Natural and surgically imposed anastomoses of the circle of Willis

The efficacy of the circle of Willis as a flow equalizer is well known. Most cerebral macrovasculatures also contain other natural anastomoses which are activated in times of stenotic stress. For the past several decades, neurosurgeons have surgically augmented the cerebral network with additional vessels which further increase the flow of blood to a defrauded region of the brain. It is desirable to know quantitatively what role these anastomoses play in the delivery of blood. Apart from computer simulation, such knowledge remains out of reach to the medical community but with modern simulation techniques, a wealth of information can be made available. This paper presents both time-dependent and period-averaged results of a detailed study of cerebral anastomoses. Four different models of the macrovasculature in the circle of Willis vicinity have been developed, two of which contain an extracranial-intracranial (EC-IC) anastomosis. Five cases were developed to show how the amount of blood flow is related to the sizes of the anastomoses. Since the EC-IC bypass is only marginally beneficial in those patients whose cerebral circulations are well-equipped with naturally occurring anastomotic vessels, procedures should be developed to screen for their presence or absence. The fluid mechanics associated with the EC-IC bypass operation dictate a beneficial result. Since the surgical procedures fail to consistently show reduction in risk even when good grafts have been made, there is an enigma in the study group results.     

The arterial patterns associated with internal carotid disease and cerebral infarcts

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.     

Effect of perfluorochemicals on experimental cerebral ischemia

It has been noted that perfluorochemicals (PFC) which were developed as artificial blood substitutes, protect against ischemic brain injury by their ability to serve as oxygen carriers. It is also known that normovolemic hemodilution (HD) improves cerebral blood flow (CBF) and neurological symptoms in cerebral infarction. However, there are few reports concerning the effect of PFC on the collateral circulation via pial anastomoses in cases of middle cerebral artery (MCA) occlusion. The ability to record the pial arterial blood pressure (PAP) without interfering blood flow now makes it possible to measure the segmental resistance of cerebral vessels. By using this method, one can measure collateral vessel resistance through pial anastomoses following MCA occlusion. In this paper, we studied the protective effects of PFC combined with HD on ischemic brain injury with the focus on the collateral circulation via pial anastomoses following occlusion of the MCA. Twenty adult cats were studied: control, 8; HD, 5; Fluosol (Fluosol-DA), 7. The systemic arterial pressure (SAP) and PeCO2 were continuously monitored. Subsequently the MCA was occluded via the transorbital approach. CBF in the ectosylvian gyrus (central area of the ischemic lesion) was measured by the hydrogen clearance method. A small pial artery about 100 microns in diameter on the exposed ectosylvian gyrus was punctured nonocclusively with a micropipette filled with 2 M sodium chloride which was connected to a servo-null micropressure system (Model 900, W-P Instruments, Inc. U.S.A.). The electroencephalogram (EEG) was recorded from the ectosylvian gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of brain death by computed tomography

The absence of cerebral circulation and electrocerebral silence have served as an accurate index of irreversible brain death. It is proposed that computed tomography (CT) findings be evaluated as confirmatory criteria of brain death. To this end, CT evaluation of 14 patients satisfying the conventional criteria of brain death was performed. A.CT finding of severe compression or disappearance of the ventricular system, or so-called "brain tamponade", was seen in 7 (50%) of the 14 patients. Enhanced contrast CT, especially dynamic CT, usually distinctly reveals the cerebral vessels whenever the cerebral blood flow is preserved; conversely, the lack of enhanced brain structures, even comparing attenuation values, indicates the absence of cerebral blood flow. In 7 (70%) of 10 patients, however, there was enhanced contrast of vascular brain structures, especially the circle of Willis, major cerebral arteries, choroid plexuses, and venous sinuses. It is suggested that this result is due to the improvement of demonstrability by CT. The usefulness of CT in the confirmation of brain death lies in visualization of the pathological changes associated with a dead brain, such as "brain tamponade", and the lack of enhanced contrast indicating the absence of cerebral blood flow. The latter point is still problematic as angiography revealed an extremely low cerebral blood flow in a few cases of "dead brain" patients. It is recommended that cerebral blood flow in brain death be evaluated by dynamic CT scanning and correlated with other methods of cerebral blood flow determination (e.g., intravenous digital subtraction angiography).     

