Inhalational Anesthesia Reduced Transient Neurological Events After Revascularization Surgery for Moyamoya Disease.

BACKGROUND AND OBJECTIVES: The choice between inhalational and total intravenous anesthesia (TIVA) in revascularization surgery for Moyamoya disease (MMD) remains a topic of debate. Anesthesia methods have changed with the advent of new anesthetics. This study investigated whether modern anesthesia methods affected the development of neurological symptoms after revascularization surgery for MMD. METHODS: This single-center retrospective study included 63 adult patients (82 hemispheres) with MMD treated with direct and indirect bypass surgeries at our hospital between 2013 and 2022. Patients were divided into inhalational anesthesia (IA) and TIVA groups based on the anesthesia maintenance method. Baseline patient characteristics; postoperative neurological symptoms, including hyperperfusion syndrome, cerebral infarction, and transient neurological events (TNEs); and cortical hyperintensity belt (CHB) sign scores (5-point scale from 0 to 4) on postoperative magnetic resonance imaging were compared between the two groups. The operation methods, anesthetics, and intraoperative hemodynamic and ventilatory parameters were compared between patients with and without TNEs. RESULTS: The IA and TIVA groups comprised 39 and 43 hemispheres, respectively. The frequency of postoperative hyperperfusion syndrome and cerebral infarction did not differ between the groups, but the number of TNEs in the IA group (5/39; 13%) was significantly lower than that in the TIVA group (16/43; 37%). Multivariate logistic regression analysis revealed that TNEs were associated with TIVA (odds ratio, 3.91; 95% CI, 1.24-12.35; P = .02). The median [IQR] postoperative CHB sign score in the IA group (2 [1-3]) was significantly lower than that in the TIVA group (4 [3-4]). CONCLUSION: The IA group had fewer postoperative TNEs and lower CHB sign scores than the TIVA group. Although further studies are needed, this study provides insights into the prevention of TNEs with IA and reconsideration of the optimal anesthesia for MMD.

Hemodynamic study about cortical hyperintensity belt sign after direct bypass surgery for moyamoya disease.

Transient neurological events (TNEs) are observed after direct bypass surgery in patients with moyamoya disease (MMD). Although a correlation between cortical hyperintensity belt signs (CHBs) and TNEs has been reported, the pathophysiology of CHBs is still unknown. The purpose of this study was to reveal the pathophysiology of CHBs by using dynamic susceptibility contrast-magnetic resonance imaging. Thirty patients with MMD were included in this study. We provided scores (0-2) for the existence of CHBs on postoperative FLAIR images. We placed the ROI for the presented area of CHBs in the images of cerebral blood flow, CBV, and MTT. We calculated the change of the hemodynamic parameters (increase ratio, IR) and analyzed the relationship between IRs, CHB scores, and TNEs. TNEs were observed in 15 cases (50%) and CHBs were detected in 28 cases (93%). TNEs showed significantly higher CHB scores than those without (p < 0.05). The group of CHB score 2 showed a significantly higher CBV IR than the group with of score 0 (p < 0.05). Patients with TNEs showed a significantly higher CBV IR than those without (p < 0.05). As for the cut-off level to predict an appearance of TNEs, the CBV IR was 1.36 by the Receiver Operating Characteristic analysis, and the sensitivity and specificity were 80% respectively. We hypothesize that the pathophysiology of the CHBs are vasogenic edemas because the postoperative CBV increase correlated with the CHBs.

Cortical Venous Reddening Predicts Remote Cerebral Infarction Post Superficial Temporal Artery-Middle Cerebral Artery Bypass in Atherosclerotic Occlusive Cerebrovascular Disease.

