INTRODUCTION Intracranial developmental venous anomalies (DVAs) are considered benign vascular dispositions; they are asymptomatic in the vast majority of cases. They represent extreme variations of the venous drainage and may rarely be responsible for focal venous ischemia leading to neurological dysfunction. The aim of the study is to analyze a group of patients with symptomatic DVAs with capillary stain at angiography. METHODS We retrospectively reviewed the clinical and radiological features of patients in which a DVA was considered the cause of a neurological event. In all the patients, the DVA was suspected by angio-CT or MRI and conventional angiography was performed to detail the angioarchitecture of the DVA. RESULTS A total of 7 patients and 11 DVAs were identified; three patients had multiple DVAs. Three DVAs were frontal, two were parietal, two were thalamic, one was in the midbrain, and three were cerebellar. Patients presented with progressive neurological deficits, seizures, or cerebral hemorrhage. All these DVAs were associated with a peculiar capillary stain at angiography. CONCLUSION Although being normal anatomical variations, DVAs may create, because of hemodynamic unbalance, venous ischemia that induces angiogenic phenomena. MRI shows the suffering of the brain and angiography witnesses this angiogenesis under the form of capillary stain. Conventional angiography can thus provide useful information to recognize "atypical" symptomatic DVAs.

Cerebrovascular venous development and intracranial vascular malformations are extensive topics for which volumes of text may be devoted. However, a basic knowledge of the embryology of cerebral venous system and venous architecture is essential for understanding of cerebral vascular malformations. The aim of this work is to provide the reader with a brief overview of the development of the cranial venous anatomy. We will highlight the superficial and deep venous systems with special attention to developmental venous anomalies and vein of Galen aneurysmal malformations.

OPINION STATEMENT: Venous angiomas are currently widely referred to as developmental venous anomalies (DVAs), reflecting the prevailing concept that they represent anomalous, but functional, venous channels within the brain parenchyma. Although DVAs are not infrequently associated with other vascular malformations that harbor hemorrhage risk or can present symptomatically, isolated DVAs themselves appear to be benign lesions with little demonstrable link to hemorrhage, seizures, or headaches. Treatments to remove or occlude DVAs are consequently unnecessary. Furthermore, obliteration of a DVA can be harmful as it can lead to impairment in regional cerebral venous drainage, with the resultant risk of venous congestion, infarction, and hemorrhagic conversion, and the potential for devastating consequences from cerebral edema and mass effect. Consequently, even in the management of associated vascular malformations, it is important to preserve the DVA. In rare cases, DVAs can produce direct compressive symptoms, leading to obstructive hydrocephalus or neurovascular compression. In such cases, cerebrospinal fluid diversion or direct microvascular decompression, respectively, without disruption of the DVA itself is appropriate. In the uncommon setting of spontaneous DVA thrombosis leading to venous infarction, anticoagulation, as recommended for dural and cortical venous thrombosis, is a reasonable consideration. Hemorrhagic presentation from a presumed isolated DVA should prompt careful evaluation for an associated vascular malformation as the true etiology of hemorrhage.

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INTRODUCTION Developmental venous anomalies (DVA) consist of dilated intramedullary veins that converge into a large collecting vein. The appearance of these anomalies was evaluated on whole-brain computed tomography (CT) digital subtraction angiography (DSA) and CT perfusion (CTP) studies. METHODS CT data sets of ten anonymized patients were retrospectively analyzed. Five patients had evidence of DVA and five age- and sex-matched controls were without known neurovascular abnormalities. CT angiograms, CT arterial-venous views, 4-D CT DSA and CTP maps were acquired on a dynamic volume imaging protocol on a 320-detector row CT scanner. Whole-brain CTP parameters were evaluated for cerebral blood flow (CBF), cerebral blood volume (CBV), time to peak (TTP), mean transit time (MTT), and delay. DSA was utilized to visualize DVA anatomy. Radiation dose was recorded from the scanner console. RESULTS Increased CTP values were present in the DVA relative to the unaffected contralateral hemisphere of 48%, 32%, and 26%; and for the control group with matched hemispheric comparisons of 2%,-10%, and 9% for CBF, CBV, and MTT, respectively. Average effective radiation dose was 4.4 mSv. CONCLUSION Whole-brain DSA and CTP imaging can demonstrate a characteristic appearance of altered DVA hemodynamic parameters and capture the anomalies in superior cortices of the cerebrum and the cerebellum. Future research may identify the rare subsets of patients at increased risk of adverse outcomes secondary to the altered hemodynamics to facilitate tailored imaging surveillance and application of appropriate preventive therapeutic measures.

