The MetaFam Server: a comprehensive protein family resource.

MetaFam is a comprehensive relational database of protein family information. This web-accessible resource integrates data from several primary sequence and secondary protein family databases. By pooling together the information from these disparate sources, MetaFam is able to provide the most complete protein family sets available. Users are able to explore the interrelationships among these primary and secondary databases using a powerful graphical visualization tool, MetaFamView. Additionally, users can identify corresponding sequence entries among the sequence databases, obtain a quick summary of corresponding families (and their sequence members) among the family databases, and even attempt to classify their own unassigned sequences. Hypertext links to the appropriate source databases are provided at every level of navigation. Global family database statistics and information are also provided. Public access to the data is available at http://metafam.ahc.umn.edu/.

Quantitative Susceptibility Mapping in Cerebral Cavernous Malformations: Clinical Correlations.

BACKGROUND AND PURPOSE: Quantitative susceptibility mapping has been shown to assess iron content in cerebral cavernous malformations. In this study, our aim was to correlate lesional iron deposition assessed by quantitative susceptibility mapping with clinical and disease features in patients with cerebral cavernous malformations. MATERIALS AND METHODS: Patients underwent routine clinical scans in addition to quantitative susceptibility mapping on 3T systems. Data from 105 patients met the inclusion criteria. Cerebral cavernous malformation lesions identified on susceptibility maps were cross-verified by T2-weighted images and differentiated on the basis of prior overt hemorrhage. Mean susceptibility per cerebral cavernous malformation lesion (χ̄lesion) was measured to correlate with lesion volume, age at scanning, and hemorrhagic history. Temporal rates of change in χ̄lesion were evaluated in 33 patients. RESULTS: Average χ̄lesion per patient was positively correlated with patient age at scanning (P < .05, 4.1% change with each decade of life). Cerebral cavernous malformation lesions with prior overt hemorrhages exhibited higher χ̄lesion than those without (P < .05). Changes in χ̄lesion during 3- to 15-month follow-up were small in patients without new hemorrhage between the 2 scans (bias = -0.0003; 95% CI, -0.06-0.06). CONCLUSIONS: The study revealed a positive correlation between mean quantitative susceptibility mapping signal and patient age in cerebral cavernous malformation lesions, higher mean quantitative susceptibility mapping signal in hemorrhagic lesions, and minimum longitudinal quantitative susceptibility mapping signal change in clinically stable lesions. Quantitative susceptibility mapping has the potential to be a novel imaging biomarker supplementing conventional imaging in cerebral cavernous malformations. The clinical significance of such measures merits further study.

A quality-of-life instrument for young hemorrhagic stroke patients.

BACKGROUND AND PURPOSE: Hemorrhagic stroke has a high initial mortality rate. While survivors often recover motor function, many experience significant changes in their quality of life (QOL). Available outcome measures assess neurological impairment, disability, or handicap, yet often inadequately characterize the full impact of a stroke on patients' lives. In this study, we develop and validate a QOL instrument specific for young patients with hemorrhagic strokes. METHODS: Methodological guidelines for instrument development were initially established. Based on the content of 40 open-ended patient interviews, a 54-item instrument (HSQuale) was developed. The reliability (test-retest and internal consistency) and validity (content and construct) of HSQuale were assessed in another 71 patients (18 to 49 years of age, 63% women, 77% white), at 1 year after their hemorrhagic stroke. Comparisons were made between HSQuale and other commonly used outcome measures. RESULTS: HSQuale demonstrated reproducibility (test-retest kappa, 0.40 to 0.96) and internal consistency (Cronbach alpha >/=0.80 for 5 of 7 domains). HSQuale scores had broad frequency distributions (

Further observations on the pathology of subcortical lesions identified on magnetic resonance imaging.

We performed postmortem magnetic resonance imaging and pathologic examinations on the brains of seven consecutive patients older than 50 years of age who died of non-neurologic causes. Multiple hyperintense subcortical lesions were identified in each patient, and a total of 29 lesions were examined histologically (eight rims, six caps, six punctate lesions, and nine patches). Rims were characterized by subependymal gliosis and loss of the ependymal lining; caps were associated with myelin pallor, gliosis, and arteriosclerosis; punctate lesions were characterized by dilated perivascular spaces and perivascular gliosis; and patches were associated with myelin pallor and dilated perivascular spaces. The pattern of myelin pallor defined the size and shape of caps and patches. Arteriosclerosis was identified in six of six caps, three of six punctate lesions, and in three of nine patches. These data indicate that (1) each type of hyperintense subcortical lesion has a distinct pathologic correlate; (2) arteriosclerosis is not invariably associated with all types of hyperintense subcortical lesions on magnetic resonance imaging; and (3) myelin pallor appears to contribute to the magnetic resonance imaging signal at 1.5 tesla.