Morphological features of holoprosencephaly

The gross and microscopic features of holoprosencephaly are described on the basis of five representative cases of the alobar and semilobar types, which were investigated by autopsy and/or magnetic resonance imaging. Alobar holoprosencephaly was distinguished from the semilobar type by its gross morphology: the brain neither separated horizontally into the hemispheres nor differentiated axially into the telencephalon and diencephalon. Dorsal cyst, which communicated with the prosencephalic common ventricle through a horseshoe-shaped cerebral mantle defect, was present in all cases. The wall of the cyst, called the ‘dorsal sac’, consisted of ependymal remnants and leptomeninges, in which a layer of dysplastic cerebral tissue or heterotopic glioneural tissue was included in some cases. The dorsal sac extended from the hippocampal ridge and attached posteriorly to the epithalamic structure. The cerebral cortex showed abnormally formed convolutions with agyria, pachygyria or polymicrogyria in all the cases examined, without distinction between the alobar and semilobar types. The microscopic features of these cortices were poorly formed lamination, marginal glioneural heterotopia and periventricular aggregates of neuroblasts. Glomerular structures, which Mere devoid of neurons and consisted of fine dendrites and axons, were found in three cases of this series. These abnormal cortical structures, resulting from disordered neuronal migration, were considered characteristic microscopic findings of the holoprosencephalic brain. The current classification system advocated by DeMyer and Zeman, which depends on surface morphology, does not reflect the maturity of the brain as investigated histopathologically in this series.     

The interplay between the pineal complex and the habenular nuclei in lower vertebrates in the context of the evolution of cerebral asymmetry

This paper presents an overview on the epithalamus of vertebrates, with particular reference to the pineal and to the asymmetrical organization of the habenular nuclei in lower vertebrates. The relationship between the pineal and the habenulae in the course of phylogenesis is here emphasized, taking data in the frog as example. Altogether the data support the hypothesis, put forward also in earlier studies, of a correlation of habenular asymmetry in lower vertebrates with phylogenetic modification of the pineal complex. The present re-visitation was also stimulated by recent data on the asymmetrical expression of Nodal genes, which involves the pineal and habenular structures in zebrafish. The comparative analysis of data, from cyclostomes to mammals, suggests that transformation of epithalamic structures may play an important role in brain evolution. In addition, in mammals, including rodents, a remarkable complexity has evolved in the organization of the habenulae and their functional interactions with the pineal gland. The evolution of these two epithalamic structures seems to open also new perspectives of knowledge on their implication in the regulation of biological rhythms.     

Origin of temperature changes evoked in the brain by sensory stimulation

Temperature was measured in lateral geniculate nucleus, ventrobasal thalamus and inferior colliculus and at the cerebral arteries which supply these structures in monkeys and cats with chronically implanted thermocouples. Animals were studied when they were conscious and when they were anesthetized, during spontaneously occurring changes in behavior and during the presentation of visual, somesthetic, and auditory stimuli. Parallel low-gain and high-gain recorders allowed absolute temperatures to be determined with an accuracy of 0.05 C and temperature changes of 0.0004 C to be resolved. In confirmation of earlier studies, we found that in behaving animals, large changes in temperature occur in cerebral arterial blood and throughout the brain during feeding, sleeping, and arousal. Brain temperature shifts follow blood temperature shifts. The cerebral arterial blood at the circle of Willis is cooler than the brain. When sensory stimuli are presented, the usual thermal response is a rise in temperature at the cerebral arteries followed by a smaller rise in brain temperature. The changes in cerebral arterial blood temperature following sensory stimulation ranged from 0.003 C to 0.133 C in lightly anesthetized animals. The temperature changes in lateral geniculate, ventrobasal thalamus, or inferior colliculus ranged from 0 to 0.067 C and followed the blood temperature changes by 7 to 71 sec. Changes in brain temperature never occurred without a previous change in blood temperature. Blood temperature responses to sensory stimulation were larger in awake animals and in light anesthesia than in deeply anesthetized animals. Blood temperature rises were associated with peripheral cranial vasoconstriction, suggesting that the initial thermal response to sensory stimulation is peripheral autonomic activity and decreased peripheral heat loss. Other investigators observing brain temperature changes following sensory stimulation did not measure cerebral arterial blood temperature and concluded that the shifts in brain temperature were due to changes in neuronal metabolism or cerebral blood flow. The results of the present study do not support this conclusion. When cerebral arterial blood temperature and brain temperature are monitored simultaneously, it is evident that the changes in brain temperature elicited by sensory stimulation are produced by changes in temperature of the cerebral arterial blood.     

