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Frey's syndrome
Frey's syndrome
Frey's syndrome
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Frey's syndrome
Other namesAuriculotemporal syndrome, Baillarger's syndrome, Dupuy's syndrome, Frey-Baillarger syndrome
Redness associated with Frey's syndrome
SpecialtyNeurology Edit this on Wikidata
SymptomsRedness and sweating of cheek area when salivating
CausesDamage to auriculotemporal nerve
Diagnostic methodStarch-iodine test
Frequency30–50% (after parotidectomy)

Frey's syndrome (also known as Baillarger's syndrome, Dupuy's syndrome, auriculotemporal syndrome,[1] or Frey-Baillarger syndrome) is a rare neurological disorder resulting from damage to or near the parotid glands responsible for making saliva, and from damage to the auriculotemporal nerve often from surgery.[1][2]

The symptoms of Frey's syndrome are redness and sweating on the cheek area adjacent to the ear (see focal hyperhidrosis). They can appear when the affected person eats, sees, dreams, thinks about, or talks about certain kinds of food which produce strong salivation.[3] Observing sweating in the region after eating a lemon wedge may be diagnostic.[2]

Signs and symptoms

[edit]

Signs and symptoms include erythema (redness or flushing) and sweating in the cutaneous distribution of the auriculotemporal nerve, usually in response to gustatory stimuli. There is sometimes pain in the same area, often burning in nature. Between attacks of pain, there may be numbness or other altered sensations (anesthesia or paresthesia). This is sometimes termed "gustatory neuralgia".

Causes

[edit]

Frey's syndrome often results as a complication of surgeries of or near the parotid gland or due to injury to the auriculotemporal nerve, which passes through the parotid gland in the early part of its course. The auriculotemporal branch of the mandibular branch (V3) of the trigeminal nerve carries parasympathetic fibers to the parotid salivary gland and sympathetic fibers to the sweat glands of the scalp. As a result of severance and inappropriate regeneration, the parasympathetic nerve fibers may switch course to a sympathetic response, resulting in "gustatory sweating" or sweating in anticipation of eating, instead of the normal salivary response.[2] It is often seen with patients who have undergone endoscopic thoracic sympathectomy, a surgical procedure wherein part of the sympathetic trunk is cut or clamped to treat sweating of the hands or blushing. The subsequent regeneration or nerve sprouting leads to abnormal sweating and salivation. It can also include discharge from the nose when smelling certain food.

Rarely, Frey's syndrome can result from causes other than surgery, including accidental trauma, local infections, sympathetic dysfunction, and pathologic lesions within the parotid gland.[4] An example of such rare trauma or localized infection can be seen in situations where a hair follicle has become ingrown and is causing trauma or localized infection near or over one of the branches of the auriculotemporal nerve.

Diagnosis

[edit]

Diagnosis is made based on clinical signs and symptoms and a starch-iodine test, also known as the Minor test. The affected area of the face is painted with iodine which is allowed to dry, then dry corn starch is applied to the face. The starch turns blue on exposure to iodine in the presence of sweat.[5]

Treatments

[edit]

Cochrane reviews of interventions to either prevent[7] or treat[8] Frey's syndrome have found little or no evidence to support their effectiveness or safety, and conclude that further clinical trials are needed.

Epidemiology

[edit]

The condition is rare, although the exact incidence is unknown.[9]

The disorder most often occurs as a complication of the surgical removal of a parotid gland (parotidectomy). The percentage of individuals who develop Frey syndrome after a parotidectomy is controversial and reported estimates range from 30 to 50 percent. In follow-up examinations, approximately 15 percent of affected individuals rated their symptoms as severe. Frey syndrome affects males and females in equal numbers.