Stenosis of a DVA may result in chronic venous ischemia. We present 6 patients (3 men, 3 women; age range, 30-79 years; mean age, 53 years) with unilateral calcification of the caudate and putamen on noncontrast CT. This calcification typically spared the anterior limb of the internal capsule. No patient presented with symptoms referable to the basal ganglia or had an underlying metabolic disorder or other process associated with calcium deposition. All patients subsequently underwent gadolinium-enhanced MR imaging and/or CTA or conventional angiography demonstrating the presence of an adjacent DVA. We hypothesize that chronic venous ischemia in the drainage territory of the DVA causes the abnormal mineralization. Greater recognition of this entity will prevent misinterpretation of this finding as acute hemorrhage and will prevent unnecessary and sometimes invasive evaluation in such patients. Furthermore, this entity should be considered in the differential diagnosis of unilateral basal ganglia hyperattenuation.

INTRODUCTION The aim of this paper was to evaluate the angioarchitectural factors that can induce concurrent cavernous malformation (CM) in the territory of developmental venous anomaly (DVA). METHODS From January 2006 to December 2007, 21 patients with 23 CMs in the territory of DVA were retrospectively analyzed (M; F = 12; 9, mean age = 53.3). Gadovist®-enhanced three-dimensional spoiled gradient-echo images on a 3 T magnetic resonance (MR) scanner were used. We investigated the presence of angioarchitectural factors: factor 1, the angulated course of curved medullary or draining vein in the distal portion of CM; factor 2, narrowing of distal draining vein; factor 3, severe medullary venous tortuosity. These were also analyzed for control group of 23 subjects (M; F = 11; 12, mean age = 46). RESULTS Factor 1 was demonstrated in 22 cases (97%) and the CM occurred in a position of 90° or less of an abrupt angulated medullary or draining vein in 15 cases (65%) of the study group. Factor 2 was found in 13 cases (57%) with the diameter reduction of 50% or more in five cases. The mean ratio of diameter reduction was 0.53. Factor 3 was found in 17 cases (74%). Analyzing the independent factors, the p values for factors 1 and 3 were <.05, i.e., statistically significant. If combination of more than two factors was present, the p values for all the combinations were <0.05, i.e., statistically significant. CONCLUSION Anatomical angioarchitectural factors might be the key factors in causing concurrent sporadic CM within the territory of DVA by causing disturbance of blood flow.

Recent clinical and experimental evidence has challenged the traditional concept of the venous system as a "passive" element in the genesis and evolution of intracranial vascular malformations. The authors review the clinical and experimental evidence linking the venous system and its anomalies to the genesis of various intracranial vascular malformations, including dural arteriovenous fistulas, cavernous malformations, parenchymal arteriovenous malformations, and capillary telangiectasia. They also describe the potential significance of different associations of these vascular anomalies.

Cerebral developmental venous anomalies are the most frequently encountered cerebral vascular malformation, and as such, are frequently reported as fortuitous findings in computed tomography (CT) and magnetic resonance imaging (MRI) studies. Developmental venous anomalies (DVAs) are generally considered extreme anatomical variations of the cerebral vasculature, and follow a benign clinical course in the vast majority of cases. Here we review current concepts on DVAs with the aim of helping clinicians understand this complex entity. Morphological characteristics that are necessary to conceptualize DVAs are discussed in depth. Images modalities used in diagnosing DVAs are reviewed, including new MRI or CT techniques. Clinical presentation, association with other vascular malformations and cerebral parenchymal abnormalities, and possible physiopathological processes leading to associated imaging or clinical findings are discussed. Atypical forms of DVAs are also reviewed and their clinical significance discussed. Finally, recommendations as to how to manage asymptomatic or symptomatic patients with a DVA are advanced. Ann Neurol 2009;66:271-283.

