Chronic Paroxysmal Hemicrania Presenting asToothache

Roben E, Delcanho. BDSc, MS

Steven B, Graff-Radford, DDS

Section of Orofaciai PainUCLA, Schooi of Dentistry10833 Le Conte AvenueLos Angeles, Califomis 90024

Correspondence to Dr Delcanho

Chronic paroxysmal hemicrania is an intermittent head-pain prob-lem that is characterized by pain paroxysms lasting about IS min-tites- The attacks usually produce pain in the frontotemporal regionand are responsive to indomethacin. A set of symptoms that defineschronic paroxysmal hemicrania is presented, and two cases inwhich the presenting symptom was toothache are reported. It isemphasized that clinicians should consider chronic paroxysmalhemicrania in the differential diagnosis of orofaciai pain.J OROFACIAL PAIN 1993;7:300-306,

Most pain problems perceived in the teeth can be adequate-ly managed by common dental techniques. However,patients may present with pain in the orofaciai region

that does not arise in the teeth but rather is referred from otherorgan systems. Such prohlems require spectahzed managetiient, notmechanical dental interventions. To formulate a differential dtag-nosis when a patient presents with orofaciai pain, the clinicianmust be familiar with all possible pain conditions that may be per-ceived in the orofaciai region. Most of these conditions have beenpreviously discussed in the dental literature,' ' Chronic paroxysmalhemicrania (CPH), a complex set of symptoms first described bySjaastad and Dale," may present in the orofaciai area but has thusfar not heen reviewed in the dental literature. This article brieflyreviews this syndrome and presents two case reports in which CPHinitially presented as maxillary tooth pain.

Clinical Features

Chronic paroxysrnal hemicrania is a rare, yet well-character i zed,*chronic unilateral headache disorder, with specific inclusionary cri-teria as determined by the International Headache Society.^Clinically similar to cluster headache, but with important differ-ences, the main features of CPH are:

1. Unilateral, intense, throhbtng periorbital/temporal pain2. Multiple attacks per day3. Attacks of short duration4. Chronic daily pattern of attacks, without remission5. Female preponderance6- Associated autonomie symptoms7. Attacks that are mechanically precipitated by neck movements

in some patients8. Absolute respotise to indomethacin

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Age and Gender

Age of onset of CPH is variable, with Antonaciand Sjaastad' finding a range of 11 to 8 I years anda mean age of onset of 33.7 years. This is very sim-ilar to the age of onset in cluster headachepatients.

In an early CPH review,' eight of the definitediagnoses and seven of the ten possible diagnosesdescribed were made for women. This was the firstremarkable difference noted when comparing thepain problem to tbat in Ekbom et AVS classic clus-ter headache study,' in which 143 patients weremale and only 20 were female. As more cases cameto light, it became apparent tbat CPH primarilyaffects women, although there are definite exam-ples of men with CPH.

The relationship of CPH to tbe female reproduc-tive cycle has been studied because of this genderdifference. In 10 pregnant CPH patients, a trendtoward reduction of or freedom from headachewas observed, but symptoms resumed immediatelyafter parturition."

Chronic paroxysmal hemicrania has also beenknown to begin after pregnancy. Tbe administra-tion of birth control pills has been sbown to baveno influence on tbe tendency of attacks, whilemenstruation has been shown to have botb posi-tive and negative effects on CPH attacks, Tbere isinsufficient evidence of the influence of menopauseto draw any conclusions at tbis time.

Location and Character of the Pain

Typically, GPH patients complain of recurrentdaily attacks of intense, throbbing, periorbitaland/or temporal pain. These attacks of severe painare unilateral, always occur on the same side, andrun a chronic course without remission. The painIS usually located in the oculotemporal or temporalregion, but it may involve the entire hemicranium,including the jaws, and so may be confused withother pain syndromes found in this region (eg,toothache]. Patients with CPH have been knownto have root canal therapy and even extraction ofteeth in an attempt to eliminate what was felt to bethe source of the pain.' The pain has also beenreported to spread down through the neck, to theipsilateral shoulder and arm.

Frequency of Attacks

In one study,' attack frequency in CPH patientshas been found to vary between 4 and 38 occur-rences over a 24-bour period (mean of 13.6),

Another study' of 84 CPH patients found themean number of attacks to be 10.8 ± 5,0 over a24-hour period. These multiple attacks are a prin-cipal characteristic that helps differentiate CPHpatients from cluster headache patients, who aver-age only 1 to 3 attacks per day (mean 1.67) duringthe cluster periods.'