BACKGROUND: The superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis (STA-MCA bypass) currently is performed to prevent atherosclerotic occlusive cerebrovascular disease. However, the benefits of the bypass surgery remain controversial. To ensure consistent surgical benefits, understanding the mechanisms of perioperative cerebral infarction (CI) is required. Moreover, appropriate patient selection procedures must be determined to decrease the rate of perioperative stroke. We retrospectively investigated patients who underwent bypass surgery at our institution and determined that the patients who presented with cortical venous reddening after anastomosis during the surgery developed perioperative CI. METHODS: A total of 45 consecutive patients who underwent bypass surgery were retrospectively investigated. Twenty-five of the 45 patients underwent bypass for atherosclerotic occlusion or stenosis of the internal carotid artery or middle cerebral artery. Preoperative iodine-123-N-isopropyl-iodoamphetamine single-photon emission computed tomography was performed with and without acetazolamide administration. Change in color of the cortical veins was observed on recorded surgical videos, and its correlation with perioperative CI was investigated. RESULTS: We experienced 2 cases of perioperative extensive CI at a region remote from the site of anastomosis. In both cases, retrospective investigation of surgical videos demonstrated reddening of cortical veins soon after the anastomosis procedure. Of all 45 patients, postoperative CI and venous reddening were observed in only these 2 cases. CONCLUSIONS: We determined that patients presenting with cortical venous reddening after anastomosis developed perioperative CI. Cortical venous reddening may be an important predictor for the occurrence of CI after STA-MCA bypass surgery for patients with atherosclerotic occlusive cerebrovascular disease.

Internal carotid artery aneurysms diagnosed after stereotactic radiosurgery for a growth hormone-secreting pituitary adenoma: a case report and literature review.

Radiation therapy is associated with the subsequent development of cerebral aneurysms; however, stereotactic radiosurgery (SRS)-associated aneurysm cases have not been well documented, with only 18 cases reported to date. We present a case of intracranial aneurysms with the rupture occurring 20 years after SRS for a growth hormone-producing pituitary adenoma. This is the first report of aneurysms diagnosed following transsphenoidal surgery and SRS for pituitary adenoma. We believe that the aneurysm reported here is a consequence of the SRS treatment, and thus this may be a very rare long-term complication following radiation treatments.

Surgical Treatment of Spontaneous Internal Carotid Artery Dissection with Abducent Nerve Palsy: Case Report and Review of Literature.

BACKGROUND: Sixth-nerve palsy often develops as a result of trauma, neoplasm, or vascular disease affecting the pons. Less commonly, this palsy can be caused by pathology of the internal carotid artery in the cavernous sinus region. Here, we describe a rare case of spontaneous dissection of the internal carotid artery in the cavernous sinus accompanied by acute sixth nerve palsy that was successfully treated with surgery. CASE DESCRIPTION: An 18-year-old man presented suddenly and spontaneously with isolated abducent nerve palsy. His magnetic resonance angiography identified a dissection of the right internal carotid artery in the cavernous sinus. We successfully treated it with high-flow bypass and ligation of the internal carotid artery (ICA). CONCLUSIONS: Intracavernous ICA dissection is a possible cause of sixth nerve palsy. While most cases likely result from compromised arterial blood supply to the affected nerve, compression of the cranial nerves by the expanded artery can occur in some cases. Surgical treatment is a safe and effective option for relieving nerve compression after intracavernous ICA dissection.

Dural arteriovenous fistula associated with intratumor hemorrhage.

Dural arteriovenous fistula (dAVF) associated with an intracranial tumor is a relatively rare condition. Furthermore, to our knowledge, this is the first case report of dAVF associated with intratumor hemorrhage. We experienced this very rare case and report it here, along with a literature review. A 59-year-old woman presented with transient aphasia and dysgraphia. Computed tomography, magnetic resonance imaging, and angiography showed left anterior cranial fossa dAVF and a tumor with an intratumor hemorrhage. Cerebral angiography demonstrated AV shunts from the left ethmoidal artery via cortical vein flow into the superior sagittal sinus. She underwent shunt-point extirpation for the dAVF and removal of the tumor. The histological finding indicated transitional meningioma. The patient was discharged without any neurological deficit. A dAVF with intratumor hemorrhage is very rare and may be due to the venous congestion of the tumor draining vein by venous hypertension caused by the dAVF.

Modified frailty index predicts postoperative outcomes of spontaneous intracerebral hemorrhage.

