Establishment of a Reproducible Ischemic Stroke Model in Nestin-GFP Mice with High Survival Rates.

An accumulation of evidence shows that endogenous neural stem/progenitor cells (NSPCs) are activated following brain injury such as that suffered during ischemic stroke. To understand the expression patterns of these cells, researchers have developed mice that express an NSPC marker, Nestin, which is detectable by specific reporters such as green fluorescent protein (GFP), i.e., Nestin-GFP mice. However, the genetic background of most transgenic mice, including Nestin-GFP mice, comes from the C57BL/6 strain. Because mice from this background strain have many cerebral arterial branches and collateral vessels, they are accompanied by several major problems including variable ischemic areas and high mortality when subjected to ischemic stroke by occluding the middle cerebral artery (MCA). In contrast, CB-17 wild-type mice are free from these problems. Therefore, with the aim of overcoming the aforementioned defects, we first crossed Nestin-GFP mice (C57BL/6 background) with CB-17 wild-type mice and then developed Nestin-GFP mice (CB-17 background) by further backcrossing the generated hybrid mice with CB-17 wild-type mice. Subsequently, we investigated the phenotypes of the established Nestin-GFP mice (CB-17 background) following MCA occlusion; these mice had fewer blood vessels around the MCA compared with the number of blood vessels in Nestin-GFP mice (C57BL/6 background). In addition, TTC staining showed that infarcted volume was variable in Nestin-GFP mice (C57BL/6 background) but highly reproducible in Nestin-GFP mice (CB-17 background). In a further investigation of mice survival rates up to 28 days after MCA occlusion, all Nestin-GFP mice (CB-17 background) survived the period, whereas Nestin-GFP mice (C57BL/6 background) frequently died within 1 week and exhibited a higher mortality rate. Immunohistochemistry analysis of Nestin-GFP mice (CB-17 background) showed that GFP+ cells were mainly obverted in not only conventional neurogenic areas, including the subventricular zone (SVZ), but also ischemic areas. In vitro, cells isolated from the ischemic areas and the SVZ formed GFP+ neurosphere-like cell clusters that gave rise to various neural lineages including neurons, astrocytes, and oligodendrocytes. However, microarray analysis of these cells and genetic mapping experiments by Nestin-CreERT2 Line4 mice crossed with yellow fluorescent protein (YFP) reporter mice (Nestin promoter-driven YFP-expressing mice) indicated that cells with NSPC activities in the ischemic areas and the SVZ had different characteristics and origins. These results show that the expression patterns and fate of GFP+ cells with NSPC activities can be precisely investigated over a long period in Nestin-GFP mice (CB-17 background), which is not necessarily possible with Nestin-GFP mice (C57BL/6 background). Thus, Nestin-GFP mice (CB-17 background) could become a useful tool with which to investigate the mechanism of neurogenesis via the aforementioned cells under pathological conditions such as following ischemic stroke.

Brain oxygen tension controls the expansion of outer subventricular zone-like basal progenitors in the developing mouse brain.

The mammalian neocortex shows a conserved six-layered structure that differs between species in the total number of cortical neurons produced owing to differences in the relative abundance of distinct progenitor populations. Recent studies have identified a new class of proliferative neurogenic cells in the outer subventricular zone (OSVZ) in gyrencephalic species such as primates and ferrets. Lissencephalic brains of mice possess fewer OSVZ-like progenitor cells and these do not constitute a distinct layer. Most in vitro and in vivo studies have shown that oxygen regulates the maintenance, proliferation and differentiation of neural progenitor cells. Here we dissect the effects of fetal brain oxygen tension on neural progenitor cell activity using a novel mouse model that allows oxygen tension to be controlled within the hypoxic microenvironment in the neurogenic niche of the fetal brain in vivo. Indeed, maternal oxygen treatment of 10%, 21% and 75% atmospheric oxygen tension for 48 h translates into robust changes in fetal brain oxygenation. Increased oxygen tension in fetal mouse forebrain in vivo leads to a marked expansion of a distinct proliferative cell population, basal to the SVZ. These cells constitute a novel neurogenic cell layer, similar to the OSVZ, and contribute to corticogenesis by heading for deeper cortical layers as a part of the cortical plate.