Developmental venous anomalies (DVAs), formerly known as venous angiomas, have become the most frequently diagnosed intracranial vascular malformation. DVAs are currently considered congenital cerebrovascular anomalies with mature venous walls that lack arterial or capillary elements. They are composed of radially arranged medullary veins, which converge in an enlarged transcortical or subependymal collector vein, and have characteristic appearances (caput medusae) on magnetic resonance imaging and angiography. DVAs were once thought to be rare lesions with substantial potential for intracerebral hemorrhage and considerable morbidity. The prevalence of incidental and asymptomatic DVAs has been more apparent since the advent of magnetic resonance imaging; recent cohort studies have challenged the once-held view of isolated DVAs as the cause of major neurological complications. The previously reported high incidence of intracerebral hemorrhage associated with DVAs is currently attributed to coexistent, angiographically occult cavernous malformations. Some patients may still have noteworthy neurological morbidity or die as a result of acute infarction or hemorrhage directly attributed to DVA thrombosis. DVAs can coexist with cavernous malformations and arteriovenous malformations. Such combination or transitional forms of malformations might suggest common pathways in pathogenesis. Recent data support a key role for DVAs in the pathogenesis of mixed vascular malformations.

Cerebral developmental venous anomalies are the most frequently encountered cerebral vascular malformation, and as such, are frequently reported as fortuitous findings in computed tomography (CT) and magnetic resonance imaging (MRI) studies. Developmental venous anomalies (DVAs) are generally considered extreme anatomical variations of the cerebral vasculature, and follow a benign clinical course in the vast majority of cases. Here we review current concepts on DVAs with the aim of helping clinicians understand this complex entity. Morphological characteristics that are necessary to conceptualize DVAs are discussed in depth. Images modalities used in diagnosing DVAs are reviewed, including new MRI or CT techniques. Clinical presentation, association with other vascular malformations and cerebral parenchymal abnormalities, and possible physiopathological processes leading to associated imaging or clinical findings are discussed. Atypical forms of DVAs are also reviewed and their clinical significance discussed. Finally, recommendations as to how to manage asymptomatic or symptomatic patients with a DVA are advanced. Ann Neurol 2009;66:271-283.

This article provides a comprehensive description of the morphology of the human petrosquamosal sinus (PSS) derived from original observations made on 13 corrosion casts of the cranial venous system combined with routine clinical imaging studies in two patients. The PSS is not a rare finding in the adult human. In particular, continuous developments in imaging techniques have made radiologists become increasingly aware of this anatomical entity in recent years. The role of the PSS as a major encephalic drainage pathway and its potential implication in pathological conditions such as intracranial venous hypertension are discussed.

BACKGROUND AND PURPOSE: Passing from the supine to the upright position favors cerebral venous outflow into vertebral venous systems rather than into the internal jugular veins. We sought to determine venous connections between dural venous sinuses of the posterior cranial fossa and craniocervical vertebral venous systems. METHODS: Corrosion casts of the cranial and cervical venous system were obtained from 12 fresh human cadavers, and anatomic confirmation was made by dissection of three previously injected fresh human specimens. MR venography was performed to provide radiologic correlation. RESULTS: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins were found to represent the venous connections between the dural venous sinuses of the posterior cranial fossa and the vertebral venous systems. This study revealed the nearly constant presence of the anterior condylar confluent (ACC) located on the external orifice of the canal of the hypoglossal nerve. The ACC offered multiple connections with the dural venous sinuses of the posterior cranial fossa, the internal jugular vein, and the vertebral venous system. All these structures were shown by MR venography. CONCLUSION: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins connect the dural venous sinuses of the posterior cranial fossa with the vertebral venous systems. These connections are clinically relevant, because encephalic drainage occurs preferentially through the vertebral venous system in the upright position. The ACC is a constant anatomic structure that may play an important role in the redirection of cerebral blood in the craniocervical region.

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INTRODUCTION: Multidetector CT (MDCT) is increasingly used for the investigation of neurovascular disorders, but restricted z-axis coverage (3.2cm for 64-MDCT) currently limits perfusion to a small portion of the brain close to the circle of Willis, and precludes dynamic angiographic appreciation of the entire brain circulation. We illustrate the clinical potential of recently developed 320-MDCT extending the z-axis coverage to 16cm in a patient with symptomatic carotid artery stenosis. METHODS: In a 74-year-old patient presenting with critical symptomatic stenosis of the left CCA, pre- and post-carotid artery stenting whole-head subtracted dynamic MDCT angiography and perfusion were obtained in addition to CT angiography of the supra-aortic trunks. Both whole-head subtracted MDCT angiography and perfusion demonstrated delayed left ICA circulation, which normalized after carotid stenting. DISCUSSION: 320-MDCT offers unprecedented z-axis coverage allowing for whole-brain perfusion and subtracted dynamic angiography of the entire intracranial circulation. These innovations can consolidate the role of MDCT as a first intention imaging technique for cerebrovascular disorders, in particular for the acute management of stroke.

