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Objective: Cerebral arteriovenous malformation during pregnancy is rare but lethal disease that usually present with new-onset seizures and headaches mimicking eclampsia. We report a rare case of cerebral arteriovenous malformation with abrupt seizures in the third trimester. Case Report: A 28-year-old primipara was brought to our emergency department at 32 6/7 weeks of gestation with new-onset acute seizures and hypertension. Owing to neurological deterioration, the patient underwent emergency cesarean delivery. However, 24 h after cesarean delivery and eclampsia treatment, the seizures worsened. Computed tomography and magnetic resonance imaging showed unruptured arteriovenous malformation of the right frontal lobe. Subsequently, intraarterial embolization was performed. The patient was discharged 5 days after surgery without neurological sequelae or obstetric complications. Conclusion: This case report highlights the differential diagnoses of sudden new-onset seizures in late pregnancy for obstetricians and emergency medicine physicians. Lethal cerebral diseases, apart from eclampsia, should be considered during pregnancy.

Arteriovenous malformations (AVMs) are a tangle of blood vessels that connects arteries and veins in which the feeding arteries are directly connected to the venous channels. Cerebral AVM needs special consideration due to high risk of bleeding and neurological deficit associated with morbidity and mortality. In pediatric population, prevalence rate of cerebral AVM is 0.02%. The systemic hemodynamic changes are seen more frequently with peripheral AVM, whereas its association with cerebral AVM is rare. We report a rare case of cerebral AVM in a 12-year-old child with severe systemic hypertension and electrocardiogram changes of biventricular hypertrophy planned for surgical resection of AVM in view of intracerebral bleed. This case illustrates the importance of detailed cardiac, renal, and endocrine evaluation in children with cerebral AVM with systemic hypertension and left ventricular hypertrophy to rule out other causes of systemic hypertension prior to surgery.

BackgroundThe disruption of intracranial fluid dynamics due to large unruptured cerebral arteriovenous malformation (AVM) commonly triggers a domino effect within the central nervous system. This phenomenon is frequently overlooked in prior clinic and may lead to catastrophic misdiagnoses. Our team has documented the world’s first case of so-called AVM Pentalogy (AVMP) induced by a AVM.Clinical presentation and resultA 30-year-old female was first seen 9 years ago with an occasional fainting, at which time a huge unruptured AVM was discovered. Subsequently, due to progressive symptoms, she sought consultations from several prestigious neurosurgical departments in China, where all consulting neurosurgeons opted for conservation treatment due to perceived surgical risks. During the follow-up period, the patient gradually presented with hydrocephalus, empty sella, secondary Chiari malformation, syringomyelia, and scoliosis (we called as AVMP). When treated in our department, she already displayed numerous symptoms, including severe intracranial hypertension. Our team deduced that the hydrocephalus was the primary driver of her AVMP symptoms, representing the most favorable risk profile for intervention. As expected, a ventriculoperitoneal shunt successfully mitigated all symptoms of AVMP at 21-months post-surgical review.ConclusionDuring the monitoring of unruptured AVM, it is crucial to remain vigilant for the development or progression of AVMP. When any component of AVMP is identified, thorough etiological studies and analysis of cascade reactions are imperative to avert misdiagnosis. When direct AVM intervention is not viable, strategically addressing hydrocephalus as part of the AVMP may serve as the critical therapeutic focus.

Spontaneous occlusion of arteriovenous malformations (AVM), characterized by complete disappearance of the AVM nidus and early venous drainage, and is a rare. The frequency of this phenomenon varied from 0.1 to 1.3 %. We analyzed two cases of spontaneous occlusion of cerebral AVMs with a non-hemorrhagic debut after 3 and 13 years in women aged 28 and 40 years, respectively. In both cases AVM was diagnosed during routine neuroimaging because of headache. Both patients had superficial small malformations. After discussing the risks of surgical treatment, both patients refused to perform any intervention. Scheduled angiography was performed 3 years after the diagnosis to follow-up the course of the disease and revealed complete disappearance of the AVM. Another patient noted persistent regression of headache after 3 years. Follow-up angiography was performed 13 years after diagnosis and confirmed spontaneous occlusion of the AVM. Given the data on the recurrence of the disease after spontaneous occlusion, such patients require long-term follow-up. When an AVM ruptures, hemodynamic changes may explain the thrombosis of the malformation, but the mechanisms of spontaneous occlusion in non-ruptured AVM remain unclear.

