The Auriculotemporal Syndrome a Clinical and Pharmacologic Study

THE AURICULOTEMPORAL SYNDROME A CLINICAL AND PHARMACOLOGIC STUDY

A. S. Freedberg, … , Robert S. Shaw, M. J. McManus

J Clin Invest. 1948;27(5):669-676. https://doi.org/10.1172/JCI102015.

Research Article

Find the latest version: https://jci.me/102015/pdf THE AURICULOTEMPORAL SYNDROME A CLINICAL AND PHARMACOLOGIC STUDY By A. S. FREEDBERG, ROBERT S. SHAW AND M. J. McMANUS (From the Department of Medicine, Harvard Medical School, and the Medical Service and Research Laboratories, Beth Israel Hospital, Boston) (Received for publication May 26, 1948)

The auriculotemporal syndrome which develops temporal nerve. There was a right facial weakness and after injury to the parotid gland, consists of ptosis of the right upper eyelid; the latter was said to flushing and profuse sweating, upon eating, over have been present since the patient's recent cerebral vas- cular accident. The cranial nerves were otherwise normal. the cutaneous distribution of the auriculotemporal Case 2: T. H., a 63 year old man, MGH No. 484270, nerve on the injured side. Although there have with a history of recent sinusitis, had had bilateral sup- been few cases reported since the original descrip- purative parotitis, of unknown etiology, twenty-five years tion by Frey (1) in 1923, the syndrome is not previously; this had been drained through incisions over rare, having been noted repeatedly, for-example, the glands on both sides. Several weeks after operation the patient noted the occurrence of profuse sweating and in clinics observing patients after operation on a a feeling of warmth on the left side of his face when eat- parotid gland (2, 3). The syndrome is of interest ing. The phenomenon had continued until admission. It to the physiologist because it affords an oppor- was brought on by eating any food, especially apples. At tunity to study the consequences of denervation of no time had the patient noticed any numbness or paralysis cholinergic end organs. It is our purpose to pre- of his face. Physical examination was not remarkable sent three instances of this syndrome with except for the old drainage scars over both parotid glands. some The parotid glands were normal to palpation and saliva observations relating to its mechanism. was easily expressed from both ducts. Sensation over the face was normal and the function of other cranial nerves CASE HISTORIES was apparently intact. Case 3: D. E. S., a 49 year old married woman 1: a (re- Case J. B., 68 year old man, BIH No. 78777, ferred entered the on of by Dr. I. T. Nathanson), had had a tumor of the hospital 9/29/44 complaining transient right parotid gland removed in 1942. weakness and dysarthria. These symptoms were believed Approximately onc. to be consequent to a recent cerebrovascular accident. year later she noted the onset of sweating following the Forty-one years ago, while in the Russian army, the eating of various foods. The sweating involved the right patient had had typhoid fever, complicated by right paro- side of the face in the region of the incision. Rarely a titis. Two attempts to drain the parotid gland by vertical sense of heat was noted but visible flushing was never incisions were unsuccessful. Two incisions, 2 cm. lateral observed. No specific food was noted to be particularly to the right upper border of the thyroid gland, resulted effective in producing the sweating reaction. Although in drainage for approximately 50 days. Approximately on rare occasions a whole meal did not produce sweating, one month after the successful drainage, and two months hot tea by itself occasionally produced profuse perspira- after the onset of the parotitis, the patient noticed the de- tion. She had had mumps as a child, but with no sequelae. velopment of profuse sweating over the right side of the face while eating. Although ingestion of many foods was OBSERVATIONS followed by sweating, the phenomenon was particularly marked when apples were eaten. On each occasion just Observations in Case 1: The observations on prior to the onset of sweating the patient experienced a sweating were made by means of the Minor sensation of warmth over the involved area. Redness, starch-iodine test (4) which consists of applying a swelling and pain, however, were absent; at no time was solution of iodine (15 cc. 1 per cent iodine, 5 cc. numbness noted over the involved area. The amount of sweating had become less pronounced during the previous of castor oil and 80 cc. 95 per cent alcohol) and three years. after drying, lightly dusting the skin with starch On physical examination, scars on the face and neck and