Commentary

Vascular malformations in and around the brain and skull base are not rare, and many cause neurological and neuro-ophthalmic signs and symptoms. When the orbit is involved, arteriovenous malformations (AVMs) may manifest with primary orbital signs, including proptosis, chemosis, and dystopia. Secondary signs may include problems associated with optic nerve function and morbidity related to orbital venous congestion. Digital subtraction angiography remains the gold standard of diagnosis, but the past 15 years have provided a revolution in neurointerventional therapeutic techniques. Small tracker catheters and more experienced neuroradiologists can maneuver into small feeders, embolizing AVMs transarterially or even transvenously.

Orbital lesions have remained on the frontier of interventional neuroradiology. The extensive connections between the internal and external carotid artery supply as well as the potential for inadvertent embolization of end arteries such as the central retinal artery have limited the role of embolization in AVMs affecting the orbit.

Embolization may be inadequate to cure a lesion permanently unless the nidus is totally obliterated (often requiring placement of glue or some other agent that completely eliminates the primary connection into the venous system). If the nidus is not removed, additional vessels will be recruited. This statement also holds true for orbital lesions. As the authors point out, surgical excision is likely to remain an important part of the treatment of AVMs involving the orbit for the foreseeable future. The use of a multidisciplinary approach to these lesions recognizes the clinical spectrum possible as well as the contributions available from radiologists and ophthalmologists. Not all of these lesions need to be approached. Only when there is evidence of clinical deterioration or interference with function does the risk:benefit ratio for various therapeutic options need to be discussed.