Dynamic Mechanism of Cerebral Venous Disruption: Longitudinal Evidence From a Community-Based Cohort.

BACKGROUND: This study aims to investigate the temporal and spatial patterns of structural brain injury related to deep medullary veins (DMVs) damage. METHODS AND RESULTS: This is a longitudinal analysis of the population-based Shunyi cohort study. Baseline DMVs numbers were identified on susceptibility-weighted imaging. We assessed vertex-wise cortex maps and diffusion maps at both baseline and follow-up using FSL software and the longitudinal FreeSurfer analysis suite. We performed statistical analysis of global measurements and voxel/vertex-wise analysis to explore the relationship between DMVs number and brain structural measurements. A total of 977 participants were included in the baseline, of whom 544 completed the follow-up magnetic resonance imaging (age 54.97±7.83 years, 32% men, mean interval 5.56±0.47 years). A lower number of DMVs was associated with a faster disruption of white matter microstructural integrity, presented by increased mean diffusivity and radial diffusion (ß=0.0001 and SE=0.0001 for both, P=0.04 and 0.03, respectively), in extensive deep white matter (threshold-free cluster enhancement P<0.05, adjusted for age and sex). Of particular interest, we found a bidirectional trend association between DMVs number and change in brain volumes. Specifically, participants with mild DMVs disruption showed greater cortical enlargement, whereas those with severe disruption exhibited more significant brain atrophy, primarily involving clusters in the frontal and parietal lobes (multiple comparison corrected P<0.05, adjusted for age, sex, and total intracranial volume). CONCLUSIONS: Our findings posed the dynamic pattern of brain parenchymal lesions related to DMVs injury, shedding light on the interactions and chronological roles of various pathological mechanisms.

Middle third falcine meningiomas-surgical nuances for cortical venous preservation.

PURPOSE: To improve postoperative outcome in middle third falcine meningiomas by cortical venous preservation. BACKGROUND: Falcine meningiomas arise from the falx and do not involve the superior sagittal sinus (SSS). Their complete resection is often associated with the risk of venous infarction in the eloquent cortex due to overlying superficial cortical veins on the tumors. METHOD: We report one case of middle third falcine meningioma, where we used the posterior interhemispheric corridor for tumor approach. CONCLUSION: Use of the posterior interhemispheric approach, carefully raised bone flap, along with sharp dissection and vein reinforcement using fibrin glue can help to preserve the cortical veins while resecting the falcine meningiomas.

Oculomotor Nerve Palsy Induced by a Cerebral Developmental Venous Anomaly: A Case Report and Comprehensive Review.

BACKGROUND Symptoms caused by developmental venous anomalies (DVAs) are usually mild and unspecific. Despite the benign nature of DVAs, they can occasionally be symptomatic. CASE REPORT A 67-year-old woman presented with sudden diplopia and left eyelid ptosis for 10 days. A neurologic examination revealed left complete oculomotor nerve palsy. Other neurologic deficits, including eye pain or pulsatile tinnitus, were not detected. Furthermore, the visual acuity was normal. Additionally, no retinal hemorrhage, venous dilatation, or fundus tortuosity were observed. No ischemia lesions or neoplasms were observed in MRI, and no widening or enhancement of the cavernous sinus was detected in post-contrast T1-weighted images, but magnetic resonance tomography cerebral angiography (MRTA) detected an offending vessel compressing the left oculomotor nerve in the fossa interpeduncular. We hypothesized that oculomotor nerve palsy (ONP) was caused by an abnormal arterial structure. However, digital subtraction angiography (DSA) revealed no aneurysm or abnormal arterial structure in the arterial phase, while a tortuous and dilated collecting vein was detected in the venous phase, connecting the left temporal lobe to the left cavernous sinus. This indicated a typical caput medusae appearance, suggesting the mechanism of oculomotor palsy caused by compressive impairment of the DVA. The patient refused microvascular decompression surgery, and ONP persisted after 30 days. Management was conservative, with spontaneous resolution at 60 days and no recurrence during the 2-year follow-up. CONCLUSIONS ONP is rarely caused by DVAs, which are easily ignored due to their benign nature. Cerebral vein examinations are advised for patients exhibiting clinical symptoms of unknown etiology.

Spontaneous thrombosis of type II vein of Galen aneurysmal malformation: a case report.