noting the onset of sweating which is signal- were noted. The opening of the right Stenson's duct was ized as black spots. Ten seconds after taking a protuberant; saliva could not be expressed from it. The bite of apple and while chewing, the patient noticed orifice of the left duct appeared normal and saliva was easily expressed. Perception of heat and cold was normal a feeling of warmth over the right face, and a and equal on both sides of the face. There was cutaneous slight flush was noted on this side. Five seconds hypaesthesia in the distribution of the right auriculo- later, sweating appeared in part of the area in- 669 670 A. S. VREDIBERG, ROBERT S. SHAW AND M. J. MCMANUS sive during the whole period of injection and for a short time afterward. A series of experiments was performed to determine whether there was hypersensitivity of the sweating mechanism in the involved area. In normal controls, local sweating was observed over and around intradermal wheals made by the injection of 0.1 cc. of various concentrations of acetylcholine bromide dissolved in isotonic saline solution. By using increasing dilutions, a measure of the sensitivity of the local sweating appa- ratus to acetylcholine might be obtained. While sensitivity was found to vary in different individuals and in different regions of the body, the end FIG. 1. THE DISTRIBUTION OF SWEATING OBSERVED IN points were consistent. In this patient, intra- CASE 1, REPRESENTED BY THE CROSS-HATCHED AREA dermal wheals in the involved area on the right side of the face produced with 0.1 cc. of isotonic cluded in the distribution of the auriculotemporal saline solution containing 0.0001-0.1 'gamma of nerve (Figure 1). The sweating could be induced acetylcholine bromide resulted in local sweating. by chewing any food, but was absent or slight Similar concentrations of acetylcholine in sym- when the patient chewed paraffin. The applica- metrical positions on the left face of the patient did tion of ice to the right face before chewing food not produce sweating. A wheal on the left side resulted in a decreased amount of sweating in the of the face which contained 0.5 gamma acetylcho- chilled area. Sweating was absent when the pa- line per 0.1 cc. produced sweating. tient held but did not chew food placed in his Iontophoresis (3.4 milliamperes for ten minutes mouth. When the tongue was swabbed with through a 1 sq. cm. pad) of a 1: 12,500 solution vinegar, a small amount of sweating appeared. of acetylcholine bromide in isotonic saline solu- The response was independent of the region of the tion, produced sweating on the involved right side tongue swabbed. When the patient chewed a of the face and no sweating on the uninvolved left pledget of cotton soaked in vinegar, the amount side on two attempts, with no sweating on either of sweating, as judged by the extent and depth of side on the third attempt. Ten mgm. of acetylcho- the starch-iodine reaction, was more marked. line bromide injected subcutaneously did not re- Psychic salivation and sweating could not be in- sult in facial sweating. duced. Sweating induced by the general appli- The possibility was examined that disturbances cation of heat to the body was irregularly dimin- in vasomotor nervous function are present in the ished over the right side of the face. auriculotemporal syndrome. The variation in skin Procainization of the right auriculotemporal temperature of the involved areas in response to was nerve resulted in anesthesia over part of the dis- cooling and heating the body and extremities measured and to unin- tribution of the nerve. In the area of anesthesia compared symmetrical volved areas. To determine the time of occur- sweating failed to appear after the usual stimulation. Novocaine injection 1 of the right superior rence of the maximal response to heating and cooling, measurements of the skin temperature of a cervical ganglion resulted in a Horner's syndrome, The measurements of skin suffusion of the conjunctiva, increased warmth, finger tip were made. temperature were made at frequent intervals with and dilation of the right hand veins. While the a thermocouple. The experiment was performed cervical sympathetics were blocked, eating an apple in a constant temperature room, 200 C. The pa- induced sweating in 45 seconds and 20 seconds in tient was seated and the legs, arms and chest were two successive trials. The patient was apprehen- uncovered. Within 20 minutes a distinct fall' in 1 The authors are indebted to Dr. Reginald Smithwick finger tip temperature was observed (Figure 2) for the procaine blocks in Cases 1 and 2. which 'reached a maximum in 70 minutes. The