OBJECTIVES: Frailty is an indispensable concept among elderly. The purpose of this study was to determine the association between modified frailty index (mFI) and the postoperative outcome of surgery for spontaneous intracerebral hemorrhage (sICH). PATIENTS AND METHODS: Outcome measures included an unfavorable outcome (modified Rankin Scale score of 4-6) or mortality at 6-8 months after hemorrhage. The prognostic ability of mFI was assessed by comparing adjusted and nonadjusted effects with the Hemphill's ICH score. The performance of the ICH score combined with mFI was assessed for discriminative ability. RESULTS: In total, 156 patients satisfied the inclusion criteria. Multivariate analyses revealed that higher mFI was significantly associated with an unfavorable outcome (p-value = 0.004) and mortality (p-value < 0.001). Compared with the ICH score alone, the ICH score combined with mFI revealed significantly higher discriminative ability for predicting postoperative outcome. CONCLUSION: mFI was a useful and reliable predictor of postoperative unfavorable outcome for sICH. Frailty may be an important essence to be considered before operation for sICS in the aging society.

High prevalence of small vessel disease long after cranial irradiation.

Accelerated atherosclerosis of intra- or extracranial large arteries is a major cause of radiation-induced strokes. Recent development of MRI techniques has enabled detection of another important vasculopathy: microinfarcts or microbleeds after cranial irradiation. The purpose of this study was to investigate the incidence and characteristics of small vessel disease after cranial irradiation. MR images and clinical records of 102 outpatients who had undergone cranial irradiation to brain tumors were retrospectively reviewed. Only those who had undergone T1WI, T2WI, FLAIR, and T2∗WI during follow-up were included. Small vessel disease including small subcortical infracts, microbleeds, and volume of white matter lesions were assessed on the latest MR images of each patient. Ischemic or hemorrhagic stroke during the follow-up period was also reviewed. Twelve patients (mean age at the latest MRI, 38.5years; 8men) were assessed. The total radiation dose was 52.3±9.7Gy in these patients, 9 of whom received whole brain irradiation. Small subcortical infarcts (mean 2.3) were detected in 8 patients, microbleeds (mean 19.4) were detected in 11, and white matter lesion volume was 38.3±11.6ml. During the follow-up period of 19.8±9.7years, 5 patients experienced stroke (4 lacunar, 1 hemorrhagic). These strokes occurred as long as a median 21.9 (range, 10.4-30.2) years after cranial irradiation. In conclusion, small vessel disease is not a rare complication after cranial irradiation, even in young patients. Patients after cranial irradiation should be followed up with MR imaging including a hemosiderin-sensitive sequence.

Remote Lesions of Synchronous Sacral and Cervical Dural Arteriovenous Fistulas: A Case Report.

BACKGROUND: Spinal dural arteriovenous fistula (DAVF) is a rare disease, and multiple concurrent lesions are extremely rare. Such multiple spinal DAVFs have similar outflow routes at neighboring levels. However, there have been no reported cases of remote lesions of multiple spinal DAVFs. The authors herein report a case of double synchronous cervical and sacral DAVFs. CASE DESCRIPTION: A 56-year-old man with no previous history of disease presented with progressive myelopathy, and spinal magnetic resonance imaging showed extensive edema of the spinal cord from the conus to T7. The initial angiography incidentally revealed a C1 DAVF, but the sacral DAVF was not diagnosed. The C1 DAVF was treated surgically, because of the risk of subarachnoid hemorrhage. A second angiography was performed 2 months after the first surgery because of high clinical suspicion, and the sacral DAVF was diagnosed at that time. The sacral DAVF was treated surgically, and the symptoms gradually resolved within 6 months after surgery. CONCLUSIONS: Spinal DAVF is a rare disease, but clinicians should be aware of the possibility of the concurrence of multiple spinal fistulas located at different levels in the same patient.

Macrophage-Derived Angiopoietin-Like Protein 2 Exacerbates Brain Damage by Accelerating Acute Inflammation after Ischemia-Reperfusion.

