Yoshinobu Kamio

Usefulness of Intraoperative Monitoring of Visual Evoked Potentials in Transsphenoidal Surgery

Postoperative visual outcome is a major concern in transsphenoidal surgery (TSS). Intraoperative visual evoked potential (VEP) monitoring has been reported to have little usefulness in predicting postoperative visual outcome. To re-evaluate its usefulness, we adapted a high-power light-stimulating device with electroretinography (ERG) to ascertain retinal light stimulation. Intraoperative VEP monitoring was conducted in TSSs in 33 consecutive patients with sellar and parasellar tumors under total venous anesthesia. The detectability rates of N75, P100, and N135 were 94.0%, 85.0%, and 79.0%, respectively. The mean latencies and amplitudes of N75, P100, and N135 were 76.8 ± 6.4 msec and 4.6 ± 1.8 μV, 98.0 ± 8.6 msec and 5.0 ± 3.4 μV, and 122.1 ± 16.3 msec and 5.7 ± 2.8 μV, respectively. The amplitude was defined as the voltage difference from N75 to P100 or P100 to N135. The criterion for amplitude changes was defined as a > 50% increase or 50% decrease in amplitude compared to the control level. The surgeon was immediately alerted when the VEP changed beyond these thresholds, and the surgical manipulations were stopped until the VEP recovered. Among the 28 cases with evaluable VEP recordings, the VEP amplitudes were stable in 23 cases and transiently decreased in 4 cases. In these 4 cases, no postoperative vision deterioration was observed. One patient, whose VEP amplitude decreased without subsequent recovery, developed vision deterioration. Intraoperative VEP monitoring with ERG to ascertain retinal light stimulation by the new stimulus device was reliable and feasible in preserving visual function in patients undergoing TSS.

Human Mesenchymal Stem Cell‐Derived Microvesicles Prevent the Rupture of Intracranial Aneurysm in Part by Suppression of Mast Cell Activation via a PGE2‐Dependent Mechanism

Activation of mast cells participates in the chronic inflammation associated with cerebral arteries in intracranial aneurysm formation and rupture. Several studies have shown that the anti‐inflammatory effect of mesenchymal stem cells (MSCs) is beneficial for the treatment of aneurysms. However, some long‐term safety concerns exist regarding stem cell‐based therapy for clinical use. We investigated the therapeutic potential of microvesicles (MVs) derived from human MSCs, anuclear membrane bound fragments with reparative properties, in preventing the rupture of intracranial aneurysm in mice, particularly in the effect of MVs on mast cell activation. Intracranial aneurysm was induced in C57BL/6 mice by the combination of systemic hypertension and intrathecal elastase injection. Intravenous administration of MSC‐derived MVs on day 6 and day 9 after aneurysm induction significantly reduced the aneurysmal rupture rate, which was associated with reduced number of activated mast cells in the brain. A23187‐induced activation of both primary cultures of murine mast cells and a human mast cell line, LAD2, was suppressed by MVs treatment, leading to a decrease in cytokine release and tryptase and chymase activities. Upregulation of prostaglandin E2 (PGE2) production and E‐prostanoid 4 (EP4) receptor expression were also observed on mast cells with MVs treatment. Administration of an EP4 antagonist with the MVs eliminated the protective effect of MVs against the aneurysmal rupture in vivo. Human MSC‐derived MVs prevented the rupture of intracranial aneurysm, in part due to their anti‐inflammatory effect on mast cells, which was mediated by PGE2 production and EP4 activation. Stem Cells 2016;34:2943–2955

Successful serial imaging of the mouse cerebral arteries using conventional 3-T magnetic resonance imaging.

Serial imaging studies can be useful in characterizing the pathologic and physiologic remodeling of cerebral arteries in various mouse models. We tested the feasibility of using a readily available, conventional 3-T magnetic resonance imaging (MRI) to serially image cerebrovascular remodeling in mice. We utilized a mouse model of intracranial aneurysm as a mouse model of the dynamic, pathologic remodeling of cerebral arteries. Aneurysms were induced by hypertension and a single elastase injection into the cerebrospinal fluid. For the mouse cerebrovascular imaging, we used a conventional 3-T MRI system and a 40-mm saddle coil. We used non-enhanced magnetic resonance angiography (MRA) to detect intracranial aneurysm formation and T2-weighted imaging to detect aneurysmal subarachnoid hemorrhage. A serial MRI was conducted every 2 to 3 days. MRI detection of aneurysm formation and subarachnoid hemorrhage was compared against the postmortem inspection of the brain that was perfused with dye. The imaging times for the MRA and T2-weighted imaging were 3.7 ± 0.5 minutes and 4.8 ± 0.0 minutes, respectively. All aneurysms and subarachnoid hemorrhages were correctly identified by two masked observers on MRI. This MRI-based serial imaging technique was useful in detecting intracranial aneurysm formation and subarachnoid hemorrhage in mice.