THE AURICULOTEMPORAL SYNDROME 671 right ear skin temperature fell from 29.50 C to served to sweat, although this had never been 25.50 C in this interval of time. At the arrow noted by the patient. Psychic salivation was eas- (70 minutes) one leg and one arm were immersed ily induced, but the syndrome of flushing and in running warm water (T 420); the patient was sweating did not occur. covered with blankets and hot water bottles were Sweating, distributed usually over the upper applied to the chest and back. Approximately 15 lip and nares, may be induced in normal subjects minutes later, a distinct and sustained rise in by the application to the tongue and chewing of finger and left ear temperature occurred. The red pepper or ginger. In this patient these foods involved right ear, however, showed no rise in resulted in sweating on -the upper lip but did not temperature in response to heating (Figure 2); induce sweating in the distribution of the auriculo- furthermore, the increase in right facial skin tem- temporal nerve. perature in response to heat was less than that ob- Novocaine injection of the superior cervical served in a symmetrical point on the uninvolved sympathetic ganglion on the left resulted in a left side. Horner's syndrome and an absence of sweating An attempt was made to measure and compare in response to heat. In the presence of this block, the secretion from the parotid glands in this pa- the auriculotemporal syndrome was observed as tient. No saliva could be collected from the right before, after the usual stimulus. parotid duct. Secretion from the left duct ap- Intradermal wheals produced with .05 gamma peared normal. acetylcholine bromide contained in 0.1 cc. isotonic Observations in Case 2: In this subject flushing saline solution produced sweating in the involved was observed over the left side of the face ten area on the left face, but none in the corresponding seconds after he began to eat an apple, and in 15 location on the right. seconds sweating was observed over the entire Saliva was collected from the right and left distribution of the auriculotemporal nerve on the parotid ducts by means of silver cups attached by left. A small area on the right cheek was also ob- suction to the parotid gland duct orifices. No

36 35 34 z 33 0 32 e) LwJ 31 w W- 30 wLL a 29 W 28 cr- D 27 C 26 O 25 w I 24 23 0 10 20 30 40 50 60 70 80 90 100 10 120 130 140 TJME - MINUTES FIG. 2. VARIATIONS IN SKIN TEMPERATURE ON COOLING AND HEATING THE BODY See text for description of figure. 672 A. S. FREEDBERG, ROBERT S. SHAW AND M. J. MCMANUS

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110 TIME- MINUTES FIG. 3. VARIATION IN SKIN TEMPERATURE ON COOLING AND HEATING THE BODY; VARIATIONS OF THE SKIN TEMPERATURE CONSEQUENT TO EATING IN THE INVOLVED SKIN AREA IN THE AURICULOTEMPORAL SYNDROME See text for description of figure. significant differences were found in the two sam- Observations in Case 3: After the patient ples in the amount or relative viscosity as meas- chewed an apple and on another occasion a lemon, ured by high pressure Ostwald viscosimeter. sweating appeared in the region of the scar 16 and Studies in the manner described in Case 1 were 12 seconds later, respectively. Chewing paraffin made of the variations of facial and ear skin tem- induced sweating in the same region in 16 seconds. perature (Figure 3) with cooling and warming of Chewing ginger resulted in sweating in the region the body and extremities. In response to cooling of the scar in 14 seconds and the upper lip in 30 of the extremities and body a distinct fall in finger seconds. Intradermal wheals were made in the temperature was obtained. The changes in skin involved area and in a symmetrical point on the temperature of the ears and face were slight and left side of the face. On the right side sweating no significant difference was observed between the occurred over and around wheals containing .005 right and left sides. At the first arrow (48 min- gamma acetylcholine bromide in 0.1 cc. isotonic utes) heat was applied and 25 minutes later a salt solution. On the left side sweating was ab- distinct rise in finger temperature occurred from sent with wheals of a similar concentration and approximately 210 C to 310 C. After maximal also with a concentration of 0.05 gamma in 0.1 cc. finger vasodilation in response to heat had been of isotonic salt solution. obtained, eating an apple (arrow at 91 minutes) produced a definite increase in temperature not COMMENT only on the involved left side of the face and ear There have been at least 35 instances of the but also on the right side. No asymmetry of auriculotemporal