We thank Kranendonk and colleagues for their interest in the treatment of facial flushing. It is unfortunate that their patient experienced muscle paralysis after treatment with 8 U of botulinum… Click to show full abstract
We thank Kranendonk and colleagues for their interest in the treatment of facial flushing. It is unfortunate that their patient experienced muscle paralysis after treatment with 8 U of botulinum toxin given in 2 U increments in four injections 1 cm apart on the right midcheek. On examination of the photograph, it appears that the levator labii superioris muscle is involved because their patient is unable to raise the middle third of the right side of the lip (above the canine) and the zygomatic muscles (seen by blunting of the modiolus). The levator labii superioris muscle is located in the right midcheek, medial to the zygomaticus minor muscle. Their patient may have developed the paralysis if the injections were placed deeper than anticipated, or the paralysis may be due to the fact that 2 U were placed in each site. In our patient, 10 injection sites were performed of 0.05 cc (1 U each) distributed evenly over the cheek extending from the malar prominence, down to the midcheek (but above the modiolus), and lateral to cover the area of prominent flushing. Our patient has had the procedure repeated four times, with no loss of muscle function. In addition, I have treated five other patients in a similar manner, on one side of the cheek only, and none have experienced any facial muscle weakness. These patients were followed every 4 weeks for 14 to 22 weeks. The authors who treated Frey’s syndrome likely stayed within the borders of the parotid gland because Frey’s syndrome is due to damage to parasympathetic salivary nerve fibers of the auriculotemporal nerve located at the parotid gland.1 In this syndrome, the regenerating cholinergic nerve fibers make contact with the sweat glands on the cheek, causing paradoxical sweating on the cheek when eating. The efficacy of this treatment for facial flushing has yet to be determined in a large-scale study. The mechanisms by which it may occur are speculative but have been partially elucidated. The vasoconstriction may be related to inhibition of release of vasoactive intestinal peptide (VIP), calcitonin gene–related peptide (CGRP), or other neuropeptides contained in presynaptic vesicles. Acetylcholine, catecholamine, VIP, atrial natriuretic peptide, CGRP, galanin, and adenosine triphosphate have been localized in the periglandular nerves. Their significance on sweat gland function is not known. CGRP, VIP, and substance P are all potent vasodilators. CGRP and substance P increase nitrite formation through increasing nitric oxide synthase (constitutively expressed on endothelial cells in the microvasculature of the human dermis).2 Nitric oxide is a potent mediator of endothelium-dependent vasodilation. CGRP and VIP (but not substance P) are cotransmitters in the sudomotor nerve terminals.3 When the release of acetylcholine is blocked from the sudomotor nerve terminals by botulinum toxin, the release of CGRP and VIP is blocked as well.4 Therefore, blockage of release of vasodilators may lead to a comparative vasoconstriction. These clinical results have been noted by experts in the field of botulinum. Carruthers and Carruthers noted that patients treated with both broadband light treatments and botulinum toxin A (BTX-A) chemodenervation had greater improvement in telangiectasias than those with broadband light treatments alone.5 Makowichuk and Carruthers noted this phenomenon when BTX-A injections were used in the treatment of facial hyperkinetic lines (personal communication, July 2001). In addition, Carl Swartling, MD, noted that his patients treated with BTXA for palmar hyperhidrosis experienced mild blanching of the treated palm (personal communication, August 2003). Dr. Andrew Roberts has noted that BTX-A is suitable for emotional blushing (personal communication, July 2003). Whether these clinical phenomena are consistently reproducible remains to be seen. It may be that the patients with severe telangiectasia at rest are better candidates for KTP or broadband light therapy to reduce the permanently dilated vessels, followed by botulinum toxin for the reduction of further facial flushing.
               
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