Hypoxia inducible factor-1α (HIF-1α) is required for neural stem cell maintenance and vascular stability in the adult mouse SVZ.

HIF-1α is a hypoxia-inducible protein that regulates many cell and molecular processes, including those involved in angiogenesis and stem cell maintenance. Prior studies demonstrated constitutive HIF-1α stabilization in neural stem cells (NSCs) of the adult mouse SVZ, but its role there has not been elucidated. Here, we tested the hypothesis that HIF-1α plays an essential role in the maintenance of adult NSCs and stabilization of the SVZ vascular niche using conditional, tamoxifen-inducible Hif1a knock-out mice. We generated nestin-CreER(T2)/R26R-YFP/Hif1a(fl/fl) triple transgenic mice, to enable tamoxifen-inducible Hif1a gene inactivation in nestin-expressing NSCs within the adult SVZ. Hif1a gene deletion resulted in a significant loss of YFP(+) NSCs within the SVZ by 45 d post recombination, which was preceded by significant regression of the SVZ vasculature at 14 d, and concomitant decrease of VEGF expression by NSCs. Loss of YFP(+) NSCs following Hif1a gene inactivation in vivo was likely an indirect consequence of vascular regression, since YFP(+) neurosphere formation over serial passage was unaffected. These results identify NSC-encoded HIF-1α as an essential factor in the maintenance of the adult SVZ, and demonstrate that NSCs within the SVZ maintain the integrity of their vascular niche through HIF-1α-mediated signaling mechanisms.

Bone morphogenetic protein inhibition promotes neurological recovery after intraventricular hemorrhage.

Intraventricular hemorrhage (IVH) results in neural cell death and white matter injury in premature infants. No therapeutic strategy is currently available against this disorder. Bone morphogenetic protein (BMP) signaling suppresses oligodendrocyte development through basic-helix-loop-helix (bHLH) transcription factors and promotes astrocytosis. Therefore, we hypothesized that IVH in premature newborns initiates degeneration and maturation arrest of oligodendrocyte lineage and that BMP inhibition alleviates hypomyelination, gliosis, and motor impairment in the survivors of IVH. To test the hypotheses, a rabbit model of IVH was used in which premature rabbit pups (E29) are treated with intraperitoneal glycerol at 2 h of age to induce IVH; and the pups with IVH exhibit hypomyelination and gliosis at 2 weeks of postnatal age. Maturation of oligodendrocyte lineage was evaluated by specific markers, and the expression of bHLH transcription factors was assessed. BMP levels were measured in both premature rabbit pups and autopsy materials from premature infants. Recombinant human noggin was used to suppress BMP action; and neurobehavioral performance, myelination and gliosis were assessed in noggin-treated pups compared with untreated controls. We found that IVH resulted in apoptosis and reduced proliferation of oligodendrocyte progenitors, as well as arrested maturation of preoligodendrocytes in rabbits. BMP4 levels were significantly elevated in both rabbit pups and human premature infants with IVH compared with controls. Importantly, BMP inhibition by recombinant human noggin restored the levels of phospho-Smad1/5/8, Olig2 transcription factor, oligodendrocyte maturation, myelination, astrocyte morphology, and motor function in premature pups with IVH. Hence, BMP inhibition might enhance neurological recovery in premature infants with IVH.

Ventriculomegaly and postoperative lateral/third ventricular blood as predictors of cerebrospinal fluid diversion following posterior fossa tumor resection.

