1241/1441. Spontaneous disappearance of a cerebral arteriovenous malformation in infancy. Case report. The authors report a case of the disappearance of an arteriovenous malformation in infancy, demostrated by follow-up angiography performed 7 months after the original angiograms. Some possible mechansims whereby a cerebral arteriovenous anomaly is thrombosed are discussed. ( info) |
1242/1441. intracranial hypertension resulting from a cerebrovascular malformation. A vascular malformation caused prominent intracranial hypertension by impairing CSF resorptive capacity rather than by its mass effect or ventricular obstruction. It was successfully treated by diversionary shunt. ( info) |
1243/1441. Dural arteriovenous malformation manifesting as tic douloureux. BACKGROUND: Although cerebral arteriovenous malformation (AVM) is an established cause of trigeminal neuralgia, dural AVM has rarely been reported to cause tic douloureux. Treatment of dural AVM in the tentorial and torcular regions by transarterial embolization is rarely curative. It has recently been proposed that many cranial dural AVMs with leptomeningeal venous drainage require only interruption of the draining vein as it enters the subarachnoid space for successful, lasting elimination. CASE REPORT: We present a case of 65-year-old man with typical trigeminal neuralgia caused by a dural AVM. Carotid angiography revealed a dural AVM in the petrotentorial region with enlarged and serpiginous draining veins, which compressed the trigeminal nerve. facial pain had been completely relieved for 2 months after successful transarterial embolization, but the symptom recurred. The patient subsequently underwent surgical interruption of the draining veins just beneath the cerebellar tentorium. The dural AVM disappeared, and the trigeminal neuralgia was completely relieved. CONCLUSION: The literature concerning the etiology of tic douloureux is reviewed and the selection of treatment modality of this case is discussed. The striking clinical and radiologic improvement in this case emphasizes the pivotal role of simple interruption of the arterialized vein for petrotentorial dural AVMs, which are not amenable to cure by endovascular procedures. ( info) |
1244/1441. An unusual complication of an inadvertent dural tap. The report describes a case of a large arteriovenous malformation of the brain becoming manifest following an inadvertent dural tap which was achieved while performing a lumbar epidural for the relief of labour pains. ( info) |
1245/1441. Sinus skeletonization: a treatment for dural arteriovenous malformations of the tentorial apex. Report of two cases. Two cases of dural arteriovenous malformation of the tentorial apex are presented. Both were treated surgically by means of a sinus skeletonization technique. The operative technique included a combined bioccipital and median suboccipital craniotomy in which the posterior third of the superior sagittal and the straight and bilateral transverse sinuses were skeletonized by incising the falx and the tentorium along the sinuses. Endovascular embolization was used prior to the surgical approach in one case. Clinical and angiographic cure was achieved in both patients, with a follow up of 4 years in the first case and 1 year in the second one. The surgical technique is described in detail. ( info) |
1246/1441. Acquired cerebral arteriovenous malformation in a child with moyamoya disease. Case report. The authors report a unique case involving a 2-year-old child with idiopathic moyamoya disease who presented with cerebral infarctions and seizures. On initial evaluation, computerized tomography (CT) showed a left parietal infarct and angiograms demonstrated early moyamoya disease with no evidence of arteriovenous malformation (AVM). Approximately 9 years later, angiography and magnetic resonance (MR) imaging revealed an AVM centered on the same region of the left parietal lobe. Angiographic, CT, and MR images are presented that demonstrate the progression of moyamoya disease and de novo development of the AVM in the infarct site. The possible role of angiogenesis in the etiology of acquired AVMs and moyamoya disease is discussed. ( info) |
1247/1441. Chronic encapsulated expanding hematoma in association with gamma knife stereotactic radiosurgery for a cerebral arteriovenous malformation. Case report. The authors report a rare case of a patient with a chronic encapsulated expanding hematoma and progressive neurological deterioration who presented 2 years after gamma knife radiosurgery for a cerebral arteriovenous malformation (AVM). A tough capsule containing multiple layers of organized hematoma resulting from previous bleeding was confirmed surgically. Histological examination revealed that the capsule consisted of a dense collagenous outer layer and a granulomatous newly vascularized inner layer with marked fibrosis. hemosiderin deposits were frequently observed in the inner layer, which suggested recurrent minor bleeding from fragile vessels in this layer. An AVM was found in the hematoma, which had degenerated as the result of radiosurgery. A cross-section of the abnormal vessels showed various stages of obliteration due to intimal hypertrophy. The clinical course, radiological features, and histological findings in this case were compatible with those of previously reported chronic encapsulated hematomas. A possible mechanism of hematoma formation and its expansion are discussed. ( info) |
1248/1441. recurrence of a cerebral arteriovenous malformation after surgical excision. Case report. Complete excision of a cerebral arteriovenous malformation (AVM) should eliminate the future risk of an associated intracranial hemorrhage. Because total removal of an AVM may be difficult to assess at the time of surgery, postoperative angiography has become the accepted standard for documenting that the removal has been accomplished. However, even angiography confirmed excision of an AVM does not completely ensure against rebleeding. Regrowth of an AVM with subsequent hemorrhage can occur. This has been documented in children and is attributed to forces acting on the immature vasculature of these younger patients. The authors report the case of an older patient whose AVM recurred when he was 28 years of age, despite an angiography proven complete excision, and emphasize that, even in adults, angiography documentation of total removal does not always eliminate the risk of reformation of an AVM. ( info) |
1249/1441. Spontaneous occlusion of an intracranial arteriovenous malformation. The case of a 2-month-old girl is described in whom an arteriovenous malformation (AVM) was observed in the paramedial region of the right cerebral hemisphere associated with an arachnoid cyst in the right fronto-parieto-temporo-occipital region. The only treatment was evacuation of the arachnoid cyst by trephination. When the child was 3 years old, images of the AVM were not found although all the intracranial vessels were angiographically explored. It is considered that the reduced pressure in the right cranial cavity due to the drainage of the arachnoid cyst may contribute to the occlusion of the AVM by causing a slight displacement of the intracranial structures towards the side of the drained cyst. ( info) |
1250/1441. Gamma knife radiosurgery for cerebral arteriovenous malformations: an autopsy report focusing on irradiation-induced changes observed in nidus-unrelated arteries. BACKGROUND: In radiosurgical treatment for an arteriovenous malformation (AVM), the effects of irradiation on the intranidal and perinidal angioarchitectures have seldom been analyzed histologically. An autopsy case is reported, studying an AVM treated by gamma knife radiosurgery. Postmortem studies following AVM-unrelated death were performed after a 2-year angiography had demonstrated complete nidus obliteration. Irradiation-induced changes were also observed in surrounding nidus-unrelated arteries and the choroid plexus, both of which were within the irradiation target. methods: Microscopic studies were performed using a coronal section of the brain including the center of the AVM, on which the percent isodose volume gradient, corrected with a magnification rate, was superimposed. RESULTS: This study disclosed that intimal hypertrophy can occur in a normal, AVM-unrelated pial artery due to irradiation of 10 Gy or more and that more remarkable intimal hypertrophy with fragmentation of the elastic laminae, or even complete occlusion, can occur in these arteries with 25 Gy. Similarly, irradiation-induced degeneration was present in the choroid plexus, which had been exposed to doses varying from 10 Gy to 25 Gy. CONCLUSIONS: A normal surrounding blood vessel may also be affected by high-dose, single-fraction irradiation though the abnormal vessels have been reported to be more susceptible. ( info) |