The number of pain attacks may be cyclic, witbperiods of increased and decreased attack frequen-cy. These periods of relative exacerbation andremission blend into each otber over weeks andmonths. Similarly, there is variation in the severityof the pain attacks, with transitions from mild tointense attack periods occurring gradually over afew days. When low-grade pain occurs there maybe difficulty in discerning the temporal pattern ofthe pain. However, unlike cluster headache, clear-cut pain remission phases do not occur in CPH,although up to 42% of patients enter a remissionphase in which the pain appears in more episodicclusters, rather than in the regular daily pattern,"The pain pattern may resemble tbat of both clusterand migraine headaches during this phase.

Duration of Attacks

The pain attacks of CPFl generally do not iasc aslong as those of cluster headache. Russell' hasfound the mean duration to be 13,3 minutes witha range of 3 to 46 minutes. By comparison, thesame study reported cluster attacks to have a meanduration of 45 minutes. More recently, Antonaciand Sjaastad" have reported CPH attacks generallylasting 10 to 30 minutes (mean 20,9 minutes) witha range of 5 to 45 minutes.

Timing of Attacks

The attacks may appear at any particular time,sometimes with clockwork regularity. Russell'sstudy' of CPH patients found that attacks seemedto occur mostly in the late afternoon or during theevening, with less than one third of CPH attacksoccurring during sleep. It seems therefore that noc-turnal pain is not as strong a feature in CPH as incluster headaches, in which the pain characteristi-cally awakens a patient from sleep.

Associated Symptoms

Autonomie symptoms are similar to, but generallymilder tban, those found in cluster headache. Suchsymptoms may include nasal congestion, lacrima-tion, conjunctival injection, rhinorrhea, ptosis, andeyelid edema on the symptomatic side. Nausea and

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vomiting, which accompany many other headachetypes, are not seen. Sweating, another ciinicaicharacteristic seen on the symptomatic side in clus-ter headache, has heen studied in six female CPHpatients using an evaporimeter.'" The results showonly two of the six patients to have increasedsweating on the symptomatic side, and it wastherefote concluded that the sweating pattern seenin cluster headache is not a characteristic of CPH.Interestingly, in patients whose attacks could beprecipitated mechanically, marked forehead sweat-ing on the symptomatic side was strongly predic-tive that a pain attack was about to ensue.

Precipitating Factors

Mechanically precipitated attacks have beendescribed in detail by Sjaastad et al.""" Clinicallythe same as spontaneous attacks, these mechanicalattacks were triggered by either flexion movementof the head and neck or by pressure applied to ten-der cervical areas. The head flexion-triggeredattacks could only be induced if the head itself,and not the entire body, was hent. The painoccurred from 5 seconds to 1 minute after thestimulus, depending on the state of the individualpatient. Rotating the head maximally to the symp-tomatic side could also precipitate such attacks.Following neck flexjon in susceptible patients, tbeautonomie phenomena appeared many secondsahead of the pain, thus indicating clearly that suchphenomena are not due to tfie pain per se."Alternatively, pressure to certain cervical triggerspots could immediately precipitate attacks ofCPH, with the pain and autonomie phenomenaappearing together. The mechanisms hehindmechanical precipitation of CPH remain unclear,although the sympathetic nervous system isthought to be the primary mediator of the impulsesfrom the neck ro the ocular region. Ingestion ofalcohol may also trigger CPH, as is the case in clus-ter headache.

Absolute Effectjveness of Appropriate Doses ofIndomethacin

The rapid treatment response to indomethacinforms part of the diagnostic criteria of CPH,allowing indomethacin to be used as a diagnostictest to differentiate CPH from other headaches.

The total response to indomethacjn'' is one ofthe most impressive factors that identify CPH as aunique entity. Tbe initial two patients studied bySjaastad and Dale' reported acctylsalicyiic acid indoses of 6 to 8 g pet day as being tbe only medica-

tion tbat had any benefit prior to ii <-' "findometbacin. In both patients, the initial responseto indomethacin {75 mg per day) occurred withintbe first 24 bours. Sometimes tbe patients benefitat smaller dose levels, and as little as 12.5 mg perday can be effective. Tbe maximum required doseappears to be 250 mg. Tbe effects of jndometbacinbave been reported to continue for several yearsafcer the initiation of treatment witbout the devel-opment of tolerance. Discontinuation of theindomethacin usually causes return of symptomswithin 2 days. Jensen et al'" have repotted onepatient who, after 3 months of indomethacin treat-ment, stopped the medication and remained painfree after 6 months.