History

[edit]

It is named after Łucja Frey-Gottesman.[10] The disorder was first reported in medical literature by Baillarger in 1853. A neurologist from Poland, Dr. Lucja Frey, provided a detailed assessment of the disorder and coined the term "auriculotemporal syndrome" in 1923.[11]

References

[edit]
[edit]
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Frey's syndrome

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from Grokipedia
Frey's syndrome, also known as auriculotemporal syndrome, is a rare characterized by unilateral gustatory sweating and facial flushing, typically occurring in the preauricular and temporal regions during or after eating, due to aberrant regeneration of damaged nerves following surgery or trauma. The condition arises primarily from injury to the or nearby parasympathetic and sympathetic fibers, most commonly during for tumors, with an incidence of 30% to 50% in affected patients; other causes include , mandibular fractures, burns, or rarely, non-surgical factors such as or zoster. In the underlying , severed parasympathetic fibers from the auriculotemporal nerve aberrantly reinnervate sympathetic nerve endings innervating sweat glands and facial blood vessels, leading to inappropriate activation by salivary stimuli rather than their normal or secretory functions. Symptoms usually manifest 6 to 18 months post-injury and include excessive sweating, redness, warmth, burning, or itching on the affected side of the face, often triggered by spicy, sour, or hot foods, though they are generally benign and not physically harmful but can cause significant social or psychological distress. is primarily clinical, based on patient history and , and can be confirmed with the Minor starch-iodine test, where iodine applied to the skin turns blue-black upon contact with sweat mixed with powder. There is no definitive cure for Frey's syndrome, but management focuses on symptom relief through topical anticholinergics (such as cream) or antiperspirants like aluminum for mild cases, while type A injections provide effective temporary inhibition of sweating for 3 to 20 months by blocking release at sweat glands, with minimal side effects. Surgical interventions, including resection or placement of barriers like acellular dermal matrix during initial procedures, are reserved for cases due to risks such as damage, though preventive techniques like flaps can reduce incidence by up to 90%. The prognosis is favorable, with symptoms often mild and manageable, and spontaneous regression occurring in up to 69% of pediatric cases.

Clinical features

Signs and symptoms

Frey's syndrome is characterized by unilateral gustatory sweating and flushing confined to the preauricular and temporal regions of the face, occurring specifically in response to eating, chewing, or even thinking about food. These symptoms typically manifest seconds after gustatory stimulation and last for a few minutes, with sweating that can be profuse enough to drench the affected area and require wiping. Patients often experience associated sensations of warmth, redness, and mild discomfort in the involved region, though pain is uncommon. Bilateral involvement is rare, and the condition does not produce systemic symptoms such as fever or widespread pain. The manifestations of Frey's syndrome can significantly impair , leading to social embarrassment from visible sweating and flushing, as well as avoidance of public meals to prevent discomfort.

Natural history

Frey's syndrome typically develops 6 to 18 months after the initial or , coinciding with the regeneration of damaged . Initial symptoms are generally mild, manifesting as subtle facial sweating and flushing during gustatory stimulation, such as eating. This delayed onset reflects the time required for aberrant reinnervation to establish functional connections. Following onset, symptoms often intensify over the next 1 to 2 years, reaching peak severity with more frequent and pronounced episodes of gustatory sweating and flushing. These episodes can be exacerbated by repeated exposure to strong gustatory stimuli, including spicy, sour, or salty foods, leading to increased discomfort during meals. In the absence of intervention, symptoms usually stabilize after this peak period but persist lifelong in most cases, with ongoing discomfort reported beyond 5 years post-injury. Spontaneous partial regression or stabilization may occur after 2 to 5 years in some patients, though complete resolution is rare, affecting about 5% of adults. Up to 69% of cases in children resolve spontaneously. This chronic course underscores the condition's benign yet persistent nature.

Pathophysiology

Etiology

Frey's syndrome most commonly results from iatrogenic injury to the and its associated nerves during , a procedure frequently performed to treat tumors, infections, or . The incidence of the syndrome following such varies widely, with objective testing revealing rates up to 100%, while symptomatic reports range from 10% to 60%, influenced by the extent of gland resection—higher in total parotidectomy than in partial superficial procedures. Traumatic etiologies, though less frequent, involve blunt or penetrating injuries to the parotid region, such as those sustained in accidents, assaults, mandibular condyle fractures, or wounds, which disrupt the relevant neural structures. Rare causes include congenital cases, such as perinatal trauma from forceps delivery, idiopathic presentations particularly in infants, and post-inflammatory conditions following , viral infections like herpes zoster, or parotid abscesses. Non-surgical etiologies overall account for less than 5% of cases and may also involve or other systemic factors.