OBJECTIVE: Postoperative hydrocephalus occurs in one-third of children after posterior fossa tumor resection. Although models to predict the need for CSF diversion after resection exist for preoperative variables, it is unknown which postoperative variables predict the need for CSF diversion. In this study, the authors sought to determine the clinical and radiographic predictors for CSF diversion in children following posterior fossa tumor resection. METHODS: This was a retrospective cohort study involving patients ≤ 18 years of age who underwent resection of a primary posterior fossa tumor between 2000 and 2018. The primary outcome was the need for CSF diversion 6 months after surgery. Candidate predictors for CSF diversion including age, race, sex, frontal occipital horn ratio (FOHR), tumor type, tumor volume and location, transependymal edema, papilledema, presence of postoperative intraventricular blood, and residual tumor were evaluated using a best subset selection method with logistic regression. RESULTS: Of the 63 included patients, 26 (41.3%) had CSF diversion at 6 months. Patients who required CSF diversion had a higher median FOHR (0.5 vs 0.4) and a higher percentage of postoperative intraventricular blood (30.8% vs 2.7%) compared with those who did not. A 0.1-unit increase in FOHR or intraventricular blood was associated with increased odds of CSF diversion (OR 2.9 [95% CI 1.3-7.8], p = 0.02 and OR 20.2 [95% CI 2.9-423.1], p = 0.01, respectively) with an overfitting-corrected concordance index of 0.68 (95% CI 0.56-0.80). CONCLUSIONS: The preoperative FOHR and postoperative intraventricular blood were significant predictors of the need for permanent CSF diversion within 6 months after posterior fossa tumor resection in children.

3D Image Analysis of the Complete Ventricular-Subventricular Zone Stem Cell Niche Reveals Significant Vasculature Changes and Progenitor Deficits in Males Versus Females with Aging.

With age, neural stem cell (NSC) function in the adult ventricular-subventricular zone (V-SVZ) declines, reducing memory and cognitive function in males; however, the impact on females is not well understood. To obtain a global view of how age and sex impact the mouse V-SVZ, we constructed 3D montages after multiplex immunostaining, and used computer-based 3D image analysis to quantify data across the entire niche at 2, 18, and 22 months. We discovered dramatic sex differences in the aging of the V-SVZ niche vasculature, which regulates NSC activity: females showed increased diameter but decreased vessel density with age, while males showed decreased diameter and increased tortuosity and vessel density. Accompanying these vascular changes, males showed significant decline in NSC numbers, progenitor cell proliferation, and more disorganized migrating neuroblast chains with age; however, females did not. By examining the entire 3D niche, we found significant sex differences, with females being relatively spared through very old age.

Consequences of intraventricular hemorrhage in a rabbit pup model.

BACKGROUND AND PURPOSE: Intraventricular hemorrhage (IVH) is a common complication of prematurity that results in neurological sequelae, including cerebral palsy, posthemorrhagic hydrocephalus, and cognitive deficits. Despite this, there is no standardized animal model exhibiting neurological consequences of IVH in prematurely delivered animals. We asked whether induction of moderate-to-severe IVH in premature rabbit pups would produce long-term sequelae of cerebral palsy, posthemorrhagic hydrocephalus, reduced myelination, and gliosis. METHODS: The premature rabbit pups, delivered by cesarean section, were treated with intraperitoneal glycerol at 2 hours postnatal age to induce IVH. The development of IVH was diagnosed by head ultrasound at 24 hours of age. Neurobehavioral, histological, and ultrastructural evaluation and diffusion tensor imaging studies were performed at 2 weeks of age. RESULTS: Although 25% of pups with IVH (IVH pups) developed motor impairment with hypertonia and 42% developed posthemorrhagic ventriculomegaly, pups without IVH (non-IVH) were unremarkable. Immunolabeling revealed reduced myelination in the white matter of IVH pups compared with saline- and glycerol-treated non-IVH controls. Reduced myelination was confirmed by Western blot analysis. There was evidence of gliosis in IVH pups. Ultrastructural studies in IVH pups showed that myelinated and unmyelinated fibers were relatively preserved except for focal axonal injury. Diffusion tensor imaging showed reduction in fractional anisotropy and white matter volume confirming white matter injury in IVH pups. CONCLUSION: The rabbit pups with IVH displayed posthemorrhagic ventriculomegaly, gliosis, reduced myelination, and motor deficits, like humans. The study highlights an instructive animal model of the neurological consequences of IVH, which can be used to evaluate strategies in the prevention and treatment of posthemorrhagic complications.

Hypothesis for lateral ventricular dilatation in communicating hydrocephalus: new understanding of the Monro-Kellie hypothesis in the aspect of cardiac energy transfer through arterial blood flow.