Ischemic stroke is a leading cause of death and disability worldwide. Several reports suggest that acute inflammation after ischemia-reperfusion exacerbates brain damage; however, molecular mechanisms underlying this effect remain unclear. Here, we report that MAC-3-positive immune cells, including infiltrating bone marrow-derived macrophages and activated microglia, express abundant angiopoietin-like protein (ANGPTL) 2 in ischemic mouse brain in a transient middle cerebral artery occlusion (MCAO) model. Both neurological deficits and infarct volume decreased in transient MCAO model mice established in Angptl2 knockout (KO) relative to wild-type mice. Acute brain inflammation after ischemia-reperfusion, as estimated by expression levels of pro-inflammatory cytokines such as interleukin (IL)-1ß and tumor necrosis factor alpha (TNF)-α, was significantly suppressed in Angptl2 KO compared to control mice. Moreover, analysis employing bone marrow chimeric models using Angptl2 KO and wild-type mice revealed that infiltrated bone marrow-derived macrophages secreting ANGPTL2 significantly contribute to acute brain injury seen after ischemia-reperfusion. These studies demonstrate that infiltrating bone marrow-derived macrophages promote inflammation and injury in affected brain areas after ischemia-reperfusion, likely via ANGPTL2 secretion in the acute phase of ischemic stroke.

Superficial temporal artery-to-middle cerebral artery bypass surgery for middle cerebral artery stenosis in a patient with cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy is a rare hereditary small vessel disease. Ischemic events are the main clinical manifestation of this condition. Here, we present a case in which superficial temporal artery-to-middle cerebral artery anastomosis was performed in a patient with cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy who developed cerebral infarctions caused by severe middle cerebral artery stenosis. Cerebral blood flow and cerebrovascular reactivity were effectively improved using double anastomoses. To our knowledge, surgical revascularization for patients with this condition has not yet been described in the literature. Superficial temporal artery-to-middle cerebral artery anastomosis is effective for patients with cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy who show marked regional cerebral hypoperfusion.

Endoscopic endonasal skull base approach for parasellar lesions: Initial experiences, results, efficacy, and complications.

BACKGROUND: Endoscopic surgery is suitable for the transsphenoidal approach; it is minimally invasive and provides a well-lit operative field. The endoscopic skull base approach through the large opening of the sphenoid sinus through both nostrils has extended the surgical indication for various skull base lesions. In this study, we describe the efficacy and complications associated with the endoscopic skull base approach for extra- or intradural parasellar lesions based on our experiences. METHODS: Seventy-four cases were treated by an endoscopic skull base approach. The indications for these procedures included 55 anterior extended approaches, 10 clival approaches, and 9 cavernous approaches. The operations were performed through both the nostrils using a rigid endoscope. After tumor removal, the skull base was reconstructed by a multilayered method using a polyglactin acid (PGA) sheet. RESULTS: Gross total resection was achieved in 82% of pituitary adenomas, 68.8% of meningiomas, and 60% of craniopharyngiomas in anterior extended approach and in 83.3% of chordomas in clival approach, but only in 50% of the tumors in cavernous approach. Tumor consistency, adhesion, and/or extension were significant limitations. Visual function improvements were achieved in 37 of 41 (90.2%) cases. Cerebrospinal fluid (CSF) leakage (9.5%), infections (5.4%), neural injuries (4.1%), and vascular injuries (2.7%) were the major complications. CONCLUSIONS: Our experiences show that the endoscopic skull base approach is a safe and effective procedure for various parasellar lesions. Selection of patients who are unlikely to develop complications seems to be an important factor for procedure efficacy and good outcome.

Rosuvastatin ameliorates early brain injury after subarachnoid hemorrhage via suppression of superoxide formation and nuclear factor-kappa B activation in rats.