Studies comparing various other anti-inflamma-tory medications found that none were any moreeffective than acetylsalicylic acid or as effective asJndomethacJn.

Laboratory Findings

The following significant findings were made vialaboratory investigation. The interested reader isreferred to Sjaastad'" for a more complete discus-sion of CPH, including the various tests and stud-ies thus far carried out on CPH patients.

Corneal Indentation Pulse CCIP) Amplitudes

The CIP amplitudes of CPH patients were foundto he at the upper range of normal betweenattacks; however, the CIP amplitudes were signifi-cantly increased on the symptomatic side duringattacks.'* Marked increases in CIP amplitudes basi-cally reflect an increase in pulsatile hlood volume.Fluorescein appearance time was studied to deter-mine if there was a change in intraocular bloodflow. Almost identical fluorescein appearance timewas seen in botb eyes, suggesting tbat the ampli-tude change is due to local changes in ocular circu-lation and not to a generalized vasodilation. ThisIS further supported by the lack of changes ininternal carotid artety blood flow, blood pressure,and CSF pressure during an attack.

Intraocular Pressure

Increased intraocular pressure of 4 to 6 mm Hghas also heen reported in CPH patients; this maybe due to the acute vasodilation that results fromthe increased volume which occurs in the ocularvascular bed during pain attacks.

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Pupitlometry

Patients with CPH tend to have a relatively smallpupil on the symptomatic side, but pupiUometricstudies have not shown that a specific sympatheticdeficit is present. By contrast, patients sufferingfrom cluster headache often present wirh an asso-ciated Horner's syndrome.

Blood Tests

Many tests were performed, but all were found tobe within normal limits. No significant alterationsin any of the blood coagulation factors were foundin parients with CPH.

Urinaty Histamine Excretion

Histamine has been closely associated with patho-genesis oí cluster headache and therefore was sttid-ied in the CPH patients. No good correlationbetween the degree of histamine excretion and theseverity of the attacks could be observed.

Proposed Mechanisms

Since the establishment of this relatively newheadache entity, many physiologic parameters havebeen studied in CPH parienrs ro hecter understandand evaluate rhe mechanisms that couid be respon-sible. Particularly the work of Ottar Sjaastad, thesestudies have led to speculation that CPH symptomsare mediated either by autonomie impulses or vas-cular factors. The latter could be associated witheither occlusion of arterial flow in the carotid orvertebral arteries, which may occur during headrotation or flexion, or vasoactive substancesreleased from cerebral (or neck) blood vessels.

It has thus been theorized that mediation ofCPH symptoms is via the blood vessels and/urautonomie impulses. Based on the response to theanti-inflammatory medication indomcthacm, it hasbeen suggested that the source of the pain in CPHis an active neurogenic inflammatory processinvolving prostaglandins and vasoactive algesicsubstances, such as bradykinin and histamine.However, this would not account for the changesseen in the CIP amplitudes, the regular pattern ofCPH attacks, or the lack of response ro orher anti-inflammatory medications. The fact chat CPHattacks can be precipitated with mechanicalmanipulation, without any refractory timeberween the manipulation and the onser of theautonomie signs, does not support the hypothesis

that there is a blood-borne subsrance released fromthe ipsilateral carotid artery. The unilaterality ofCPH is also difficult ro explain by rhis proposedmechanism,

("erebral angiography studies have failed to elu-cidate any consistent finding that may producetracrion on the blood vessels and so stimularerelease of vasoacrive substances that can mediatepain. Nor was any evidence found of externalcompression of either the internal or commoncarotid arteries, effectively disproving the hypothe-sis that reduced cerebral blood flow subsequent toarterial compression is the cause of the headache,

A conflicting hypothesis suggests that changes incerebral blood flow patterns related to rhe openingof arreriovenous anastomoses may result in pain.This hypothesis is based on rhe finding that reduc-tion in cerehral blood flow is known to occur withadministration of indomethacin." By exclusion, itseems the mosr likely cause for precipitation ofattacks is via the aurononiic nervous system. Thesympathetic system is most likely involved, as theparasympathetics to the end organs are hardlyaffected when the head is flexed, Sjaastad'' has con-cluded that in CPH it was most likely rhat pain andauronomic phenomena are triggered in parallel.

