✓ This is a report of spontaneous regression of intracranial arteriovenous malformations (AVM's) in three female patients; two of these patients had complete angiographic disappearance of the AVM, including an instance of intimate association of the AVM with an astrocytoma. The AVM's in these two patients were unicompartmental medium- to large-sized lesions supplied by a single feeder and draining principally through one large vein; spontaneous thrombosis is suggested as a cause of the AVM regression. Partial regression in the third patient might have been partially due to embolism from a clot-filled aneurysm on the feeding vessel. The significance of such disappearance of AVM's in relation to persistence or otherwise of the neurological status of these patients is discussed.
Report of three cases
Matthew F. Omojola, Allan J. Fox, Fernando V. Viñuela, and Charles G. Drake
Matthew F. Omojola, Allan J. Fox, Roland N. Auer, and Fernando V. Viñuela
✓ A selective non-occlusive technique was developed for administration of BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) into the internal carotid artery of the dog, and the neuropathological effects in the brain were studied. One out of three dogs showed ipsilateral hemorrhagic necrotizing encephalitis at doses of 102 mg/sq m, and all of three dogs showed similar but more severe pathology at doses of 215 to 232 mg/sq m. This study and previous studies in the dog and monkey suggest definite thresholds above which cerebral toxicity occurs when BCNU is administered via the intracarotid route. Greater dilution of drug in the larger territory of supply of the human internal carotid artery allows somewhat higher doses in man. The pathology of the lesion induced by BCNU suggests a primary vascular injury as a pathogenic mechanism, consonant with similar findings following high-dose systemic BCNU administration in man. Investigators conducting ongoing and future trials of intracarotid BCNU in the human for the treatment of intracranial neoplasms should be especially vigilant for a similar toxic effect.