Nasopharyngeal carcinoma presenting with rapidly progressive severe visual disturbance: a case report

IntroductionNasopharyngeal carcinoma is one of the most difficult tumors to diagnose correctly at the initial phase because of the occasional lack of nasal symptoms. The perineural spread of the trigeminal nerve is one of the most common and important routes in the intracranial paracavernous extension of nasopharyngeal carcinoma, but visual loss is very rare.Case presentationWe report the case of a 54-year-old Japanese man with nasopharyngeal carcinoma, who presented with rapid and severe disturbance of left monocular visual acuity and eye movement with a 10-month history of ipsilateral otitis media and facial pain. Magnetic resonance imaging revealed a lesion in the left fossa of Rosenmüller, pterygopalatine fossa, sphenoid and ethmoid sinus, and the left cavernous sinus extending to the orbital apex through the superior orbital fissure. The histopathological diagnosis was nonkeratinizing undifferentiated nasopharyngeal carcinoma. Epstein–Barr virus was detected by in situ hybridization. Although focal radiotherapy induced remarkable tumor shrinkage and relieved ocular motor disturbance and facial pain, his visual acuity did not improve.ConclusionThe awareness of cranial nerves in addition to intracranial and orbital apex involvement, as in this case, is important for appropriate diagnosis and treatment planning of nasopharyngeal carcinoma.

Prevention Effect of Antiplatelets on Aneurysm Rupture in a Mouse Intracranial Aneurysm Model

Background and Purpose: Subarachnoid hemorrhage (SAH) from intracranial aneurysm rupture results in significant morbidity and mortality. In the present study, we examined the effect of most widely used antiplatelet drugs, aspirin and cilostazol, on aneurysm rupture prevention using a mouse intracranial aneurysm model. Materials and Methods: Intracranial aneurysms were induced by a combination of deoxycorticosterone acetate-salt and a single injection of elastase into the cerebrospinal fluid in mice. Treatment with aspirin or cilostazol was started 1 day after aneurysm induction. Aneurysm rupture was detected by neurological symptoms and the presence of intracranial aneurysm with SAH was confirmed by post-mortem examination. Results: Aspirin (10 mg/kg) significantly reduced aneurysm rupture (control:aspirin = 80%:31%, p < 0.05) without affecting the overall incidence of aneurysm formation (60%:62%). Cilostazol (3 mg/kg, 30 mg/kg) did not reduce both rupture rate (control:3 mg/kg:30 mg/kg = 81%:67%:77%) and the overall incidence of aneurysm formation (control:3 mg/kg:30 mg/kg = 72%:71%:76%). Tail vein bleeding time prolonged significantly in both aspirin and cilostazol groups (p < 0.01). Conclusion: Aspirin prevented aneurysm rupture in a mouse intracranial aneurysm model, while cilostazol did not. Aspirin, the most frequently used drug for patients with ischemic myocardial and cerebral diseases, is also effective in preventing cerebral aneurysmal rupture.

Cerebellar Hemorrhage due to a Direct Carotid-Cavernous Fistula after Surgery for Maxillary Cancer.

Infratentorial cerebral hemorrhage due to a direct carotid–cavernous fistula (CCF) is very rare. To our knowledge, only four such cases have been reported. Cerebellar hemorrhage due to a direct CCF has not been reported. We describe a 63-year-old female who presented with reduced consciousness 3 days after undergoing a maxillectomy for maxillary cancer. Computed tomography showed a cerebellar hemorrhage. Magnetic resonance angiography showed a left-sided direct CCF draining into the left petrosal and cerebellar veins through the left superior petrosal sinus (SPS). Her previous surgery had sacrificed the pterygoid plexus and facial vein. Increased blood flow and reduced drainage could have led to increased venous pressure in infratentorial veins, including the petrosal and cerebellar veins. The cavernous sinus has several drainage routes, but the SPS is one of the most important routes for infratentorial venous drainage. Stenosis or absence of the posterior segment of the SPS can also result in increased pressure in the cerebellar and pontine veins. We emphasize that a direct CCF with cortical venous reflux should be precisely evaluated to determine the hemodynamic status and venous drainage from the cavernous sinus.

