Despite remarkable progress, the microsurgical extirpation of cerebral arteriovenous malformations (AVMs) even by experienced neurosurgeons is not always easy or safe. This article focuses on how to render AVM surgery safer, and offers strategies and tactics for avoiding perilous bleeding and preserving postoperative neurological function. Our treatment strategies and surgical techniques are offered from the operating surgeon's perspective. An understanding of pathophysiology of cerebral AVMs is important for their appropriate surgical treatment. Sophisticated neuroimaging techniques and scrupulous neurophysiological examinations alert to possible complications, and improved surgical approaches help to minimize the sequelae of unanticipated complications. At the early stage of cerebral AVM surgery, extensive dissection of the sulci, fissures, and subarachnoid cistern should be performed to expose feeders, nidus, and drainers. Problems with the surgery of large and/or deep-seated lesions are exacerbated when arterial bleeding from the nidus continues even after all major feeders are thought to have been occluded. We routinely place catheters for angiography at the surgery of complex AVMs to find missing feeding arteries or to identify the real-time hemodynamic status of the lesion. Temporary clip application on feeders and less coagulation of the nidus is necessary to control intranidal pressure and to avoid uncontrollable bleeding from the nidus and adjacent brain. Intraoperative navigation images superimposed on tractography images can provide us with valuable information to minimize neurological deficits. Deeper insight into AVM nature and into events that occur during AVM surgery as well as the inclusion of molecular biological approaches will open new horizons for the safe and effective treatment of AVMs.
Summary: Proper assessment of endovascular patency after carotid stent (CS) placement with carotid color-coded duplex sonography (CCCD) can be difficult. We investigated the usefulness of contrast-enhanced (CE) CCCD for post-CS follow-up. CCCD images could not depict the entire bloodstream in overlapped stents and in highly positioned stents. CE-CCCD images, however, did provide anatomic information almost equivalent to that of intra-arterial angiography. CE-CCCD is useful in screening for post-CS restenosis.
A 64-year-old woman presented with the history of transient global amnesia. Magnetic resonance imaging with contrast medium showed a lobulated heterogeneously enhanced cystic lesion attached to the superior surface of the right tentorium, indenting the right temporal lobe laterally and midbrain medially. A small part of the lesion was located under the right tentorium and did not involve the right trigeminal nerve. The lesion was subtotally resected via the subtemporal approach and did not affect the trochlear and trigeminal nerves. Histological examination showed that the lesion was schwannoma. Intracranial schwannomas usually arise from the cranial nerves. The present case of tentorial schwannoma not associated with the cranial nerves is extremely rare. Schwannoma should be included in the differential diagnosis of tumors arising from the tentorium.
Given the social importance of intracranial aneurysm as a major cause of a lethal subarachnoid hemorrhage, clarification of mechanisms underlying the pathogenesis of this disease is essential for improving poor prognosis once after rupture. Previous histopathological analyses of human aneurysm walls have revealed the presence of T cells in lesions suggesting involvement of this type of cell in the pathogenesis. However, it remains unclear whether T cell actively participates in intracranial aneurysm progression. To examine whether T cell is involved in aneurysm progression, intracranial aneurysm model of rat was used. In this model, aneurysm is induced by increase in hemodynamic force loaded on bifurcation site of intracranial arteries where aneurysms are developed. Deficiency in T cells and pharmacological inhibition of T cell function were applied to this model. CD3-positive T cells were present in human aneurysm walls, whose number was significantly larger compared with that in control arterial walls. Deficiency in T cells in rats and pharmacological inhibition of T cell function by oral administration of Cyclosporine A both failed to affect intracranial aneurysm progression, degenerative changes of arterial walls and macrophage infiltration in lesions. Although T cells are detectable in intracranial aneurysm walls, their function is dispensable for macrophage-mediated inflammation and degenerative changes in arterial walls, which presumably leads to intracranial aneurysm progression.
Subarachnoid hemorrhage due to the rupture of a cerebral aneurysm is a life-threatening disease. Despite this, the detailed mechanisms underlying the initiation and progression of cerebral aneurysm are unclear. The relation of hypercholesterolemia and apolipoprotein E (ApoE) to cerebral aneurysm formation, has been unclear until now. We used, in the present study, a previously established cerebral aneurysm model of rats and mice whose histological features were closely similar to human cerebral aneurysms. ApoE protein was expressed mainly in the endothelial cells of arterial walls both in control arteries and cerebral aneurysms. The expression of ApoE was reduced during aneurysm formation in the immunohistochemistry. The mRNA expression of ApoE in arterial walls was not different between the controls and cerebral aneurysms. Owing to the deficiency of ApoE, mice presented marked hypercholesterolemia, but there was no difference in cerebral aneurysm formation. In the present study, we clarified that ApoE was not responsible for cerebral aneurysm formation.