Aberrant reinnervation

Frey's syndrome arises from damage to the and its contained parasympathetic secretomotor fibers during trauma or surgery, leading to misdirected axonal during the regeneration process. This injury disrupts the normal innervation pathway to the , prompting regenerating axons to seek alternative targets in the surrounding tissues. The aberrant regrowth results in salivary secretomotor fibers innervating nearby denervated sweat glands and vasodilatory structures in the overlying skin, thereby rerouting gustatory stimuli—such as eating or salivating—to provoke inappropriate (sweating) and (flushing and warmth) responses rather than . The underlying neural pathway exclusively involves the , originating from preganglionic fibers in the that in the before traveling via the to the . Postganglionic parasympathetic fibers, which release to stimulate muscarinic receptors on sweat glands and vascular —structures normally under sympathetic control—undergo this misdirected reinnervation, with regenerating axons often following sympathetic pathways to reach denervated sweat glands and vasodilatory structures. This peripheral explains the typical delayed onset of symptoms, often 6 to 18 months after injury, allowing time for axonal sprouting and functional reconnection. Histological evidence supporting this mechanism includes findings from human skin biopsies demonstrating the presence of parasympathetic fibers innervating sweat glands in affected areas, as well as animal models showing crossover of fibers to structures without alterations in the . Seminal studies, such as those using samples from patients post-parotidectomy, have confirmed the absence of involvement and highlighted the peripheral nature of the fiber misdirection, reinforcing the aberrant reinnervation theory first detailed in mid-20th-century research.

Diagnosis

Clinical evaluation

The clinical evaluation of Frey's syndrome begins with a detailed patient history to identify key features suggestive of the condition. Clinicians inquire about prior parotid surgery, neck surgery, trauma, or in the parotid region, as these are common precipitating events. Symptoms typically manifest as unilateral facial sweating and flushing triggered by gustatory stimuli such as sour or spicy foods, with onset occurring weeks to years after the initial insult. The history also emphasizes the unilateral nature of involvement, usually in the preauricular or temporal area, and the absence of bilateral or generalized symptoms. Physical examination focuses on the affected region, often revealing signs of prior surgical scarring or trauma in the parotid area. To elicit symptoms, clinicians may perform simulated gustatory stimulation by having the patient suck on a slice or similar acidic substance for about one minute, observing for asymmetry in sweating or flushing compared to the contralateral side. The examination also assesses for the absence of other neurological deficits, such as facial weakness or sensory loss, to support the localized aberrant reinnervation characteristic of Frey's syndrome. Differential diagnosis involves targeted questioning to distinguish Frey's syndrome from mimicking conditions. Food allergies are ruled out by noting the absence of rapid-onset systemic symptoms like urticaria or gastrointestinal distress, and the specificity to gustatory triggers without other atopic features. Primary is differentiated by its non-gustatory triggers and potential bilateral involvement, while emotional sweating typically affects palms, soles, and axillae rather than the facial region. Other considerations, such as gustatory tearing or , are excluded based on the lack of ocular or nasal symptoms. Symptom severity is documented using validated scales to establish a baseline for monitoring. One proposed system assigns points based on symptomatology (0-1 point for presence), affected area size (1-3 points: <2 cm, 2.1-4 cm, >4 cm), and sweat intensity or odor (up to 3 points), classifying cases as mild (<4 points total) or severe (≥4 points). This approach quantifies the extent of gustatory sweating and flushing, aiding in clinical characterization without relying on advanced testing.

