Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:611-616

Facial flushing after thermocoagulation of theGasserian ganglionPD DRUMMOND, A GONSKI, JW LANCE

From the Departments ofNeurology and Neurosurgery, The Prince Henry Hospital, Sydney, Australia

SUMMARY The development of a facial flush during thermocoagulation of the Gasserian ganglionwas monitored in 16 patients with pulse recording techniques and in a further 17 patients withthermography. There was a close association between the development of the facial flush in thedistribution of one or more divisions of the trigeminal nerve and the subsequent demonstration ofpostoperative analgesia. In regions where significant changes took place, vascular pulsationsincreased 25-233% (mean 96%) and facial temperature rose 0*5-2-0°C. The response persistedfor up to an hour postoperatively, and was not diminished in patients with pre-operativeanalgesia from a previous procedure. Possible mechanisms for the facial flush, including stimula-tion of an active vasodilator system, the antidromic release of vasoactive substances from trigem-inal nerve terminals and the release of tonic vasoconstriction are discussed. A practical applica-tion of the pulse recording technique used in the present investigation would be to monitor thedistribution of vasodilatation at operation to avoid unwanted first division sensory loss.

Flushing on one side of the face may follow anattack of trigeminal neuralgia' and has beenobserved after injection of alcohol into the ipsilat-eral trigeminal (Gasserian) ganglion.2 Rowbotham2commented that facial temperature and skin colourdid not alter after tractotomy, root section or intra-cranial neurectomy, and attributed the rise in skintemperature after alcohol injection of the ganglionto involvement of sympathetic fibres either in theganglion or adjacent to it. Oka3 reported that temp-erature increased on one or both sides of the facefollowing injection of alcohol into the Gasserianganglion, the response reaching its peak 10-30minutes after injection and persisting for 40-120minutes.

Similar observations have been made afterthermocoagulation of the Gasserian ganglion. Sweetand Wepsic4 commented that flushing was limited tothe skin distribution of the appropriate division ofthe trigeminal nerve. Onofrio5 confirmed this andremarked that the blush did not appear if the sen-sory root, ganglion or sensory division had previ-ously been damaged sufficiently to cause denseanaesthesia. He considered that the phenomenonwas more likely to be caused by stimulation of a

Address for reprint requests: Professor JW Lance, The PrinceHenry Hospital, Little Bay, 2036, New South Wales, Australia.

Received 2 November 1982. Accepted 20 November 1982

vasodilator system than destruction of sympatheticfibres.The aim of the present investigation was to pro-

vide an objective assessment of these clinical obser-vations, to determine the localization and timecourse of facial flushing after thermocoagulation andto ascertain, if possible, whether it was caused byexcitation of vasodilator fibres, destruction of a tonicvasoconstrictor influence, or both.

Patients and methods

PatientsObservations were made on 33 patients, 17 male and 16female, aged 33-90 years (mean 63 years) undergoingthermocoagulation of the Gasserian ganglion. The indica-tions for the procedure were trigeminal neuralgia (27),atypical facial pain (3), carcinoma invading the trigeminalnerve (2) and cluster headache (1). Two patients whoexperienced recurrence of pain postoperatively werestudied a second time when the procedure was repeated.Facial sensation was examined clinically before and afteroperation.

ProcedureThe operative technique was similar to that described bySweet and Wepsic4 and Onofrio.' A thermistor needle wasinserted through the foramen ovale under local anaes-thesia, the position of the tip being monitored fluoroscopi-cally and confirmed by radiographs. While the patient wasconscious, the Gasserian ganglion was stimulated electri-

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cally (10 v peak, 0-5-1-0 ms pulses, 5 Hz for 10-30 s) tocheck that paraesthesiae were referred to the appropriatedivision or divisions. The patient was then fully anaesthet-ised for a brief period during thermocoagulation (70°C for1-2 minutes). In some instances a second lesion was madeafter repositioning the needle slightly.