Sclerosing vasculopathy of the central nervous system in nonelderly demented patients.

Three nonelderly patients without hypertension whose clinical and radiologic features otherwise resembled Binswanger's subcortical arteriosclerotic encephalopathy underwent biopsy of the hyperintense periventricular lesions seen on magnetic resonance imaging. The pathologic findings of the periventricular lesions consisted of gliosis with mild rarefaction and edema of the white matter. All patients had a sclerosing vasculopathy of unknown cause, which involved numerous small vessels within the periventricular lesions. The vessels stained negatively for amyloid, amyloid precursors, desmin, vimentin, keratin, immunoglobulin, and complement. On electron microscopy, small arteries, arterioles, venules, and capillaries were characterized by swollen astrocytic foot processes surrounding the vessels; dense, perivascular collagen packing; crystalline arrays of filaments within basement membrane; giant lipid-laden lysosomes within perivascular cells; and narrowing of the vascular lumina. Similar changes were not seen in a control group of 19 patients. The pathologic features of the vessels in these cases are distinct from the vasculopathy associated with Binswanger's subcortical arteriosclerotic encephalopathy. We suggest that a spectrum of vasculopathies may be associated with dementia and periventricular hyperintense lesions on magnetic resonance imaging.

Surgery for intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) represents 8 to 15% of all strokes in the United States and 20 to 30% of all strokes in Japan and China. Although ICH represents a relatively small fraction of total strokes, it is a formidable disease, with a 30-day mortality rate two- to sixfold higher than that for ischemic stroke. Furthermore, it is a major cause of disability, with only 20% of patients becoming independent at 6 months. The most common risk factors for ICH are age, hypertension, and amyloid angiopathy, which are associated with damage to and weakening of the arterial/arteriolar wall leading to vessel rupture. The pathology is a dynamic one that continues to evolve over the first few days after onset. In 20 to 30% of ICH, clot volume increases over the first 24 hours and is generally associated with neurologic worsening. The final outcome from ICH is related not only to clot volume, compression, and destruction but also to potential neurotoxicity from the blood degradation products and associated neuronal ischemia. The treatment of ICH has been one of the most controversial and least well-studied areas from a medical or surgical perspective. Surgical treatment has evolved over the years and can be grouped into open and stereotactically guided surgery for hematoma evacuation. Seven thousand operations per year are performed in the United States for hematoma evacuation, although this approach has not been adequately investigated. Adjuvant medical therapies with neuroprotective agents require further investigation and may potentially have additive benefits.

Prediction of cognitive change as a function of preoperative ability status among temporal lobectomy patients seen at 6-month follow-up.

The relationship between preoperative ability levels and postoperative changes in cognitive function was examined among 23 left (LTL) and 19 right (RTL) temporal lobectomy patients using a battery of memory, language, and visuospatial tasks administered approximately 3 months before surgery and at 6 months follow-up. Higher preoperative performances on the memory and language measures were associated with larger decrements in postsurgical scores among the LTL patients. The RTL group showed no consistent relationship between preoperative ability levels and subsequent postsurgical cognitive changes. Based on the present data, we constructed base-rate tables for the Wechsler Memory Scale-Revised indicating the likelihood of measurable gains or losses in memory as a function of presurgical ability level for patients undergoing LTL. While tentative, these data provide a useful and practical guide for counseling prospective epilepsy patients of the attendant cognitive risks of LTL.

Endovascular therapeutic approach to peripheral aneurysms of the superior cerebellar artery.

Peripheral aneurysms of the superior cerebellar artery may be difficult to treat surgically owing to their inaccessibility and to the frequent inability to preserve the involved parent artery. In fact, for most cases, surgical treatment consists of proximal parent artery occlusion and/or trapping with surgical clips. An equivalent endovascular therapeutic approach to these lesions may be an attractive alternative method of management. We describe two cases of peripheral superior cerebellar artery aneurysms that were treated successfully with endovascular embolization.