This paper summarized the nursing management for a patient with intracerebral hemorrhage due to ruptured cerebral arteriovenous malformation and neurogenic pulmonary edema. Based on the monitoring of postoperative vital signs of the patient, efforts were made in the following aspects: Early identification and intervention on normal perfusion pressure breakthrough syndrome; Ensuring the effective cerebral perfusion pressure during control of blood pressure and intracranial pressure; Early identification and nursing of neurogenic pulmonary edema; Enhancing the postoperative airway, fluid and volume management; Providing lung protective ventilation strategy; Carrying out awakenings and awareness recovery for the patient with chronic disorders of consciousness. (本文总结1例脑动静脉畸形破裂出血并发神经源性肺水肿患者的护理体会。术后在严密监测神志、瞳孔、生命体征变化基础上, 对正常灌注压突破综合征进行早期识别及干预, 在控制性降压及颅内压的同时保证有效的脑灌注压; 做好神经源性肺水肿的早期识别及护理, 在扩容的同时预防肺水肿进一步加重; 做好患者的呼吸道管理及容量管理, 给予正确的肺保护通气策略, 细化出入量; 对慢性意识障碍进行促醒康复, 促进患者早日康复。)

目的 探究散发性脑动静脉畸形组织中Kirsten大鼠肉瘤病毒癌基因同源物（Kirsten rat sarcoma viral oncogene homolog，KRAS）突变与临床特征之间的关系。 方法 回顾性收集散发性动静脉畸形（brain arteriovenous malformation，BAVM）术后病变组织的福尔马林固定石蜡包埋（formali n-fixation and paraffin-embedding，FFPE）样本和对应患者的临床信息，从FFPE样本中提取DNA，通过PCR扩增KRAS的指定区域（以chr12：25398284为靶点）并进行超深扩增子测序。根据是否存在KRAS突变分为突变组和无突变组，比较2组的临床特征差异。 结果 本研究共纳入145例BAVM患者的FFPE样本。其中63例（43.4%）存在KRAS 体细胞突变。其中41例（28.3%）中检测到c.35G→A（G12D）突变，14例（9.7%）中检测到c.35G→T（G12V）突变。此外，还发现了几种罕见报道的KRAS突变，包括c.34G→T（G12C）突变8例（5.5%）、c.34G→A（G12S）突变7例（4.8%）、c.35G→C（G12A）突变2例（1.4%）、c.34G→C（G12R）突变1例（0.7%）。KRAS基因突变组与无突变组的临床特征差异无统计学意义。 结论 本研究发现43.4%的BAVM患者存在KRAS基因突变，其中G12D是最常见的KRAS突变类型。此外，还发现了一些罕见报道的突变类型，包括G12C和G12A等。未发现KRAS突变与临床特征之间的关系. Abstract: Objective To investigate the relationship between Kirsten rat sarcoma viral oncogene (KRAS) mutation in brain arteriovenous malformation (BAVM) and clinical features. Methods The sporadic BAVM formalin-fixation and paraffin-embedding (FFPE) samples and the corresponding clinical features were collected. DNA was extracted from the BAVM FFPE samples, the specified region of KRAS (targeting chr12:25398284) was amplified by PCR and ultra-deep amplicon sequencing was performed. According to having KRAS mutation or not, the patients were divided into mutation group and no mutation group, the clinical features of the two groups were compared. Results A total of 145 BAVM FFPE samples were collected, with 63 (43.4%) samples with KRAS somatic mutation. Of these KRAS mutations, c.35G→A(G12D) were detected in 41 samples (28.3%), and c.35G→T(G12V) in 14 samples (9.7%). In addition, several infrequent KRAS variants rarely reported were identified, including 8 cases (5.5%) with c.34G→T(G12C), 7 cases (4.8%) with c.34G→A(G12S), 2 cases (1.4%) with c.35G→C(G12A) and 1 cases (0.7%) with c.34G→C(G12R). There were no statistical differences in clinical characteristics between the KRAS mutation group and no-mutation group. Conclusions In this study, KRAS gene mutation was found in 43.4% of BAVM patients, of which G12D was the most common mutation type of KRAS. In addition, several infrequent mutant types such as G12C and G12A were found. No relationship between KRAS mutations and clinical features were found.