Vein of Galen malformations (VGAMs) are rare and complex congenital brain vascular anomalies that pose significant diagnostic and treatment challenges. The natural history of this type of vascular anomaly is very poor, with many patients succumbing to complications such as congestive heart failure, hydrocephalus, and brain parenchymal injury. Although the clinical course of most VGAMs was considered unfortunate, with meticulous imaging, a group of lesions with a more placid presentation and course can be identified.

In vivo mapping of hippocampal venous vasculature and oxygenation using susceptibility imaging at 7T.

Mapping the small venous vasculature of the hippocampus in vivo is crucial for understanding how functional changes of hippocampus evolve with age. Oxygen utilization in the hippocampus could serve as a sensitive biomarker for early degenerative changes, surpassing hippocampal tissue atrophy as the main source of information regarding tissue degeneration. Using an ultrahigh field (7T) susceptibility-weighted imaging (SWI) sequence, it is possible to capture oxygen-level dependent contrast of submillimeter-sized vessels. Moreover, the quantitative susceptibility mapping (QSM) results derived from SWI data allow for the simultaneous estimation of venous oxygenation levels, thereby enhancing the understanding of hippocampal function. In this study, we proposed two potential imaging markers in a cohort of 19 healthy volunteers aged between 20 and 74 years. These markers were: 1) hippocampal venous density on SWI images and 2) venous susceptibility (Δχvein) in the hippocampus-associated draining veins (the inferior ventricular veins (IVV) and the basal veins of Rosenthal (BVR) using QSM images). They were chosen specifically to help characterize the oxygen utilization of the human hippocampus and medial temporal lobe (MTL). As part of the analysis, we demonstrated the feasibility of measuring hippocampal venous density and Δχvein in the IVV and BVR at 7T with high spatial resolution (0.25 × 0.25 × 1 mm3). Our results demonstrated the in vivo reconstruction of the hippocampal venous system, providing initial evidence regarding the presence of the venous arch structure within the hippocampus. Furthermore, we evaluated the age effect of the two quantitative estimates and observed a significant increase in Δχvein for the IVV with age (p=0.006, r2 = 0.369). This may suggest the potential application of Δχvein in IVV as a marker for assessing changes in atrophy-related hippocampal oxygen utilization in normal aging and neurodegenerative diseases such as AD and dementia.

Intracranial dural arteriovenous fistulas: association with cerebral venous thrombosis, baseline aggressiveness, and clinical outcomes. A retrospective multicenter study on 263 consecutive patients and literature review.

OBJECTIVE: The pathogenesis of intracranial dural arteriovenous fistulas (icDAVFs) is controversial. Cerebral vein thrombosis (CVT) and venous hypertension are recognized predisposing factors. This study aimed to evaluate the incidence of association between icDAVF and CVT and describe baseline aggressiveness and clinical outcomes for icDAVFs associated with CVT. The authors also performed a literature review of studies reporting icDAVF associated with CVT. METHODS: Two hundred sixty-three consecutive patients in two university hospitals with confirmed icDAVFs were included. A double-blind imaging review was performed to determine the presence or absence of CVT close or distant to the icDAVF. Location, type (using the Cognard classification), aggressiveness of the icDAVF, clinical presentation, treatment modality, and clinical and/or angiographic outcomes at 6 months were also collected. All prior brain imaging was analyzed to determine the natural history of onset of the icDAVF. RESULTS: Among the 263 included patients, 75 (28.5%) presented with a CVT concomitant to their icDAVF. For 18 (78.3%) of 23 patients with previous brain imaging available, CVT preceding the icDAVF was proven (6.8% of the overall population). Former/active smoking (OR 2.0, 95% CI 1.079-3.682, p = 0.022) and prothrombogenic status (active inflammation or cancer/coagulation trouble) were risk factors for CVT associated with icDAVF (OR 3.135, 95% CI 1.391-7.108, p = 0.003). One hundred eighty-seven patients (71.1%) had a baseline aggressive icDAVF, not linked to the presence of a CVT (p = 0.546). Of the overall population, 11 patients (4.2%) presented with spontaneous occlusion of their icDAVF at follow-up. Seven patients (2.7%) died during the follow-up period. Intracranial DAVF + CVT was not associated with a worse prognosis (modified Rankin Scale score at 3-6 months: 0 [interquartile range {IQR} 0-1] for icDAVF + CVT vs 0 [IQR 0-0] for icDAVF alone; p = 0.055). CONCLUSIONS: This was one of the largest studies focused on the incidence of CVT associated with icDAVF. For 6.8% of the patients, a natural history of CVT leading to icDAVF was proven, corresponding to 78.3% of patients with previous imaging available. This work offers further insights into icDAVF pathophysiology, aiding in identifying high-risk CVT patients for long-term follow-up imaging. Annual imaging follow-up using noninvasive vascular imaging (CT or MR angiography) for a minimum of 3 years after the diagnosis of CVT should be considered in high-risk patients, i.e., smokers and those with prothrombogenic status.

