Taketo Hatano

Intraprocedural detection of cerebral hyperperfusion by flat detector computed tomography in the evaluation of cerebral blood volume during carotid artery stenting. A case report.

Cerebral blood volume (CBV) can be measured using a C-arm flat detector angiographic system. The present report describes a case in which cerebral hyperperfusion was detected with the Neuro parenchymal blood volume (PBV) system (syngo Neuro PBV IR, Siemens Medical Solutions, Erlangen, Germany) during carotid artery stenting (CAS). An 89-year-old man was referred to our hospital for cerebral brain infarction and severe stenosis of the left carotid artery. CAS was performed, and Neuro PBV was used to measure CBV both during and after the procedure. Postoperative Neuro PBV revealed dramatically increased CBV, and a hyperperfusion state was suspected. The next day, subarachnoid hemorrhage along the sulcus of the left hemisphere was revealed on computed tomography. Strict management of blood pressure was instituted just after the detection of hyperperfusion, and the patient was ultimately discharged from the hospital without any new neurological deficits. Neuro PBV has the advantage that it can be performed in the angiography suite and does not require patient transfer to an alternate setting. Therefore, intracranial hemodynamic changes can be detected during the procedure. We conclude that the Neuro PBV system is useful for monitoring intracranial hemodynamics during endovascular procedures.

Surgical treatment of tentorial dural arteriovenous fistulae located around the tentorial incisura

Tentorial dural arteriovenous fistulae (DAVF) are relatively uncommon and are the most dangerous type of DAVF. Because of a high incidence of hemorrhage and subsequent neurological deficits, treatment is mandatory. A consecutive series of nine surgically treated patients with symptomatic tentorial DAVF were analyzed in this study. All lesions were located around the tentorial incisura and were treated microsurgically using a subtemporal approach in eight cases and a supracerebellar approach in one case. The dural bases of the lesions were located adjacent to the tentorial edge in six patients and the tentorial apex in three patients. Complete obliteration was achieved in all treated tentorial DAVF. In one patient, the torcular fistula remained untreated without cortical venous reflux. Postoperative asymptomatic temporal lobe hemorrhage was diagnosed in one patient with a tentorial apex DAVF; however, no new neurological symptoms were present after surgical treatment. The subtemporal approach for unilateral tentorial DAVF is a favorable and direct approach for the highly skilled surgeon. Perimesencephalic venous dilatation or varix is an important finding on MRI to help localize tentorial DAVF in the tentorial edge or apex.

Stenting for stenoses of the proximal vertebral artery.

We report our initial experience of stenting for symptomatic stenoses of the proximal vertebral artery. A total of 25 lesions affecting the proximal vertebral artery were treated by PTA with stent in 23 patients. The lesions involved the vertebral artery ostium in 20 lesions and the nonostial V1 portion in five lesions. The mean stenosis rate of those lesions was 81% pre-stenting and was reduced to 4% post-stenting. There were two transient neurological complications: hemiparesis in one patient and visual acuity disturbance in another. Angiographic follow-up studies more than three months after treatment demonstrated restenosis in three patients. One of these patients was symptomatic. These restenoses were successfully treated by PTA. Our initial results demonstrated that stenting is a feasible and safe method of treating stenosis of the proximal vertebral artery.

Stenting for abrupt closure of the intracranial vertebral artery complicating balloon angioplasty. A case report.

We report a case of stenting for abrupt closure of the intracranial vertebral artery complicating balloon angioplasty. A 58-year-old man with symptomatic restenosis of the intracranial vertebral artery underwent balloon angioplasty, which was complicated by acute occlusion due to wall dissection. The acute occlusion of the lesion was completely recanalized by implanting a balloon-expandable stent designed for the coronary artery. Follow-up angiography 15 months after stenting did not show severe restenosis and the patients symptoms disappeared after stenting. This therapeutic option may be useful as a means to bail out from acute occlusion of the intracranial artery caused by endovascular procedures.