MethodsIn 16 patients, infrared photocells (Narco Bio-Systems)were fastened with adhesive washers to the forehead,cheek, or chin of the symptomatic side and one area (usu-ally the cheek) of the opposite side. Providing that thephotocells are not placed over a superficial artery theymeasure changes in capillary perfusion,6 a techniqueknown as photoplethysmography. Recordings were madebeforevand during preliminary electrical stimulation (sixpatients) and before, during and after thermocoagulation(16 patients). Measurements were taken 15, 30 and 60seconds after the tip of the needle reached 70°C, fromwhich the mean amplitude was calculated and expressed asa percentage of pre-coagulation amplitude for statisticalpurposes. Recordings were continued for 10 minutes afterthe procedure in seven patients and for up to 60 minutes inthree patients.Heat loss from the face was measured in 17 patients

before, during and after the procedure, using an AGAthermovision camera sensitive to infrared radiation. Toobtain thermograms during the operative procedure a mir-ror, angled at 450, was positioned above the face of thesupine patient 23 cm in front of the thermovision camera.The thermogram was photographed on Polaroid film witheach isotherm, separated by 0*5°C, being photographedthrough a different coloured filter. The thermogram wasthus a photograph portraying in colour each facial isotherm(Plate 1), the isotherms being calibrated by reference to adisc maintained at 34°C placed next to the patient's head.Observations were continued for up to 30 minutes after theprocedure in eight patients and another measurement wastaken the following day in seven patients.

Results

PHOTOPLETHYSMOGRAPHYVascular pulsations did not change significantlyfrom baseline in any of the six patients during pre-liminary electrical stimulation. On the non-symptomatic side of the face, pulsations varied inamplitude during thermocoagulation from -47% to+25% of the control value (mean -7%, SD 15%),presumably as a non-specific reaction to anaesthesiaand operative intervention. For assessment of dilata-tion on the operated side, any increase in vascularpulsation in excess of two standard deviations of themean on the unoperated side, that is in excess of23%, was deemed to be significant.

In the cutaneous distribution of the trigeminalnerve where significant changes took place, pulsa-tions increased 25-233% (mean 96%, SD 62%)(fig 1). The response became apparent as the tip ofthe needle reached 70°C and was of similar mag-

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_ItIIAUWWAW_ADuring

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Fig 1 Increase in amplitude ofpulsation in the distributionofthe second and third divisions of the right trigeminalnerve during thermocoagulation. Analgesia was detectedpostoperatively in the two divisions showing increasedvascular pulsations during thermocoagulation.

nitude in each of the three divisions, mean increasesbeing 92% for the first division, 111% for the sec-ond division and 85% for the third division. Pulsa-tions remained increased for up to an hour afterthermocoagulation (fig 2) but the change was statis-tically significant for only the first 10 minutesbecause of the relatively small numbers studied.Two lesions were made during the one procedure

in nine patients. Vascular pulsations increased byonly 10% after the second lesion, an insignificantchange.The increase in vascular pulsation in the cutane-

ous distribution of each division correlated posi-tively with the demonstration of postoperativeanalgesia in that division (table 1, fig 3). In a furtherfive patients with pre-operative analgesia from aprevious procedure, augmentation of vascular pulsa-tion was observed in 8 of the 12 divisions studied(fig 3).

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Coagulated side

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0 5 10 30Time after thermocoagulation ( minutes )

Fig 2 Time course ofincreased vascular pulsationfollowing thermocoagulation.

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Facial flushing after thermocoagulation of the Gasserian ganglion

b

c dPlate Temperature changes during thermocoagulation. Thermograms are calibrated by reference to the green discmaintained at 34°C. Each colour represents an isotherm of0-5°C ranging from 33-0-33-50C (blue) to 36-0-36-50C(white). Thermograms ofa patient (a) before and (b) during thermocoagulation, demonstrating an increase of05-1 0°C on the operated side during thermocoagulation, (c) Thermograms 15 min and (d) 30 min after theprocedure, showing the time course ofthe facial flush.

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Drummond, Gonski, Lance

Table 1 Association between increased vascular pulsationin the distribution ofa given division ofthe trigeminal nervewith the subsequent finding ofanalgesia in that division

Analgesia Increased vascular pulsation Chi-squared

Yes No Total

Yes 13 5 18 8-13No 3 11 14 (p < 0-01)Total 16 16 32

Post operative analgesia Pre and post operativeanalgesia

V2 29=

0 5

I Increased vascular pulsations

] Post operative analgesia

Fig 3 Increased vascular pulsation in regions whereanalgesia was detected postoperatively.