VICTR: Venous transit time imaging by changes in T1 relaxation.

PURPOSE: Abnormalities in cerebral veins are a common finding in many neurological diseases, yet there is a scarcity of MRI techniques to assess venous hemodynamic function. The present study aims to develop a noncontrast technique to measure a novel blood flow circulatory measure, venous transit time (VTT), which denotes the time it takes for water to travel from capillary to major veins. METHODS: The proposed sequence, venous transit time imaging by changes in T1 relaxation (VICTR), is based on the notion that as water molecules transition from the tissue into the veins, they undergo a change in T1 relaxation time. The validity of the measured VTT was tested by studying the VTT along the anatomically known flow trajectory of venous vessels as well as using a physiological vasoconstrictive challenge of caffeine ingestion. Finally, we compared the VTT measured with VICTR MRI to a bolus-tracking method using gadolinium-based contrast agent. RESULTS: VTT was measured to be 3116.3 ± 326.0 ms in the posterior superior sagittal sinus (SSS), which was significantly longer than 2865.0 ± 390.8 ms at the anterior superior sagittal sinus (p = 0.004). The test-retest assessment showed an interclass correlation coefficient of 0.964. VTT was significantly increased by 513.8 ± 239.3 ms after caffeine ingestion (p < 0.001). VTT measured with VICTR MRI revealed a strong correlation (R = 0.84, p = 0.002) with that measured with the contrast-based approach. VTT was found inversely correlated to cerebral blood flow and venous oxygenation across individuals. CONCLUSION: A noncontrast MRI technique, VICTR MRI, was developed to measure the VTT of the brain.

Occipital emissary vein existence and its impact on the diagnosis of idiopathic intracranial hypertension in pediatric patients.

PURPOSE: This study aimed to investigate the efficacy of occipital emissary vein (OEV) detection in the diagnosis of idiopathic intracranial hypertension (IHH) in the pediatric age group, and to compare the prevalence and luminal diameter of OEV in patients with IHH and in healthy control subjects. METHODS: Conventional magnetic resonance imaging findings were assessed in the patients with IHH and in healthy control subjects who were under the age of 18, by two observers. The presence and luminal dimension of OEV and transverse sinus stenosis were also evaluated and compared between these two groups with magnetic resonance venography techniques. RESULTS: The rate of OEV existence was 7 times higher in the IIH group compared to the control group based on the second observer outcome (p = 0.010, OR = 7.0), with a very good interobserver agreement (Ƙ = 0.85). The dimension of OEV ranged between 0.6 and 2.5 mm. There was no correlation found between the opening pressure and the dimension of OEV (p = 0.834). CONCLUSION: In conclusion, OEV existence could be an additional radiological finding for diagnosing IHH among pediatric patients, alongside other conventional findings.

The Basal or Sphenopetrosal Superficial Middle Cerebral Vein Type.

Background and Objectives: The adult superficial middle cerebral vein (SMCV) commonly drains into the middle cranial fossa. However, different embryonic types persist, in which the SMCV drains into the lateral sinus. The basal type of SMCV coursing on the middle fossa floor is a scarce variant. Materials and Methods: During a retrospective study of archived computed tomography angiography (CTA) and magnetic resonance angiography (MRA) files, three rare adult cases of the basal or sphenopetrosal type of SMCV were found and further documented. Results: In the first case, which was evaluated via CTA, the basal type of SMCV formed a sagittal loop. It continued on the middle fossa floor, over a dehiscent tegmen tympani, to drain into the lateral sinus. In the second case, documented via MRA, the basal type of SMCV's anterior loop was in the coronal plane and closely related to the internal carotid artery and the cavernous sinus. It continued with the basal segment over a dehiscent glenoid fossa of the temporomandibular joint (TMJ). In the third case, documented via CTA, the initial cerebral part of the SMCV had a large fenestration. The middle fossa floor coursed within a well-configured sulcus of the SMCV and received a tributary through the tympanic roof. Its terminal had a tentorial course. Conclusions: Beyond the fact that such rare variants of the SMCV can unexpectedly interfere with specific approaches via the middle fossa, dehiscences of the middle fossa floor beneath such variants can determine otic or TMJ symptoms. Possible loops and fenestrations of the SMCV should be considered and documented preoperatively.