syndrome reported in the litera- facial sweating in response to heat could be ob- ture (1, 5-15). In the majority of cases the orig- served. inal episode involved both infection in and opera- THE AURICULOTEMPORAL SYNDROME 673 tion on the parotid gland. The most common in- Proposed theories: citing circumstance was a parotitis, complicating I. It has been suggested (17) that the sweating typhus or typhoid fever, which had been drained phenomenon results from the diffusion of acetyl- surgically. The syndrome has also followed paro- choline or cholinergic substances from the injured titis complicating syringomyelia, mumps, opera- parotid gland. The speed of the reaction, the tion on the parotid without infection (2, 16), and distribution in the course of the entire auriculo- parotitis of unknown etiology in the absence of temporal nerve and the occurrence of the phe- suppuration and operation. The sweating makes nomenon in patients in whom the involved paro- its appearance from a few days (14) to three tid gland is in all likelihood completely destroyed years (9) after the original episode, and lasts the (Case 1) are against this interpretation. rest of the patient's life. One case is reported II. Needles (12) noted the appearance of the with gradual disappearance of the syndrome over auriculotemporal syndrome coincident with the a three-year period (11). Uniformly the sweat- closure of a salivary fistula, and felt that the syn- ing appears over part or all of the distribution of drome might be caused by the irritation of su- the auriculotemporal nerve on the injured side. domotor nerve fibers passing through or near the It is usually accompanied by visible flushing, and parotid gland by the swelling of the gland on patients without visible flushing describe a sen- mastication. This appears unlikely, since the sation of warmth over the involved area. Minor syndrome may appear in the presence of an atro-' disturbances in sensation and decreased phied and functionless parotid gland (Case 1). sweating III. Ford has suggested (8) that the auriculo- response to heat over the distribution the auric- of temporal syndrome may be explained by injury ulotemporal nerve of the involved side are fre- to the auriculotemporal nerve and subsequent quently noted. aberrant regeneration of parotid secretary fibers The severity of sweating varies from patient along'sudomotor and vasomotor pathways. The to patient, being slight in some (Case 3) and pro- auriculotemporal nerve contains, in addition to fuse in others (Cases 1 and 2). The studies de- sensory fibers, secretary fibers to the parotid scribed above suggest that relief may be obtained gland, sudomotor fibers, and vasodilator fibers to in instances of severe flushing and sweating by in- the area of sensory distribution of the nerve (18); terruption of the efferent arc by alcohol injection the parotid secretary fibers, sudomotor and va- or surgical section of the auriculotemporal nerve. sodilator fibers are all cholinergic. The following facts are in support of this hypothesis: Mechanism of auriculotemporal syndrome- anatomic pathway 1. The time interval between the original injury and the appearance of the syndrome, usually one It appears that the disorder in the auriculo- month or longer, is consistent with a period of temporal syndrome lies in the efferent arc. The nerve degeneration and subsequent regeneration. pathway of the afferent arc is variable since sweat- One case, however, is reported (14) where the ing may be initiated by stimulation of the seventh syndrome appeared two to three days following or ninth nerves and has been reported to result injury. 2. The frequently noted abnormalities from psychic stimulation. The efferent pathway in sensation and decreased sweating response to involves fibers in the region of the auriculo- heat over the distribution of the auriculotemporal temporal nerve as demonstrated by the effect of nerve, and, as in one of our cases, defective va- procainization (Case 1). Since procainization of somotor response over the distribution of the au- the superior cervical ganglion resulted in the disap- riculotemporal nerve, are consistent with injury to pearance of sweating in response to heat over the all components of the auriculotemporal nerve. face but did not affect the occurrence of the auricu- Although hypersensitivity of the sweat glands over lotemporal syndrome, it is clear that the fibers in the affected region is consistent with the inter- the efferent arc do not pass through the cervical pretation that the involved sweat glands have been sympathetics. partially denervated, it is difficult to explain