A 13-year-old boy, with a history of intermittent headache and transient diplopia, was found to have non-hemorrhagic cerebral arteriovenous malformation in the midbrain tegmental region associated with hydrocephalus. Gamma knife radiosurgery was performed at 16 Gy with 75% marginal dose. Posttreatment course was uneventful. Follow-up MR imaging at one year after the treatment revealed complete disappearance of the abnormal vascular flow voids. The size of each ventricle at the treatment and at one year after treatment were as follows; 60.2 cc and 20.9 cc in the lateral ventricles, 3.7 cc and 2.7 cc in the third ventricle. The hydrocephalus might be caused by obstructive mechanism but mostly by high venous pressure due to the shunt blood flow. The goal of treatment for hydrocephalus should be nidus obstruction and normalizing the vascular flow.

Endovascular embolization is a critical component in the treatment of cerebral arteriovenous malformations. It can be used as an independent treatment modality or as an adjunct to microurgery or radiosurgery. The published literature in the PubMed database until September 2021 was reviewed with reference to the results of cerebral arteriovenous malformations embolization using liquid embolic agents. More scientific data reporting about total embolization of the cerebral arteriovenous malformations with a final cure. Although complications and mortality after arteriovenous malformations embolization have decreased significantly, but they still exist, and decisions about it usage should be weighed against its benefits during the planning phase. Treatment of arteriovenous malformations of the brain requires a multidisciplinary approach involving vascular neurosurgeons, endovascular interventionists and radiation oncologists, with a deep understanding of the natural course and combination of risks of multimodal treatment. Only such approach can increase the likelihood of a positive outcome of the cerebral arteriovenous malformations treatment.

Cases of low-grade cerebral arteriovenous malformations (cAVMs) showing dynamic changes and large areas of brain edema on short-term MRI follow-up have rarely been reported. This report describes an incidentally discovered and initially misdiagnosed cAVM in a patient with malignancies. The presence of abnormal signals surrounded by large areas of brain edema combined with tortuous or dilated vessels indicates the possibility of an AVM, especially in young people.

The primitive trigeminal artery (PTA), an abnormal carotid-basilar anastomosis, forms the vascular anomaly connection between the internal carotid artery and vertebrobasilar system. Rarely, PTA can be complicated by several other cerebrovascular disease, including arteriovenous malformations (AVMs), intracranial aneurysms, moyamoya disease, and carotid-cavernous malformations. Herein, we reported a rare case of PTA combined with an AVM in a male patient. The patient was a 28-year-old male with epileptic seizures at the onset of symptoms. Magnetic resonance imaging showed abnormal signal foci and localized softening foci formation with gliosis in the right parietal temporal lobe. Furthermore, using a digital subtraction angiogram (DSA), it was found that an abnormal carotid-basilar anastomosis had developed through a PTA originating from the cavernous portion of the right internal carotid artery (ICA) and a large AVM on the surface of the right carotid artery. The lesion of AVM tightly developed and draining into superior sagittal sinus. A hybrid operating room was used for the surgery. The main feeding arteries of the AVM originating from three major arteries, including the right middle cerebral artery, the right anterior cerebral artery, and the right posterior cerebral artery, were clipped and subsequently, then the AVM was thoroughly removed. The intraoperative DSA showed that the AVM had been resected completely. Postoperative pathological examination of the resected specimen indicated the presence of an AVM. The patient recovered well after surgery and has been symptom-free for more than 3 months. In summary, the pathogenesis of the coexistence of PTA and AVM remains unknown. As highlighted in this case report, hybrid surgery can be used to remove AVMs and can improve the patients' prognosis. To our best knowledge, this is the first case in the literature of successful AVM treatment using hybrid surgery.

