal fluid cap and in 26 (63.4%) of those without this sign. The preservation rate of facial nerve function increased in a time-dependent manner after surgery in patients with a fundal fluid cap but plateaued by 3 months postoperatively in those without a fundal fluid cap; the difference was statistically significant at 12 months (96.1% vs 82.9%, p = 0.013) and 24 months (97.1% vs 82.9%, p = 0.006) after surgery. The presence of a fundal fluid cap had a significantly positive effect on long-term facial nerve function at 24 months after surgery when tumor size and intraoperative neuromonitoring response were taken into account (OR 5.55, 95% CI 1.12–27.5, p = 0.034). CONCLUSIONS Neuromonitoring-guided microsurgery for total resection of VSs is more likely to be successful in terms of preservation of facial nerve function if a fundal fluid cap is present. This preoperative radiographic sign could be helpful when counseling patients and deciding the treatment strategy.

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.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 levels135 mEq/L were maintained until day 14.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.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).

A purely intrasellar chordoma is rare among skull base chordomas and is recognized as originating from ectopic embryological notochord located in the sella turcica. In view of its rarity and nonspecific symptoms, clinicians may misdiagnose intrasellar chordoma as pituitary adenoma based on preoperative radiographic images. In this report, we present an intrasellar chordoma that clinically mimicked pituitary macroadenoma with hyperprolactinemia and hypopituitarism and was successfully resected by endoscopic endonasal transsphenoidal surgery. This case demonstrated radiographic features that chordoma should be suspected in sellar lesions. The enlarged sellar with thinned remodeled bone without clival destruction was firstly reminiscent of pituitary adenoma, whereas the very high signal on T2-weighted images and heterogeneous enhancement characteristically suggested chordoma. This rare diagnosis must be considered in the preoperative evaluation of sellar lesions because it can affect how the neurosurgeon prepares for surgery and the surgical goals.

BACKGROUND: Although there have been reports of Raeder’s syndrome developing after carotid artery dissection, to our knowledge, no case of Raeder’s syndrome occurring after carotid stenting has been reported. CASE REPORT: A 46-year-old man was urgently treated with a self-expanding stent for idiopathic right carotid artery dissection. However, the patient complained of moderate oppressive pain in the right orbit and forehead immediately after stent placement. Further examination revealed a right eye miosis and right ptosis. No anhidrosis was noted. A diagnosis of Raeder’s syndrome was made based on partial Horner’s syndrome and pain in the first branch of the trigeminal nerve. We noticed that he had hypertension and started antihypertensive medication. After starting the antihypertensive medication, his blood pressure stabilized, and his periorbital pain disappeared dramatically as his blood pressure fell. However, Horner’s symptoms (miosis and ipsilateral ptosis) were still present. CONCLUSION: We experienced a case of Raeder’s syndrome that occurred after stenting of the carotid artery. Neuralgia improved by treatment of hypertension. It should be noted that the paratrigeminal neuralgia of Raeder’s syndrome after carotid stenting can be caused by hypertension. KEY WORDS: Antihypertensive medication, Horner’s symptoms, Raeder’s syndrome, stenting of the carotid artery

Coagulation factor XIII (F13) deficiency has been known to be a rare disease with estimated one per two million and one of the possible reasons of postoperative hemorrhage; however, it still remains unpenetrated to physicians. We report a case of acute ventriculoperitoneal (VP) shunt dysfunction due to delayed intraventricular hemorrhage, which could be because of F13 deficiency. The patient was a 48-year-old man with a history of post-meningitis hydrocephalus followed by VP shunt placement. He was found unconscious and transferred to our hospital. A brain CT scan demonstrated shunt malfunction, and he underwent emergency shunt revision. The postoperative course was uneventful except for unexpected neck bruises and continuous minor bleeding from the surgical wound. Three days after surgery, he suddenly became comatose and a CT scan revealed the recurrence of hydrocephalus with newly identified small volume of intraventricular hemorrhage. Emergency shunt revision was performed again. The shunt valve was filled with a hematoma and bloody cerebrospinal fluid was drained from the ventricle. Postoperative blood sample examination demonstrated no abnormal findings but a decreased level of F13 activity, which was thought to be a possible cause of postoperative hemorrhage and the shunt valve hematoma. F13 deficiency causes delayed intracranial hemorrhage 24–48 h after neurological surgery. It can only be diagnosed by checking F13 activity with suspicion. If diagnosed accurately beforehand, unexpected postoperative bleeding can be preventable with proper treatment, such as F13 concentrate and cryoprecipitate. The actual number of the patient with F13 deficiency may be more than estimated ever.

Intracranial artery occlusion due to a foreign body is a complication associated with cardiac surgery that is treated by various techniques. However, little is known about appropriate strategies for symptomatic intracranial artery stenosis due to an unknown embolic source. We reported a case of middle cerebral artery (MCA) stenosis after mitral valve repair (MVR) for infective endocarditis (IE). An 80-year-old man presented with right hemiplegia. MR angiography findings were normal, and diffusion-weighted imaging revealed subtle ischemic change in the left MCA territory. The patient was diagnosed with cardioembolic stroke owing to IE and performed MVR. Four days later, he suddenly presented with consciousness disorder and left hemiplegia. Computed tomography (CT) confirmed a very low-density area within the right MCA. MR angiography revealed right MCA stenosis, which corresponded to the low-density area on CT images. Diffusion-weighted imaging revealed new ischemic change in the right MCA territory. Angiography confirmed an irregular stenosis at the right M2 with antegrade blood flow, and the hemiplegia resolved during angiography. Conservative therapy was performed; however, the resting 123 I-IMP-single photon emission CT revealed moderate perfusion defect in the right MCA territory, and transient left hemiplegia appeared every few days. Therefore, 19 days after the initial transient ischemic attack, the patient was performed superficial temporal artery–MCA anastomosis, and the patient responded with a good clinical course without recurrence of the ischemic symptoms. This strategy may be a safe and effective treatment for symptomatic intracranial artery stenosis due to an unknown embolic source.