To clarify the clinical usefulness of preoperative fibre-tracking in affected pyramidal tracts for intraoperative monitoring during the removal of brain tumours from patients with motor weakness.We operated on 10 patients with mild to moderate motor weakness caused by brain tumours located near the pyramidal tracts under local anaesthesia. Before surgery, we performed fibre-tracking imaging of the pyramidal tracts and then transferred this information to the neuronavigation system. During removal of the tumour, motor function was evaluated with motor evoked potentials elicited by cortical/subcortical electrical stimulation and with voluntary movement.In eight patients, the locations of the pyramidal tracts were estimated preoperatively by fibre-tracking; motor evoked potentials were elicited on the motor cortex and subcortex close to the predicted pyramidal tracts. In the remaining two patients, in which fibre-tracking of the pyramidal tracts revealed their disruption surrounding the tumour, cortical/subcortical electrical stimulation did not elicit responses clinically sufficient to monitor motor function. In all cases, voluntary movement with mild to moderate motor weakness was extensively evaluated during surgery and was successfully preserved postoperatively with appropriate tumour resection.Preoperative fibre-tracking could predict the clinical usefulness of intraoperative electrical stimulation of the motor cortex and subcortical fibres (ie, pyramidal tracts) to preserve affected motor function during removal of brain tumours. In patients for whom fibre-tracking failed preoperatively, awake surgery is more appropriate to evaluate and preserve moderately impaired muscle strength.
Changes in the density of cerebroarterial nerve fibers containing calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP)-like substance, as well as changes in dilatory responses of isolated cerebral arteries to these neuropeptides, after subarachnoid hemorrhage (SAH) were examined in dogs. Moreover, the effects of these neuropeptides to the experimentally produced cerebral arterial spasm were also examined in dogs. SAH was produced by a single injection of fresh autologous arterial blood (1 ml/kg body weight) or double injection of arterial blood (0.5 ml/kg body weight, 48 hours apart) into the cisterna magna. Constriction of basilar artery was most prominent on Day 3 in the single injection model, and on Day 7 in the double injection model. The density of nerve fibers with CGRP-or VIP-like immunoreactivity (LI) was markedly decreased during 7-14 days or 3-7 days after SAH. Vasodilatory actions of CGRP and VIP to isolated basilar artery in vitro were markedly impaired during acute stage of post-SAH period and significantly enhanced during chronic stage of post-SAH period. Intracisternal bolus injection of 10(-10) mol/kg CGRP completely reversed cerebral arterial constriction on Day 3 of single injection SAH model, and intracisternal injection of 10(-11) to 2 x 10(-10) mol/kg CGRP reversed cerebral vasospasm dose-dependently. Intraarterial injection of CGRP could not reversed cerebral arterial constriction. The effects of VIP was much weaker than CGRP.
Japan has been reported to have the highest (and increasing) incidence of subarachnoid hemorrhage (SAH) in the world. However, there has never been a report on the nationwide incidence rate and recent trends for SAH in Japan. In this register-based study, the authors aimed to clarify the estimated nationwide SAH incidence rate and the recent trend in SAH incidence in Japan and the reasons for any changes in this trend.
The treatment of dural arteriovenous fistulas (DAVFs) at the foramen magnum remains controversial by reason that DAVFs appearing from the foramen magnum represent only a minority of spinal DAVFs. We present our treatment for an asymptomatic patient suffering from a foramen magnum DAVF. A 53-year-old man presented to our hospital with the complaint of a floating sensation. Although there was no subarachnoid hemorrhage or cerebral infarction on magnetic resonance imaging, a magnetic resonance angiography revealed a number of dilated veins and a large varix surrounding the medulla oblongata. Cerebral digital subtraction angiography (DSA) showed a foramen magnum DAVF fed by the neuromeningeal branch of the left ascending pharyngeal artery and occipital artery, draining into the posterior spinal vein. Occlusion of the fistula was achieved by a microsurgical technique combined with a feeder occlusion using transarterial coil embolization, without complications. We verified the complete occlusion on post-operative cerebral DSA. While this combined therapy was already established for the treatment of DAVFs, there were no reports of the combined therapy for foramen magnum DAVFs. This treatment was considered to be useful for foramen magnum DAVFs, especially those DAVFs at the foramen magnum with a number of dilated veins and a large varix.