The PTEN hamartoma tumor syndrome, manifestations of which include Cowden disease and Bannayan-Riley-Ruvalcaba syndrome, is caused by various mutations of the PTEN gene located at 10q23. Its major criteria are macrocephaly and a propensity to develop breast and thyroid cancers as well as endometrial carcinoma. Minor diagnostic criteria include hamartomatous intestinal polyps, lipomas, fibrocystic disease of the breasts, and fibromas. Mutations of PTEN can also be found in patients with Lhermitte-Duclos disease (dysplastic gangliocytoma of the cerebellum). The authors report the case of a 17-year-old girl who had a severe cyanotic cardiac malformation for which surgery was not advised and a heterozygous missense mutation (c.406T>C) in exon 5 of PTEN resulting in the substitution of cysteine for arginine (p.Cysl36Arg) in the protein, which was also found in her mother and sister. The patient presented in the pediatric emergency department with severe spastic paraparesis. A magnetic resonance imaging study of the spine showed vertebral hemangiomas at multiple levels, but stenosis and compression were maximal at level T5-6. An emergency T5-6 laminectomy was performed. The decompression was extremely hemorrhagic because the rapid onset of paraparesis necessitated prompt treatment, and there was no time to perform preoperative embolization. The patient's postoperative course was uneventful with gradual recovery. This represents the first report of an association of a PTEN mutation and multiple vertebral angiomas. The authors did not treat the remaining angiomas because surgical treatment was contraindicated without previous embolization, which in itself would present considerable risk in this patient with congenital cyanotic heart disease.

Aim: Can monovoxel magnetic resonance spectroscopy (MRS) reliably follow tumour progression in low-grade glioma? Materials and Methods: 21 patients with low-grade glioma underwent at least 3 MRS. Results: For progression from a grade II to grade III tumour, a sensitivity of 57.1% and specificity of 60% were observed, with a positive predictive value (PPV) of 48.8% and a negative predictive value (NPV) of 54.5%. For progression under treatment, we obtained a sensitivity of 57.1% by N-acetylaspartate (NAA)/choline (Cho) and myoinositol/creatine (Cr) and a specificity of 100% by Cho/Cr and lipids, with a PPV of 80% and a NPV of 63.6%. Conclusion: We found that NAA/Cho is the best marker of tumour progression before therapy, with a sensitivity of 53.9%. For the therapeutic response, sensitivity was only 28.2%. Copyright (c) 2007 S. Karger AG, Basel.

BACKGROUND AND PURPOSE: The assessment of blood flow speed by imaging modalities is of increasing importance for endovascular treatment, such as stent implantation, of cerebral aneurysms. The subtracted vortex centers path line method (SVC method) utilizes image postprocessing for determining flow quantitatively. In current practice, intra-aneurysmal flow in an in vitro model is visualized by laser sheet translumination and digitally recorded. In this study, we applied this method to cinematic angiography (CA), which is the preferred imaging method for endovascular interventions, to analyse hemodynamic changes. The SVC method was applied to the images and compared with results of the slipstream line method with colored fluid.METHODS: A transparent tubular model was constructed of silicone which included an aneurysm 10 mm in diameter and having a 5 mm neck on a straight parent artery with a diameter of 3.5 mm. The model was integrated into a pulsatile circulation system. By CA, successive images at 25 frames/s with injection of contrast were obtained. RESULTS AND CONCLUSION: Rotating vortexes of contrast, which advanced along the wall of the aneurysm, were observed in successive images of the aneurysm cavity. This phenomenon was also observed in the successive images with the slipstream line method. The speed of the vortex center was calculated and the results show that the vortex speed of CA was the same as that under the slipstream line method. This indicates the possibility of applying the SVC method to medical imaging equipment for analysis of the flow in aneurysms containing stent.