Background The differences between 3-dimensional (3D) high definition (HD) and 2-dimensional (2D) 4-K ultra-HD (4K) endoscopy and their respective advantages remain unclear. Objective To evaluate the utility of these endoscopy systems in endonasal skull base surgery. Methods Consecutive series of endoscopic endonasal surgeries performed after introduction of 3D/HD and 2D/4K systems (July 2017) were retrospectively evaluated. Sporadic cases treated with either system, or a conventional 2D standard definition (SD) system, during the rental period from March 2016 were also included. Objective comparisons between the systems were made for newly diagnosed Knosp grade 0 to 3 pituitary adenomas. Surgical procedures were divided into nasal, sphenoidal, and intradural phases, and the surgical procedural time was compared for each phase. The time required for and accuracy of suturing the sellar floor dura was also evaluated. Results A total of 74 cases were treated with 3D/HD and/or 2D/4K, and 12 cases with 2D/SD. 3D/HD was advantageous in the nasal phase because of its intuitive depth perception. 2D/4K was advantageous in the intradural phase because of its superior image quality. Surgical time of the nasal phase with 3D/HD, and that of the intradural phase with 2D/4K, were significantly shorter than that with 2D/SD. The time required for and accuracy of sellar floor dural suturing showed a trend toward improving in the order of 2D/SD, 2D/4K, and 3D/HD. Conclusion 3D/HD and 2D/4K endoscopy systems have different advantages, which are useful in distinct surgical phases. Understanding the characteristics of endoscopy systems is important for selecting the most appropriate system for distinct surgical situations.

Objective Postoperative headache (POH) is a disturbing symptom following vestibular schwannoma (VS) resection. However, there are currently no treatment guidelines. The aim of this study was to evaluate the usefulness of symptom-based opioid-free treatments for persistent POH following VS resection. Methods Of 137 patients in whom sporadic VS was resected via the retrosigmoid approach, 74 had persistent POH beyond 3 postoperative months. Their symptoms were classified as tension-type headache, migraine, neuralgia, or other and were treated. We retrospectively analyzed the treatment outcomes during 2 postoperative years. Results Patients with persistent POH were significantly younger (P = 0.003) and had significantly smaller tumors (P = 0.001) and greater extent of resection (P = 0.04) than patients without POH. The most common simple symptom was tension-type headache in 56 patients, followed by migraine in 6 patients and neuralgia in 5 patients. All 7 patients with complex symptoms had a mixture of tension-type headache and migraine. Complete disappearance of POH was achieved in 40 (54%) patients, and a medication-free condition was achieved in 51 (69%). No patients had residual severe POH that could not be controlled with medication. Achievement of a medication-free outcome that included complete disappearance of persistent POH was significantly more common in patients with preserved facial nerve function (P = 0.008) and patients with simple symptoms (P < 0.001). Conclusions A symptom-based approach is appropriate for understanding and managing persistent POH after VS resection with excellent pain control. Preserved facial nerve function and simple symptoms are significant prognostic factors for a medication-free outcome.

Langerhans cell histiocytosis (LCH) is characterised by tissue destruction caused by the abnormal proliferation of pathogenic dendritic cells. We report a rare case of multi-system LCH with local invasion of the orbital apex.A 56-year-old woman suffered from a decrease of visual acuity in the left eye caused by central scotoma and the limitation of eye movement in all directions. Magnetic resonance imaging revealed an enhanced lesion in the left orbital apex, suggesting optic nerve compression. She had been diagnosed with eosinophilic granuloma 24 years previously. Two weeks after the current presentation, we admitted the patient for optic canal and orbital apex decompression and subtotal tumour resection. Histopathological analysis confirmed the diagnosis of LCH. Post-surgical treatment with low-dose cytarabine was initiated for the residual tumour. However, it was ceased because of myelosuppression-induced pyelonephritis. After surgery, the central scotoma disappeared on day 5 and eye movement palsy resolved by 6 months. After the cessation of cytarabine, she has received low-dose steroid therapy for 2 years with no recurrence. Early surgical intervention with low-dose steroid therapy can lead to recovery of visual acuity and resolve eye movement palsy in patients with lesions of the orbital apex caused by multi-system LCH.

Background A small number of reports have described subarachnoid hemorrhage resulting from a ruptured aneurysm embedded within a prolactinoma. To the best of our knowledge, no reports have described an embedded carotid cavernous fistula. We report a patient with carotid cavernous fistula secondary to a ruptured internal carotid artery aneurysm embedded within a prolactinoma. Case Description A 61-year-old woman was referred to our hospital with sudden headache, vomiting, and dizziness. Magnetic resonance imaging demonstrated a small acute subdural hematoma, recurrent prolactinoma, and left cavernous carotid aneurysm. Conservative therapy was initiated. Her serum prolactin level at hospitalization was 11,300 μg/L; therefore, we initiated cabergoline therapy. Twenty days after cabergoline administration, she suddenly presented with left conjunctival injection and pulsatile tinnitus. Angiography showed a left direct carotid cavernous fistula with a connection between the cavernous internal carotid artery and the cavernous sinus via the aneurysm and venous congestion. To prevent hemorrhagic stroke, we scheduled staged surgery. First, we urgently performed embolization of the cavernous sinus and fistula. One month later, to prevent aneurysm rerupture, we performed a radical operation with superficial temporal artery–middle cerebral artery double anastomosis with proximal occlusion of the left internal carotid artery at the cervical portion. The patient was discharged 2 weeks after surgery without neurological deficits. Follow-up angiography revealed complete occlusion of the aneurysm 2 months postoperatively. Conclusions An aneurysm embedded within a prolactinoma should be closely observed when cabergoline administration is started.

Secure reconstruction in transsphenoidal surgery (TSS) is important for the prevention of the major and serious complication of postoperative cerebrospinal fluid (CSF) leak. Although abdominal fat can be safely and effectively used as a reconstruction tissue, harvesting it from the abdominal wall is traumatic and invasive, resulting in cosmetic problems. In this report, we present a method of harvesting abdominal fat using a minimally invasive liposuction technique to avoid cosmetic issues. Since 2016, we have been using fat harvested from the abdominal wall by suctioning with a dedicated syringe for reconstruction after TSS in selected cases. The liquefied fat obtained by the liposuction technique was wrapped with an oxycellulose sheet and changed its form to what we termed "fatty candy". In this form, the fat maintained its configuration and could be handled almost as easily as a conventional fat graft. In our experienced series, there was no case with wound complication nor postoperative or late-onset CSF leak during a postoperative follow-up of at least 3 months. The fat harvested by this simple and minimally invasive liposuction technique can be expected to provide an autologous graft that is adequate not only for prevention of cosmetic problems but also for prevention of postoperative CSF leak.