False recognition depends on depth of prior word processing: a magnetoencephalographic (MEG) study

Brain activity was measured with a whole head magnetoencephalograph (MEG) during the test phases of word recognition experiments. Healthy young subjects had to discriminate between previously presented and new words. During prior study phases two different levels of word processing were provided according to two different kinds of instructions (shallow and deep encoding). Event-related fields (ERFs) associated with falsely recognized words (false alarms) were found to depend on the depth of processing during the prior study phase. False alarms elicited higher brain activity (as reflected by dipole strength) in case of prior deep encoding as compared to shallow encoding between 300 and 500 ms after stimulus onset at temporal brain areas. Between 500 and 700 ms we found evidence for differences in the involvement of neural structures related to both conditions of false alarms. Furthermore, the number of false alarms was found to depend on depth of processing. Shallow encoding led to a higher number of false alarms than deep encoding. All data are discussed as strong support for the ideas that a certain level of word processing is performed by a distinct set of neural systems and that the same neural systems which encode information are reactivated during the retrieval.     

Effects of depth electrode montage and single-pulse electrical stimulation sites on neuronal responses and effective connectivity

ObjectiveTo determine the optimal depth electrode montages for the assessment of effective connectivity based on single-pulse electrical stimulation (SPES). To determine the effect of SPES locations on the extent of resulting neuronal propagations.MethodsWe studied 14 epilepsy patients who underwent invasive monitoring with depth electrodes and measurement of cortico-cortical evoked potentials (CCEPs) and cortico-cortical spectral responses (CCSRs). We determined the effects of electrode montage and stimulus sites on the CCEP/CCSR amplitudes.ResultsBipolar and Laplacian montages effectively reduced the degree of SPES-related signal deflections at extra-cortical levels, including outside the brain, while maintaining those at the cortical level. SPES of structures more proximal to the deep white matter, compared to the cortical surface, elicited greater CCEPs and CCSRs.ConclusionsOn depth electrode recording, bipolar and Laplacian montages are suitable for measurement of near-field CCEPs and CCSRs. SPES of the white matter axons may induce neuronal propagations to extensive regions of the cerebral cortex.SignificanceThis study helps to establish the practical guidelines on the diagnostic use of CCEPs/CCSRs.     

脑损害昏迷患者意识/昏迷深度的无创监测及量化研究

目的探索通过脑状态监测仪（cerebral state monitor，CSM）获取患者数字化处理的脑电（EEG）信号：脑电指数（脑状态指数cerebral state index，CSI）、肌电指数（eleetromyographic，EMG）、爆发抑制指数（bunt suppression，BS），量化昏迷深度及脑功能损害程度。方法对50例临床脑损害昏迷患者进行CSM监测，分析这些指标与患者的体征反射、听觉诱发电位（AEP）、格拉斯哥昏迷评分（GCS）及格拉斯哥预后评分（GOS）改变的关系。结果CSl0—100是从清醒到深昏迷、脑死亡的一个连续不断的刻度范围，与患者昏迷深度确切相关，与GCS昏迷评分、体征反射相应消涨；特别在恒定刺激作用下的CSI变化，结合BS、EMG能够准确判断患者预后，量化脑功能的改变并赋予其相应的临床意义。结论通过CSM无创实时监测获得量化的、数字化的脑功能损害程度，可以建立起量化的、数字化的脑功能损害临床标准，客观地指导临床救治和把握预后。     

