Crayfish medial giant axons (MGAs) transected in physiological saline form vesicles which interact with each other, pre-existing vesicles, and͞or with the plasmalemma to form an electrical and a physical barrier that seals a cut axonal end within 60 min. The formation of this barrier (seal) was assessed by measuring the decay of injury current at the cut end; its location at the cut end was determined by the exclusion of f luorescent hydrophilic dye at the cut end. When a membrane-incorporating styryl dye was placed in the bath prior to axonal transection and a hydrophilic dye was placed in the bath just after axonal transection, many vesicles near the barrier at the cut axonal end had their limiting membrane labeled with the styryl dye and their contents labeled with the hydrophilic dye, indicating that these vesicles originated from the axolemma by endocytosis. This barrier does not form in Ca 2؉ -free salines. Similar collections of vesicles have been observed at regions of plasmalemmal damage in many cell types. From these and other data, we propose that plasmalemmal lesions in most eukaryotic cells (including axons) are repaired by vesicles, at least some of which arise by endocytosis induced by Ca 2؉ inf low resulting from the plasmalemmal damage. We describe several models by which vesicles could interact with each other and͞or with intact or damaged regions of the plasmalemma to repair small (1-30 m) plasmalemmal holes or a complete transection of the plasmalemma.To survive plasmalemmal damage, a cell must rapidly form a barrier which prevents the gain of deleterious substances (e.g., Ca 2ϩ ) and the loss of essential substances (e.g., proteins). Such a barrier (seal) must consist of a nonconducting lipid layer (i.e., membranous material) that is continuous except for submicroscopic (Ͻ10 nm) pores or channels. The repair of plasmalemmal damage has not been well studied. Repair of transected axons has usually been assumed to occur by a complete collapse and fusion of the axolemmal leaflets at the cut end (1-5) or by the formation of a single, continuous membranous partition at the cut end (6). In contrast, we recently showed that the sealing of transected myelinated earthworm medial giant axons (MGAs) was associated with the aggregation of vesicles at incompletely closed cut ends (7). However, we had no direct evidence whether this accumulation of vesicles and͞or myelin delaminations created a diffusion barrier and where such a barrier might be located with respect to the vesicular aggregation. Furthermore, we did not know the origin of any of the vesicles, whether such vesicles collected at regions of lesser axolemmal damage (e.g., 1-to 30-m holes), or whether vesicles collected at sites of plasmalemmal damage in other axons or in other cell types of other phyla.We now report that crayfish MGAs (unmyelinated) transected in physiological salines containing Ca 2ϩ form vesicular aggregations at incompletely closed cut ends. These vesicles and other membranous structures constitute a barrier to the d...

Vesicles and/or other membranous structures that form after axolemmal damage have recently been shown to repair (seal) the axolemma of various nerve axons. To determine the origin of such membranous structures, (1) we internally dialyzed isolated intact squid giant axons (GAs) and showed that elevation of intracellular Ca2+ >100 microM produced membranous structures similar to those in axons transected in Ca2+-containing physiological saline; (2) we exposed GA axoplasm to Ca2+-containing salines and observed that membranous structures did not form after removing the axolemma and glial sheath but did form in severed GAs after >99% of their axoplasm was removed by internal perfusion; (3) we examined transected GAs and crayfish medial giant axons (MGAs) with time-lapse confocal fluorescence microscopy and showed that many injury-induced vesicles formed by endocytosis of the axolemma; (4) we examined the cut ends of GAs and MGAs with electron microscopy and showed that most membranous structures were single-walled at short (5-15 min) post-transection times, whereas more were double- and multi-walled and of probable glial origin after longer (30-150 min) post-transection times; and (5) we examined differential interference contrast and confocal images and showed that large and small lesions evoked similar injury responses in which barriers to dye diffusion formed amid an accumulation of vesicles and other membranous structures. These and other data suggest that Ca2+ inflow at large or small axolemmal lesions induces various membranous structures (including endocytotic vesicles) of glial or axonal origin to form, accumulate, and interact with each other, preformed vesicles, and/or the axolemma to repair the axolemmal damage.

Arteriovenous malformations (AVMs) of the posterior fossa are complex neurovascular lesions that are less common than their supratentorial counterparts, accounting for < 15% of all AVMs. The majority of patients with these lesions present with intracranial hemorrhage, a factor that has been consistently shown to increase one's risk for subsequent bleeding. Studies have additionally shown a posterior fossa or deep AVM location to portend a more aggressive natural history. The authors reviewed the literature on posterior fossa AVMs, finding their annual rupture rates to be as high as 11.6%, an important factor that underscores the importance of aggressive treatment of lesions amenable to intervention as therapeutic options and results continue to improve.

Adenosine appears to allow safe flow arrest during intracranial aneurysm surgery. This can enhance the feasibility and safety of clipping in select circumstances.

Aneurysmal subarachnoid hemorrhage continues to have high rates of morbidity and mortality for patients despite optimal medical and surgical management. Due to the fact that aneurysmal rupture can be such a catastrophic event, preventive treatment is desirable for high-risk lesions. Given the variability of the literature evaluating unruptured aneurysms regarding basic patient population, clinical practice, and aneurysm characteristics studied, such as size, location, aspect ratio, relationship to the surrounding vasculature, and the aneurysm hemodynamics, a metaanalysis is nearly impossible to perform. This review will instead focus on the various anatomical and morphological characteristics of aneurysms reported in the literature with an attempt to draw broad inferences and serve to highlight pressing questions for the future in our continued effort to improve clinical management of unruptured intracranial aneurysms.