Structured Abstract Objective 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 method. Therefore, it is necessary to develop a useful decision support tool to identify an appropriate patient-specific treatment for carotid artery stenosis. Our objective is to develop an accurate post-CEA/CAS outcome prediction model using machine learning (ML) algorithms that will serve as a basis for a new decision support tool for patient-specific treatment planning. Methods Retrospectively collected data from 165 consecutive patients with carotid artery stenosis underwent CEA or CAS at a single institution were divided into training and test samples. The following six ML algorithms were tuned, and their predictive performance evaluated by comparison with surgeon predictions: an artificial neural network, logistic regression, support vector machine, Gaussian naive Bayes, random forest, and extreme gradient boosting (XGBoost). A total of 17 clinical parameters were used for the ML model development. These parameters consisted of age, pretreatment modified Rankin scale, hypertension, diabetes mellitus, medical history of arteriosclerotic disease, serum low-density lipoprotein cholesterol value, internal carotid artery peak systolic velocity, symptomatic, crescendo transient ischemic attack or stroke in evolution, previous neck irradiation, type III aorta, contralateral carotid occlusion, stenosis at a high position, mobile plaque, plaque ulceration, vulnerable plaque, and procedure (CEA or CAS). Outcome was defined as any ischemic stroke within 30 days after treatment. Results The XGBoost model performed the best in the evaluation; its sensitivity, specificity, positive predictive value, and accuracy were 66.7%, 89.5%, 50.0%, and 86.4%, respectively. The average of the outcome predictions made by four surgeons had a sensitivity of 41.7%, specificity of 75.0%, positive predictive value of 20.1%, and accuracy of 70.5%. Internal carotid artery peak systolic velocity, serum low density lipoprotein cholesterol, and procedure (CEA or CAS) were the most contributing factors according to the XGBoost algorithm. Conclusions We were able to develop a post-CEA/CAS 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.

Cancer cells optimize nutrient utilization to supply energetic and biosynthetic pathways. This metabolic process also includes redox maintenance and epigenetic regulation through nucleic acid and protein methylation, which enhance tumorigenicity and clinical resistance. However, less is known about how cancer cells exhibit metabolic flexibility to sustain cell growth and survival from nutrient starvation. Here, we find that serine and glycine levels were higher in low-nutrient regions of tumors in glioblastoma multiforme (GBM) patients than they were in other regions. Metabolic and functional studies in GBM cells demonstrated that serine availability and one-carbon metabolism support glioma cell survival following glutamine deprivation. Serine synthesis was mediated through autophagy rather than glycolysis. Gene expression analysis identified upregulation of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) to regulate one-carbon metabolism. In clinical samples, MTHFD2 expression was highest in the nutrient-poor areas around “pseudopalisading necrosis.” Genetic suppression of MTHFD2 and autophagy inhibition caused tumor cell death and growth inhibition of glioma cells upon glutamine deprivation. These results highlight a critical role for serine-dependent one-carbon metabolism in surviving glutamine starvation and suggest new therapeutic targets for glioma cells adapting to a low-nutrient microenvironment. Electronic supplementary material The online version of this article (10.1186/s40478-020-01114-1) contains supplementary material, which is available to authorized users.

Accurate diagnosis and treatment of sellar and parasellar inflammatory lesions is difficult. We report six patients with sellar and parasellar inflammatory lesions and impaired visual function, who underwent endonasal endoscopic surgery. These patients included one with aspergillosis, one with hypertrophic pachymeningitis, one patient with abscess, and three with idiopathic granulomatous lesions. Following surgery and medication, visual function improved in patients with aspergillosis, hypertrophic pachymeningitis, and abscess. In patients with idiopathic granulomatous inflammation, visual function improved in one out of three patients. The treatment outcome for sellar and parasellar inflammatory lesions with impaired visual function depends on the surgery as well as on the reaction to postoperative medication. In the present study, the functional prognosis of patients with idiopathic granulomatous lesions was relatively poor when compared with that of patients with other inflammatory lesions.

Background The endoscopic endonasal trans-lacerum approach (EETLA) is useful in handling skull base tumors around inferior petrous apex (IPA); however, its surgical corridor is exclusively a triangular space (supra-eustachian triangle [SET]), between the internal carotid artery (ICA) and eustachian tube. Methods We investigated correlation between SET size and extent of resection around the IPA (lateral extent of resection [EOR]) through a retrospective analysis of 15 surgeries using EETLA. Results Of 15 cases (9 chordomas, 4 chondrosarcomas, and 2 meningiomas), 20 sides of IPA were affected by the tumor. When being restricted to sides with severe lateral tumor extension beyond the midpoint of petrous ICA (10 sides), the SET size was significantly broader in the group with lateral EOR of ≥90% (p value = 0.019). Conclusions The SET size was a powerful index of tumor resectability in EETLA, especially in cases with severe tumor extension. The individual anatomical variations should be considered when determining EETLA application.

The nasal cavity is the exclusive surgical corridor for endoscopic endonasal surgery; however, it is sometimes too narrow to allow extensive surgical maneuvering. Here we show the technique of submucosal inferior turbinectomy (SIT) to widen this surgical corridor. Its effectiveness is evaluated quantitatively by comparing pre- and intraoperative magnetic resonance images. Between March 2015 and October 2018, we performed endoscopic endonasal resection of 57 skull base tumors with 3T intraoperative magnetic resonance imaging (iMRI). Among these resections, cases with previous endonasal surgery and cases for which the iMRI did not cover the entire nasal cavity were excluded. Finally, six cases with and 19 cases without SIT were included in the subsequent retrospective analysis. We measured the dimensions of the narrowest area in inferior nasal cavity on pre- and intraoperative coronal plane gadolinium (Gd)-enhanced T1-weighted MR images using dedicated software, and compared them. The incidence rates of postoperative nasal complaints at outpatient clinics were also compared. Considerable widening of the inferior nasal cavity could be achieved with the SIT, which was statistically significant compared with those without the SIT (111.1 ± 56.5% vs. 39.4 ± 59.4%, respectively; P = 0.0093). In terms of the incidence rate of postoperative nasal complaints at 6 months, there was no statistical difference between the groups (33.3% vs. 15.8%, respectively; P = 0.35). SIT is effective for widening the surgical corridor while keeping nasal function and is especially helpful for lower clivus and laterally extended skull base lesions.