Pathophysiology of age-related cerebral white matter changes

The pathogenesis of age-related cerebral white matter changes (WMC) is still a matter of investigation. Alterations of deep small vessels, such as arteriolosclerosis, are considered to play a central role in the development of WMC. Stenosis or occlusion of small vessels may cause sudden or more chronic ischemia resulting in small areas of necrosis (lacunar infarction) or diffuse alterations consistent with the definition of white matter incomplete infarct. Moreover, the arteriolosclerotic changes may cause loss of autoregulation in the deep white matter and consequent cerebral blood flow fluctuations in response to changes of systemic blood pressure. Both these types of mechanisms may be particularly harmful because the blood supply of the white matter is of the terminal type with scarce anastomoses. Other pathophysiological hypotheses on the origin of WMC have been raised, and they can probably be considered as complementary to the ischemic one. The small vessel alterations could lead to damage of the blood-brain barrier and chronic leakage of fluid and macromolecules in the white matter. The increased interstitial fluid concentration in abnormal white matter may be also a consequence of arterial hypertensive bouts. Genetically determined factors could play an important role in the development of WMC, and at least one disease (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy - CADASIL) characterized by severe leukoencephalopathy exists with a determined genetic origin. It is possible that other genetic factors contribute, by interaction with conventional risk factors, to the development of white matter injury in nonfamilial cases.     

Excitatory amino acid changes in the brains of rhesus monkeys following selective cerebral deep hypothermia and blood flow occlusion

Selective cerebral deep hypothermia and blood flow occlusion can enhance brain tolerance to ischemia and hypoxia and reduce cardiopulmonary complications in monkeys. Excitotoxicity induced by the release of a large amount of excitatory amino acids after cerebral ischemia is the major mechanism underlying ischemic brain injury and nerve cell death. In the present study, we used selective cerebral deep hypothermia and blood flow occlusion to block the bilateral common carotid arteries and/or bilateral vertebral arteries in rhesus monkey, followed by reperfusion using Ringer’s solution at 4°C. Microdialysis and transmission electron microscope results showed that selective cerebral deep hypothermia and blood flow occlusion inhibited the release of glutamic acid into the extracellular fluid in the brain frontal lobe and relieved pathological injury in terms of the ultrastructure of brain tissues after severe cerebral ischemia. These findings indicate that cerebral deep hypothermia and blood flow occlusion can inhibit cytotoxic effects and attenuate ischemic/ hypoxic brain injury through decreasing the release of excitatory amino acids, such as glutamic acid.     

Successive depth variations in microvascular distribution of rat somatosensory cortex

Although hemodynamic-based functional brain imaging techniques are powerful tools to explore the brain functions noninvasively, hemodynamic-based signal is strongly affected by spatial configuration of microvessels. Understanding the quantitative relations between microvascular structure and functional activity is therefore significant to make a valid signal interpretation for the imaging techniques. In the present study, we evaluated depth profiles of microvascular distributions in rat somatosensory subfields (barrel field, forelimb region, trunk region and hindlimb region) and characterized depth variations in microvascular structures, such as locations, lengths and directions of microvessels, throughout the cortical layers (I-VI). To obtain the accurate microvascular structure, we made a customized casting method by using confocal laser scanning microscope. We observed that microvascular distribution successively varied throughout the cortical layers (I-VI) and that the maximum number density of microvessels was consistently found in middle layers (III-V). In addition, superficial layers had relatively long microvessels, almost perpendicular to the cortical surface, whereas middle layers had short microvessels propagating in all directions. These regional differences in microvascular structures were closely related to the somatosensory subfields, e.g., barrel field was the greatest number density of microvessels among the investigated subfields. Based on these observations, we compared microvascular profiles with previously reported distribution patterns of tissue partial pressure of oxygen (pO2). The results showed that tissue pO2 was correlated with microvascular distribution in some but not all of the subfields. This finding shows that detailed microvascular profiles are helpful to investigate causal relationships between microvascular structure and functional activities in cerebral cortex.     