Abstract Background Cerebral arteriovenous malformation (AVM) is a serious life-threatening congenital cerebrovascular disease. Specific anatomical features, such as nidus size, location, and venous drainage, have been validated to affect treatment outcomes. Until recently, molecular biomarkers and corresponding molecular mechanism related to anatomical features and treatment outcomes remain unknown. Methods RNA N6-methyladenosine (m6A) Methyltransferase METTL3 was identified as a differentially expressed gene in groups with different lesion sizes by analyzing the transcriptome sequencing (RNA-seq) data. Tube formation and wound healing assays were performed to investigate the effect of METTL3 on angiogenesis. In addition, Methylated RNA Immunoprecipitation Sequencing technology (MeRIP-seq) was performed to screen downstream targets of METTL3 in endothelial cells and to fully clarify the specific underlying molecular mechanisms affecting the phenotype of cerebral AVM. Results In the current study, we found that the expression level of METTL3 was reduced in the larger pathological tissues of cerebral AVMs. Moreover, knockdown of METTL3 significantly affected angiogenesis of the human endothelial cells. Mechanistically, down-regulation of METTL3 reduced the level of heterodimeric Notch E3 ubiquitin ligase formed by DTX1 and DTX3L, thereby continuously activating the Notch signaling pathway. Ultimately, the up-regulated downstream genes of Notch signaling pathway dramatically affected the angiogenesis of endothelial cells. In addition, we demonstrated that blocking Notch pathway with DAPT could restore the phenotype of METTL3 deficient endothelial cells. Conclusions Our findings revealed the mechanism by which m6A modification regulated the angiogenesis and might provide potential biomarkers to predict the outcome of treatment, as well as provide suitable pharmacological targets for preventing the formation and progression of cerebral AVM.

Yu-Chen Jia,1,* Jia-Yue Fu,2,* Ping Huang,3 Zhan-Pu Zhang,3 Bo Chao,3 Jie Bai3 1Inner Mongolia Key Laboratory of Molecular Biology, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, People’s Republic of China; 2Inner Mongolia Medical University, Hohhot, People’s Republic of China; 3Department of Neurosurgery, Affiliated Hospital, Inner Mongolia Medical University, Hohhot, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jie BaiDepartment of Neurosurgery, Affiliated Hospital, Inner Mongolia Medical University, No. 1 Tongdao North Road, Hohhot City, Inner Mongolia 010000, People’s Republic of ChinaTel +86-471-6351352Fax +86-471-6351184Email baijie0611@126.comIntroduction: Cerebral arteriovenous malformation (cAVM) is a disease characterized by the angiogenesis and remodeling of veins. However, whether vascular endothelial cells (ECs) exhibit morphological and functional changes during cAVM remains unclear. This study aimed to investigate the role of ECs in the pathogenesis of cAVM.Methods: Rat model of cAVM was established by anastomosing the common carotid artery with the external jugular vein. The digital subtraction angiography (DSA), HE, Masson and immunohistochemical staining were performed to evaluate the model. ECs were isolated from AVM rat model or control rats, and characterized by MTT, cell scratch, and tube formation assays. The secretion of vascular endothelial growth factor (VEGF) was detected by ELISA.Results: AVM rat model showed typical pathological characteristics of cAVM. In addition, the proliferation, migration and tube formation abilities of ECs of arterialized vein (AV-ECs) were significantly better than those of ECs of normal vein (NV-ECs). Moreover, the levels of secreted VEGF were significantly higher in AV-ECs than in NV-ECs.Conclusion: AV-ECs isolated from AVM rat model showed increased proliferation, migration and angiogenesis and may be potential target for the treatment of cAVM.Keywords: cerebral arteriovenous malformation, endothelial cell, angiogenesis, VEGF

