Key points
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Frey syndrome is a common sequela of parotid gland surgery, affecting up to 64% of patients with varying degrees of severity.
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Frey syndrome is secondary to synkinesis of postganglionic parasympathetic nerve fibers within the transected parotid gland reinnervating the overlying sweat glands.
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Many surgical techniques, which are aimed at creating a barrier between the transected parotid gland and the overlying skin, have been used with varying degrees of success to prevent the development of Frey syndrome.
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Subcutaneous injection of botulinum toxin A into affected areas can be used to treat the postoperative symptoms of Frey syndrome.
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Surgical treatment for Frey syndrome refractory to medical management has been described, but clinical data to support its utilization are limited.
Introduction
Frey syndrome is a postoperative phenomenon following salivary gland surgery and less commonly neck dissection, facelift procedures, and trauma that is characterized by gustatory sweating and flushing. Frey syndrome was first described by Lucie Frey in 1923 and was termed auriculotemporal syndrome. It described sweating and flushing in the preauricular area in response to mastication or a salivary stimulus. Initially thought to be rare, it was later recognized as a common occurrence after salivary gland surgery, occurring in 4% to 62% of postparotidectomy patients 6 to 18 months after surgery.
The synkinetic mechanism for Frey syndrome is aberrant reinnervation of postganglionic parasympathetic neurons to nearby denervated sweat glands and cutaneous blood vessels. Consequently, this results in flushing and sweating in the sympathetically void skin in response to mastication and salivation. The previous sympathetic responses of sweating and flushing are now controlled by postganglionic parasympathetic fibers. Mastication, which releases acetylcholine from the parasympathetic nerve endings, now induces sweating and flushing, which was a sympathetic cholinergic response before synkinesis of parasympathetic nerve fibers ( Fig. 1 ).
The symptoms of Frey syndrome can include flushing, sweating, burning, neuralgia, and itching. Generally, the symptoms are mild but can result in discomfort as well as social anxiety and avoidance. A survey conducted by Baek and colleagues revealed that Frey syndrome was the most commonly self-perceived consequence of parotidectomy in a group undergoing parotidectomy for benign disease. With significant psychosocial morbidity resulting from Frey syndrome, interventions to prevent the development and to treat this sequela of parotid surgery have been the topic of focus in the literature.
Diagnosis of Frey syndrome is based on clinical history, but confirmatory testing can be done with a Minor starch-iodine test. The starch-iodine test consists of painting the patient’s postsurgical affected region with iodine. Once dry, dry starch is then applied to the painted area, and a salivary stimulus is given. The starch turns blue/brown in the presence of iodine and sweat ( Fig. 2 ). Patients who underwent parotidectomy had a positive Minor starch-iodine test in 62% of cases, whereas the self-reported incidence of symptoms was only 23% in the same group. These numbers attest both to the high incidence of the synkinesis and to the subclinical nature of Frey syndrome.
Introduction
Frey syndrome is a postoperative phenomenon following salivary gland surgery and less commonly neck dissection, facelift procedures, and trauma that is characterized by gustatory sweating and flushing. Frey syndrome was first described by Lucie Frey in 1923 and was termed auriculotemporal syndrome. It described sweating and flushing in the preauricular area in response to mastication or a salivary stimulus. Initially thought to be rare, it was later recognized as a common occurrence after salivary gland surgery, occurring in 4% to 62% of postparotidectomy patients 6 to 18 months after surgery.
The synkinetic mechanism for Frey syndrome is aberrant reinnervation of postganglionic parasympathetic neurons to nearby denervated sweat glands and cutaneous blood vessels. Consequently, this results in flushing and sweating in the sympathetically void skin in response to mastication and salivation. The previous sympathetic responses of sweating and flushing are now controlled by postganglionic parasympathetic fibers. Mastication, which releases acetylcholine from the parasympathetic nerve endings, now induces sweating and flushing, which was a sympathetic cholinergic response before synkinesis of parasympathetic nerve fibers ( Fig. 1 ).
The symptoms of Frey syndrome can include flushing, sweating, burning, neuralgia, and itching. Generally, the symptoms are mild but can result in discomfort as well as social anxiety and avoidance. A survey conducted by Baek and colleagues revealed that Frey syndrome was the most commonly self-perceived consequence of parotidectomy in a group undergoing parotidectomy for benign disease. With significant psychosocial morbidity resulting from Frey syndrome, interventions to prevent the development and to treat this sequela of parotid surgery have been the topic of focus in the literature.
Diagnosis of Frey syndrome is based on clinical history, but confirmatory testing can be done with a Minor starch-iodine test. The starch-iodine test consists of painting the patient’s postsurgical affected region with iodine. Once dry, dry starch is then applied to the painted area, and a salivary stimulus is given. The starch turns blue/brown in the presence of iodine and sweat ( Fig. 2 ). Patients who underwent parotidectomy had a positive Minor starch-iodine test in 62% of cases, whereas the self-reported incidence of symptoms was only 23% in the same group. These numbers attest both to the high incidence of the synkinesis and to the subclinical nature of Frey syndrome.
Surgical methods for the prevention of Frey syndrome
Prevention of Frey syndrome has been guided by the alteration of surgical techniques or the addition of procedures focused on preventing synkinesis. The overarching theme for the surgical prevention of Frey syndrome has been the incorporation and maintenance of a barrier between the underlying postganglionic parasympathetic nerve endings within the transected parotid and the overlying cutaneous tissue. Many techniques aimed at accomplishing this have been described and include increased skin flap thickness, local fascia or muscle flaps, and the use of acellular dermal matrix (ADM) or free fat grafts.
Increased Skin Flap Thickness
Within the facial skin, the sweat glands are positioned at the same level or slightly deeper than the base of the hair follicles. Based on this, it has been presumed that increasing the thickness of the elevated skin flap, to keep the sweat glands from being exposed, affords protection from the aberrant parasympathetic nerve regeneration that results in Frey syndrome. Early studies suggested that there was a significant increase in the rate of Frey syndrome when a thin flap was elevated compared with that of a thick flap (12.5 vs 2.6%, P <.05). Although this study did lay a foundation for surgical technique, its measurements for flap thickness were crude, and the diagnosis of Frey syndrome lacked objective measurements.
More recent studies, which objectively measured flap thickness and assessed Frey syndrome by clinical symptoms as well as starch-iodine testing, have failed to demonstrate a reduction in the incidence of Frey syndrome with increased flap thickness. Although flap thickness did not decrease the incidence of Frey syndrome in these studies, it did show a decrease in the total skin surface area affected and perhaps the overall severity of the disease.
Transposition Muscle or Fascia Flaps
Similar to increasing the thickness of the elevated skin flap to shield the facial sweat glands from aberrant reinnervation, pedicled muscle and fascia flaps have been used to cover the resected parotid gland in an attempt to create a physical barrier between the overlying dermis and the transected nerve fibers within the parotid.
Temporoparietal fascia flap
The temporoparietal fascia flap (TPFF) is a broad, vascularized fascia flap that is based off the superficial temporal artery ( Fig. 3 ). It was first described as a composite flap for ear reconstruction in 1976 by Fox and Edgerton and was later adapted to a fascia flap. Given its accessibility, predictable vasculature, and low donor site morbidity, it became a common method for reconstruction of the cheek, ear, nasal cavity, and orbit.