Exceptional multiplicity of cerebral arteriovenous malformations associated with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome).

PURPOSE: To describe the clinical and imaging features of seven patients with hereditary hemorrhagic telangiectasia and an exceptional number of cerebral arteriovenous malformations (AVMs). METHODS: One hundred thirty-six patients from a dedicated hereditary hemorrhagic telangiectasia clinic were screened systematically for cerebral AVMs by means of MR imaging. Thirty-one were found to have abnormalities suggestive of a vascular malformation. Eighteen of these 31 patients subsequently underwent diagnostic cerebral angiography. RESULTS: Of the 18 patients who had cerebral angiography, all were found to have at least one AVM and seven were found to have three or more AVMs. The number of cerebral AVMs detected ranged from three to nine. At angiography, the AVMs varied in size from 3 to 25 mm in maximal dimension and consisted of a poorly defined plexiform nidus that typically had a single arterial feeding pedicle and a single draining vein. The two largest AVMs (20- and 25-mm nidus, respectively) contained intranidal aneurysms. Treatment included embolization, surgical excision, or follow-up management. CONCLUSIONS: Multiple cerebral AVMs are associated with hereditary hemorrhagic telangiectasia and further highlight the uniqueness of central nervous system involvement by this systemic angiodysplasia. MR imaging can underestimate the number and size of cerebral AVMs; therefore, catheter angiography is necessary to establish the extent of central nervous system involvement in this disorder.

MR of hereditary hemorrhagic telangiectasia: prevalence and spectrum of cerebrovascular malformations.

PURPOSE: Our goal was to describe the prevalence and types of cerebral vascular malformations (CVMs) seen with MR imaging in patients with hereditary hemorrhagic telangiectasia (HHT). METHODS: We reviewed retrospectively the brain MR images of 184 consecutive patients with HHT. Catheter angiography was performed in 17 patients with CVMs detected on MR images. RESULTS: MR imaging revealed 63 CVMs in 42 patients. Classic arteriovenous malformations (n = 10) had a conspicuous network of vessels with flow voids and enlarged adjacent pial vessels. Apparent venous malformations (n = 5) were best seen after administration of contrast material as a prominent vessel coursing through normal brain parenchyma. Indeterminate vascular malformations (n = 48) had a spectrum of appearances characterized by variable combinations of heterogeneous signal intensity, enhancement, or hemosiderin. Angiography in 17 patients revealed 47 CVMs. Forty-six were arteriovenous malformations (AVMs), including 25 CVMs not seen with MR imaging and 21 CVMs that by MR criteria included 8 AVMs and 13 indeterminate vascular malformations. Angiography confirmed 1 venous malformation seen with MR imaging but failed to detect 3 indeterminate lesions revealed by MR imaging. CONCLUSION: MR imaging of a large cohort of consecutive patients with HHT revealed a CVM prevalence of 23% (42/184). Most CVMs (48/63) have an atypical appearance for vascular malformations on MR images. Angiographic correlation suggests that MR imaging underestimates the prevalence of CVMs and that the majority of indeterminate CVMs, despite their variable MR appearance, are AVMs.

Intracranial cavernous malformations: lesion behavior and management strategies.

Intracranial cavernous malformations are vascular anomalies consisting of endothelium-lined caverns filled with blood at various stages of thrombosis and organization and separated by a collagenous stroma devoid of mature vessel wall elements. They occur in an estimated 0.45 to 0.9% of the population, with male and female patients equally affected and all ages represented. They commonly manifest as seizures, gross intracranial hemorrhage, and focal neurological deficits. Lesions are frequently multiple in the same patient, and 10 to 30% are associated with familial clustering. Several reports have documented a dynamic clinical-radiological lesion behavior with de novo lesion genesis, intralesional and perilesional hemorrhage, and corresponding fluctuations in lesion size. Hemorrhagic risk and neurological disability seem to be related to multiple factors, including lesion location, age, gender, state of reproductive cycle, and previous hemorrhage. Lesions may behave aggressively with repetitive hemorrhages and cumulative disability or may remain quiescent for many years. Management strategies include expectant follow-up in patients with asymptomatic or inaccessible lesions, excision of symptomatic and accessible lesions, and radiosurgery of progressively symptomatic lesions in inoperable locations. Relevant disease-specific outcome parameters are proposed to guide clinical decisions and future research. Prospective, stratified, hypothesis-driven studies using rigorous epidemiological methods must be undertaken to delineate patient and lesion factors influencing clinical aggressiveness. Biological studies are essential to uncover strategies to predict and modify lesion behavior.