Background: As essential techniques, intraoperative indocyanine green video angiography (ICG-VA) and FLOW 800 have been widely used in microsurgery for arteriovenous malformations (AVMs). In the present report, we introduced a supplementary technical trick for judging the degree of lesion resection when there were superficial drainage veins. FLOW 800 analysis is used to verify our conjecture. Methods: A retrospective analysis of a 33 case cohort treated surgically from June 2020 to September 2022 was conducted and their lesions were removed by superficial drainage veins as a supplementary technical trick and analyzed with FLOW800. Results: In our 33 AVMs, the feeding artery was visualized earlier than the draining vein. Intraoperatively, the T1/2 peak and slope of the draining vein were significantly higher than that of the lesion. However, the maximum fluorescence intensity (MFI) of the draining vein decreased as the procedure progressed (p < 0.001). After reducing the blood flow to the nidus by progressive dissection of the feeding artery, the arteriovenous transit time (AVTT) decreased from 0.64 ± 0.47 s, was prolonged to 2.38 ± 0.52 (p < 0.001), and the MFI and slope of the nidus decreased from the pre-resection 435.42 ± 43.90 AI and 139.77 ± 27.55 AI/s, and decreased to 386.70 ± 48.17 AI and 116.12 ± 17.46 AI/s (p < 0.001). After resection of the nidus, the T1/2 peak of the draining vein increased from 21.42 ± 4.70 s, prolonged to after dissection of the blood feeding artery, 23.07 ± 5.29 s (p = 0.424), and after resection of the lesion, 25.13 ± 5.46 s (p = 0.016), with a slope from 135.79 ± 28.17 AI/s increased to 210.86 ± 59.67 AI/s (p < 0.001). Conclusions: ICG-VA integrated with FLOW 800 is an available method for determining the velocity of superficial drainage veins. Whether the color of the superficial drainage veins on the cortical surface returns to normal can determine whether the lesion is completely resected and can reduce the possibility of residual postoperative lesions.

Background: Spontaneous regression of arteriovenous malformations (AVMs) is usually associated with bleeding, but sometimes asymptomatic regression occurs. Case description: We describe a case of spontaneous regression of AVM without evidence of hemorrhagic event. A 60-year-old otherwise healthy woman came to our hospital with complaints of headache. Digital subtraction angiography (DSA) showed an AVM with a 1.4 × 1.0 × 0.9 cm nidus in the right temporal lobe. The patient decided on observation without treatment rather than stereotactic radiation therapy or direct surgery. Seven years later, DSA revealed partial regression of the AVM. Venous ectasia and the nidus had decreased in size, and the nidus was obscure, especially around the feeding artery. No obvious features of hemorrhage were detected. Conclusions: Spontaneous regression of AVM is the result of multiple interacting factors. Structural changes to the AVM and histopathological changes may be important.

Vein of Galen malformations (VoGMs) are rare vascular malformations resulting from persistent shunting of primitive choroidal vessels into the median prosencephalic vein of Markowski. VoGMs are associated with poor clinical outcome with a reported 76.7% mortality if left untreated. We present an exceedingly rare case of a giant, untreated VoGM measuring 7.8 × 5.5 × 7 cm in a 42-year-old man. The embryologic origin, classification, clinical manifestations, and treatment options of VoGMs are discussed with a review of pertinent literature.