Confirmatory tests

The diagnosis of Frey's syndrome is often suspected based on clinical history and examination, but confirmatory tests provide objective evidence of gustatory sweating and associated vasodilation. The most widely used confirmatory test is the Minor starch-iodine test, which directly visualizes areas of aberrant sweating. In this procedure, an iodine solution (typically 2-5% tincture) is applied to the affected facial skin, allowed to dry, and then covered with a fine starch powder, such as lycopodium or cornstarch. A gustatory stimulus, such as chewing a lemon wedge or sour candy, is introduced to provoke sweating; where perspiration occurs, the iodine-starch mixture reacts to form a blue-black discoloration, delineating the extent of the affected region. This test is considered the gold standard for confirming the diagnosis due to its simplicity, low cost, and ability to map subclinical involvement, though it may detect cases not reported symptomatically by patients. Infrared thermography offers a noninvasive alternative or complementary method to assess the syndrome by capturing temperature changes indicative of the aberrant response, often showing asymmetry such as a cold spot due to evaporative cooling from sweating (e.g., mean differences of approximately 0.8°C between sides). The technique involves using an infrared camera to image the facial skin before and after a salivary stimulus, such as eating; this allows for quantitative mapping of the involved region and is particularly useful in cases where sweating is minimal or the Minor test is inconclusive, providing a visual thermogram of the response. Thermography has been validated in clinical studies for its qualitative and quantitative reliability in diagnosing post-parotidectomy. Emerging techniques like laser Doppler flowmetry provide precise quantification of cutaneous blood flow changes during gustatory stimulation, measuring vasodilation via laser light scattering from red blood cells. Probes are placed on the affected and contralateral cheek, recording flux units before and after eating; significant increases (often >20-50% over baseline) in the ipsilateral area confirm the hyperemic response. While highly sensitive for research purposes, this method is not yet routine in due to equipment costs and complexity.

Management

Nonsurgical treatments

Nonsurgical treatments for Frey's syndrome primarily aim to alleviate gustatory sweating and flushing through reversible interventions that target activity or neural signaling, offering low-risk options for symptom management in mild to moderate cases. Topical antiperspirants, such as 20% aluminum chloride hexahydrate, are applied to the affected to occlude eccrine sweat ducts and reduce . Patients typically apply the solution nightly or 30 minutes before meals, with studies demonstrating significant symptom improvement in mild cases, as confirmed by starch-iodine testing. Treatment intervals vary from 1 to 50 days based on response, though long-term compliance is often limited due to recurrence upon discontinuation and potential irritation. Anticholinergic agents like glycopyrrolate inhibit parasympathetic stimulation of sweat glands and are administered topically in concentrations of 0.25% to 2% as a cream or solution. Application protocols involve daily or as-needed use on the affected area, providing effective control of severe gustatory sweating in post-parotidectomy patients with minimal systemic absorption. Common side effects include localized dry mouth, but the treatment is generally safe and well-tolerated. Botulinum toxin type A (BTX-A) injections offer a targeted approach by temporarily paralyzing nerve endings at sweat glands, with a reporting an rate of 98.5% across multiple studies. Injections are administered intradermally at doses of 2.0 to 5.0 units per mL, with 0.1 mL per site and spacing of 10 to 20 mm, totaling up to 380 units depending on the affected area; effects typically last 6 to 12 months, requiring repeat treatments. Adverse effects are uncommon, including transient dry mouth in about 1-2% of cases and mild injection-site pain. Lifestyle modifications, such as avoiding trigger foods like spicy, acidic, or caffeinated items that exacerbate gustatory sweating, can provide modest symptom relief for some patients. Patient-reported outcomes indicate that dietary adjustments and reassurance alone suffice for controlling mild symptoms in up to 77% of cases without further intervention.