Many theories have been postulated to date regarding mechanisms involved in non-enlargement of the subarachnoid space and enlargement of the ventricles in patients with communicating hydrocephalus, but none have been prove to be definite. Cerebrospinal fluid (CSF) movement is known not to bulk flow but rather pulsatile flow that develops from the energy of the blood flow ejected from the heart, in an isolated system of the intracranial cavity surrounded by a solid skull, as in the Monro-Kellie hypothesis. The authors attempt to explain the mechanisms involved in selective enlargement of the lateral ventricle in patients with communicating hydrocephalus by re-addressing the Monro-Kellie hypothesis with respect to cardiac energy transfer and dissipation by the Windkessel effect. The authors present a concept whereby the large energy of blood flow from the heart that is conveyed to the intracranial artery, arteriole, brain parenchyme, ventricle, and CSF within the confined cranial space as in the Monro-Kellie hypothesis, and which ultimately dissipates to maintain an intracranial energy equilibrium. In the same context, if, for some reason the intracranial equilibrium in the energy transfer and dissipation is changed or disrupted, then structural changes would have to occur to achieve and maintain a new intracranial equilibrium. We postulate that the above described mechanisms are those responsible for the development enlarged of lateral ventricles in patients with communicating hydrocephalus. Structural enlargement of the lateral ventricles in communicating hydrocephalus is a consequence of CSF pathway obstruction and resultantly increased CSF absorption function in the lateral ventricle which markedly increases the pulsatile CSF energy flow returning to the lateral ventricles, thus causing collision of pulsatile CSF flow with the brain parenchyme at the ventricular wall, which subsequently leads to structural enlargement of the lateral ventricles. Also, the collision between the CSF pulsation and brain parenchyme pulsation reduces the Windkessel effect of the brain parenchyme which increases the intracranial artery pulse pressure, which in turn is transmitted to the CSF and increases CSF pulse pressure. This vicious circle results in the high pulse pressure within the lateral ventricle structurally dilating the lateral ventricle. Our theory also explains the relationship between ventricle dilatation and idiopathic intracranial hypertension, venous sinus thrombosis, achondroplasia.

Intraventricular haemorrhage caused by the rupture of a dural arteriovenous malformation of the middle cranial fossa.

Dural arteriovenous malformations of the middle cranial fossa are very rare. Venous drainage flows either through superficial leptomeningeal veins or through the sphenoparietal, sphenopetrous and/or sphenobasilar sinuses. They often have an aggressive course and therefore poor outcome. It is essential to analyse and understand the angioarchitecture of the dural arteriovenous malformations in order to select and plan the correct treatments. We describe an exceptional case of intraventricular haemorrhage caused by the rupture of a dural arteriovenous malformation of the middle cranial fossa. To our knowledge, this is the first case report of such characteristics described in the literature.

The variations of the anterior choroidal artery: an intraoperative study.

AIM: Increasing use of surgical magnification for operations in the territory of the anterior choroidal artery (AChA) has created a need for detailed knowledge of their anatomical variations. The aim of the present study is to examine the anatomical variations of the AChAin patients operated via pterional approach. MATERIAL AND METHODS: The origin and branching pattern of AChAs were observed intraoperatively in 130 patients who were operated via a pterional approach at our center. RESULTS: AChAs arose from the internal carotid artery (ICA) and distal to the posterior communicating artery (PCoA) at a ratio of 70%, from just distal to the original point of the PCoA in 20%, and from just proximal to the ICA bifurcation in 10% of the patients. In 95 cases, AChAs arose from the inferolateral aspect of the ICA in the posterolateral aspect in 27 and from its lateral part in 8 cases. AChAs were found as a single branch at the origins from ICA in 110 patients, as double in 17 cases and as triple in 3 patients. CONCLUSION: Recognition of anatomical variations and microvascular relationships of AChA will allow neurosurgeons to construct a better and safer microdissection plan, to save time and can prevent postoperative neurological deficits.

Heterogeneous Expression of SDF1 Retains Actively Proliferating Neural Progenitors in the Capillary Compartment of the Niche.