Background: Cerebral arteriovenous malformation (cAVM) is a type of vascular malformation associated with vascular remodeling, hemodynamic imbalance, and inflammation. We detected four angioarchitecture-related cytokines to make a better understanding of the potential aberrant signaling in the pathogenesis of cAVM and found useful proteins in predicting the risk of cerebral hemorrhage. Methods: Immunohistochemical analysis was conducted on specimens from twenty patients with cAVM diagnosed via magnetic resonance imaging and digital subtraction angiography and twenty primary epilepsy controls using antibodies against vascular endothelial growth factor receptor-2 (VEGFR-2), matrix metalloproteinase-9 (MMP-9), vascular cell adhesion molecule (VCAM-1), and endothelial nitric oxide synthase (eNOS). Western blotting and real-time fluorescent quantitative polymerase chain reaction (PCR) were performed to determine protein and mRNA expression levels. Student's t-test was used for statistical analysis. Results: VEGFR-2, MMP-9, VCAM-1, and eNOS expression levels increased in patients with cAVM compared with those in normal cerebral vascular tissue, as determined by immunohistochemical analysis. In addition, Western blotting and real-time PCR showed that the protein and mRNA expression levels of VEGFR-2, MMP-9, VCAM-1, and eNOS were higher in the cAVM group than in the control group, all the differences mentioned were statistically significant (P < 0.05). Conclusions: VEGFR-2, MMP-9, VCAM-1, and eNOS are upregulated in patients with cAVM and might play important roles in angiogenesis, vascular remodeling, and migration in patients with cAVM. MMP-9, VEGFR-2, VCAM-1, and eNOS might be potential excellent group proteins in predicting the risk of cerebral hemorrhage at arteriovenous malformation.

Cerebral arteriovenous malformation (AVM) or aneurysm in pregnancy is a complex situation and there is no definite recommendation regarding mode of anesthesia for patient with this type of intracranial pathology. We present a case series on the anesthetic management in two pregnant patients with either cerebral AVM or aneurysm presenting for elective cesarean section. Our case series highlights the following: (1) team working and collaboration with neurosurgeon and obstetrician to improve patient outcome; (2) crucial role of anesthetic management in reducing perioperative complications; (3) anesthetic management goals so as to minimize the risk of hemorrhage from an AVM or aneurysm.

Heterozygous loss of activin receptor-like kinase 1 (Alk1) can lead to hereditary hemorrhagic telangiectasia (HHT), which is a kind of vascular disease characterized by direct connections between arteries and veins with the lacking of capillaries, and develops into arteriovenous malformations (AVMs) in later stage. However, the changes of Alk1 in human sporadic cerebral AVMs (cAVMs) remain unknown. In the present study, we used endothelial cells (ECs) derived from human cAVMs (cAVM-ECs) specimens, to explore the characteristics of cAVM-ECs and the relationship between Alk1 and human sporadic cAVMs. Our data showed that there were obvious morphological changes in cAVM-ECs, and they could trans-differentiate into mesenchyme-like cells easily in a short period. In addition, the abilities of migration of cAVM-ECs were poorer than that in human aortic endothelial cells (HA-ECs). The abilities of proliferation of cAVM-ECs in patients with different ages were lower than HA-ECs. Immunofluorescent staining and Western blot showed that the levels of Alk1 mRNA and protein in the HA-ECs were both higher than that in cAVM-ECs. In addition, the levels of Alk1 mRNA had no significant differences between different ages in cAVM-ECs groups. The levels of VEGF-A mRNA in the cAVM were higher than HA-ECs. Besides, levels of VEGF-A mRNA expression were lower in older cAVM patients. Therefore, we conclude that Alk1 might induce the formation of sporadic human cAVMs through affecting migration and proliferation of endothelial cells combined with VEGF-A.