Case 1

A 53-year-oId wbite woman presented with rhecomplaint of an intermittent sharp pain that waslocalized in the left maxillary and temporalregions. The pain was described as occurring sev-eral times a day and was often associated withtearing in the ipsilareral eye and sweating.

History

The pain attacks were inirially felt as pain in rheupper premolar area, prompting the parienr ro visither dentist. The dentist proceeded ro perform roorcanal treatment on rhe premolar, which did notsubstantially reduce the pain. The patient thenconsulted numerous physicians, including internalmedicine and neurologic specialists, and was even-tually diagnosed as suffering from migraine. Trialsusing a number of migraine prophylactic medica-tions, including propranolol and amirripryline,were attempted without any benefit. The parientreported that her pain had been most successfullyredticed by the use of 6 to 12 aspirin per day. Thepain could be triggered by rhe parient exrendingher head up and back, as would occur when thepatient reached to get a teacup from a cupboard

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located above her head. The paiti had also beennoted ro be worse during cold weather.

Examination

The medical history revealed a family history ofmigraine, and the patient reported a previous his-tory of some intermittent migrainous symptoms.The review of systems was within normal hmits.Psychosocial questioning revealed a happily mar-ried woman with two children and no major Stres-sors or financial problems. The MinnesotaMultiphasic Personality Inventory ¡MMPI} wasadministered and the scales were found Co be unel-evated. The dental, stomatognathic, myofascial,cervical spine, and cranial nerve examinationswere all within normal limits.

Impressions

The intermittent chronic nature of the attacks,occurring several times a day with associated auto-nomie features and triggerable by certain headmovements, led to a preliminary diagnosis of CPH.The fact that only aspirin had been helpful wasalso .suggestive of CPH. The patient was started ona triai of 25 mg of indomethacin three times perday. The patient called 48 hours later to advisethat she was pam free. The mitial controlhng dosewas found to be 125 mg per day, but she is nowbeing maintained on 25 mg without any sideeffects. The patient has found that the longest shecan stay off the indomethacin is 7 days before hersymptoms will return.

Case 2

A 67-year-old, retired white man presented withthe complaint of intermittent daily attacks of painthat was localized to the maxillary molar area. Thepain was described as feeling as if a dentist weredrilling the tooth without using local anesthesia.The attacks generally lasted 10 to 20 minutes,occurred regularly in the afternoon and then duringthe night, and occasionally woke him from sleep.

History

These pain attacks had been present ovet a 3-yearperiod and no triggers had been identified thatwould precipitate the attacks. There were no asso-ciated autonomie symptoms with the pain. Whenasked if anything aggravated the pain, the patientreported that stress could be a factor. Aspirin was

the only alleviating factor described by the patientand was also reported to help stave off an attack.The patient had initially thought the pain was ofdental origin and so had consulted a dentist, whofailed ro find any dental pathology, A physicianthought that trigeminal neuralgia was a possibilityand prescribed Dilantln (100 mg three times aday), but this failed to produce any relief from theattacks. The patient was referred to a neurosur-geon, who thought trigeminal neuralgia was anunlikely diagnosis, and was then referred on to anotolaryngologist. The ensuing examination,together with sinus radiography, proved negativefor pathology, and it was suggested to the patientthat perhaps a temporomandibular joint (TMJ)problem was present. The patient then consulted asecond dentist, who felt the problem was unlikelyto be related to TMJ, and was referred to theCedars-Sinai Anesthesia Pain Center.

Examination

The medical history and review of systems were allwithin normal limits. Dental, stomatognathic,myofascial, cervical spine, and cranial nervescreening examinations were negative or withinnormal limits. Psychosocial questioning was nega-tive for possible depression and did not reveal aneed for psychometric evaluation.

Impressions

Assessment of the chronic nature of the attacks,combined with the unilaterality, regularity, dura-tion, and lack of remission periods or triggers, ledto a preliminary diagnosis of CPH. It was there-fore thought that indomethacin trial may be help-ful, and the patient was started on 75 mgindomethacin SR per day, which was increased to75 mg twice per day after 4 days. One week laterthe patient reported total relief from the attacks.One month later he was still free of pain and wasbeing maintained on 75 mg indomethacin SR perday.