[Posterior Fossa Anatomy for Microvascular Decompression Surgery].

In most microvascular decompression surgeries, surgical maneuvers are performed within normal anatomical structures without any neoplasms. Thus, detailed anatomical knowledge is essential to perform safe and efficient procedures. "Rule of 3" by Rhoton AL Jr. is helpful for understanding not only the anatomy of the posterior fossa but also the three neurovascular compression syndromes. The cerebellar arteries and posterior fossa veins have substantial variability, but a basic understanding of their typical patterns is useful to explore individual cases. To use adequate surgical approaches through the cerebellar tentorial or petrosal surface in individual trigeminal neuralgia surgeries, anatomical knowledge of the bridging veins on the tentorial(the bridging veins into the tentorial sinus)and petrosal surfaces(the superior petrosal vein)is crucial. Fissure openings help to minimize cerebellar retraction, similarly to the sylvian fissure dissection in supratentorial surgeries.

[Microvascular Decompression for Trigeminal Neuralgia Due to Venous Compression].

In microvascular decompression surgery for trigeminal neuralgia, the veins are essential as an anatomical frame for the microsurgical approach and as an offending vessel to compress the trigeminal nerve. Thorough arachnoid dissection of the superior petrosal vein and its tributaries provides surgical corridors to the trigeminal nerve root and enables the mobilization of the bridging, brainstem, and deep cerebellar veins. It is necessary to protect the trigeminal nerve by coagulating and cutting the offending vein. We reviewed the clinical features of trigeminal neuralgia caused by venous decompression and its outcomes after microvascular decompression. Among patients with trigeminal neuralgia, 4%-14% have sole venous compression. Atypical or type 2 trigeminal neuralgia may occur in 60%-80% of cases of sole venous compression. Three-dimensional MR cisternography and CT venography can help in detecting the offending vein. The transverse pontine vein is the common offending vein. The surgical cure and recurrence rates of trigeminal neuralgia with venous compression are 64%-75% and 23%, respectively. Sole venous compression is a unique form of trigeminal neuralgia. Its clinical characteristics differ from those of trigeminal neuralgia caused by arterial compression. Surgical procedures to resolve venous compression include nuances in safely handling venous structures.

Neuroimaging of Neonatal Stroke: Venous Focus.

Perinatal venous infarcts are underrecognized clinically and at imaging. Neonates may be susceptible to venous infarcts because of hypercoagulable state, compressibility of the dural sinuses and superficial veins due to patent sutures, immature cerebral venous drainage pathways, and drastic physiologic changes of the brain circulation in the perinatal period. About 43% of cases of pediatric cerebral sinovenous thrombosis occur in the neonatal period. Venous infarcts can be recognized by ischemia or hemorrhage that does not respect an arterial territory. Knowledge of venous drainage pathways and territories can help radiologists recognize characteristic venous infarct patterns. Intraventricular hemorrhage in a term neonate with thalamocaudate hemorrhage should raise concern for internal cerebral vein thrombosis. A striato-hippocampal pattern of hemorrhage indicates basal vein of Rosenthal thrombosis. Choroid plexus hemorrhage may be due to obstruction of choroidal veins that drain the internal cerebral vein or basal vein of Rosenthal. Fan-shaped deep medullary venous congestion or thrombosis is due to impaired venous drainage into the subependymal veins, most commonly caused by germinal matrix hemorrhage in the premature infant and impeded flow in the deep venous system in the term infant. Subpial hemorrhage, an underrecognized hemorrhage stroke type, is often observed in the superficial temporal region, and its cause is probably multifactorial. The treatment of cerebral sinovenous thrombosis is anticoagulation, which should be considered even in the presence of intracranial hemorrhage. ©RSNA, 2024 Test Your Knowledge questions in the supplemental material and the slide presentation from the RSNA Annual Meeting are available for this article.

Use of greyscale and Doppler ultrasound in initial evaluation and follow-up of neurovascular malformations in children.

Pediatric intracranial arteriovenous shunts are rare vascular malformations that can be diagnosed prenatally or postnatally, as an incidental finding or due to complications. We propose a review of cerebral vascular malformations in newborns and infants with special emphasis on neurosonography and Doppler ultrasound as the first diagnostic method. Sonography can thus contribute in the planning of further studies that are always necessary, and in post-therapy follow-up.