Extracranial-intracranial bypass surgery: a critical analysis in light of the International Cooperative Study.

The ability of extracranial-intracranial bypass surgery to alter favorably the natural history of ischemic cerebrovascular disease remains in question. A recently completed prospective randomized multicenter cooperative trial failed to confirm the hypothesis that the procedure prevents further cerebral ischemia in patients with atherosclerotic internal carotid artery or middle cerebral artery disease. We analyze findings of the study in detail, including possible effects on the natural history of the disease beyond the immediate perioperative period. Potential sources of bias that may have unpredictably affected the study are discussed. These include observational bias (patient and therapist not blinded), "randomization-to-treatment" bias (high morbidity after randomization but before operation), and "prerandomization" or allocation bias (patients in the study representing a selected sample of the population with cerebrovascular disease). The extensive analysis of secondary subgroups with small numbers of patients is discussed in light of the statistical methods used. Two particular classes of patients not addressed in the study who might benefit from the procedure are defined. They are patients failing the best available medical therapy and patients with clearly documented hemodynamic compromise. Possible indications for bypass surgery are suggested for the various lesions in light of the trial and of recent reports on the natural history and pathophysiology of ischemic cerebrovascular disease. Selected cases illustrating these indications are presented.

Giant aneurysms of the proximal anterior cerebral artery: report of three cases.

Aneurysms of any size involving the A1 segment of the anterior cerebral artery are unusual, but giant aneurysms in this location are exceedingly rare, with only five cases previously reported in the literature. We report three cases of A1 segment giant aneurysms presenting with mass effect that were successfully treated. A discussion of the salient features of diagnosis and treatment are presented, along with a brief review of the literature describing these aneurysms. The role of newer imaging modalities, including magnetic resonance imaging, magnetic resonance angiography, and intraoperative angiography, is discussed. The three patients were treated by direct exploration, trapping, and endaneurysmal decompression. Giant A1 segment aneurysms present a unique opportunity to safely trap and decompress the aneurysm with definitive cure.

Extent of mesiobasal resection determines outcome after temporal lobectomy for intractable complex partial seizures.

The extent of resection was assessed in 94 patients who underwent temporal lobectomy for medically intractable complex partial seizures originating from a unilateral seizure focus in the anteromesial temporal lobe. Postoperative magnetic resonance imaging in the coronal plane was used to quantify the extent of resection of lateral and mesiobasal structures according to a 20-compartment model of the temporal lobe. Successful seizure outcome (greater than or equal to 90% reduction in seizure frequency) was accomplished in 83% of the patients (all followed up for more than 1 year; mean duration of follow-up, 25.2 months) and correlated significantly (P less than 0.05) with the extent of mesiobasal resection, regardless of the extent of resection of lateral structures. Successful seizure outcome was accomplished in 81% of the patients with no structural lesions, and also correlated significantly (P less than 0.05) with the extent of mesiobasal resection regardless of the extent of lateral resection. A successful seizure outcome was accomplished in 90% of the 21 patients with structural lesions documented by neuroimaging studies. Two patients who underwent extensive lobectomy without resection of the structural lesion had no reduction in seizure frequency postoperatively. We conclude that the most important factor in determining the outcome of temporal lobectomy in patients with unilateral anteromesial temporal lobe epileptogenicity is the extent of resection of structures in the mesiobasal temporal lobe. In patients with structural lesions, lesion resection may be an added contributor to successful seizure outcome.

Delayed facial nerve palsy after temporal lobectomy for epilepsy: report of four cases and discussion of possible mechanisms.