Surgical treatments

Surgical treatments for Frey's syndrome primarily aim to prevent aberrant reinnervation by creating physical barriers during or to interrupt neural pathways in established cases. These approaches are indicated for high-risk surgeries or severe, symptoms, focusing on structural interventions to mitigate gustatory sweating and flushing. Interpositional grafts are a cornerstone prophylactic strategy, placed between the elevated skin flap and the parotid bed to block parasympathetic nerve fibers from the from regenerating into sweat glands, thereby preventing the aberrant reinnervation underlying the syndrome. Common materials include the sternocleidomastoid (SCM) muscle flap, which is rotated to cover the defect and has demonstrated reduced subjective Frey's syndrome incidence (12.5% versus 47.1% without flap). The superficial musculoaponeurotic system (SMAS) flap, involving rotation and advancement of the facial soft tissue layer or preservation, serves as an autologous barrier with reported objective incidence rates of 8.3% versus 38.7% without. Acellular dermis grafts, such as AlloDerm or Insuregraf, provide a biocompatible, non-immunogenic alternative that integrates well, achieving low Frey's syndrome rates (e.g., 0% versus 20.3% without). Overall, these grafts yield prevention success rates of 70-90% in reducing clinical manifestations, depending on material and surgical technique. A 2024 study of 82 patients found acellular dermal matrix significantly reduced incidence (P<0.05) and delayed onset to 7.54 months versus 3.43 months without. For patients with severe, persistent Frey's syndrome unresponsive to conservative measures, selective denervation procedures offer targeted relief by severing involved neural pathways. Tympanic neurectomy, which transects the tympanic branch of the glossopharyngeal nerve (Jacobson's nerve) via a transcanal or endoscopic approach, interrupts parasympathetic supply to the parotid and has historically been effective, though its use has declined since the 1990s in favor of less invasive options; a 2025 review reported complete symptom resolution in 56% of cases. Auriculotemporal nerve section directly divides the affected nerve trunk, providing symptom resolution in select cases but carrying risks such as transient taste disturbances (dysgeusia or ageusia on the posterior tongue) due to proximity to glossopharyngeal fibers. These procedures are reserved for debilitating symptoms, with potential for partial symptom recurrence if collateral reinnervation occurs. The SMAS flap rotation is particularly valued as a prophylactic measure in high-risk parotidectomies, leveraging the patient's own tissue for minimal donor-site morbidity while enhancing cosmetic outcomes through contour restoration. In modern practice, advancements including refined use of acellular dermal matrices have improved outcomes, with long-term recurrence rates below 10% attributed to better barrier durability and surgical precision. Endoscopic-assisted techniques incorporating preventive flaps or grafts have also emerged to reduce complications.

Epidemiology

Prevalence

Frey's syndrome is a rare disorder in the general population, with an incidence of less than 1%, as it predominantly manifests as a complication following surgery rather than occurring spontaneously. Following , the condition exhibits a wide range of reported incidences, with subclinical cases—detected via objective tests such as the Minor's iodine-starch test—occurring in 50% to 100% of patients, while symptomatic cases, involving noticeable gustatory sweating and flushing, affect 2% to 30%. The discrepancy between subclinical and symptomatic rates underscores the condition's variable clinical expression, with many instances remaining asymptomatic or mild enough to evade routine detection. Incidence varies significantly by surgical approach, with higher rates after total (up to 96% objective incidence) compared to superficial or partial procedures (as low as 4%). Underreporting is common, particularly for mild cases that do not prompt medical consultation; recent studies from 2023 to 2024 indicate stable incidence rates despite advancements in surgical techniques, with a 2024 reporting 77.9% prevalence of symptoms at least one year post-superficial parotidectomy, over 85% of which were mild to moderate and 74.6% of affected patients desiring treatment.

Risk factors

Frey's syndrome is most commonly associated with surgical procedures involving the , where the extent of dissection plays a key role in elevating risk. Extensive parotid dissection, including superficial or total , significantly increases the likelihood of the condition due to greater exposure and potential damage to the and surrounding tissues, with risk ratios ranging from 4.4 to 8.2 compared to more limited approaches. The lack of protective flaps, such as or dermal grafts, further heightens this risk, as these interventions have been shown to decrease the incidence by approximately 81% by creating a barrier to aberrant regrowth. Surgeon experience may also influence outcomes, though specific data linking less experienced operators to higher rates remain limited in the literature. Patient-related factors such as age and sex do not appear to be associated with incidence. Trauma to the represents another major category of risk, where the severity of correlates with higher likelihood of the syndrome. More extensive trauma, such as mandibular condyle fractures or deep lacerations, disrupts a larger area of glandular and neural tissue, promoting aberrant connections. Delays in treatment following such injuries can compound this by allowing uncontrolled scarring and inflammation, though quantitative data on delay duration is sparse. can rarely cause Frey's syndrome independently by causing glandular and nerve damage. Non-modifiable factors are less common but noteworthy. Genetic predispositions to Frey's syndrome are rare, typically manifesting in familial patterns without prior trauma or surgery, as documented in isolated case series. A family history of may compound susceptibility by predisposing individuals to exaggerated responses, potentially amplifying gustatory sweating upon nerve injury. Overall, while post-parotidectomy prevalence ranges from 20% to 60%, these risk factors help explain variations in individual cases.