Background: Symptomatic vasospasm is a major cause of morbidity and mortality in subarachnoid hemorrhage patients. Hyponatremia and dehydration due to natriuresis after subarachnoid hemorrhage are related to symptomatic vasospasm. Therefore, most institutions are currently targeting euvolemia and eunatremia in subarachnoid hemorrhage patients to avoid complications. We retrospectively investigated the predictors of symptomatic vasospasm with respect to water and sodium homeostasis, while maintaining euvolemia and eunatremia after subarachnoid hemorrhage. Methods: We monitored changes in serum sodium levels, serum osmolarity, daily sodium intake, daily urine volume, and daily water balance for 14 days after subarachnoid hemorrhage. Outcomes were assessed using the modified Rankin scale at 1 month after subarachnoid hemorrhage. Results: Among 97 patients, 27 (27.8%) had symptomatic vasospasm. Patients with symptomatic vasospasm were older than those without symptomatic vasospasm; the occurrence of symptomatic vasospasm affected outcomes. Serum sodium levels were sequentially significantly decreased, but within the normal range from 1 day before the occurrence of symptomatic vasospasm. Serum osmolarity of the spasm group was lower than that of the non-spasm group. Conclusions: Symptomatic vasospasm occurs more often in older patients and affects outcomes. A decrease in serum sodium levels occurs a day before symptomatic vasospasm. This observation may help predict symptomatic vasospasm.

The epidemiology of patients with traumatic brain injury (TBI) has changed dramatically over recent decades as a result of rapid advances in aging societies. We assessed the influence of age on outcomes of patients with TBI and sought to identify prognostic factors for in-hospital mortality of TBI among elderly patients.Using a nationwide database, we analyzed data from 5651 patients with TBI. Univariate analysis was conducted to compare patient demographics, neurologic status on admission, radiologic findings, systemic complication rates, length of hospital stay, in-hospital mortality, and home discharge rates between elderly and nonelderly groups. Multivariable analysis was conducted to determine prognostic factors for in-hospital mortality among elderly patients.Overall in-hospital mortality was significantly higher in elderly patients (12.8% vs. 19.3%; P0.001). In-hospital mortality of elderly patients with mild TBI increased significantly at7 days after admission, whereas that of elderly patients with moderate or severe TBI was significantly higher immediately after admission. Age (odds ratio [OR], 1.62; P = 0.024), male sex (OR, 1.30; P = 0.004), Japan Coma Scale score on admission (OR, 5.95, P0.001), and incidence of acute subdural hematoma (OR, 1.89; P0.001) were associated with in-hospital mortality in elderly patients with TBI.Elderly patients with TBI showed significantly higher in-hospital mortality. Delayed increases in in-hospital mortality were observed among elderly patients with mild TBI. Level of consciousness on admission was the strongest predictor of in-hospital mortality among elderly patients.

Background: The recent progress of medical therapy has made the surgical indication for carotid artery stenosis more stringent. Therefore, surgical outcome of patients resistant to medical therapy were compared with those non-resistant to medical therapy. Methods: Between August 2006 and September 2017, 320 consecutive carotid revascularizations (CEA/CAS) were performed in our institute. Resistant (R) group was defined as patients with crescendo TIA, repeated TIA/infarction despite of medical therapy (n=15) or patients with symptomatic mobile plaque (n=5) (total 18; 2 patients overlapped). Other patients with symptomatic (116) and asymptomatic (186) stenosis were defined as non-resistant (N) group (total 302). Clinical characteristics, magnetic resonance (MR) plaque imaging, plaque pathology, and long-term outcomes with survival analysis were investigated. Results: 13 CEA and 5 CAS were performed in R group. 181 CEA and 121 CAS were performed in N group. The periprocedural stroke & death rate was higher in R group (1/18 [5.6%]; CEA 0/13, CAS 1/5 [20%]) than in N group (9/302 [3.0%]; CEA 4/181 [2.2%], CAS 5/121 [4.1%]) but no significant difference was observed. Signal intensity ratio of plaque relative to sternocleidomastoid muscle was significantly higher in R group than in N group (1.9 vs 1.5, p = 0.007; Fig. 1A) in MR plaque imaging study, which was consistent with intraplaque hemorrhage in pathological findings of R group. Estimates of the 4-year event rate of primary end point (stroke/death/MI within 30 days, and any ipsilateral stroke thereafter) using competing risk analysis were 18% for R group and 4.5% for N group (P = 0.022; Fig. 1B). ALL recurrence occurred after CAS. Conclusion: The resistance to medical therapy was likely to be due to severe intraplaque hemorrhage, which might explain relatively poor outcome of CAS in R group. Appropriate indication is critical for good outcome of R group.

Background: Symptomatic vasospasm (SVS) is one of the major causes of morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Hyponatremia and dehydration due to natriuresis after SAH is related to SVS and predicts it. Therefore, nowadays most institutions target to euvolemia and eunatremia in SAH patients to avoid complications. In this study, we retrospectively investigated the predictors of SVS in terms of water and sodium homeostasisunder maintaining euvolemia and eunatremia after SAH. We also analyzed the relationship between hyponatremia and the effect of treatment modality (clipping and endovascular coiling). Methods: We monitored changes in serum sodium levels, serum osmolarity, daily sodium intake, daily urine volume, and daily water balance during 14 days after SAH. Outcome was assessed using the modified Rankin scale one month after subarachnoid hemorrhage. Results: Among 105 patients, 29 (27.6%) had SVS. Patients with SVS were older than those without SVS and SVS affected outcome. Serum sodium levels were sequentially significantly decreased within normal range from one day before occurrence of SVS.Among the patients, 67 (63.8%) were treated with surgical clipping and 38 (36.2%) were treated with endovascular coiling. The group with coiling suffered significantly more severe hyponatremia and had less urine volume compared with the clipping group. Conclusions: SVS occurs more often in older patients and affects outcome. Serum sodium level decrease occurs one day before SVS. This observation may help predict SVS. A further large prospective study is necessary to resolve the detailed relationships among hyponatremia, urine volume, treatment modality and SVS in patients with SAH.