The benefit of favorable venous outflow profile is mediated through reduced microvascular dysfunction in acute ischemic stroke.

INTRODUCTIONS: Venous outflow (VO) is emerging as a marker of microvascular integrity in acute ischemic stroke. Using hemorrhagic transformation (HT) and infarct growth as mediators, we tested whether a favorable VO profile benefited functional outcome by reducing consequences of microvascular dysfunction. PATIENTS AND METHODS: Patients receiving thrombectomy in three comprehensive stroke centers due to acute anterior circulation occlusion were included. VO was assessed semi-quantitatively by the opacification of ipsilateral vein of Labbé, Trolard and superficial middle cerebral vein. HT was graded on follow-up CT. Infarct growth volume (IGV) was the difference of final infarct volume and baseline core volume. The association of VO and functional independence (90-day modified Rankin Scale ⩽ 2) was examined by logistic regression. Mediation analysis was performed among VO, HT or IGV, and functional outcome in patients with or without recanalization, respectively. RESULTS: In 242 patients analyzed, VO was strongly correlated with functional independence and VO ⩾ 4 was defined favorable. In 175 patients recanalized, favorable VO was associated with a reduced risk of HT (OR = 0.82, 95% CI 0.71-0.95, p = 0.008), which accounted for 13.1% of the association between VO and favorable outcome. In 67 patients without recanalization, favorable VO was associated with decreased IGV (ß = -0.07, 95% CI -0.11 to -0.02, p = 0.007). The association of favorable VO and functional independence was no longer significant (aOR = 4.84, 95% CI 0.87-38.87, p = 0.089) after including IGV in the model, suggesting a complete mediation. DISCUSSION AND CONCLUSION: In patients with acute anterior large vessel occlusion, the clinical benefit of VO may be mediated through reduced microvascular dysfunction.

Cortical Brush Sign: A Novel Finding on Thin-slice 3T Susceptibility-weighted Imaging in Acute Cerebral Infarct and Cerebral Venous Thrombosis.

We observed a new SWI finding, "cortical brush sign," that represents prominent venous structures in the cortex of patients with acute cerebral infarct with or without moyamoya disease and cerebral venous thrombosis. The cortical brush sign disappeared on follow-up SWI in all cases. Cortical brush sign may help to understand the pathophysiology of venous structures in the cortex at acute phase.

Early neurological deterioration in patients with acute ischemic stroke is linked to unfavorable cerebral venous outflow.

INTRODUCTION: Early neurological deterioration (END) is associated with poor outcomes in patients with acute ischemic stroke due to large vessel occlusion (AIS-LVO). Causes of END after mechanical thrombectomy (MT) include unsuccessful recanalization and reperfusion hemorrhages. However, little is known about END excluding the aforementioned causes. We aimed to investigate factors associated with unexplained END (ENDunexplained) with regard to the cerebral collateral status. PATIENTS AND METHODS: Multicenter retrospective study of AIS-LVO patients with successful MT (mTICI 2b-3). On admission CT angiography (CTA), pial arterial collaterals and venous outflow (VO) were assessed using the modified Tan-Scale and the Cortical Vein Opacification Score (COVES), respectively. ENDunexplained was defined as an increase in NIHSS score of ⩾ 4 within the first 24 hours after MT without parenchymal hemorrhage on follow-up imaging. Multivariable regression analyses were performed to examine factors of ENDunexplained and unfavorable functional outcome (modified Rankin Scale score 3-6). RESULTS: A total of 620 patients met the inclusion criteria. ENDunexplained occurred in 10% of patients. While there was no significant difference in pial arterial collaterals, patients with ENDunexplained exhibited more often unfavorable VO (81% vs. 53%; P < 0.001). Unfavorable VO (aOR [95% CI]; 2.56 [1.02-6.40]; P = 0.045) was an independent predictor of ENDunexplained. ENDunexplained was independently associated with unfavorable functional outcomes at 90 days (aOR [95% CI]; 6.25 [2.06-18.94]; P = 0.001). DISCUSSION AND CONCLUSION: Unfavorable VO on admission CTA was associated with ENDunexplained. ENDunexplained was independently linked to unfavorable functional outcomes at 90 days. Identifying AIS-LVO patients at risk of ENDunexplained may help to select patients for intensified monitoring and guide to optimal treatment regimes.