BACKGROUND: Statins, or 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, have been suggested to possess pleiotropic effects, including antioxidant and anti-inflammatory properties. We investigated the protective effects of pretreatment with rosuvastatin, a relatively hydrophilic statin, on early brain injury (EBI) after a subarachnoid hemorrhage (SAH), using the endovascular perforation SAH model. METHODS: Eighty-six male Sprague-Dawley rats were randomly divided into 3 groups: (1) sham operation, (2) SAH+vehicle, and (3) SAH+10 mg/kg rosuvastatin. Rosuvastatin or vehicle was orally administered to rats once daily from 7 days before to 1 day after the SAH operation. After SAH, we examined the effects of rosuvastatin on the neurologic score, brain water content, neuronal cell death estimated by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate nick end labeling staining, blood-brain barrier disruption by immunoglobulin G (IgG) extravasation, oxidative stress, and proinflammatory molecules. RESULTS: Compared with the vehicle group, rosuvastatin significantly improved the neurologic score and reduced the brain water content, neuronal cell death, and IgG extravasation. Rosuvastatin inhibited brain superoxide production, nuclear factor-kappa B (NF-κB) activation, and the increase in activated microglial cells after SAH. The increased expressions of tumor necrosis factor-alpha, endothelial matrix metalloproteinase-9, and neuronal cyclooxygenase-2 induced by SAH were prevented by rosuvastatin pretreatment. CONCLUSIONS: The present study demonstrates that rosuvastatin pretreatment ameliorates EBI after SAH through the attenuation of oxidative stress and NF-κB-mediated inflammation.

Prolonged and regionally progressive symptomatic cerebral hyperperfusion syndrome after superficial temporal artery-middle cerebral artery anastomosis in a patient with moyamoya disease.

BACKGROUND: The incidence of symptomatic hyperperfusion syndrome after superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis for patients with moyamoya disease (MMD) approaches 30%. In most cases, hyperperfusion occurs in a localized area and disappears within 1-2 weeks. CASE DESCRIPTION: A 59-year-old female diagnosed with asymptomatic MMD for 4 months became rapidly symptomatic with transient ischemic attacks (TIAs). After left STA-MCA anastomosis surgery, she developed symptomatic hyperperfusion, initially (1-2 weeks after surgery) manifesting with severe headache and lesions located in the left basal ganglia. She then developed (2-5 weeks after surgery) aphasia and right hemiparesis caused by new hyperperfusion lesions located in the left frontal area. At discharge (7 weeks after surgery), she recovered fully without any remaining neurologic deficit and no ischemic lesions. CONCLUSION: This report details a rare case of a patient with MMD who presented with regionally progressive hyperperfusion lesions after STA-MCA anastomosis and symptoms that persisted for 5 weeks following surgery. Results from this case suggest that regional differences exist in the functional recovery of cerebrovascular reactivity (CVR) in a patient with rapidly progressive MMD.

RAGE mediates vascular injury and inflammation after global cerebral ischemia.

The receptor for advanced glycation end products (RAGE) is a multi-ligand receptor involved in a diverse range of pathological conditions. To analyze the roles of RAGE and its decoy receptor, endogenous secretory RAGE (esRAGE), in the global cerebral ischemia, three different mouse cohorts, wild-type, RAGE⁻/⁻, and esRAGE transgenic (Tg) mice were subjected to bilateral common carotid artery occlusion (BCCAO). RT-PCR and immunohistochemical analysis revealed that expression of RAGE was induced in the vascular cells at 12 h, and then in the neurons and glia from 3 to 7 days in the hippocampus after BCCAO. The numbers of surviving neurons in the hippocampal CA1 region were significantly higher in RAGE⁻/⁻ and esRAGE Tg mice than those in wild-type mice in the periods between 24 h and 7 days after BCCAO. Lower levels of 3-nitrotyrosine (3-NT) and higher levels of endothelial nitric oxide synthase (eNOS), together with enlarged vascular areas were observed in RAGE⁻/⁻ and esRAGE Tg mice at 12 h after BCCAO. In the later periods, expressions of glia-derived inflammatory mediators TNFα and inducible nitric oxide synthase (iNOS) were reduced in RAGE⁻/⁻ and esRAGE Tg mice. These results suggest that RAGE may contribute to delayed neuronal death after global cerebral ischemia by enhancing vascular injury and deleterious glia-mediated inflammation.

Purinergic signaling induces cyclooxygenase-1-dependent prostanoid synthesis in microglia: roles in the outcome of excitotoxic brain injury.