Discussion

Chronic paroxysmal hemicrania is a rare headpain syndrome, but one that should be consideredin the differential diagnosis of throbbing or boringpain in the maxillary region. This is particularly sowhere there is a chronic daily pattern of multiplepain attacks of short duration. Dental pathologyshould be ruled out Brst, and the use of local anes-

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Table 1 Organ System Classification of Headache Problems That Present asToothache'

Organ system

In traerá nial

Extraerá nia i

(vluscuioskeietai

Neurovascular

Neuroganic

Sympatheticnervous system

Psychogenic

Diagnosis

InfarctTumor

Sinusitis

Myofaseiai pain

MigraineCiusterChronic paroxysmal hemicraria

Tngeminai neuralgiaPretrigeminal neuralgia

Atypical odontaigia

Psychogenic pain

Presence

Continuousintermittent

Conlinuoits

Conlinuous

intermittentintermittentintermittent

intermittentContinuous

Continuous

Vanabie

Quality

Steady, du i iSteady, duii

Duil

Duil, aching

ThrobbingThrobbmgThrobbing

Sharp, shootingDuii, aching

Duii, burning

Variable

thetic blocks may he required to ascertain that thepain is not pulpal in origin. The presence of inter-mittent throbbing pains that are not detital in ori-gin is generally suggestive of a neurovascular dis-order (Table 1), Sinus, myofascial, and TMJproblems are also far more common than CPHand should be ruled out by the appropriate diag-nostic procedures.

The chronic, unremitting nature of the attacks,which are often associated with autonomie signssuch as lacritnation, nasal stuffiness, conjunctivalinjection, and rhinorrhea, should alert the clinicianto the possibility of CPH. An indomethacin trial isthe best test for establishing the diagnosis of CPH,with a lack of response effectively ruling out CPH,Sjaastad'" has utilized indomethacin trial to ruleout CPH whenever headache attack frequencyexceeds 4 occurrences in a 24-hour period. Itshould be noted that cerebrovascular disease andother tntracranial pathology may cause headachewith simtlar features to CPH, and neuroimaging isrecommended wherever CPH-type symptoms arepresent.-*'

The indomethacin effect, although absolute, isdose dependent, and the dose should be titratedfor each patient. For an indomethacin trial startthe patient with 75 mg per day and increase by 25mg every 3 days, up to a maximum of 250 mg. Ifno effect is noted within a few days, a CPH diag-nosis can be virtually excluded. The indomethacinshould be taken with food ro reduce the possibilityof gastric side effects. For those parients in whomgastric side effects are significant, the use of eitherthe sustained release preparation or suppositoriesmay be helpful. However, these preparations result

in lower blood levels, and higher doses may herequired for equivalent effects to be achieved. If apositive effect occurs, the dosage can be varied up(to a maximum 250 mg per day) or down to find amatntenance dose that keeps the pattent headachefree. The cyclic nature of CPH should be kept inmind, recognizing that the patient may enter aperiod of exacerbation that requires dosage read-justment. Tolerance does not seem to occur,indeed it has been reported that the amount ofdrug required may even decrease over time,-'

Conclusion

Little is known about the nature of this uncom-mon facial pain condition, other than it is con-trolled by indomethacin. At this stage the basis forthe absolute effect of this tnedication is unknown.Any proposed mechanism presented at this time toexplain CPH is also speculative.

References

1, Bell WE, Toothaches of nonodontogenm origin, J CalifDent Assocl976; 23:50-78,

2, Bdl WE, OrofacJal Pains, Classification, Diagnosis andManagement, ed 4. Chicago: Year Book, 1989,

3, Graff-Radford SB, Headache problems that can present astoothache. Dental Gin North Am 1991;5(l):155-170,

4, Sjaastad O, Dale I, A new (?) clinical headache entity"Chronic Paroxysmal Hetnicrania," Acta Neurol Scand1976;54:140-159,

5, Sjaastad O, Apfelbaum R, Casltey W, et al. Chronicparoxysmal hemicrania (CPH), The clLnicd manifesta-tions. A review, Upssala J Med Sci 1980;31(suppl):37-40.