Cerebral hyperperfusion syndrome after endovascular reperfusion therapy in a patient with acute internal carotid artery and middle cerebral artery occlusions

BACKGROUND Cerebral hyperperfusion syndrome (CHS) is known to be a rare but devastating complication of carotid artery revascularization. Because patients with acute ischemic stroke due to acute major cerebral and/or cervical artery occlusion treated with endovascular reperfusion therapy may have impaired autoregulation in the cerebral vasculature, these patients may also develop CHS. Despite the growing number of endovascular reperfusion procedures for acute ischemic stroke, this complication has only rarely been reported. CASE DESCRIPTION A 77-year-old man developed acute cerebral infarction as the result of occlusions of the right internal carotid artery and right middle cerebral artery. After systemic intravenous injection of recombinant tissue-type plasminogen activator, endovascular reperfusion therapy was initiated. The occluded arteries were successfully recanalized with thrombectomy by using a stent retriever for the middle cerebral artery and stent placement for the origin of the internal carotid artery. However, head computed tomography obtained 12 hours after treatment showed acute intracranial hemorrhage that did not involve the ischemic lesions. Under evaluation with transcranial near-infrared spectroscopy and single-photon emission computed tomography, the hemorrhage was considered to have been caused by CHS after reperfusion therapy. CONCLUSIONS CHS may lead to unfavorable outcomes after reperfusion therapy for acute ischemic stroke. Recognizing clinical deterioration caused by CHS can be challenging in patients with neurologic disorders of acute ischemic stroke. Therefore, it is important to perform routine monitoring of regional cerebral oxygen saturation by using near-infrared spectroscopy, perform single-photon emission computed tomography promptly to evaluate cerebral blood flow, and maintain strict antihypertensive therapy to prevent CHS after reperfusion therapy.

Improving treatment times for patients with in-hospital stroke using a standardized protocol

BACKGROUND Previous reports have shown significant delays in treatment of in-hospital stroke (IHS). We developed and implemented our IHS alert protocol in April 2014. We aimed to determine the influence of implementation of our IHS alert protocol. METHODS Our implementation processes comprise the following four main steps: IHS protocol development, workshops for hospital staff to learn about the protocol, preparation of standardized IHS treatment kits, and obtaining feedback in a monthly hospital staff conference. We retrospectively compared protocol metrics and clinical outcomes of patients with IHS treated with intravenous thrombolysis and/or endovascular therapy between before (January 2008-March 2014) and after implementation (April 2014-December 2016). RESULTS Fifty-five patients were included (pre, 25; post, 30). After the implementation, significant reductions occurred in the median time from stroke recognition to evaluation by a neurologist (30 vs. 13.5min, p<0.01) and to first neuroimaging (50 vs. 26.5min, p<0.01) and in the median time from first neuroimaging to intravenous thrombolysis (45 vs. 16min, p=0.02). The median time from first neuroimaging to endovascular therapy had a tendency to decrease (75 vs. 53min, p=0.08). There were no differences in the favorable outcomes (modified Rankin scale score of 0-2) at discharge or the incidence of symptomatic intracranial hemorrhage between the two periods. CONCLUSION Our IHS alert protocol implementation saved time in treating patients with IHS without compromising safety.

Follow-up after undersized dilatation of targeted lesions in carotid artery stenting

Background and purpose. We assessed whether intentional undersized dilatation of targeted lesions during carotid artery stenting (CAS) carried a higher risk of in-stent restenosis (ISR) and correlation to subsequent ischemic stroke in qualifying arteries in the follow-up period. Methods. Consecutive patients undergoing CAS between April 2003 and May 2010 were retrospectively reviewed. The use of a filter device as a distal embolic protection device (EPD) was first approved by Japanese governmental health insurance in April 2008; previously, transient balloon occlusion was used off-label. Until March 2008 (Group A), the target diameter of balloon dilatation was 80–100% of the normal vessel diameter just distal to the stenotic lesion. Moderately undersized dilatation (70–80% of the normal vessel diameter) using the distal EPD was adopted in April 2008 (Group B) in an attempt to reduce the amount of released plaque debris. Results. We analyzed 132 CAS procedures (125 patients) in Group A and 53 CAS procedures (52 patients) in Group B. The mean follow-up period was 35.4 months (35.3 months in Group A and 36.0 months in Group B). Eight lesions (4.3%; 7 in Group A and 1 in Group B) developed ISR. None of the patients had symptomatic ISR, and ISR did not increase in Group B (odds ratio, 0.34; 95% confidence interval, 0.04–2.86; p = 0.32). Conclusions. Undersized dilatation of targeted lesions did not increase the risk of developing ISR, and we suggest it as a viable treatment option to prevent ischemic events during CAS.