Cyclooxygenases (COX) are prostanoid synthesizing enzymes constitutively expressed in the brain that contribute to excitotoxic neuronal cell death. While the neurotoxic role of COX-2 is well established and has been linked to prostaglandin E(2) synthesis, the role of COX-1 is not clearly understood. In a model of N-Methyl-D-aspartic acid (NMDA) induced excitotoxicity in the mouse cerebral cortex we found a distinctive temporal profile of COX-1 and COX-2 activation where COX-1, located in microglia, is responsible for the early phase of prostaglandin E(2) synthesis (10 minutes after NMDA), while both COX-1 and COX-2 contribute to the second phase (3-24 hours after NMDA). Microglial COX-1 is strongly activated by ATP but not excitatory neurotransmitters or the Toll-like receptor 4 ligand bacterial lipopolysaccharide. ATP induced microglial COX-1 dependent prostaglandin E(2) synthesis is dependent on P2X7 receptors, extracellular Ca(2+) and cytoplasmic phospholipase A2. NMDA receptor activation induces ATP release from cultured neurons leading to microglial P2X7 receptor activation and COX-1 dependent prostaglandin E(2) synthesis in mixed microglial-neuronal cultures. Pharmacological inhibition of COX-1 has no effect on the cortical lesion produced by NMDA, but counteracts the neuroprotection exerted by inhibition of COX-2 or observed in mice lacking the prostaglandin E(2) receptor type 1. Similarly, the neuroprotection exerted by the prostaglandin E(2) receptor type 2 agonist butaprost is not observed after COX-1 inhibition. P2X7 receptors contribute to NMDA induced prostaglandin E(2) production in vivo and blockage of P2X7 receptors reverses the neuroprotection offered by COX-2 inhibition. These findings suggest that purinergic signaling in microglia triggered by neuronal ATP modulates excitotoxic cortical lesion by regulating COX-1 dependent prostanoid production and unveil a previously unrecognized protective role of microglial COX-1 in excitotoxic brain injury.

Endoscopic surgical treatment for pituitary apoplexy in three elderly patients over the age of 80.

OBJECTIVES: As the population continues to live longer, the diagnosis of pituitary adenoma-induced apoplexy becomes more common in the elderly. The standard treatment options for pituitary apoplexy are debatable. Although there is little information regarding the treatment of pituitary apoplexy in elderly patients, the optimal treatment needs to be determined for this age group. The current study examined the surgical treatment of pituitary apoplexy in three patients over the age of 80. CASE DESCRIPTION: Three patients over the age of 80 with pituitary apoplexy were admitted to our hospital. Some symptoms caused by pituitary apoplexy, including decreased visual acuity, double vision and oculomotor paresis, had persisted for more than 14 days. Magnetic resonance imaging revealed suprasellar mass lesions extending into the cavernous sinus. The general condition of the patients was good, and we performed endoscopic transsphenoidal surgery in each of these cases. The masses were removed, and the histological findings were diagnosed as non-functioning pituitary adenoma with presence of hemorrhagic or ischemic necrosis. Perioperative courses and general conditions were good, and the neurological deficits of each patient improved immediately. CONCLUSIONS: Endoscopic transsphenoidal surgery has the advantage of visualization of the structures surrounding the pituitary gland. Moreover, the complication rate is relatively low because stress on the pituitary gland can be reduced by using this procedure. Even in patients over 80 years of age during the subacute phase, endoscopic surgical management is a good treatment candidate for pituitary apoplexy with mass lesion extension into the cavernous sinus.

Strategy for treating unruptured vertebral artery dissecting aneurysms.

BACKGROUND: The natural course of unruptured vertebral artery dissecting aneurysms (VADAs) remains unclear. OBJECTIVE: The purpose of this retrospective study was to develop a strategy for treating unruptured VADAs based on long-term follow-up. METHODS: Our study population consisted of 100 patients with unruptured VADAs; in 66, the initial symptom was headache only, 30 presented with ischemic symptoms and 4 with mass effect. All underwent magnetic resonance imaging and magnetic resonance angiography at the time of admission and 2 weeks and 1, 3, 6, 12, and 24 months after the onset. If the dissection site was demonstrated to be enlarged on magnetic resonance imaging and magnetic resonance angiography without the manifestation of new symptoms, the patients received additional treatment to prevent bleeding. RESULTS: Of the 100 patients, 4 underwent early intervention because of symptom exacerbation. The other 96 were initially treated conservatively; during follow-up, 5 manifested lesion enlargement on magnetic resonance angiography. Nine patients received additional treatment; 1 underwent direct surgery with trapping of the dissection site, and 8 underwent coil embolization. The other 91 patients continued to be treated conservatively; the dissection site remained unchanged in 70, improved or healed in 18, and disappeared in 3 patients. We treated 38 patients with recurrent ischemic attacks with antiplatelet therapy. No patients experienced bleeding or permanent neurological deficits during follow-up. CONCLUSION: The nature of an unruptured VADA is not highly aggressive. However, if the dissection site enlarges without the manifestation of new symptoms, it should be occluded. In patients with recurrent ischemic attacks antiplatelet therapy should be considered.