History

Early descriptions

The earliest documented description of what is now recognized as Frey's syndrome appeared in 1853, when French neurologist Jules Baillarger reported five cases of gustatory sweating, with two particularly illustrative examples involving patients who developed facial sweating and flushing during meals following incision and drainage for parotid abscesses; he attributed the phenomenon to irritation of the . Throughout the remainder of the 19th century, scattered reports emerged in European medical literature, primarily linking similar symptoms—such as unilateral facial sweating triggered by eating—to parotid region trauma or , though without a cohesive explanatory framework. For instance, in 1859, French surgeon Hippolyte Rouyer described three cases of gustatory hyperhidrosis, one following a to the and the others after drainage, suggesting local involvement but not establishing a unified . Additional cases were noted by Russian physician Sergei Botkin in 1875, who detailed gustatory sweating on the cheek after parotid resolution, and by British physician Frederick Parkes Weber in 1897, who reported the first English-language instance of bilateral symptoms stemming from parotid suppuration scars. These accounts, drawn from surgical and neurological observations across , , and Britain, highlighted associations with parotid injury but remained isolated, often interpreted through the lens of local rather than aberrant regeneration. In the pre-20th century context, surgical texts occasionally referenced autonomic disturbances following parotid interventions, such as excessive salivation or localized sweating, but these were typically viewed as transient complications of infection or , without recognition as a distinct . Early physiological studies, like those by in 1850, explored gustatory-induced facial sweating in healthy individuals, providing a backdrop for later interpretations but not connecting it to . Overall, these observations underscored autonomic irregularities in the parotid area yet lacked integration into a broader clinical entity. Systematic investigation into the condition remained absent until the early 1900s, with initial reports emphasizing infectious etiologies—such as parotid abscesses—over iatrogenic factors like surgical trauma, delaying a comprehensive understanding of its mechanisms.

Naming and recognition

Frey's syndrome was first systematically described and explained by Polish neurologist Łucja Frey in 1923 through a detailed clinical and anatomical study of a patient who developed gustatory sweating and flushing following trauma to the parotid region. In her publication, Frey proposed the parasympathetic misdirection theory, hypothesizing that severed parasympathetic fibers from the auriculotemporal nerve aberrantly regenerated to innervate sympathetic sweat glands, leading to the characteristic symptoms triggered by eating. This work built on earlier isolated reports but provided the first comprehensive pathophysiological framework linking the auriculotemporal nerve's dual innervation to the disorder. Born in 1889 in Lwów (now , ), Frey earned her medical degree in 1923 and established herself as a neurologist in during Poland's , amid rising and professional challenges for Jewish physicians. Her contributions to , including the auriculotemporal syndrome, gained international notice in the 1920s, but her career was cut short by the Nazi occupation. In 1942, during the liquidation of the , she was deported to the Bełżec extermination camp and presumed murdered, one of countless Holocaust victims whose scientific legacies were nearly erased. The "Frey's syndrome" emerged shortly after her paper and achieved widespread adoption in surgical literature during the 1930s and 1940s, particularly as procedures increased and the condition was identified as a common postoperative complication. This recognition persisted despite debates over historical priority, including an earlier 1853 description by French neurologist Jules Baillarger of similar gustatory sweating without a mechanistic explanation. Following , interest in Frey's work resurged amid renewed focus on peripheral nerve regeneration, with the parasympathetic misdirection theory gaining validation through animal experiments in the that replicated the aberrant reinnervation process in models of parotid injury. These studies solidified the eponym's place in medical nomenclature, even as discussions on attribution continued, honoring Frey's foundational insights into the syndrome's etiology.

References

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