Katsuya Goto

Treatment of scalp arteriovenous malformation.

We report seven patients with scalp arteriovenous malformations, including two patients with lesions > 10 cm in diameter, who were successfully treated. The principal complaint of each patient was a deforming mass. Each of four patients had a history of blunt traumatic injury. The lesions, each consisting of the nidus, feeders, and draining veins, evolved in all patients. The nidus consisted of fistulae, which exhibited various angioarchitectures as revealed by angiography. A hemangiomatous component was histologically recognized in one patient. In five patients, in whom the lesions were relatively small and whose nidi included only large fistulae, the malformations were remedied by surgical intervention alone or were cured with embolization alone using liquid adhesives. In the two patients with lesions > 10 cm, the nidi consisted of numerous large fistulae and plexiform fistulae in one patient and plexiform fistulae and a hemangiomatous component in the other patient. These patients were treated with a combination of transarterial embolization and surgical intervention. Preoperative embolization greatly reduced blood loss during resection. Total excision and scalp reconstruction using a soft tissue expander were performed in both patients. The cosmetic results were excellent in all of the patients, and no recurrence has been recognized during the follow-up period, which ranges from 31 to 99 months. The treatment of scalp arteriovenous malformations should strive to improve deforming features and to attain a permanent cure. Because each nidus includes a variety of anomalous angioarchitectural features, there should be different means and a combination of treatments for each patient. Embolization alone could be adequate treatment in relatively small lesions, the nidi of which consist only of several large fistulae. For malformations with more extensive, large fistulae or with anomalous components other than large fistulae, a combined endovascular and surgical approach and scalp reconstruction seems to be the best treatment.

Vertebral arteriovenous fistula that developed in the same place as a previous ruptured aneurysm: a case report

BACKGROUND Aneurysms of the extracranial vertebral artery (VA) and vertebral arteriovenous fistulas (VAVFs) are relatively rare diseases. The most frequent cause of both diseases is trauma. Atraumatic lesions are less common. Presented here is a case of atraumatic AVF of the extracranial VA that developed in the same location as a previous ruptured aneurysm of the ipsilateral VA that was originally treated by proximal occlusion 11 years earlier. METHODS A 40-year-old woman presented with a massive hematoma in the upper posterior neck region caused by the rupture of an extracranial VA aneurysm. Proximal occlusion of the VA was performed by use of a detachable balloon. She enjoyed good health for 11 years, then she noticed a pulsatile bruit. Angiograms revealed an AVF between the left VA that was fed by collateral circulation and the paravertebral venous plexus. Incidentally found were soft tissue masses in the left retroauricular and the right suboccipital regions. Also, skull X-ray films showed multiple bony defects. Biopsy of the subcutaneous mass was performed in the hope of obtaining clues as to which pathological processes had weakened the artery. RESULTS As direct transarterial access to the fistula was out of the question, the fistulous compartment of the paravertebral venous plexus was tightly packed with multiple platinum coils effected by the transfemoral approach. A histological examination of the specimen revealed features of a neurofibroma, and a diagnosis of neurofibromatosis Type 1 was established. CONCLUSIONS In this case, transvenous embolization of the VAVF was successfully performed. The fragility of the arterial wall, related to neurofibromatosis Type 1, was considered to contribute to the development of the aneurysm and AVF.

A case of intracranial arteriovenous fistula in an infant with neurofibromatosis type 1

Abstract.Introduction: Reported cases of arteriovenous fistula (AVF) with neurofibromatosis type1 (NF1) are rare. Case report: In this paper we report the first case of intracranial AVF in an NF1 infant who developed heart failure. Endovascular treatment using coils successfully obliterated the AVF. The mechanism underlying the AVF in this case was believed to be a congenital mesenchymal abnormality of the intracranial vessels. Discussion: The mechanism underlying the development of heart failure in this case is also discussed.

Intraarterial injection of colforsin daropate hydrochloride for the treatment of vasospasm after aneurysmal subarachnoid hemorrhage: preliminary report of two cases

We describe two patients with symptomatic vasospasms after aneurysmal subarachnoid hemorrhage who were successfully treated with intraarterial injection of colforsin daropate hydrochloride (HCl). Colforsin daropate HCl is capable of directly stimulating adenylate cyclase, which in turn causes vasorelaxation via elevated intracellular concentrations of cyclic adenosine monophosphate. We suggest that colforsin daropate HCl might be a useful therapeutic tool in treating cerebral vasospasm.

Spinal intradural perimedullary arteriovenous fistula with varix in infant

A rare occurrence of type IV spinal arteriovenous malformation (intradural perimedullary arteriovenous fistula) is described in an 18-month-old boy initially misdiagnosed with Guillain-Barré syndrome. An intramedullary mixed-intensity mass lesion at Th1 was demonstrated by magnetic resonance imaging together with flow voids over the dorsal aspect of the swollen spinal cord. Angiography demonstrated an intradural perimedullary arteriovenous fistula including an intraparenchymal vascular pocket. After partial embolisation of the posterior spinal arteries through the left intercostal-radicular artery, the arteriovenous fistula was removed completely together with an organised haematoma. The fistula directly opened into a vascular pocket, which was confirmed pathologically to be a varix. The postoperative course was uneventful, and the patient resumed ambulation within 4 months. The case, subclassifiable as a type IVb spinal perimedullary AVF, was unique given its location and the patients age at presentation.

Improved technique for liquid embolization of cerebral arteriovenous malformation: catheter-tip position and flow control

This paper outlines the problems currently limiting the success and safety of embolization of cerebral arteriovenous malformations (AVMs) based upon the experiences of 110 cases. In cases where liquid embolic material was deposited mainly in arterial feeders, there was a reconstitution of the nidus through residual primary feeders and recruitment of blood flow via collateral tracts. A recent improvement of flexible microcatheters with minimal friction has made it possible to place the tip of a microcatheter into the nidus with greater success and safety. In order to obtain better filling of the AVM nidus and slower penetration to the draining veins, it is important to perform a temporary balloon occlusion of another main feeding pedicle to reverse the dynamic balance in favor of the pedicle being injected. In order to successfully occlude arteriovenous shunts in the nidus, appropriate flow control and optimal setting time of n-butyl-2 cyanoacrylate have prime importance.

Surgery or γ -knife for the treatment of arteriovenous malformations?

Abstract Decision making for either surgery or γ-knife for the treatment of arteriovenous malformations (AVMs) cannot be uniform. The skill of the neurosurgeon in operating on AVMs is now being compared with that of the γ-knife. The decision varies from case to case and is to be taken by the neurosurgeon. This report presents three cases in which such decision making was not easy. Case 1 was a non-ruptured cingulate AVM of 2.5 cm diameter in the cingulate cortex. The operative field was anticipated to be very narrow between the parietal bridging veins. Case 2 was a tiny ruptured AVM in the speech-motor area which was buried underneath the cortex. Case 3 was a large ruptured thalamo-stiriate-capsular AVM with feeders from the anterior and posterior choroidal arteries. All cases were operated without serious morbidity. A combination of pre-operative intravascular surgery (cases 1 and 3) or postoperative γ-knife (case 3) was adopted. In conclusion, there is no unitary rule to decide on surgery or γ-knife for the treatment of AVMs. It depends on what good or harm the responsible surgeon or the γ-knife does.