Four cases of idiopathic peripheral facial nerve palsy were documented after 110 consecutive resections of the temporal lobe for intractable epilepsy. In 3 of the 4 cases, the palsy was ipsilateral to the side of the temporal lobectomy. The onset of facial weakness was delayed 7 to 13 days after surgery (mean, 9.7 days). One patient underwent facial electroneurography, which documented 17% of normal facial motor function at the height of his weakness and the absence of the acoustic stapedius reflex. All patients were treated with prednisone (60-80 mg per day by mouth for 10-14 days, tapering off throughout the subsequent week). Facial function recovered fully in all patients within 6 to 8 weeks. Possible mechanisms are discussed, including heat and/or mechanical trauma to the facial nerve near the geniculate ganglion during resection of mesial temporal lobe structures.

Second operation after the failure of previous resection for epilepsy.

We present our surgical experience with second operations in 15 patients with recurrent intractable partial seizures after resection for epilepsy. The interval from the first operation until the first recurrence of seizures ranged from 1 day to 7 months (mean, 62 days). The interval between the first and second operations ranged from 3 months to 12 years (mean, 38 months). Detailed video-electroencephalographic interictal and ictal recording was performed in all patients (invasive electrodes were used in 11 patients). Ictal onset was shown to be remote from the zone of previous resection in 3 of 15 cases (all 3 extratemporal and in the ipsilateral hemisphere). Recurrent seizures arose from the area of previous extratemporal resection in 2 of 15 patients, and from the area of previous temporal resection in 10 of 15 patients. Both cases of extratemporal recurrences and 3 of the 10 cases of temporal lobe recurrences in the area of previous resection were associated with residual unresected structural lesion. Of the 10 patients with local temporal recurrence, 6 had proven epileptogenicity in the residual mesial structures, and 4 had residual epileptogenicity in the unresected lateral temporal lobe. The patients have been monitored for 8 to 82 months (mean, 18 months) after the second operation: 7 patients (47%) have remained seizure-free and another 5 (33%) have achieved a reduction in seizure frequency of more than 90%. There was no mortality or significant morbidity in this series. We conclude that the extent and distribution of residual epileptogenicity after failed epilepsy surgery are highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)

Mixed vascular malformations of the brain: clinical and pathogenetic considerations.

The clinical relevance of any scheme for classification of vascular malformations of the brain remains controversial. Widely accepted pathologic classifications include discrete venous, arteriovenous, capillary, and cavernous malformations. Of 280 cases of possible vascular malformations evaluated by a single cerebrovascular service during a 5-year period, 14 were instances of mixed vascular malformations including definite features of more than one pathologically discrete type of malformation within the same lesion. There were six instances of mixed cavernous and venous malformations in the same lesion; in all instances, the cavernous malformation accounted for the clinical presentation. There were three cases of mixed venous and arteriovenous malformations (arterialized venous malformations), presenting with the typical histoarchitectural appearance of a venous malformation, but with arteriovenous shunting; all cases were symptomatic, two with hemorrhage and one with focal neurological symptoms. There were five cases of predominantly cavernous malformations with features of arteriovenous malformation or capillary telangiectasia in the same lesion. These five cases presented clinically as angiographically occult lesions indistinguishable from a cavernous malformation. Lesions including a venous malformation were recognizable preoperatively because of characteristic imaging features of the venous malformation. Other mixed vascular malformations were indistinguishable on diagnostic studies from pure cavernous malformations. Of the 14 mixed vascular malformations, 11 included a cavernous malformation that was usually responsible for the symptomatic presentation. In the other three cases, manifestations of clinical lesions were due to arteriovenous shunting within a venous malformation. We conclude that mixed vascular malformations of the brain are rare entities with distinct clinical, radiological, and pathological profiles. Their identification generates several hypotheses about common pathogenesis or causation-evolution among different types of lesions.

Reversal of a dense, persistent, holohemispheric neurological deficit after an endarterectomy of the carotid artery: case report.

The role and timing of a carotid endarterectomy in the setting of an acute ischemic stroke-in-evolution remain controversial. Although computed tomographic (CT) scans typically show no abnormalities in the acute stage, it is generally agreed that a dense neurological deficit (hemiplegia) and/or multiple modality neurological disturbance (involving motor, sensory, gaze, and visual field impairment) represent contraindications to surgical intervention. We present a case of an acute right holohemispheric neurological deficit including dense hemiplegia, hemisensory loss, gaze disturbance, hemineglect, and impaired level of consciousness. This persisted for 4 days while serial CT scans showed no evidence of infarction. Angiography revealed pre-occlusive stenosis of the right internal carotid artery with sluggish antegrade flow. The anterior collaterals of the circle of Willis were impaired, and the right middle cerebral artery territory filled via the posterior communicating artery. Despite the dense neurological deficit persisting for 4 days, a carotid endarterectomy was performed. Gradual neurological improvement was noted within hours of the operation, and all neurological deficits resolved within the subsequent 3 days. This case is consistent with prolonged holohemispheric hemodynamic compromise below the threshold of neurological dysfunction, but above the threshold of tissue infarction ("idling neurons"). Features assisting in the recognition of this unusual scenario and the indications and risks of revascularization in this setting are discussed.