Transvenous Embolization of a Dural Arteriovenous Fistula Involving the Suboccipital Cavernous Sinus

Arnautovic et al. [1] termed the venous structures surrounding the extraspinal segment of the vertebral artery (VA; V3) the suboccipital cavernous sinus (SCS) [1, 4]. We experienced a rare dural arteriovenous fistula (AVF) involving the SCS, which differed from dural AVFs involving the anterior condylar confluence (ACC). Here we present a case of SCS dural AVF with pulsatile tinnitus treated by transvenous embolization (TVE).

Dissecting Aneurysm at the Proximal Segment of the Anterior Cerebral Artery Associated with Infraoptic Course Anterior Cerebral Artery

A 48-year-old man presented a subarachnoid hemorrhage caused by a rupture of a dissecting aneurysm at the proximal segment (A1 segment) of the right anterior cerebral artery (ACA). He also had an anomalous artery named infraoptic course ACA and an agenesis of the contralateral ACA A1 segment. Balloon occlusion test at the bifurcation of the right internal carotid artery demonstrated that the distal segments of the bilateral ACAs were perfused through the infraoptic course ACA. Therefore, we surgically trapped the A1 segment including the aneurysm. The patient got discharged without any neurological deficit. Natural course of ACA dissecting aneurysms is unclear because of rarity of the disease and treatment strategy is still controversial. Most of the dissecting aneurysms in the A1 segment are surgically treated, because they often present with massive hemorrhage and poor prognosis. In the present case, the contralateral A1 segment was absent but trapping of the dissecting aneurysm could be achieved without vascular reconstruction (e.g., bypass surgery) because of the presence of the infraoptic course ACA.

Protective Effect of Mesenchymal Stem Cells Against the Development of Intracranial Aneurysm Rupture in Mice.

BACKGROUND Mesenchymal stem cells (MSCs) are multipotent stem or stromal cells found in multiple tissues. Intravenous MSC injections have been used to treat various diseases with an inflammatory component in animals and humans. Inflammation is emerging as a key component of pathophysiology of intracranial aneurysms. Modulation of inflammation by MSCs may affect sustained inflammatory processes that lead to aneurysmal rupture. OBJECTIVE To assess the effect of MSCs on the development of aneurysm rupture using a mouse model. METHODS Intracranial aneurysms were induced with a combination of a single elastase injection into the cerebrospinal fluid and deoxycorticosterone acetate salt-induced hypertension in mice. We administered allogeneic bone marrow-derived MSCs or vehicle, 6 and 9 d after aneurysm induction. RESULTS MSC administration significantly reduced rupture rate (vehicle control vs MSCs, 90% vs 36%; P < .05). In cell culture experiments with an MSC and mast cell coculture, MSCs stabilized mast cells through cyclooxygenase-2 (COX-2)-dependent production of prostaglandin E2, thereby reducing the release of proinflammatory cytokines from mast cells. Pretreatment of MSCs with COX-2 inhibitor, NS-398, abolished the protective effect of MSCs against the development of aneurysm rupture. CONCLUSION Intravenous administration of MSCs after aneurysm formation prevented aneurysmal rupture in mice. The protective effect of MSCs against the development of aneurysm rupture appears to be mediated in part by the stabilization of mast cells by MSCs.

Dural Arteriovenous Fistula of the Transverse and Sigmoid Sinus Manifesting Ascending Dysesthesia: Case Report and Literature Review

Cases involving intracranial dural arteriovenous fistulas (AVFs) with spinal perimedullary venous drainage exhibit variable presentations, which results in delayed diagnoses. We describe a case of a 66-year-old female with a transverse-sigmoid sinus dural AVF with spinal perimedullary venous drainage who developed dysesthesia and hypalgesia that ascended from the peripheral lower extremities. Sixty cases of intracranial dural AVFs resulting in myelopathy have been reported, and an absence of brainstem signs significantly correlated with a delay in diagnosis (positive group: 3.4 months vs. negative group: 9.6 months, P < 0.05). Intracranial dural AVFs with brainstem signs should be diagnosed without delay because the myelopathy and bulbar symptoms could progress aggressively without alternative drainage routes besides the perimedullary veins. We emphasize that intracranial dural AVFs should be considered as a differential diagnosis in case presenting with symptoms, such as atypical dysesthesia and hypalgesia ascending from the toes, without brainstem signs. Moreover, we should perform cerebral angiography as early as possible because dural AVFs with slow-flow venous drainage can produce false negatives on magnetic resonance angiography.