the 674 A. S. FREEDBERG, ROMERT S. SHAW AND M. J. MCMANUS evident hypersensitivity after regeneration has reported cases of the auriculotemporal syndrome, taken place. hypersensitivity to pilocarpine as manifested by The resemblance of the case described by early sweating in the involved area, and our ob- Uprus, Gaylor and Carmichael (16) to those ex- servations of local hypersensitivity to acetylcholine hibiting the auriculotemporal syndrome is so strik- in the involved regions as demonstrated by intra- ing as to suggest a common mechanism. They cutaneous wheals or iontophoresis of acetylcholine, described an instance of flushing and gustatory clearly show that there is a hypersensitivity of the sweating over the distribution of the right cu- sweat glands in the involved region. That hyper- taneous colli nerve appearing one to two years sensitivity to cholinergic substances may occur in following the removal of cervical lymph glands organs following denervation has been demon- through a horizontal incision over the mid right strated in the submaxillary gland (19), skeletal sternocleidomastoid muscle. In the involved area, muscle (20) and iris (21). In these latter studies sensations to pin prick and light touch were di- hypersensitivity developed in from one to two minished. There was diminished sweating re- weeks. Observations on the time relationship of sponse to heat and an impaired vasomotor re- the development of hypersensitivity following de- sponse after thermal stimuli. Procainization of nervation of sweat glands are necessary. the cutaneous colli nerve (sensory and vasomotor Other data are available consistent with the in- to the area) had no effect upon the flushing and the terpretation that a cranial supply of sudomotor sweating reaction induced by food. Blocking the fibers exists. It is a common observation that lingual nerve proximal to the origin of the chorda facial sweating occurs in normal individuals with tympani resulted in cessation of salivation and the the eating of hot spicy foods. More unusually, it disappearance of the phenomena. In this in- may occur with the eating of chocolate (9) and stance the primary injury was to the cutaneous the drinking of vinegar (22). Gustatory sweat- colli nerve and injury to. the secretary fibres in ing in normal individuals, as produced by the eat- the lingual nerve appears unlikely because of the ing of ginger, has been studied by us. The sweat- level of the incision. With absence of injury to ing occurs maximally about the mouth and nose. submaxillary secretary fibers, aberrant regenera- Observations were also made in a patient who had tion is unlikely in this case. a unilateral preganglionic cervical sympathectomy IV. The explanation offered here is that the for Raynaud's syndrome. In this patient who had auriculotemporal syndrome may represent the no Horner syndrome, there was absence of heat response of denervated and hypersensitive sweat sweating on the denervated side. Gustatory sweat- glands to previously unapparent cranial sudomotor ing induced by eating ginger was marked on the impulses. List and Peet observed (18) marked normal side of the face but scarcely perceptible facial gustatory sweating following postganglionic on the denervated side. This would suggest that cervical sympathectomy. In these patients, the the nervous pathways involved in gustatory sweat- sweating appeared following the eating of foods ing consequent upon the eating of ginger passed which were similar to those foods causing sweat- through the cervical sympathetics. The pathways ing in patients with the auriculotemporal syn- concerned in the auriculotemporal syndrome do drome. List and Peet (18) suggested that this not, as demonstrated by the fact that the syndrome type of sweating was an "exaggeration of nor- is not affected by cervical sympathetic block. mal gustatory sweating" caused by denervation Furthermore in Case 2 sweating induced by ginger hypersensitivity of the sweat glands, but they was observed to occur independently from the felt that denervation hypersensitivity was not the auriculotemporal syndrome sweating. The failure explanation of the auriculotemporal syndrome, be- to block the syndrome by procainization of the cause the diminution of heat sweating over the superior cervical ganglion (Cases 1 and 2), al- area involved in the auriculotemporal syndrome though heat sweating was abolished, is also con- was so slight as to suggest that the denervation of sistent with the presence of cranial sudomotor the sweat glands was negligible. However, in the fibers. That the facial sweat glands may have a THE AURICULOTEMPORAL SYNDROME 675 