Development of a kit to treat subarachnoid hemorrhage by intrathecal simple urokinase infusion (ITSUKI) therapy: preliminary results in patients with World Federation of Neurological Surgery (WFNS) grade V subarachnoid hemorrhage.

OBJECTIVE: To report the effectiveness of intrathecal selective administration of urokinase infusion (ITSUKI) therapy delivered via a special kit (ITSUKit), developed to prevent vasospasm in patients with ruptured aneurysms who had undergone Guglielmi detachable coil (GDC) placement, in patients with World Federation of Neurological Surgery (WFNS) grade V subarachnoid hemorrhage (SAH). METHODS: A study of ITSUKI therapy with or without ventricular drainage enrolled 6 patients with WFNS grade V SAH owing to ruptured intracranial aneurysms who were eligible for coil embolization. The procedures were performed within 48 hours of the occurrence of aneurysmal SAH. The incidence of symptomatic vasospasm and the clinical outcomes based on the Glasgow Outcome Scale (GOS) were assessed at 6 months after SAH onset. RESULTS: All patients underwent complete coil embolization. There were no side effects or adverse reactions attributable to ITSUKI therapy. Symptomatic vasospasm occurred in one patient (16.7%). There were no patients with hydrocephalus. Based on the GOS, one patient had a good outcome, two manifested moderate disability, and three manifested severe disability. CONCLUSIONS: The results showed that the ITSUKit was useful for ITSUKI therapy. Although the combination of coil embolization and ITSUKI therapy did not completely eliminate WFNS grade V SAH, it significantly improved the treatment outcome in some patients.

Granulocyte colony-stimulating factor enhances the angiogenetic effect of indirect bypass surgery for chronic cerebral hypoperfusion in a rat model.

BACKGROUND: Granulocyte colony-stimulating factor (G-CSF) mobilizes hematopoietic bone marrow cells into systemic circulation and has been used clinically to treat chemotherapy-induced neutropenia. Recently, G-CSF was shown to have neuroprotective and angiogenetic effects in acute cerebral infarction. OBJECTIVE: To evaluate the effects of G-CSF for angiogenesis after indirect bypass surgery. METHODS: : Chronic cerebral hypoperfusions were induced in male Wistar rats by permanent bilateral internal carotid artery occlusion (BICAO). After BICAO, unilateral indirect bypass and encephalogaleosynangiosis (EGS) were performed, and human recombinant G-CSF (10 µg/kg) or saline was injected intramuscularly for 5 consecutive days. We measured regional cerebral blood flow (rCBF) by laser Doppler flowmetry and performed immunohistochemical analysis 21 days after BICAO. RESULTS: BICAO decreased rCBF to 62.52% ± 5.8% of control (P < .01). The rCBF increased significantly 21 days after BICAO in all treatment groups (n = 10; P < .05) except the G-E- group. The rCBF increase observed in the G+E+ group was significantly higher than that observed in other groups. Both G-CSF and EGS treatments significantly increased the number of small vessels (P < .01), and G-CSF and EGS showed additive effect in increasing the number of small vessels. CONCLUSION: Combined use of G-CSF and indirect bypass surgery induces an increase in rCBF and angiogenesis under conditions of cerebral chronic hypoperfusion. This is the first report to demonstrate that G-CSF can enhance angiogenesis induced by indirect bypass surgery, and that this combined therapy is a safe and easy method of treatment.