Ultrastructural pathological features of cerebrovascular malformations: a preliminary report.

OBJECTIVE: Although cerebrovascular malformations have been characterized histologically, a systematic examination of such lesions by transmission electron microscopy has not been previously published. In this preliminary study, we describe the ultrastructural pathological features of cerebral arteriovenous malformations (AVMs) and cavernous malformations (CMs). METHODS: Using transmission electron microscopy, we examined three CMs and three AVMs microsurgically harvested from patients, for conventional indications. Normal control cerebral tissue was obtained from two patients undergoing surgery for epilepsy. Specific attention was directed at components of the vascular wall, endothelial cell (EC) morphology, intercellular tight junctions, and the subendothelial layer. RESULTS: In embolized AVM vessels, ECs were disrupted, with preservation of the underlying subendothelial vessel wall. Nidal vessel walls of AVMs showed disorganized collagen bundles. In CM specimens, ECs lined attenuated cavern walls that were composed of an amorphous material lacking organized collagen. Peripheral to the CMs, capillaries were often surrounded by rings of hemosiderin. Tight junctions between ECs were present in AVMs and control specimens, but substantial inter-EC gaps were found in CMs. Subendothelial smooth muscle cells were present in AVM and control specimens, but they were sparse or poorly characterized in CMs. CONCLUSION: Surgically resected vascular malformations demonstrate abnormal ultrastructural pathological features. The preoperative embolization of AVMs results in EC denudation, with preservation of vessel wall structural integrity. The thin walls of CMs, lacking significant subendothelial support, along with the rarity of intact tight junctions between ECs, may contribute to the known propensity of CMs for recurrent microhemorrhage.

Spontaneous angiographic obliteration of cerebral arteriovenous malformations.

OBJECTIVE: The factors associated with spontaneous angiographic obliteration of cerebral arteriovenous malformations (AVMs) are not well understood. We present a review of the literature and a report of our experience with six cases (four with no previous treatment intervention and two postoperative residual malformations) that were identified as having occurred during a 20-year period and describe the clinical and lesion features associated with this rare phenomenon. We present the first detailed histological study of a spontaneously thrombosed AVM specimen, including immunohistochemical analysis of angiogenesis factor expression. METHODS: A combined experience in the management of approximately 700 AVMs during 20 years identified six cases of spontaneous angiographic obliteration of cerebral AVMs. A literature review revealed another 24 cases with angiographic documentation of the initial AVMs and follow-up data showing nonfilling of the lesions. Histological analysis of a recently excised lesion included immunostaining with monoclonal antibodies to the antigens of Factor VIII, Tie, vascular endothelial growth factor, and its receptors, Flt-1 and Flk. RESULTS: A single draining vein was a feature in each of our 6 cases and in 12 of 14 (86%) cases from the literature. Hemorrhage as the presenting symptom was identified in 5 of our 6 (83%) cases and in 17 of 24 (71%) of the literature cases. The size of the AVM was less than 6 cm in each of our 6 cases and in 22 of 24 (92%) of the literature cases. A histological examination of a thrombosed AVM surgical specimen revealed persistent patent vascular channels within the lesion. Immunohistochemical analysis with angiogenesis and endothelia-specific factors showed expression of these factors within the lumen of the thrombosed nidus vessels. CONCLUSION: We propose that the occlusion of a single draining vein may lead to total venous outflow obstruction and lesion thrombosis. Hemorrhagic presentation and small nidus may also predispose to this phenomenon. Immunohistochemical analysis of a thrombosed AVM revealed possible ongoing angiogenic changes within the AVM vessels 1 month after angiographically documented thrombosis. It is possible that neovascularization within a thrombosed AVM may lead to lesion recanalization; however, this phenomenon seems to be clinically exceedingly rare.