We present a novel access for transvenous embolization of a dural arteriovenous fistula of the laterocavernous sinus through the external jugular vein and the pterygoid plexus. The anatomy of the laterocavernous sinus is reviewed, and its clinical implications discussed in light of the case of a patient whose management was modified after identifying this anatomical variation.

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Stenosis of a DVA may result in chronic venous ischemia. We present 6 patients (3 men, 3 women; age range, 30-79 years; mean age, 53 years) with unilateral calcification of the caudate and putamen on noncontrast CT. This calcification typically spared the anterior limb of the internal capsule. No patient presented with symptoms referable to the basal ganglia or had an underlying metabolic disorder or other process associated with calcium deposition. All patients subsequently underwent gadolinium-enhanced MR imaging and/or CTA or conventional angiography demonstrating the presence of an adjacent DVA. We hypothesize that chronic venous ischemia in the drainage territory of the DVA causes the abnormal mineralization. Greater recognition of this entity will prevent misinterpretation of this finding as acute hemorrhage and will prevent unnecessary and sometimes invasive evaluation in such patients. Furthermore, this entity should be considered in the differential diagnosis of unilateral basal ganglia hyperattenuation.

The majority of cases of leukoencephalopathy related to hypertensive crisis show brain lesions predominantly in the posterior lobe. Such cases are usually classified as reversible posterior leukoencephalopathy syndrome (RPLS). A multifocal distribution pattern is also possible, but occurs seldom. Here we report two patients with extensive white matter lesions that affect the entire brain, related to hypertensive crisis associated with a non-dipper pattern of blood pressure during the night as well as renal dysfunction. This nocturnal blood pressure abnormality may be relevant for the distribution pattern of cerebral white matter lesions and underlines the concept that in these cases a 24-h ambulatory blood pressure monitoring is needed.

INTRODUCTION The aim of this paper was to evaluate the angioarchitectural factors that can induce concurrent cavernous malformation (CM) in the territory of developmental venous anomaly (DVA). METHODS From January 2006 to December 2007, 21 patients with 23 CMs in the territory of DVA were retrospectively analyzed (M; F = 12; 9, mean age = 53.3). Gadovist®-enhanced three-dimensional spoiled gradient-echo images on a 3 T magnetic resonance (MR) scanner were used. We investigated the presence of angioarchitectural factors: factor 1, the angulated course of curved medullary or draining vein in the distal portion of CM; factor 2, narrowing of distal draining vein; factor 3, severe medullary venous tortuosity. These were also analyzed for control group of 23 subjects (M; F = 11; 12, mean age = 46). RESULTS Factor 1 was demonstrated in 22 cases (97%) and the CM occurred in a position of 90° or less of an abrupt angulated medullary or draining vein in 15 cases (65%) of the study group. Factor 2 was found in 13 cases (57%) with the diameter reduction of 50% or more in five cases. The mean ratio of diameter reduction was 0.53. Factor 3 was found in 17 cases (74%). Analyzing the independent factors, the p values for factors 1 and 3 were <.05, i.e., statistically significant. If combination of more than two factors was present, the p values for all the combinations were <0.05, i.e., statistically significant. CONCLUSION Anatomical angioarchitectural factors might be the key factors in causing concurrent sporadic CM within the territory of DVA by causing disturbance of blood flow.

BACKGROUND AND PURPOSE CCMs are commonly associated with DVAs, but the incidence of association in familial CCM is unknown. The presence of a DVA significantly complicates surgical management of a CCM because of the risk of compromised venous drainage. In this investigation, we compared the incidence of a DVA in the presence of a CCM in sporadic and familial CCM cases comprising predominantly familial CCM with the Southwestern US common Hispanic mutation (or Q455X mutation) of CCM1. MATERIALS AND METHODS Retrospective review was performed of 112 patients identified with CCM. MR imaging review included the presence or absence of a DVA and number, location, size, and signal-intensity characteristics of CCMs. Record review included patient and family history and documented genetic mutations. Statistical analysis was performed by using the Fisher exact and 2-sample t tests. RESULTS Eighty-one cases were familial, 18 were sporadic, and 13 were indeterminate. There were a total of 2212 CCMs: 2176, 21, and 15 in the familial, sporadic, and indeterminate groups, respectively. There was a close association of CCM and DVA (an apparent combined vascular lesion) in 8 of 18 (44%) sporadic cases and only 1 possible such association in the familial cases. The difference was highly statistically significant (P <.0001). CONCLUSIONS Familial CCMs are unlikely to be associated with DVAs, and sporadic CCMs have a high rate of association with DVA. This difference in imaging features of familial and sporadic CCMs suggests the possibility of a different developmental mechanism.