Aneurysms involving the lenticulostriate arteries are rare and are described in the literature in small case series or single-case reports. In this report, we discuss a case of a young woman who presented with acute lateral ventricular bleed and was found to have an arteriovenous malformation within the corona radiata and an aneurysm involving the distal lenticulostriate artery. The aneurysm was treated successfully by endovascular embolization. In deep-seated arteriovenous malformations (AVMs) that are conventionally treated by stereotactic radiosurgery, a targeted approach for treatment of an associated aneurysm could be considered to reduce the risk of rebleed until the AVM is obliterated.

In this study, we successfully established a stable method for the isolation of endothelial cells (ECs) from human cerebral arteriovenous malformation (cAVM) tissues. Despite human cAVM tissues having a minor population of ECs, they play an important role in the manifestation and development of cAVM as well as in hemorrhagic stroke and thrombogenesis. To characterize and understand the biology of ECs in human cAVM (cAVM-ECs), methods for the isolation and purification of these cells are necessary. We have developed this method to reliably obtain pure populations of ECs from cAVMs. To obtain pure cell populations, cAVM tissues were mechanically and enzymatically digested and the resulting single cAVM-ECs suspensions were then labeled with antibodies of specific cell antigens and selected by flow cytometry. Purified ECs were detected using specific makers of ECs by immunostaining and used to study different cellular mechanisms. Compared to the different methods of isolating ECs from tissues, we could isolate ECs from cAVMs confidently, and the numbers of cAVM-ECs harvested were almost similar to the amounts present in vessel components. In addition to optimizing the protocol for isolation of ECs from human cAVM tissues, the protocol could also be applied to isolate ECs from other human neurovascular-diseased tissues. Depending on the tissues, the whole procedure could be completed in about 20 days.

Se presenta una paciente que fue investigada y operada en el Hospital Universitario "Gral. Calixto García", portadora de una malformación arteriovenosa cerebral, que desapareció espontáneamente después de un cuadro neurológico de intensa gravedad. Arteriográficamente se comprobó que estaba asociada a un aneurisma arterial en su mismo sistema vascular cerebral. La paciente había sufrido 3 eventos neurológicos en orden ascendente de gravedad, y fue el último motivo de ingreso en la Unidad de Terapia Intensiva, con un nivel de 5 en la escala de Glasgow para el coma y sin signos meníngeos evidenciables. La lesión valorada como malformación arteriovenosa cerebral en las tomografías axiales cumputarizadas previas, no se evidenció en la panangiografía cerebral realizada en la fase de mejoría clínica relativa después de su etapa más crítica. Dicha angiografía demostró un aneurisma arterial homolateral a la malformación arteriovenosa ya desaparecida, el cual fue excluido de la circulación por presillamiento de su cuello sin eventos transoperatorios ni posoperatorios relevantes. Se realiza una revisión de la literatura al respecto.Authors present the case of a patient researched and operated on in the "General Calixto García" University Hospital presenting with a cerebral arteriovenous malformation disappeared spontaneously after a neurologic picture of intense severity. From the arteriographic point of view it was verified that it was associated with an arterial aneurysm present in her same cerebral vascular system. The patient has had three neurological events in rising order of severity which was the last reason for admission in the Intensive Therapy Unit (ITU) with a level of 5 in the Glasgow scale for the coma and without obvious meningeal signs. The injury classified as a cerebral arteriovenous malformation according to the previous computerized axial tomographies was not evidenced in the cerebral panangiograpy carried out in the clinical phase improvement after its more critical stage. Such angiography demonstrated the presence of a arterial aneurysm homolateral to the already disappeared arteriovenous malformation, which was excluded of the circulation by means of stitching of neck without transoperative and postoperative significant events. In this respect, author made a literature review.

We present a case of a patient with a ruptured temporo-occipital arteriovenous malformation, grade 3 on Spetzler-Martin scale, with an unpredictable evolution. A spontaneous occlusion of the malformation was found at 4 months after the initial partial endovascular embolization. We reviewed and discuss some aspects concerning clinical and angiographic finding, the angioarchitectural remodelling and evolution of the AVMs after partial occlusion treatment.