Magnetic resonance evaluation of the cerebral circulation in obstructive arterial disease

BACKGROUND: The aim of the current overview is to highlight the possibilities of magnetic resonance imaging (MRI) in the assessment of patients with obstructive arterial disease. The anatomic and hemodynamic aspects of the extra- and intracranial cerebral circulation were analyzed and show the importance of combining both aspects in studying cerebral hemodynamic changes. RESULTS: Three levels of cerebral circulation are distinguished: blood flow to the brain (level 1); the distribution of blood flow in the brain (level 2), and finally perfusion of the brain (level 3). To investigate the anatomy of the arteries in the neck and the circle of Willis, contrast-enhanced, time-of-flight and phase contrast MR angiography (MRA) are available. To evaluate the hemodynamics at the 1st and 2nd level of the cerebral circulation two-dimensional phase contrast (volume flow and flow direction) MRA can be used. In addition, the distribution of blood via the circle of Willis can be visualized with dynamic MRA. At the 3rd level, measurements of regional brain perfusion can be obtained by injecting gadolinium, dynamic susceptibility contrast MRI, or noninvasively with arterial spin labeling (ASL) MRI. In addition, selective ASL MRI is able to evaluate the perfused territories of individual brain-feeding arteries. CONCLUSION: The currently available MR techniques allow evaluation of the cerebral circulation from the aortic arch upwards towards the microvasculature and brain tissue perfusion in a comprehensive 20-min protocol. The combined use of the described MR methods in patients with steno-occlusive disease will further clarify the pathophysiological relations between the vasculature, perfusion and brain function.     

The anatomy of the late radiation encephalopathy.

The clinico-pathological data and the topography of the lesions were determined in 13 cases of late radiation encephalopathy. In one case the arterial vascularisation was studied by the translucidation technique after filling of the blood vessels with a colloidal barium sulphate solution. The radiation lesions consisted of areas of focal necrosis and of diffuse demyelination and necrosis of the deep cerebral structures and the brain stem. Demyelination was predominantly present in cases of late appearance of the neurological symptoms while necrosis was found in cases with a short latency period. The cerebral cortex and the arcuate fibres were always the most preserved structures. The topography of the focal lesions in the cerebral hemispheres and in the brain stem corresponded well to the vascular supply areas of the deep perforating arteries, while the diffuse lesions always had a predominant distribution in the periventricular arterial end- and border-zones. These observations were also confirmed by a post mortem angiographic study. The present report argues once more for a vascular aetiology as cause of the late radiation encephalopathy.     

Local cerebral blood flow and glucose metabolism in experimental meningeal carcinomatosis

Patients with meningeal carcinomatosis often evolve signs of impairment in higher mental function. Yet, common findings of histological observation are only a sheet of tumor cells on the cortical surface, and no intracerebral mass are noted. To elucidate mechanism of mental disturbances in meningeal carcinomatosis, local cerebral blood flow and glucose metabolism were evaluated in a model of experimental meningeal carcinomatosis. Viable cells (1 X 10(4) of Walker 256 tumor were inoculated into cisterna magna of Wistar rats. Animals were used for autoradiographic study at 1 to 12 days after tumor inoculation. Local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were measured with quantitative autoradiographic technique using 14C-iodoantipyrine and 14C-deoxyglucose as a tracer, respectively. In the early stage of tumor growth (1 to 3 days after tumor inoculation), reduction of LCGU was averaged to be 31% in the cerebral cortex and 28% in the deep structures, whereas reduction of LCBF was 28% in cerebral cortex and 19% in deep structures on average. In the late stage of tumor growth (4 to 12 days after tumor inoculation), average reduction of LCGU was 57% in the cerebral cortex and 47% in the deep structures. On the other hand, reduction of LCBF was averaged to be 42% in the cerebral cortex and 38% in the deep structures in the late stage of the disease. Reduction of LCGU and LCBF was especially evident in the sensory cortices such as parietal cortex, visual cortex and auditory cortex, and in the auditory centers of the brain stem such as medial geniculate body and inferior colliculus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arterial supply of limbic structures in the guinea pig.