THERMOGRAPHYIn the 17 patients studied, heat loss from the skinsupplied by each of the three divisions of the trigem-inal nerve on the symptomatic side was comparedwith the non-symptomatic side before, during andafter the operative procedure. On the non-symptomatic side, skin temperature increased by atleast 0 5°C in 25 of 51 divisions and decreased bythe same extent in only two divisions. These changeswere attributed to a generalised autonomic reactionresulting from anaesthesia and operation. Beforethermocoagulation, skin temperature on the symp-tomatic side was greater than on the non-symptomatic side by at least 05°C in 21 of the 51divisions and was cooler in only two divisions. Thisasymmetry presumably was caused by injection oflocal anaesthetic, insertion of the thermistor needleor other operative procedures.

For these reasons, increases in skin temperatureon the operated side during thermocoagulation wereregarded as significant only when they exceeded by0-5°C the ipsilateral pre-operative temperature andthe contralateral postoperative temperature in theappropriate division. According to these criteria, aflush developed on the operated side in 30 of 51divisions (Plate 1), increases being 0-5-1-00C in thefirst and second division and up to 2-00C in the thirddivision (table 2). There was a significant associationbetween the appearance of the flush and thedevelopment of postoperative analgesia (fig 4)although the flush sometimes spread to adjacent reg-ions that were not rendered analgesic (table 3). The

Table 2 Number ofpatients showing increases in skintemperature in the distribution ofeach ofthe three divisionsofthe trigeminal nerve

Division Temperature Increase

050C 1-00C 1-5-2-0°C

First 5 2 0Second 6 7 0Third 3 5 2

Table 3 Association between facial flush (detectedthermographically) in the distribution ofa given division ofthe trigeminal nerve with the subsequent finding ofanalgesiain that division

Analgesia Flush Chi-squared

Yes No Total

Yes 15 4 19 7-20No 11 17 28 (p < 0-01)Total 26 21 47

flush also became apparent in two patients withanalgesia from previous thermocoagulations and inone patient with analgesia of the second and thirddivisions as the result of a partial section of thetrigeminal root central to the ganglion 10 years pre-viously (fig 4). Analgesia developed in four regionswithout facial flushing (table 3). The face was 0-5-1.00C hotter than the contralateral side pre-operatively in three of these regions, which mayhave masked facial flushing during thermocoagula-tion.

In nine patients who showed a flush during ther-mocoagulation, a second lesion was made afterrepositioning the thermistor needle. The flush wasaccentuated in three patients but did not alter in theother six patients.

Flushing persisted in 1 1 of 17 divisions in patientsexamined 10-15 minutes postoperatively and in fiveof 11 regions in those studied 30 minutes after theprocedure. There was no evidence of flushing inseven patients examined the following day.

Post-operative analgesia

VI I

V2

V3.

5

Pre and postoperativeanalgesia

III I

*III*I

Wi~

r--,iI I* Facial flushingL--J

D Post-operative analgesia

Fig 4 Facial flushing in regions where analgesia wasdetected postoperatively.

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Facial flushing after thermocoagulation of the Gasserian ganglion

Discussion

The present findings confirm previous clinical obser-vations of unilateral facial flushing in a divisionaldistribution during and after thermocoagulation of-the Gasserian ganglion. In most instances the flushwas limited to the distribution of the division or divi-sions in which analgesia was detected postopera-tively but it was occasionally observed in an adjacentdivision. Vasodilatation was usually maximal within15-30 seconds of the start of the coagulation and asecond lesion made during the same procedure hadlittle or no additional effect.

Possible mechanisms for the flushing phenome-non include the stimulation of a vasodilator path-way,5 the antidromic release of substance P or othervasoactive substances from terminals of the trigemi-nal nerve7 or the destruction of a tonic vasoconstric-tor system. There is physiological evidence for bothconstrictor and dilator mechanisms in man. Bystudying skin temperature after blocking the supra-orbital, greater auricular, external nasal, infraorbitaland mental nerves, Fox, Goldsmith and Kidd8 con-cluded that the cutaneous circulation of the ear, lipand nose was subject to a tonic vasoconstrictorinfluence whereas active dilatation in response toheat was more important in controlling skin temper-ature of the forehead and chin.