Background Extension of a pituitary adenoma to the oculomotor cistern harbors the risk of oculomotor nerve impairment and further extension into the interpeduncular cistern. The role of endoscopic endonasal surgery for those lesions was investigated. Methods The medical records were retrospectively analyzed. Attention was paid to the oculomotor nerve function and removal rate of the tumor within the oculomotor and interpeduncular cisterns. Results Six patients were eligible for the study, including 2 with oculomotor nerve palsy. The tumor from the oculomotor and interpeduncular cistern was removed in all except on one side of the case with bilateral tumor extension. The oculomotor nerve palsy demonstrated partial recovery in both cases during the 3-month follow-up. Conclusion The pituitary adenoma extending to the oculomotor cistern can be removed under the endoscope. Improvement of oculomotor nerve palsy can be achieved, and further tumor extension into the interpeduncular cistern can be prevented.

Changes in the perihemorrhagic zone (PHZ) of intracerebral hemorrhage (ICH) are variable. Different mechanisms contribute to secondary neuronal injury after ICH. This multimodal monitoring study investigated early changes in the PHZ of ICH. Twenty-four swine were anesthetized, ventilated, and underwent monitoring of vital parameters. Next to an intracranial pressure-probe (ICP), microdialysis (MD), thermodiffusion cerebral blood flow (td-CBF), and oxygen probes (PbrO2) were placed into the gray white matter junction for 12 h of monitoring. ICH was induced using the autologous blood injection model. Pre-defined volumes were 0 ml (sham), 1.5 ml ipsilateral (1.5 ml), 3.0 ml ipsilateral (3.0 ml), and 3.0 ml contralateral (3.0 ml contra). ICP equally increased in all groups after ICH. In the 3.0 ml group tissue oxygenation decreased to ischemic values of 9 ± 7 mmHg early after 6 h of monitoring. This decrease was associated with a significant perfusion reduction from 36 ± 8 ml/100 g/min to 20 ± 10 ml/100 g/min. MD correlated with a threefold lactate/pyruvate ratio increase. Measurements in all other groups were unchanged. Multimodal monitoring demonstrates volume-dependent changes of tissue oxygenation, blood flow, and ischemic MD markers in the PHZ independent of increased ICP suggesting early moderate ischemia. No evidence was found for the existence of a perihemorrhagic ischemia in the small hematoma groups.

Background Varicella zoster virus (VZV) is known as one of the rare, but important, causes of both ischemic and hemorrhagic stroke. Most previously reported VZV-related hemorrhagic stroke and cerebral vasculitis are associated with anterior circulation because VZV spreads from trigeminal ganglia to the anterior circulation of Willis. The present study presents a patient with cerebellar hemorrhage, who was diagnosed with VZV encephalitis and vasculitis of the posterior inferior cerebellar artery. Case Report A 75-year-old man with stupor was admitted to our hospital. Computed tomography revealed right intracerebellar hemorrhage, and magnetic resonance imaging revealed multiple high-intense signals throughout the brainstem and temporal lobe on fluid attenuation inversion recovery, suggestive of encephalitis. Cerebral angiography revealed stenosis of left posterior inferior cerebellar artery. Based on cerebrospinal fluid analysis, including anti-VZV IgG antibody and VZV DNA polymerase chain reaction, the patient was diagnosed with VZV encephalitis, vasculitis, and cerebellar hemorrhage. Conclusions Both cerebral vasculitis and hemorrhagic stroke due to VZV can occur in the vertebrobasilar system. VZV may enter the central nervous system not only from trigeminal ganglia but also from other pathways. We should be aware that a VZV infection could cause cerebral vasculitis and hemorrhagic stroke in the vertebrobasilar system and in anterior circulation.

Chronic subdural hematomas (SDHs) associated with non-operated moyamoya disease are extremely rare. A 68-year-old woman underwent burr-hole surgery for a right SDH, which resolved completely. On day 3, however, the patient suffered cerebral infarction in the right parietal lobe. Cerebral angiography demonstrated total occlusion of the bilateral internal carotid arteries with transdural anastomoses via branches of the right occipital artery and middle meningeal artery, feeding the left parietal cortex. A branch of the right middle meningeal artery passed near the burr hole, but was preserved. The patient was diagnosed of moyamoya disease. We thought that the main cause of chronic SDH might be the disruption of transdural anastomoses. Furthermore, we also hypothesized that we might have coagulated the small vessels of the transdural anastomoses which were undetectable by postoperative angiography, and that cerebral infarction might occur.

Background and Objective: Brain function is highly dependent on cerebral blood flow (CBF). The precise mechanisms by which blood flow is controlled by NIR laser irradiation on the central nervous system (CNS) have not been elucidated. In this study, we examined the effect of 808 nm laser diode irradiation on CBF in mice. Study Design/Materials and Methods: We examined the effect of NIR irradiation on CBF at three different power densities (0.8, 1.6 and 3.2 W/cm 2 ) and directly measured nitric oxide (NO) in brain tissue during NIR laser irradiation using an amperometric NO-selective electrode. We also examined the contribution of NO and a neurotransmitter, glutamate, to the regulation of CBF by using a nitric oxide synthase (NOS) inhibitor, N g -nitro-Larginine methyl ester hydrochloride (L-NAME), and an N-methyl-D-aspartate (NMDA) receptor blocker, MK-801, respectively. We examined the change in brain tissue temperature during NIR laser irradiation. We also investigated the protection effect of NIR laser irradiation on transient cerebral ischemia using transient bilateral common carotid artery occlusion (BCCAO) in mice. Results: We showed that NIR laser irradiation (1.6 W/cm 2 for 15–45 minutes) increased local CBF by 30% compared to that in control mice. NIR laser irradiation also induced a significant increase in cerebral NO concentration. In mice that received L-NAME, NIR laser irradiation did not induce any increase in CBF. Mice administered MK-801 showed an immediate increase but did not show a delayed additional increase in local CBF. The increase in brain tissue temperature induced by laser irradiation was estimated to be as low as 0.88C at 1.6 W/cm 2 , indicating that the heating effect is not a main mechanism of the CBF increase in this condition. Pretreatment with NIR laser irradiation improved residual CBF and reduced the numbers of apoptotic cells in the hippocampus. Conclusion: Our data suggest that NIR laser irradiation is a promising experimental and therapeutic tool in the field of cerebral circulation research. Lasers Surg. Med. 42:566– 576, 2010. 2010 Wiley-Liss, Inc.