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6, International Headache Society, Classification and diag-nostic criteria for headache disorders, cranial neuralgiasand facial pain, Cephalalgia 19B8;7(suppl 8):1-96,

7, Antonaci F, Sjaastad O, Chronic paroxysmal hemicrania¡CPH): A review of the clinical manifestations. Headache1989;29:648-656.

8, Ekbom K, Olivarius B, de Fine D, Chronic migrainousneuralgia—Diagnostic and therapeutic aspects. Headache

9, Russell D, Chronic paroxysmal hemicrania; severity, dura-tion and time of occurrence of attacks. Cephalalgia19S4;4:53-S6,

10, Sjaastad 0 , Russell D, Saunte C. Chronic paroxysmalhemicrania, VIII, The sweating pattern, Cephalalgia1983;3:45-S2,

11, Sjaastadt O, Egge K, Horven I, et al. Chronic paroxysmalhemicrania: Mechanical precipitation of at tacks.Headache 1979:19:31-36,

12, Sjaastad O, Russell D, Saunte C, Horven I. Chronicparoxysmal hemicrania, VI, Precipitation of attacks.Further studies on the precipitation mechanism,Cephalalgia I982;2:211-214,

13, Sjaastaii O, Saunte C, Graham JR, Chronic paroxysmalhemicrania. VII, Mechanical precipitation of attacks: Newcases and localization of trigger points, Cephaialgia

14, Sjaastad O, Aasly J, Fredriksen T, Wysocka-BakowskaMM. Chronic paroxysmal hemicrania, X, On the auto-nomie involvement, Cephalalgia 1986:6:113-124,

15, Price RW, Posner JB, Chronic paroxysmal hemicrania: Adisabling headache syndrome responding to indomethacin,AnnNeurol 197g;3(2}:183-184,

16, Jensen NB, Joensen P, Jensen J, Chronic paroxysmal hemi-crania: Continued remission of symptoms after discontin-uation of indomethacin, Cephalalgia 1982;2:163-164,

17, Sjaastad O, Cluster Headache Syndrome, Major Problemsin Neurology, vol 23, London: Saunders, 1992:291-352.

18, Horven I, Nornes H, Sjaastad O, Different corneal inden-tation pulse pattern in cluster headache and migraine.Neurology 1972;22i92-98,

19, Shigeno S, Fritschka E, Shigeno T, Brock M, Effects ofIndomethacin on rCBF during and after focal cerebralischemia in the cat. Stroke 1985;] 6:235-240,

20, Newman LC, Herskovitz S, Lipton RB, Solomon S,Chronic paroxysmal headache: Two cases with cere-hrovascular disease. Headache 1992;32:75-76.

21, Sjaastad O, Antonaci F. Chronic paroxysmal hemicrania:A case report. Longstanding remission in the chronicstage, Cephalalgia 1987^7:203-205.

Resumen

Hemicréneo Paroxistico Crónico Presentado como unaOdontalgia

El hemicréneo paroxistico crónico es un problema de cefaleaintermitente caracterizado por paroxismos de dolor de 15 minu-tos de duración, aproximadamente. Los ataques están locsiiza-dos UEuaimente en ia región fron tote m pora i y responden al usode ia indometacina. Se presenta un grupo de síntomas quedefinen ei hemicráneo paroxistico crónico, también se reportandos casos en ios cuaies se presentó la odontalgia como sín-toma. Se enfatiza ei hecho de que ios clínicos deberian consid-erar ei hemicráneo paroiíistico crónico en ei diagnóstico diferen-cial del doior orofacial.

Zusammenfassung

Zahnschmerzen als Symptom von chronischer paroxys-maler Hem i krame

Chronische paroxysmale Hemikranie (CPH) ist ein schubweiseverlaufender Typ von Kopfschmerzen, der durch ca. 1 5 Minutenandauernde Schmerzattacken im frontotemporalen Bereichcharakterisiert. Typischerweise spricht die CPH aufindomethacin-Therapie an. Dieser Artikei unifasst eineLit eraturdu roh sieht über die Symptome der CPiH und berichtetüber zwei Fälie, bei denen Zahnschmerzen im Bereich derOberkieferprämoiaren und -molaren das Hauptsymptom warenDie Autoren weisen darajf hin, dass die CPH in dieDifferentia i diagnose orofacialer Schmerlen miteinbezogen wer-den muss.

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