Gonzalez, Onofrio and Kerr9 reported that stimu-lation of each division of the trigeminal nerve in thecat (9-12v, 1 ms pulses, 100 Hz for 2-3 min) causedan increase in skin temperature in the appropriatecutaneous distribution of up to 3°C for the thirddivision, 2-20C for the second division and 1-0°C forthe first. The response began after a latency of 5-8 sand lasted for 6-8 min. The vascular response wasnot altered by acute transection of the trigeminalroot, was slightly depressed by chronic transectionof the root, and was abolished by a combined lesionof trigeminal root and facial nerve. Stimulation ofthe facial nerve or its greater superficial petrosalbranch evoked temperature increases which wereabolished in the distribution of a particular divisionof the trigeminal nerve by transection of that divi-sion. It was concluded that the flushing responsedepended to a minor degree on fibres emerging fromthe brainstem in the trigeminal root but mainly upongreater superficial petrosal fibres which joined theGasserian ganglion and were distributed with eachof the three divisions of the trigeminal nerve. Thisquestion must remain open because meticulous dis-section of the heads of five cats by Dr N Bogduk inour laboratory could not demonstrate any anatomi-cal connection between the greater superficial pet-rosal nerve and the Gasserian ganglion.On the other hand, there is anatomical evidence

in the cat that the internal carotid nerve suppliessympathetic fibres to the third,'0 second'0 and first"divisions of the trigeminal nerve, joining the Gas-serian ganglion on its under surface and being distri-buted with each trigeminal branch. Matthews andRobinson'0 showed that sectioning the cervical sym-pathetic trunk in two cats led to a sustained rise inlip temperature of 1.0°C and 1-7°C respectively, arelease phenomenon which has also been noted inman after sympathectomy.'2 Conversely, stimulationof the distal end of the cut sympathetic trunk in fivecats caused a fall in lip temperature of up to 3-0°C.When the constrictor response was blocked byintravenous phentolamine in two animals, stimula-tion of the inferior alveolar nerve caused a tempera-ture increase of 2-3°C and 2*5°C respectively. Thereis thus a tonic vasoconstrictor system present inperipheral branches of the cat trigeminal nerve,originating from the cervical sympathetic system,mediated at least in part by fibres from the internalcarotid nerve which traverse the Gasserian ganglion.There is also an active vasodilator system present inbranches of the trigeminal nerve which is unmaskedwhen sympathetic activity is blocked by phen-tolamine.'0 The experiments of Gonzalez, Onofrioand Kerr9 suggested that this vasodilator systemoriginates in the greater superficial petrosal branchof the facial nerve and can be influenced by stimula-tion of the Gasserian ganglion although we have notbeen able to demonstrate an anatomical connectionbetween the greater superficial petrosal and trigem-inal nerves in the cat. "I The suggestion of Moskowitzet a17 that stimulation of the trigeminal nerve mayrelease a vasodilator such as substance P from affer-ent terminals in the skin must therefore be seriouslyentertained. There is evidence that stimulation ofthe trigeminal ganglion releases substance P in theeye and tooth pulp in the cat3 14 and increases pulpblood flow.'4 Capillary transudation is increased inthe trigeminal distribution by stimulation of the rattrigeminal ganglion.'5What is the most likely mechanism for the sus-

tained flush in man? It is unlikely to be the result ofa centrally-mediated reflex since we observed theflushing response in a patient with previous sectionof that part of the trigeminal root containing fibresfrom divisions in which the flush appeared. It couldnot be the release of tonic sympathetic vasoconstric-tion because the only demonstrable connection bet-ween the sympathetic nervous system and thetrigeminal nerve in man is a branch of the internalcarotid nerve which runs briefly with the sixth cra-nial nerve before being distributed solely to the firsttrigeminal division.'6 It is unlikely that it depends onthe antidromic release of vasodilator substancesfrom trigeminal nerve terminals responsible for pain