We report two cases of intracraneal brain haemorrhage secondary to developmental venous anomaly trombosis recently treated at our Department. First patient was a 28-year old woman on oral contraceptive treatment for a month who was referred to our Department with sudden-onset conscious level deterioration after presenting 24 hours previously with headache, vomits and hemiparesis. Computed Tomography revealed a predominant hypodense area containing hyperdense foci causing mild mass effect and midline-shift in keeping with a haemorrhagic infarction occupying almost completely the right frontal lobe. On CT, magnetic resonance (MR) and magnetic resonance angiography (MRA) there was a prominent tubular structure adjacent to the hematoma in keeping with a partly thrombosed vessel. Urgent craniotomy and partial hematoma evacuation was performed. Digital subtraction angiography confirmed the presence of a filling defect within the draining vein of a typical caputmedusae pattern developmental venous anomaly (DVA). Systemic anticoagulation was started and four days after surgery sedation was reversed and the patient awoke with normal conscious level although mild (4/5) hemiparesis persisted. Second patient was a 38-year old male evaluated in the Emergency Department due to tonic-clonic seizures in the left side followed by altered sensation in the same distribution. Initial CT revealed an intracranial bleed. After contrast administration there was an anomalous vessel in the same location that was confirmed angiographically represented a partly thrombosed DVA. Conservative management was favoured and the patient was discharged from hospital without clinical neurological deficits.

Developmental venous anomalies (DVAs) are common congenital venous drainage anomalies. Although they typically have a benign clinical course and a low symptomatic rate, thrombosis of a drainage vein may occur, leading to potentially debilitating complications. We report imaging findings of posterior fossa DVA with a thrombosed drainage vein in a patient with nonhemorrhagic cerebellar infarct. We also review the relevant literature on the subject.

Developmental venous anomalies (DVAs) represent a rare cause of intraparenchymal hemorrhage. This case demonstrates an unusual DVA associated with venous hypertension, arteriovenous shunting, and a ruptured transitional aneurysm. The authors describe the first use of embolization as a treatment method for an unstable ruptured transitional aneurysm associated with a DVA. This 33-year-old man suffered acute onset of headache, gait ataxia, and left hemiparesis. Computed tomography brain scans demonstrated a deep paramedian right frontal intraparenchymal hemorrhage. No cavernous malformation was apparent on MR imaging. Diagnostic angiography revealed arteriovenous shunting from the right anterior and middle cerebral arteries to a large DVA with an associated arteriovenous fistula, with a 3-mm aneurysm in the transition from pericallosal artery to the collecting vein. Both surgical and endovascular treatment options were considered. The patient underwent repeat angiography on hospital Day 7, at which time the aneurysm had increased to 5 mm, and endovascular treatment was selected. Acrylic occlusion of the aneurysm was performed and confirmed angiographically. The patient's neurological symptoms resolved throughout the hospital stay, and he remains symptom free in the 10 months since treatment. Developmental venous anomalies are not usually associated with arteriovenous shunting and aneurysms as a source of intraparenchymal hemorrhage. Endovascular occlusion of the aneurysm without blockage of physiologically necessary venous structures is a possible method of treatment for this complex mixed vascular lesion, and has proven safe and effective in this patient. To the authors' knowledge, this is the first presentation of this situation in the literature.

Developmental venous anomalies (DVAs) are hemodynamically low flow, low resistance vascular malformations without clinical significance. Although most DVAs are asymptomatic and are found incidentally, sometimes they can be symptomatic with intracerebral hemorrhage, many of which are usually caused by associated cavernous malformations (CMs) rather than the DVAs themselves. Only a few cases have been reported in the literature where an intracerebral hemorrhage has been caused by a DVA alone. This report describes a case of an intracerebral hemorrhage due to DVA alone with review of the literature.

A case of venous congestion associated with developmental venous anomaly (DVA) in a 5-year-old girl who presented with acute deterioration of consciousness is reported. Susceptibility-weighted imaging revealed abnormal structures connected to the central collector of a DVA, which were not shown on other sequences. These structures were considered to be presumably thrombosed medullary veins.