dual innervation from the brain and cervical to adrenalin which occurs after post-ganglionic sympathetics was suggested by Takino (23) who division of sympathetic fibers. observed both medullated and non-medullated 6. In instances of severe flushing and sweating, nerves around the sweat glands of the face. The the described studies suggest that relief may be latter evidence is not decisive and further studies obtained by interruption of the efferent arc by al- on this point are necessary. cohol injection or surgical section of the auriculo- It would seem, therefore, that the auriculotem- temporal nerve. poral syndrome, post-sympathectomy gustatory sweating and the case of Uprus, Gaylor and Car- BIBLIOGRAPHY michael represent sweating responses to nervous 1. Frey, L., Le Syndrome du Nerf Auriculo-temporal. impulses in sweat glands made hypersensitive by Rev. neurol., 1923, 2, 97. 2. Nathanson, I. T., Personal Communication. denervation. Although as noted above, in the 3. Bailey, H., Parotidectomy: Indications and Results. discussion of Ford's-hypothesis, these nervous im- Brit. M. J., 1947, 1, 404. pulses may be from abnormally regenerated sali- 4. Minor, V., Eines neues Verfahren zu der Klinischen vary secretary fibers, if cranial sudomotor fibers Untersuchung der Schweissabsonderung. Deutsches Ztschr. f. Nervenh., 1928, 101, 302. exist, they might be the efferent pathway in the 5. Kaminsky, S. D., Das "auriculo-temporale (Parotitis) three types of gustatory sweating under considera- Syndrom" bie Syringomyelie. Deutsches Ztschr. f. tion. The three syndromes would then represent Nervenh., 1929, 109, 296. complete or partial severance of the sudomotor 6. Thomas, A., Le double reflex vaso-dilatateur et re- sudoral de la face consecutif aux blessures de la and vasomotor sympathetics to the involved loge parotidienne; les parareflexes. Rev. neurol., gions leading to hypersensitivity of the sweat 1927, 1, 447. glands and exaggeration of normal and hitherto 7. Fridberg, D., Das Auriculo-temporale Syndrom. not obvious cranial sudomotor and vasomotor im- Deutsches Ztschr. f. Nervenh., 1931, 121, 225. pulses. 8. Ford, F. R., Paroxysmal lacrimation during eating as a sequel of facial palsy (syndrome of crocodile tears): report of four cases with a possible inter- SUMMARY AND CONCLUSIONS pretation and comparison with the auriculotemporal syndrome. Arch. Neurol. & Psychiat., 1933, 29, 1. The auriculotemporal syndrome is charac- 1279. terized by gustatory sweating and flushing over 9. Bassoe, P. N., Auriculotemporal syndrome and other the cutaneous distribution of the auriculotemporal vasomotor disturbances about the head: "auriculo- nerve. Three who ex- temporal syndrome" complicating diseases of paro- patients have been studied tid gland, angioneurotic edema of the brain. M. hibited this syndrome. Clin. of North America, 1932, 16, 405. 2. The gustatory sweating and flushing seen in 10. Noica and Bagdasar, Syndrome du nerf auriculo- the auriculotemporal syndrome is a manifestation temporal. Rev. neurol., 1926, 1, 225. of a reflex in which the efferent arc is through 11. Trioumphoff, A., Une forme particuliere de l'hyperhidrose locale de la face. Presse med., 1926, II, the auriculotemporal nerve or through adjacent 86, 1350. autonomic fibers and not through the cervical 12. Needles, W., The auriculotemporal syndrome, with sympathetic nerves. The afferent arc is non- suggestion regarding therapy. Arch. Neurol. & specific; the syndrome may be induced by stimu- Psychiat., 1936, 35, 357. 13. Karnosh, L. J., The syndrome of the auriculotemporal lating the seventh and ninth nerves. nerve. Cleveland Clin. Quart., 1946, 13, 194. 3. There may be a deficiency in sudomotor, 14. Souques, A., Hyperhidrose unilaterale de la face con- thermo-regulatory and sensory innervation over s~cutive a un traumatisme de la region sourciliere the involved area. et provoquee par les excitations gustatives et par la chaleur. Des hemihyperhidroses d'origine cere- 4. A local hypersensitivity of the sweat glands bro-spinale. Rev. neurol., 1927, 2, 145. in the involved region to acetylcholine bromide is 15. Guttmann, L., and List, C. F., Zur Topik und Patho- present. physiologie der Schweissekretion. Ztschr. f. d. 5. The mechanism of this syndrome is ap- ges. Neurol. u. Psychiat., 1928, 116, 504. 16. Uprus, V., Gaylor, J. B., and Carmichael, E. A., parently related to denervation hypersensitivity of Localized abnormal flushing and sweating on eat- the sweat glands analogous to the hypersensitivity ing. Brain, 1934, 57, 443. 676 A. S. FREEDBERG, ROBERT S. SHAW AND M. J. MCMANUS

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