We describe three rare cases of dissecting aneurysms in the anterior cerebral artery (ACA) treated by surgical reconstruction, and reviewed 79 previously reported cases with the ACA dissecting aneurysm. We found that 35 (77.8%) of 45 patients with ischemic event and 15 (40.5%) of 37 patients with hemorrhagic event were treated conservatively, with 11.4% (4/35 cases) and 13.3% (2/15) risk of bleeding and rebleeding, respectively. Furthermore, half of these patients died. The other 32 patients were treated surgically, and their outcome was favorable, especially after surgical reconstruction. Simultaneous treatment of both hemorrhagic and ischemic events is essential. We recommend early treatment with revascularization for patients with ACA dissection that has hemorrhaged and for patients presenting with signs of clinical deterioration with ischemic event.

A 74-year-old man presented with subarachnoid hemorrhage (SAH) and underwent neck clipping of a left middle cerebral artery (MCA) aneurysm 10 years ago. This patient presented with SAH again due to rupture of a de novo aneurysm of the anterior communicating artery (A-com. aneurysm). The A-com. aneurysm was clipped successfully. The “old” left MCA aneurysm was then inspected. A collapsed “old” aneurysmal dome and a previously applied clip were identified. The “old” aneurysmal dome was resected for histopathological examination. The wall of this aneurysmal dome varied in thickness and consisted of a thin layer of fibrous connective tissue. Fibroblasts were scattered in the aneurysmal wall and either the muscular layer or internal elastic lamina was absent. The aneurysmal dome collapsed to a certain degree, but the lumen of the dome was completely intact. In addition, neovascularization of microcapillaries was observed both inside and outside the aneurysmal dome. Some of these microcapillaries were filled with fresh erythrocytes. Thus the aneurysmal wall was apparently “vigorous.” The previous orifice of the aneurysm did not fuse together at all and could be opened widely with ease during preparation for histopathologic examination. We speculated that the clipped aneurysmal dome survived for 10 years for the following reasons: 1) Although the mechanism of neovascularization of the microcapillaries is unclear, the clipped aneurysmal dome may have obtained nourishment from the microcapillaries. 2) The cerebrospinal fluid may have incubated the dome and provided optimal circumstances for its survival. Considering the radical cure for ruptured cerebral aneurysms by neck clipping or coil embolization, the findings described in this report will be valuable for neurosurgeons and neurointerventionists. Regardless of the time since treatment, ruptured aneurysms treated by either neck clipping and/or coil embolization are at risk of recurrent subarachnoid hemorrhage when the blood re-enters the aneurysms in cases such as clip slip-off or coil compaction.

Cerebral salt wasting syndrome (CSWS) is defined as the renal loss of sodium associated with intracranial diseases (e.g., aneurysmal subarachnoid hemorrhage [SAH]) that leads to hyponatremia and decreased extracellular fluid volume. CSWS increases the risk of symptomatic vasospasm (SVS) in SAH patients. To prevent SVS, CSWS was managed by administering physiological saline and sodium chloride so as to maintain a positive water balance and serum sodium level of >140 mEq/l. The study population comprised 115 patients; the above-mentioned treatment was administered just after surgery, which was performed within 72 h after SAH. SVS occurred in 7 patients (6.09%): 5 (4.35%) presented with permanent deficits and 2 (1.74%) with transient deficits. Further, SVS occurred within a week in 6 of these patients. On Day 2, the accumulative water balance was significantly higher in the non-SVS group than in the SVS group; the water balance tended to decline in the SVS group for a few days. Until Day 6, the amount of sodium chloride administered to maintain the serum sodium level to >140 mEq/l was higher in the SVS group than in the non-SVS group. However, on Days 3-5, the serum sodium level was lower in the SVS group than in the non-SVS group. The use of physiological saline and sodium chloride therapy to maintain a positive accumulated water balance and control the serum sodium level in the management of CSWS, especially within the initial 7 days after SAH, can effectively prevent SVS.

We retrospectively studied 133 patients with subarachnoid hemorrhage (SAH) to assess whether there was any gender disparity in serum electrolytes levels throughout the clinical course. Serum concentrations of sodium and potassium were measured in all patients, while catecholamines or antidiuretic hormone were assessed in a number of cases. Female SAH-patients had lower potassium level (3.29 ± 0.47 mEq/L) than did male patients (3.68 ± 0.38) on the first day of SAH. This gender disparity continued to the beginning of the chronic phase and disappeared several months later. Mean serum sodium level was lower in the male group than in the female group throughout the clinical course. Mean serum levels of adrenaline and antidiuretic hormone were characterized by their prominent high value on the first day. Serum potassium levels were inversely related to serum levels of catecholamines, especially adrenaline, during the acute and subacute phases, particularly on the first day.

A 30-year-old female developed moyamoya syndrome after gamma knife surgery (GKS) for cerebral arteriovenous malformation (AVM), and was treated with bypass surgery. She suffered from flittering scotoma, right transient hemianopsia, and headache for 1 year. Cerebral angiography revealed a Spetzler-Martin grade III AVM located in the left occipital lobe. After staged embolization, GKS was performed with a minimum dose of 20 Gy to the periphery of the nidus at the 50% isodose level of the maximum target dose. Gradual nidus regression was achieved, and the clinical symptoms disappeared completely. However, at 30 months after GKS, the patient suffered transient ischemic attack. Cerebral angiography showed left middle cerebral artery occlusion with moyamoya vessels. The patient underwent direct and indirect bypass surgery. After surgery, the patient was free from ischemic symptoms. Chronic inflammation and long-term changes in expression of cytokines and growth factors after GKS may have triggered this case.