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sensibility7 since a flush of equal intensity wasobserved after re-operation on patients withanalgesia from previous surgery in whom a substan-tial proportion of pain fibres must have degenerated.Facial flushing may have resulted from spread ofstimulation to the greater superficial petrosal nervewhich lies in close proximity to the Gasserian gang-lion in man,'7 although it is difficult to see how theflush could be limited to the distribution of only oneor two divisions of the trigeminal nerve if this werethe case. The possibility remains that the flush maydepend on antidromic release of chemical transmit-ters such as substance P from large diameter fibresor pain fibres which survive thermocoagulation. Noinference can be drawn from the failure of prelimi-nary electrical stimulation to alter vascular pulsa-tions in our patients since only low-frequency pulses(5/sec) were used. Further elucidation of themechanism will depend on animal experimentation.A practical application of the techniques emp-

loyed in this study would be to monitor the distribu-tion of vasodilatation at operation, since surgeonsusually wish to avoid implicating the first division.Photoplethysmography would be preferable tothermography for this purpose because it is simpler,cheaper, and detects the onset of vasodilatationbefore a visible flush appears.

This study received generous support from the JAPerini Family Trust. The illustrations were photo-graphed by the Department of Medical Illustration,University of New South Wales.

References

'Jefferson G. Observations on trigeminal neuralgia. BrMed J 193 1;2:879-83.

2 Rowbotham GF. Observations on the effects of trigemi-nal denervation. Brain 1939;62:364-80.

3Oka M. Experimental study on the vasodilator innerva-tion of the face. Med J Osaka Univ 1950;2:109-16.

4 Sweet WH, Wepsic JG. Controlled thermocoagulation

of trigeminal ganglion and rootlets for differential des-truction of pain fibers. Part. 1: Trigeminal neuralgia. JNeurosurg 1974;39:143-56.

Onofrio BM. Radiofrequency percutaneous Gasserianganglion lesions. Results in 140 patients with trigemi-nal pain. J Neurosurg 1975;42:132-9.

6 Drummond PD, Lance JW. Extracranial vascular reac-tivity in migraine and tension headache. Cephalalgia1981 ;1: 149-55.

7 Moskowitz MA, Reinhard JF Jr, Romero J, Melamed E,Pettibone DJ. Neurotransmitters and the fifth cranialnerve: is there a relation to the headache phase ofmigraine? Lancet 1979;2:883-5.

' Fox RH, Goldsmith R, Kidd DJ. Cutaneous vasomotorcontrol in the human head, neck and upper chest. JPhysiol 1962;161:298-312.

9 Gonzalez G, Onofrio BM, Kerr FWL. Vasodilator sys-tem for the face. J Neurosurg 1975;42:696-703.

Matthews B, Robinson PP. The course of post-ganglionic sympathetic fibres distributed with thetrigeminal nerve in the cat. J Physiol (Lond)1980;303:391-401.

IBarlow CM, Root WS. The ocular sympathetic pathbetween the superior cervical ganglion and the orbit inthe cat. J Comp Neurol 1949;91:195-207.

12 Lewis T, Landis EM. Some physiological effects of sym-pathetic ganglionectomy in the human being and itseffect in a case of Raynaud's malady. Heart1930;15: 151-76.

'3 Bill A, Stjemschantz J, Mandahl A, Brodin E, NilssonG. Substance P: Release on trigeminal nerve stimula-tion, effects in the eye. Acta Physiol Scand1980;106:371-3.

Brodin E, Gazelius B, Lundberg JM, Olgart L. Sub-stance P in trigeminal nerve endings: Occurrence andrelease. Acta Physiol Scand 1981;111:501-3.

,s Jancso N, Jancso-Gabor A, Szolcsanyi J. Direct evidencefor neurogenic inflammation and its prevention bydenervation and by pretreatment with capsaicin. Br JPharmac Chemother 1967;31: 138-51.

16 Parkinson D, Johnston J, Chaudhuri A. Sympatheticconnections to the fifth and sixth cranial nerves. AnatRec 1978;191:221-6.

7Gray's Anatomy (35th ed). Warwick R, Williams PL,eds. Norwich: Longman, 1973.

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