Dural and Pial Arteriovenous Fistulas Connected to the Same Drainer in the Middle Cranial Fossa: A Case Report

BACKGROUND Dural arteriovenous fistulas (AVFs) in the middle cranial fossa are rare. Pial AVFs are similarly rare but differ from dural AVFs in that they derive their arterial supply from pial or cortical arterial vessels and do not lie within the intradural region. We report an extremely rare case of dural and pial AVF connected to the same drainer in the middle cranial fossa. CASE DESCRIPTION In a 58-year-old man with a subcortical hemorrhage in the right temporal lobe, digital subtraction angiography showed a dural AVF in the middle cranial fossa fed by the middle meningeal artery (MMA) and draining into the sphenopetrosal vein. A combination with a small pial AVF connected to the same sphenopetrosal vein was suspected. Open surgery was performed to directly observe the shunt points. Transarterial indocyanine green (ICG) angiography using the MMA via the superficial temporal artery on a skin flap was performed to repeatedly and distinctly evaluate the dural shunt points and to prevent cerebral thromboembolism. Although the dural supply was completely disconnected, the sphenopetrosal vein remained arterialized. ICG angiography revealed pial AVF, which was fed by the cortical arteries draining into the same drainer. The pial supply was completely disconnected, and disappearance of the dural and pial AVF was confirmed. CONCLUSIONS We report an extremely rare case of dural and pial AVF connected to the same drainer in the middle cranial fossa. To our knowledge, this is the first such case report described in the literature.

Elevated end-diastolic ratio of the common carotid artery due to cerebral arteriovenous malformation: Two case reports

An elevated end-diastolic (ED) ratio of the common carotid artery (CCA) is an indicator of occlusive lesions of the distal portion of the internal carotid artery. We report 2 cases of cerebral arteriovenous malformation (AVM) showing an elevated ED ratio of the CCA, which decreased after surgery. Case 1 was a 28-year-old man with chronic recurrent headache with aura, and case 2 was a 29-year-old woman with sudden-onset headache and intracerebral hemorrhage without neurologic abnormality. In both cases, digital subtraction angiography revealed a Spetzler-Martin Grade IV AVM, which was mainly fed by branches of the left middle cerebral artery with venous drainage into superficial and deep cerebral veins. Preoperative carotid ultrasonography showed an elevated CCA ED ratio (1.38 in case 1 and 1.47 in case 2; left > right) without atherosclerotic lesions. Patients’ AVMs were successfully resected. In both cases, the ED ratio was decreased after surgery (to 1.05 in case 1 and 1.20 in case 2). A decrease in vascular resistance on 1 side caused by cerebral AVM can result in an increase in the CCA ED ratio comparable to that of carotid axis occlusion.

International multicentre validation of the arteriovenous malformation-related intracerebral haemorrhage (AVICH) score

Objective The recently published arteriovenous malformation-related intracerebral haemorrhage (AVICH) score showed better outcome prediction for patients with arteriovenous malformation (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH scores. Here we present the results of a multicentre, external validation of the AVICH score. Methods All participating centres (n=11) provided anonymous data on 325 patients to form the Spetzler-Martin (SM) grade, the supplemented SM (sSM) grade, the ICH score and the AVICH score. Modified Rankin score (mRS) at last follow-up (mean 25.6 months) was dichotomized into favourable (mRS 0-2, n=210) and unfavourable (mRS 3-6;n=115). Univariate and AUROC analyses were performed to validate the AVICH score. Results Except nidus structure and AVM size, all single parameters forming the SM, sSM, ICH and AVICH score and the scores itself were significantly different between both outcome groups in the univariate analysis. The AVICH score was confirmed to be the highest predictive outcome score with an AUROC of 0.765 compared with 0.705 for the ICH score and 0.682 for the sSM grade. Conclusion The multicentre-validated AVICH score predicts clinical outcome superior to pre-existing scores. We suggest the routine use of this score for future clinical outcome prediction and in clinical research. Trial registration number NCT02920645.