Background: Adiponectin is a hormone secreted exclusively by adipose tissue, and is important in the regulation of tissue inflammation and insulin sensitivity. Adiponectin exerts its effects through two cell-surface receptors: Adiponectin receptor 1 (ADR1) and ADR2. However, the relationship between ADR1/2 expression and progression of atherosclerosis or plaque vulnerability remains unclear. Aims: To investigate the relationship between ADR1/2 expression and plaque characteristics in patients with carotid artery atherosclerosis. Materials and Methods: Forty-three patients who underwent carotid endarterectomy for treatment of carotid artery stenosis were reviewed. Immunohistochemical staining for ADR1 and ADR2 was performed in the specimens of carotid plaque. The relationships between ADR1/2 expression and clinical characteristics were analyzed statistically. Results: Plaque was stable in 7 patients and vulnerable in 36 patients. ADR1 expression was considered weak in 29 patients and strong in 14 patients. The formation of vulnerable plaques was significantly correlated with weak ADR1 expression (P < 0.003). ADR2 expression was considered weak in 14 patients and strong in 29 patients. Rates of formation of vulnerable plaque did not differ between patients with weak and strong ADR2 expression. Conclusions: Based on previous and the present results, ADR1 may be strongly related to the stabilization of established atherosclerotic plaques via inactivating macrophages. Enhancement of ADR1 expression could serve as a therapeutic target for the prevention of the formation of vulnerable plaque.

AIM Adiponectin plays an important role in the regulation of tissue inflammation. Recently, it has been reported that the plasma adiponectin levels in several acute illnesses decrease periodically, thus indicating that adiponectin may play a role in the inflammatory response in patients with acute illness. However, little is known about the effects of adiponectin following TBI. The aim of the present study was to examine the changes in the plasma adiponectin levels and the immunoreactivity of adiponectin in the brain after TBI. MATERIAL AND METHODS Adult male Sprague-Dawley rats were subjected to lateral fluid percussion injury using the Dragonfly device. Plasma adiponectin levels were determined by ELISA kit. Immunohistochemistry and Western blot analysis were performed to assess the immunoreactivity of adiponectin. RESULTS The plasma adiponectin levels gradually decreased and were significantly lower at 48 h and 72 h after injury than before injury. Immunohistochemistry and Western blot analysis showed that the adiponectin immunoreactivity was increased in the cerebral cortex at 24 hours after injury and in the hippocampus at 72 hours after injury. CONCLUSION Our findings suggest that adiponectin might participate in the pathophysiological process occurring after TBI.

Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin.Adult male Sprague-Dawley rats were subjected to lateral fluid percussion injury using the Dragonfly device. Immuno-histochemical studies showed that the adiponectin expression was increased in the cerebral cortex at 24 h after injury and in the hippocampus at 72 h after injury. Our findings suggest that adiponectin might participate in the pathophysiological process occurring after traumatic brain injury.

Background: The role of decompressive craniectomy (DC) in aneurysmal subarachnoid hemorrhage (aSAH) patients is still controversial. In this study we evaluated the effect of DC for aSAH patients. Methods: A matched-pair analysis was performed to compare the outcomes of patients with DC to those of patients without DC. Among 295 consecutive aSAH patients, 56 required DC. Of the remaining group, 56 matched controls were found. The match was conducted on the basis of epidemiological and potential prognostic factors, such as age, gender, World Federation of Neurosurgical Societies (WFNS) grade, Fisher group and occurrence of vasospasm. Results: Fifty-four of 56 (96.4%) patients with DC were dependent or dead at 1 month, compared with 49 of 56 (87.5%) without DC. There was no significant difference between the groups (p = 0.16). One-year outcomes were available for 108 patients (96.4%). Thirty-nine of 54 (72.2%) patients treated with DC were dependent or dead at 1 year, compared with 30 of 54 (55.6%) patients in the control group. There was no significant difference between the groups (p = 0.11). This result was unaffected by age, sex and WFNS grade. Subgroup analyses whether DC was performed primarily or delayed, and whether DC was performed due to spasm, hematoma or vessel occlusion failed to detect any significant difference. Conclusion: There was no significant advantage for patients treated with DC, but more than 25% achieved a good long-term outcome. While the value of DC is deemed uncertain, it may be effective for a very specific subset of aSAH patients. Further comparative studies are needed to resolve this matter.

Brain tissue is highly vulnerable to ischemia/hypoxia, and real-time monitoring of its viability is important. By fiber-based measurements for rat brain, we previously observed a unique triphasic reflectance change (TRC) after a certain period of time after hypoxia. After TRC, rats could not be rescued, suggesting that TRC can be used as an indicator of loss of brain tissue viability. In this study, we investigated this diffuse-reflectance change due to hypoxia in three parts. First, we developed and validated a theoretical method to quantify changes in the absorption and reduced scattering coefficients involved in TRC. Second, we performed charge-coupled-device-based reflectance imaging of the rat brain during hypoxia followed by reoxygenation to examine spatiotemporal characteristics of the reflectance and its correlation with reversibility of brain tissue damage. Third, we made simultaneous imaging and fiber-based measurement of the reflectance for the rat to compare signals obtained by these two modalities. We observed a nontriphasic reflectance change by the imaging, and it was associated with brain tissue viability. We found that TRC measured by the fibers preceded the reflectance-signal change captured by the imaging. This time difference is attributable to the different observation depths in the brain with these two methods.

Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin.

BACKGROUND xCT is a light chain of the cystine/glutamate antiporter system xc. Glutamate that is released by system xc plays an important role in the infiltration of glioblastoma (GBM) cells. Furthermore, increased glutathione synthesis by system xc may protect tumor cells against oxidative stress induced by radiotherapy and chemotherapy. OBJECTIVE To investigate whether the levels of xCT expression correlated with infiltrative imaging phenotypes on magnetic resonance imaging and outcomes in patients with GBMs. METHODS Forty patients with histologically confirmed primary GBMs were included in the study. Patient charts were retrospectively reviewed for age, sex, Karnofsky Performance Status Scale score, Mini-Mental State Examination score, magnetic resonance imaging features, xCT expression, isocitrate dehydrogenase 1 R132H expression, O-methylguanine-DNA methyltransferase promoter methylation status, type of surgery, progression-free survival, and overall survival. RESULTS In invasive margins, xCT expression was weak in 20 patients and strong in 20 patients. A Cox regression model revealed that a Karnofsky Performance Status Scale score less than 60 (hazard ratio [HR]: 4.525; P = .01), partial removal (HR: 2.839; P = .03), and strong xCT expression (HR: 4.134; P < .001) were significantly associated with shorter progression-free survival and that partial removal (HR: 2.865; P = .03), weak isocitrate dehydrogenase 1 R132H expression (HR: 15.729; P = .01), and strong xCT expression (HR: 2.863; P = .04) were significantly associated with shorter overall survival. CONCLUSION These findings suggest that xCT is an independent predictive factor in GBMs.

