Mechanisms of Blepharoptosis following Cosmetic Glabellar Chemodenervation

Sir: Chemodenervation with botulinum toxin type A has gained widespread use in various cosmetic procedures. Its long-lasting but impermanent effects make it attractive for several reasons. First-time and repeated consumers alike are drawn by convenience, cost, and efficacy. For relatively risk-averse patients, repeated chemodenervation is a viable alternative to the permanence and complications associated with incisional cosmetic surgery.1,2 Facial muscles of expression, especially those in the periorbital region, offer high-impact results.3 Although inevitable, unexpected results including brow and lid ptosis are frustrating for patients and providers. Two forms of botulinum toxin type A are commercially available in the United States today, onabotulinumtoxinA (Botox; Allergan, Inc., Irvine, Calif.) and abobotulinumtoxinA (Dysport; Medicis Aesthetics, Inc., Scottsdale, Ariz.). As many as 5.4 percent of glabellar treatments with Botox, and 3 percent with Dysport, yield undesirable blepharoptosis.4,5 This study proposes and validates two mechanisms by which cosmetic corrugator chemodenervation may lead to blepharoptosis. First, botulinum toxin may contact the levator palpebrae superioris muscle as it traverses the preperiosteal plane in deep injections. Second, the toxin may track along tributaries of the superior ophthalmic vein, which courses in along the levator muscle. A human cadaver was injected with colored latex to define arteries (red) and veins (blue). Methylene blue (1%, 1 cc) was injected into the right and left corrugator muscles, at the level of the supraorbital foramina. On the right, the injection needle was inserted deep to the bulk of the muscle belly, approaching the periosteal plane. On the left, the needle was inserted into the muscle belly, with a trajectory toward the supraorbital foramen. The superior orbital tissues were dissected and inspected for tracking of dye along relevant lid and orbital structures. Dissection through the upper lids was conducted through a horizontal incision running 15 mm superior to the upper lid margin. The anterior orbital septum and anterior surface of the levator aponeurosis were stained bilaterally. Viewed through a craniotomy approach, on the right, dye stained the orbital surface of the periosteum and the periorbita. Dissection of the left orbit revealed dye staining the superior surface of the levator palpebrae superioris and adjacent tissues, including the superior ophthalmic vein and some of its tributaries (Fig. 1).Fig. 1.: Orbital dissection. (Left) Left orbit viewed through the craniotomy approach. Dye stains the anterior body of the levator palpebrae superioris muscle (black arrow). Tiny tributaries feeding the superior ophthalmic vein are seen lying on the belly of the muscle (white arrow). (Right) Right orbit viewed through the craniotomy approach. The periorbita is seen as a blue-stained, glistening structure extending posteriorly to the orbital apex.This study was limited by unavoidable use of nonphysiologic conditions. Cooling of the cadaver for preservation and latex fixation may theoretically have altered tissue-diffusion properties. Omission of latex fixation would, however, limit visibility of minute vascular structures that may be inadvertently dissected or destroyed. In this study, two mechanisms of blepharoptosis from corrugator chemodenervation have been proposed. First, toxin may reach the levator muscle as it traverses the preperiosteal plane. Second, toxin may track along tributaries of the superior ophthalmic vein, which travels along the levator for part of its course. Blepharoptosis may be avoided through careful superficial positioning of the injection needle, using appropriately low volumes. Deep injections, particularly those overlying the bulk of the supraorbital nerve or near branches of the superior ophthalmic vein, should be avoided to prevent perineural or perivascular infiltration around the levator palpebrae superioris. DISCLOSURE The authors have no financial interest to declare in relation to the content of this article. Nicholas A. Ramey, M.D. Julie A. Woodward, M.D. Duke University Eye Center Durham, N.C.