The vascular compartment of the adult brain ventricular-subventricular zone (V-SVZ) is a critical regulator of neural stem cell and progenitor function. Blood enters the V-SVZ via arteries and arterioles to capillaries that then connect with venules and veins to return blood to the heart. We found that stromal cell-derived factor 1 (SDF1) is expressed by a subpopulation of V-SVZ vessels, the capillaries, and that actively proliferating neural stem cells (NSCs) and progenitors are preferentially associated with these SDF1-positive vessels. In contrast, slowly dividing or quiescent NSCs are most prevalent near SDF1-negative vessels. By conditional knockout, we found that loss of SDF1 signaling in NSCs stimulates lineage progression and NSC displacement from the vessel niche. With aging, SDF1/CXCR4 signaling is dysregulated, coincident with reduced proliferation and increased displacement of dividing cells from the vasculature. Our findings demonstrate SDF1-based vascular heterogeneity in the niche and suggest that reduced SDF1 signaling contributes to age-related declines in adult neurogenesis.

The microvascular architecture of the choroid plexus in fetal human brain lateral ventricle: a scanning electron microscopy study of corrosion casts.

The microvascular architecture of developing lateral ventricle choroid plexus was investigated by corrosion casting and scanning electron microscopy in human fetuses aged 20 gestational weeks. The areas with different microvascular patterns corresponded to the particular parts of the mature plexus: anterior part, glomus, posterior part, the villous fringe and the free margin. In the posterior part, densely packed parallel arterioles and venules were surrounded by sheath-like capillary networks. Other areas contained compact capillary plexuses of the primary villi: the most prominent, protruding basket- and leaf-shaped plexuses were observed in the villous fringe, whilst less numerous and smaller plexuses occurred in the anterior part and glomus. The capillaries of the plexuses had a large diameter and sinusoidal dilations, and showed the presence of occasional short, blind sprouts indicative of angiogenesis. Short anastomoses between arterioles supplying the plexuses and venules draining them were only rarely observed. In the upper area of the choroid plexus, the superior choroidal vein was surrounded by a capillary network forming small, glomerular or rosette-shapes plexuses. The free margin of the choroid plexus was characterized by flat, multiple, arcade-like capillary loops. The general vascular architecture of the human choroid plexus at 20 gestational weeks seems to be similar to that of postnatal/mature plexus, still lacking, however, the complex vascular plexuses of the secondary villi.

Arterial supply and venous drainage of the choroid plexus of the human lateral ventricle in the prenatal period as revealed by vascular corrosion casts and SEM.

The topography of the arterial supply and venous drainage was visualised by corrosion casting and scanning electron microscopy in the human foetal (20 weeks) choroid plexus of the lateral ventricle. Although secondary villi were not yet present at that developmental stage, the topography of the large arteries and veins almost fully corresponded to that described in adult individuals. The only major difference observed was a lack of the typical tortuosity of the lateral branch of the anterior choroidal artery and of the superior choroidal vein, which probably develops during further expansion of the vascular system associated with the formation of secondary villi.

Effects of electroacupuncture at the conception vessel on proliferation and differentiation of nerve stem cells in the inferior zone of the lateral ventricle in cerebral ischemia rats.

OBJECTIVE: To observe the effects of electroacupuncture (EA) at the Conception Vessel on proliferation and differentiation of the nerve stem cells in the inferior zone of the lateral ventricle in cerebral ischemia rats. METHODS: The model rats were prepared by occlusion of the middle cerebral artery for 2 hours and then by reperfusion. They were randomly divided into two groups: a control group and an EA group. Changes in differentiation and proliferation of the nerve stem cells were observed 7, 14 and 28 days after successful modeling. RESULTS: As compared with the 7-day control group (C-7d group), there was no significant difference (P > 0.05) in the numbers of 5-bromodeoxyuridine (Brdu) positive cells, Brdu/GFAP, Brdu/Nestin and Brdu/Nse double-labeled cells in the inferior zone of the lateral ventricle in the EA group 7 days after modeling. However, in the 14-day EA group (R-14d group) and the 28-day EA group (R-28d group), the numbers of Brdu positive cells and Brdu/GFAP, Brdu/Nestin, Brdu/Nse double-labeled cells significantly increased as compared respectively with the 14-day control (C-14d group) and the 28-day control (C-28d) group (P < 0.05 or P < 0.01). CONCLUSIONS: EA at the Conception Vessel promotes differentiation and proliferation of the nerve stem cells in the inferior zone of the lateral ventricle in the cerebral ischemia rats, and may stimulate differentiation of the proliferous nerve stem cells towards the astrocytes.