Limitation of cerebral blood flow by increased venous outflow resistance in elevated ICP.

Extensive investigation and modeling efforts have been dedicated to cerebral pressure autoregulation, which is primarily regulated by the ability of the cerebral arterioles to change their resistance and modulate cerebral blood flow (CBF). However, the mechanisms by which elevated intracranial pressure (ICP) leads to increased resistance to venous outflow have received less attention. We modified our previously described model of intracranial fluid interactions with a newly developed model of a partially collapsed blood vessel, which we termed the "flow control zone" (FCZ). We sought to determine the degree to which ICP elevation causing venous compression at the FCZ becomes the main parameter limiting CBF. The FCZ component was designed using nonlinear functions representing resistance as a function of cross-sectional area and the pressure-volume relations of the vessel wall. We used our previously described swine model of cerebral edema with graduated elevation of ICP to calculate venous outflow resistance and a newly defined parameter, the cerebral resistance index (CRI), which is the ratio between venous outflow resistance and cerebrovascular resistance. Model simulations of cerebral edema and increased ICP led to increased venous outflow resistance. There was a close similarity between model predictions of venous outflow resistance and experimental results in the swine model (cross-correlation coefficient of 0.97, a mean squared error of 0.087, and a mean absolute error of 0.15). CRI was strongly correlated to ICP in the swine model (r2 = 0.77, P = 0.00012, 95% confidence interval [0.15, 0.45]). A CRI value of 0.5 was associated with ICP values above clinically significant thresholds (24 mmHg) in the swine model and a diminished capacity of changes in arteriolar resistance to influence flow in the mathematical model. Our results demonstrate the importance of venous compression at the FCZ in determining CBF when ICP is elevated. The cerebral resistance index may provide an indication of when compression of venous outflow becomes the dominant factor in limiting CBF following brain injury.NEW & NOTEWORTHY The goal of this study was to investigate the effects of venous compression caused by elevated intracranial pressure (ICP) due to cerebral edema, validated through animal experiments. The flow control zone model highlights the impact of cerebral venous compression on cerebral blood flow (CBF) during elevated ICP. The cerebral venous outflow resistance-to-cerebrovascular resistance ratio may indicate when venous outflow compression becomes the dominant factor limiting CBF. CBF regulation descriptions should consider how arterial or venous factors may predominantly influence flow in different clinical scenarios.

A new classification of parasagittal bridging veins based on their configurations and drainage routes pertinent to interhemispheric approaches: a surgical anatomical study.

OBJECTIVE: Opening the roof of the interhemispheric microsurgical corridor to access various neurooncological or neurovascular lesions can be demanding because of the multiple bridging veins that drain into the sinus with their highly variable, location-specific anatomy. The objective of this study was to propose a new classification system for these parasagittal bridging veins, which are herein described as being arranged in 3 configurations with 4 drainage routes. METHODS: Twenty adult cadaveric heads (40 hemispheres) were examined. From this examination, the authors describe 3 types of configurations of the parasagittal bridging veins relative to specific anatomical landmarks (coronal suture, postcentral sulcus) and their drainage routes into the superior sagittal sinus, convexity dura, lacunae, and falx. They also quantify the relative incidence and extension of these anatomical variations and provide several preoperative, postoperative, and microneurosurgical clinical case study examples. RESULTS: The authors describe 3 anatomical configurations for venous drainage, which improves on the 2 types that have been previously described. In type 1, a single vein joins; in type 2, 2 or more contiguous veins join; and in type 3, a venous complex joins at the same point. Anterior to the coronal suture, the most common configuration was type 1 dural drainage, occurring in 57% of hemispheres. Between the coronal suture and the postcentral sulcus, most veins (including 73% of superior anastomotic veins of Trolard) drain first into a venous lacuna, which are larger and more numerous in this region. Posterior to the postcentral sulcus, the most common drainage route was through the falx. CONCLUSIONS: The authors propose a systematic classification for the parasagittal venous network. Using anatomical landmarks, they define 3 venous configurations and 4 drainage routes. Analysis of these configurations with respect to surgical routes indicates 2 highly risky interhemispheric surgical fissure routes. The risks are attributable to the presence of large lacunae that receive multiple veins (type 2) or venous complex (type 3) configurations that negatively impact a surgeon's working space and degree of movement and thus are predisposed to inadvertent avulsions, bleeding, and venous thrombosis.