A 30-year-old female developed moyamoya syndrome after gamma knife surgery (GKS) for cerebral arteriovenous malformation (AVM), and was treated with bypass surgery. She suffered from flittering scotoma, right transient hemianopsia, and headache for 1 year. Cerebral angiography revealed a Spetzler-Martin grade III AVM located in the left occipital lobe. After staged embolization, GKS was performed with a minimum dose of 20 Gy to the periphery of the nidus at the 50% isodose level of the maximum target dose. Gradual nidus regression was achieved, and the clinical symptoms disappeared completely. However, at 30 months after GKS, the patient suffered transient ischemic attack. Cerebral angiography showed left middle cerebral artery occlusion with moyamoya vessels. The patient underwent direct and indirect bypass surgery. After surgery, the patient was free from ischemic symptoms. Chronic inflammation and long-term changes in expression of cytokines and growth factors after GKS may have triggered this case.

In brain anoxia or ischemia, spreading depolarization is a key event that deterimines brain tissue survival. After onset of anoxia/ischemia, impairment of energy metabolism causes anoxic/ischemic depolarization (AD), which considerably consumes energy, leading to acute neuronal death in the brain. Our previous intrinsic-optical-signal imaging for the rat brains showed that about 2 min after starting hypoxia, AD-related light-scattering waves were focally generated in the bilateral outermost regions in the cortex and spread toward the midline, indicating that AD can be monitored by light-scattering signal. The behaviors of the scattering waves were found to be correlated with the su rvival of the rats. In the present study, we used the scattering signal-based monitoring method for AD and examined whether near-infrared laser irradiation can control AD in the rat brains. The left hemisphe re was irradiated with 808-nm laser transcranially at 7.5 mW/cm 2 before (30 min) and during hypoxia. The onset time of the scattering wave (AD) was significantly delayed in the irradiated hemisphere when compared with that in the non-irradiated hemisphere (3.4 s, n=8). The area of AD spreading in the irradiated hemisphere was significantly smaller than that in the non-irradiated hemisphere (27-90% reduction at 10-50 s after AD onset). These results suggest that near-infrared light can delay and reduce anoxic depolarization in the brain, which is probably due to increa se in the cerebral ATP by near-infrared laser irradiation. Keywords: low-level light therapy, anoxic depolarization, intrinsi c optical signal imaging, light scattering, cytochrome c oxidase

Global cerebral ischemia and reperfusion (I/R) often result in high mortality. Free radicals have been reported to play an important role in global cerebral I/R, and therefore, reduction of these might improve the outcome. Here, we investigated the effect of hydrogen gas (H2) (a strong free radical scavenger) on the survival rate of mice following global cerebral I/R. We further examined the histopathological outcome and also the brain water content (as a possible determinant of mortality). Male C57BL/6J mice were subjected to global cerebral I/R by means of 45-min bilateral common carotid artery occlusion (BCCAO). A total of 160 mice were divided into three groups: sham surgery (sham group), BCCAO without H2 (BCCAO group), and BCCAO treated with 1.3% H2 (BCCAO + H2 group). We observed that H2 treatment significantly (P = 0.0232) improved the 7-day survival rate of mice, from 8.3% (BCCAO group, n = 12) to 50% (BCCAO + H2 group, n = 10). Histopathological analysis revealed that H2 treatment significantly attenuated neuronal injury and autophagy in the hippocampal cornu ammonis 1 sector and also brain edema, after 24 h of reperfusion. The beneficial effects of H2 treatment on brain injury were associated with significantly lower levels of oxidative stress markers (8-hydroxy-2'-deoxyguanosine and malondialdehyde) in the brain tissue. Thus, we believe that H2 may be an effective treatment for global cerebral I/R.

We correlated oxygen, flow, and pressure indices of cerebrovascular reactivity (CR) with extracellular cerebral metabolite concentrations in a porcine model of intracerebral hemorrhage (ICH).Continuous advanced multimodal monitoring including microdialysis, cerebral blood flow and P(br)O(2) probes were placed 1 cm in front of the coronal suture in the grey/white matter junction. Following a period of 1 h of monitoring, an autologous arterial ICH with defined volumes (3 mL) was induced. Pressure-, oxygen-, and flow-related autoregulation indices (PRx, ORx, and FRx) were simultaneously calculated and correlated hourly with extracellular cerebral metabolites, including glucose, lactate, pyruvate, and glutamate.Seventeen swine were monitored on average 12 continuous hours per animal. FRx correlated highly with ORx (0.96, P =0.001), but values of both FRx and ORx0.2 did not correlate with any microdialysis metabolite. Values of PRx0.2 correlated highly (0.65, P0.001) with the lactate/pyruvate ratio, values of PRx0.3 correlated with glutamate (0.67, P0.05), the lactate/pyruvate ratio (0.60, P0.01), and P(br)O(2) (-0.65, P0.01).We found evidence for impaired CR in a porcine model of ICH. The findings suggest that, among other parameters of CR, positive PRx coefficients have the highest significance and could be associated with microdialysis alterations during hypoxic events.

To evaluate whether cortical spreading depolarizations (CSD) occur in the early stage after cortical intracerebral hemorrhage (ICH).Ten anesthetized male swine were examined over 19 h. Two cerebral probes were inserted around the ICH (microdialysis and thermodiffusion cerebral blood flow), ICP was monitored contralaterally and up to two electrocorticographic grid electrodes were positioned over the hemisphere after hemicraniectomy and dural opening. A right frontal autologous, arterial ICH (3.0 mL) was induced in all the animals studied.Using a modified injection technique an 80% success rate in ICH formation could be achieved. Eight animals with cortical ICH could be analyzed finally. After induction of ICH, ICP increased non-significantly. Overall, six out of eight animals had CSDs, of either single type or clusters. In one animal a CSD occurred as early as 2 h after ICH; in all other animals the first CSD did not occur before 5 h after onset.CSD's occur in cortical experimental ICH. As ICP remained stable owing to the hemicraniectomy we cannot argue in favor of ICP-related triggering of CSD. Modifications of the experimental setup avoiding hemicraniectomy may better describe the pathophysiology of CSD related to ICH in future studies.