Prevention of the Rerupture of Collateral Artery Aneurysms on the Ventricular Wall by Early Surgical Revascularization in Moyamoya Disease: Report of Two Cases and Review of the Literature.

BACKGROUND: Collateral artery aneurysms are a source of intracranial hemorrhage in moyamoya disease. Several reports have shown that surgical revascularization leads to the obliteration of collateral artery aneurysms. However, its effect on the prevention of rebleeding has not been established, and the optimal timing of the operation remains unclear. The purpose of the present study is to evaluate the effects of surgical revascularization and to investigate the optimal operation timing in patients with moyamoya disease who have ruptured collateral artery aneurysms on the ventricular wall. CASE DESCRIPTION: Two patients with moyamoya disease who presented with intraventricular hemorrhage caused by rupture of collateral artery aneurysms on the wall of the lateral ventricle are presented here. In both cases, the aneurysms reruptured approximately 1 month after the initial hemorrhage. Both patients successfully underwent superficial temporal artery-middle cerebral artery anastomosis combined with indirect bypass in the subacute stage. The aneurysms decreased with the development of collateral circulation through the direct bypasses, and rebleeding did not occur after the surgery. CONCLUSIONS: Because ruptured collateral artery aneurysms on the wall of the lateral ventricle in moyamoya disease are prone to rerupture within 1 month, surgical revascularization may be recommended as soon as the patients are stable and able to withstand the operation.

Warfarin-associated intraventricular hemorrhage.

OBJECTIVE: In this study, we have reviewed our experience with anticoagulation-associated intraventricular hemorrhage (IVH). Our goal was to determine if IVH is also an independent prognosticator of fatal outcome in patients with anticoagulation-associated intracerebral hemorrhage (ICH). METHODS: This study is a retrospective analysis of medical records and computed tomographic imaging. Eighty-eight patients with warfarin-associated ICH were analysed, including eight patients with predominant IVH. RESULTS: There was a very low rate of hemorrhage extension in patients with predominant IVH. Despite that, those patients had 50% 30 day mortality. Overall patients with ICH had 45% 30 day mortality. Ventricular extension raised mortality in ICH patients to 75%, while the absence of ventricular extension carried only 23% 30 day mortality. IVH was significantly associated with 30 day mortality (p<0.001). Panventricular extension was uniformly fatal in patients with ICH and carried 75% 30 day mortality in patients with predominant IVH. On a multivariate logistic regression model including age, ICH volume and IVH, ICH volume (p<0.001) and IVH (p = 0.003) remained independently associated with early mortality. CONCLUSION: Extension of anticoagulation-associated ICH into ventricular system caused a high mortality, especially in patients with panventricular involvement. IVH is an independent predictor of early death in these patients. In our experience, the majority of IVH do not expand over time and poor outcome appears to be related to the magnitude of the initial insult.

Intraventricular meningioma with fatal haemorrhage: clinical and autopsy findings.

Only a few cases of intraventricular meningioma have been reported and the association with intracranial haemorrhage is even rarer. More than ever, autopsy findings are scarce. Here, we report a case of primary intraventricular meningioma with intraventricular haemorrhage in a 57-year-old woman. A CT scan of the head initially suggested a malignant brain tumour as the lesion was quite inhomogeneous with hyper- and hypodense sections accompanied by fresh haemorrhage. At autopsy, the tumour was histologically diagnosed as a fibroblastic meningioma WHO-Grade I. The source of haemorrhage was most likely the tumour itself as it contained focally rather large angiomatous and additionally small cavernous vessels and acute haemorrhage in various sections. The assumptive adherence of the tumour to the choroid plexus was probably disrupted by the haematoma.