This study outlines the vascular territories of the cerebral arteries that originate from the Willis circle to supply limbic structures in the guinea pig brain. The entire cerebral vascular system was visualized in four preliminary experiments by performing superselective microangiographic studies with iodine contrast medium perfusion of the whole brain after in vitro isolation according to a technique described previously (de Curtis et al. [1991] Hippocampus 1:341-354). Subsequently, the perfusion territory of the different arteries that originate from the Willis circle was characterized after cannulation and perfusion of individual arteries with a gelatin solution that contained waterproof black ink. The analysis was performed by identifying the brain regions that contained the black stain on 150-microm-thick coronal sections that were cut after brain fixation with paraformaldehyde for at least 1 week. The middle cerebral artery and the rostral and caudal posterior cerebral arteries supply the limbic cortices and some related subcortical regions. In particular, large portions of the hippocampal formation are supplied by both the rostral posterior cerebral artery and the rostral branch of the caudal posterior cerebral artery, whereas the ventral temporal part of the hippocampus is served exclusively by the rostral posterior cerebral artery. The amygdala, the periamygdaloid cortex, and the piriform cortex are served by the middle cerebral artery and in part by the perforating arteries. The entorhinal, perirhinal, and postrhinal cortices are vascularized by the posterior and middle cerebral arteries, with a very broad overlap between the distal territories of these vessels. The demonstration of an extensive superimposition between the arterial supply of the entorhinal and the perirhinal regions suggests the presence of anastomotic connections that potentially are protective against ischemic events. Such an arrangement was not observed for the arteries that supply the ventral portion of the hippocampal formation and the basolateral amygdala, which showed nonoverlapping boundaries. The pathophysiological consequences of a similar vascular organization are discussed.     

Scalp and depth recordings of induced deep cerebral potentials

A balanced square wave was introduced between two adjacent depth electrodes implanted in the course of studying patients with intractable epilepsy and who were being considered for surgery. The stimulus current was designed so that charge density loading was well within limits of safety to avoid tissue damage. No neuronal activation was seen, and the stimulus intensity was significantly less than that used in subsequent stimulation session for the purpose of eliciting a clinical response and after-discharges. Averaging techniques were used to record the stimulus at distant electrodes both within the cerebrum and on the scalp. The recorded voltage decrement from the source was nearly identical with the theoretical voltage decrement predicted using principles of electric field theory in which the brain was assumed to be a homogeneous conductive medium. When the voltage recorded on the scalp was compared with the voltages recorded from depth electrodes, it was found that the effect of the highly resistive skull on voltage decrement was relatively less the more centric the source. This result also confirmed predictions based on electric field theory. Most significantly, voltages well within the physiologic range introduced in deep mesial temporal lobe structures were recorded from the scalp.     

Dynamic spatio-temporal imaging of early reflow in a neonatal rat stroke model

The aim of the study was to better understand blood-flow changes in large arteries and microvessels during the first 15 minutes of reflow in a P7 rat model of arterial occlusion. Blood-flow changes were monitored by using ultrasound imaging with sequential Doppler recordings in internal carotid arteries (ICAs) and basilar trunk. Relative cerebral blood flow (rCBF) changes were obtained by using laser speckle Doppler monitoring. Tissue perfusion was measured with [¹⁴C]-iodoantipyrine autoradiography. Cerebral energy metabolism was evaluated by mitochondrial oxygen consumption. Gradual increase in mean blood-flow velocities illustrated a gradual perfusion during early reflow in both ICAs. On ischemia, the middle cerebral artery (MCA) territory presented a residual perfusion, whereas the caudal territory remained normally perfused. On reflow, speckle images showed a caudorostral propagation of reperfusion through anastomotic connections, and a reduced perfusion in the MCA territory. Autoradiography highlighted the caudorostral gradient, and persistent perfusion in ventral and medial regions. These blood-flow changes were accompanied by mitochondrial respiration impairment in the ipsilateral cortex. Collectively, these data indicate the presence of a primary collateral pathway through the circle of Willis, providing an immediate diversion of blood flow toward ischemic regions, and secondary efficient cortical anastomoses in the immature rat brain.     

Increased vessel diameter of leptomeningeal anastomoses after hypoxic preconditioning

Recently, cerebral blood flow changes were re-discussed to contribute to tissue protection after preconditioning. In the present study, we demonstrate increased vessel diameters of the leptomeningeal anastomoses after hypoxic preconditioning by visualization of the brain angioarchitecture using the latex perfusion technique. This finding may display the anatomical correlate to previously described perfusion changes after preconditioning.