Intraoperative Visualization of Subependymal Arteries at the Atrium Supplying the Descending Motor Pathway.

OBJECTIVE: We previously disclosed that damage to the subependymal arteries (SEAs) caused by coagulation of the choroid plexus at the atrium can result in infarction within the lateral posterior choroidal artery territory, followed by hemiparesis. The present study describes the intraoperative anatomical findings of the SEAs and choroid plexus at the atrium, which were verified only by a few cadaveric studies. METHODS: Locations of the SEA and descending motor pathway were determined with the neuronavigation system and subcortical electrical stimulation in 8 cases of periatrial brain tumor. Indocyanine green videoangiography was performed to verify the blood flow in the choroid plexus and SEAs. RESULTS: Intraoperative visualization of the SEAs was performed successfully in all patients. The neuronavigation system and subcortical electrical stimulation mapping demonstrated that these SEAs penetrated into the descending motor pathway. Indocyanine green depicted the blood flow of the SEAs entering the wall of the lateral ventricle and adjacent brain parenchyma. The blood flow directions between the SEAs and choroid plexus were not uniform, because the SEAs were filled ahead of the choroid plexus in 3 cases, whereas the choroid plexus was filled first in the other 2 cases. CONCLUSIONS: Manipulations to the inner side of the choroid plexus at the transition from the atrium to the body of lateral ventricle can damage the SEAs. Not only coagulation of the SEAs themselves, but also coagulation of choroid plexus itself may reduce the blood flow in the SEAs, resulting in ischemic complications at descending motor pathway.

Specific Features of SVZ Neurogenesis After Cortical Ischemia: a Longitudinal Study.

Stroke is a devastating disease with an increasing prevalence. Part of the current development in stroke therapy is focused in the chronic phase, where neurorepair mechanisms such as neurogenesis, are involved. In the adult brain, one of the regions where neurogenesis takes place is the subventricular zone (SVZ) of the lateral ventricles. Given the possibility to develop pharmacological therapies to stimulate this process, we have performed a longitudinal analysis of neurogenesis in a model of cortical ischemia in mice. Our results show an initial decrease of SVZ proliferation at 24 h, followed by a recovery leading to an increase at 14d and a second decrease 28d after stroke. Coinciding with the 24 h proliferation decrease, an increase in the eutopic neuroblast migration towards the olfactory bulb was observed. The analysis of the neuroblast ectopic migration from the SVZ toward the lesion showed an increase in this process from day 14 after the insult. Finally, our data revealed an increased number of new cortical neurons in the peri-infarct cortex 65d after the insult. In summary, we report here critical check-points about post-stroke neurogenesis after cortical infarcts, important for the pharmacological modulation of this process in stroke patients.

Surgical approaches to the atrium of the lateral ventricle: microsurgical anatomy.

BACKGROUND: Managing lesions situated in the atrium of the lateral ventricle remains a challenging neurosurgical problem. The purposes of this study were to examine the microsurgical anatomy of the atrium of the lateral ventricle and the optic radiation and to define the differences in the exposure obtained by various surgical approaches. METHODS: Fifteen adult cadaveric specimens were studied using magnification x3 to x40 after perfusion of the arteries and veins with colored silicone. The microsurgical anatomy of the atrium of the lateral ventricle was examined. The relationship between the optic radiation and the atrium was studied using the white matter fiber dissection technique. Surgical approaches to the atrium of the lateral ventricle were examined in stepwise dissection. RESULTS: The medial and inferior walls of the atrium were free from optic radiation fibers. Surgical approaches to the atrium of the lateral ventricle are divided into 3 routes: (1) anterior approach: transsylvian approach, (2) posterior approaches: posterior transcortical, posterior transcallosal, occipital, and supracerebellar transtentorial approaches, and (3) lateral approaches: transtemporal and subtemporal approaches. CONCLUSION: Knowledge of the microsurgical anatomy of the atrium of the lateral ventricle and surrounding vital structures and the choice of an appropriate surgical approach will help surgeons perform safe and minimally invasive surgery.