CASE REPORT

Cerebellopontine Angle (CPA) Tumor Mimicking Dental Pain Following Facial Trauma
Jutiad Khan, M.D.S., M.P.H.; Gary M. Heir, D.M.D.; Samuel Y.P. Quek, D.M.D.. M.P.H.

0886-9634/2803205S05,00/0, THE JOURNAL OF CRANIOMANDIBULiR PRACTICE, Copyright2010 by CHROMA, Inc. Manuscripl received February 10, 2010; accepted March 15.2010 Address for correspondence: Dr. Junad Khan Dept. of Diagnostic Sciens New Jersey Dental School University of Medicine and Dentistry of New Jersey t o Bergen St., Rm. C880 Newark, NJ 07103 E-mail: junadkhan @ gmail.com

ABSTRACT: Facial injuries are common during workplace accidents. These incidents are also associated with an increase in both mortality and morbidity rates. The following case describes a 40 year-old white Hispanic patient with paroxysmal facial pain on the right side, one year in duration. The patient reported facial trauma as a result of a direct fall thought to be related to his pain complaints five months prior to arriving at the New Jersey Dental School emergency unit. The facial pain was progressively worsening ever since the accident. Upon arrival at the emergency unit, a comprehensive intraoral and extraoral examination was performed. Application of a local anesthetic at the site of the pain produced equivocal results. After obfaining a complete history and clinical examination, an MRl was ordered to rule out the possibility of a space-occupying lesion in the brain considered as a possible source of the pain. This case focuses on different aspects relative to dental care: the importance of a complete history and pafient evaluation in order to make an accurate diagnosis; the complexity of orofacial pain; and the training required for dental health care providers who treat unusual oral and facial pain complaints.

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Dr. Junad Khan is the chief resident at tlie Orofacial Pain Clinic at the University of Medicine and Dentistry of New Jersey, Newark. NJ. He has also completed his Masters in Public Heath and a Masters in Dental Sciences from UMDNJ. He has a fellowship in orofacial pain and TMJ disorders. Currentiy. he is in the second year of his PIt.D. program in oral biology. His major area of focus is pain management.

ental physicians are constantly required to diagnose odontogenic pain. Identifying the source of a toothache can be challenging. Dentists possess, within their dental armamentarium, an array of devices and procedures that aid them in diagnosing the source of pain. Percussion of the tooth, pulp vitality testing,, thermal challenges, and similar tests are often utilized. Xrays may help detect caries and gross apical pathology. Tooth pressure testing may detect potential fractures in the tooth that may contribute to the pain process. Referred pain from the maxillary sinus or from myofascial trigger points must also be suspected if all the above tests result in equivocal findings. If uncertainty remains as to a diagnosis, a diagnostic anesthetic block may provide information that confirms or refutes a local peripheral source of pain. If all odontogenic sources of pain are eliminated, a central process may be considered. Case Report A 40 year-old white Hispanic male presented lo the Orofacial Pain clinic at the University of Medicine and

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Dentistry of New Jersey-New Jersey Dental School tor emergency treatment of facial pain that had been present for one year. At his first visit, the chief complaint was of facial pain located in the right anterior segment of the maxi I la. The pain extended from the tip of the nose to the cheek. The patient was not able to localize the pain to one area, but described it as heing in the region of the maxillary division of the trigeminal nerve (Figure 1), The patient mentioned gradual worsening of the pain over the past five months following trauma to the right side of his face after a fall at work, during which he struck his face. At the time of the falK he was examined at a local hospital and treated for impact injuries, facial bruise.s, and muscle pain. After the accident, the maxillary pain abated. Three weeks later the maxillary pain returned. This time the pain attacks were more frequent, intense, and longer in duration. The patient reported that the pain progressively worsened. Upon physical examination, hlood pressure was 121 /69. Body temperature was 98.4C with a pulse of 73. The patient's physical appearance was of a healthy and responsive individual. His inedical history was negative, and he was not utilizing any medication with the exception of over-the-counter pain medications as needed (acetaminophen and ibuprofen). After the fall, as pain worsened, the patient consulted with his private dentist who attempted managing his complaints by first removing tooth #8. As pain persisted. the dentist then decided to remove tooth #7. Both extractions had no effect on the pain. Instead, the pain gradually worsened. The quality of pain one year prior to his visit was initially paroxysmal, lasting for only seconds. At the time of the current evaluation, it had progressed to 2-3

minutes duration. The frequency of the attacks had also increased from two attacks per day to almost seven attacks per day. The intensity of the attacks was moderate to severe. Pain was spontaneous with no known aggravating factors. The patient reported an increased use of overthe-counter medications (acetaminophen and ibuprofen) that were ineffective in completely eliminating the pain. There was no report of pain awakening the patient during his sleep. Objective findings included a loss of sensatittn of both light touch and pinprick in the affected area. This altered sensation was present in a small region adjacent to the apex of the right maxillary canine extra orally. A palpatory examination of the masticatory musculature revealed slight discomfort to the right masseter, but did not reproduce the chief complaint. TMJ palpation was negative. A dental examination found evidence of the recently extracted right central and lateral incisors. After reviewing the history and examining the patient both intra- and extraorally, the patient's pain could not be reproduced and no associated intraoral pathology was found. Application of topical anesthetic had no effect. A diagnostic somatic block was than administered at the site of the pain and had equivocal results. The negative dental findings prompted consideration of a central mechanism for the patient's pain. Theretbre, he was referred for an MRI of the brain. The objective was to rule out any intracranial pathology. MRI Conclusions A multiplanar, multi-sequenced MRI was performed on the patient without the administration of intravenous

Figure t The patient was tiot able to localize the pain to one area, hut described it as being it the region ot the maxillary division <t} the trigeminal nerve.
Areas of Pain Masseter trigger point tender but unable to produce chief complaint

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gadolinium. A large heterogeneous extra-axial mass lesion extending from the right cerebellopontine angle (CPA) to involve the right side ofthe perimesencephalic cistern and the posterior aspect of the suprasellar cistern was tbund. This mass encased the right cranial nerve V and the basilar artery and caused a severe mass-effect on the pons. The MRI was negative for any infarct. intracranial hemorrhage, or hydrocephalus. Normal llow-related voids were seen within the tnajor intracranial vessels (Figure 2 a-d).

Discussion The dental practitioner must always consider neuropathic pain and trigeminal neuralgia (TN) in a differential diagnosis. Clinically. TN is classified as idiopathic or symptomatic. The presentation and symptoms are typically the same but the underlying pathology is different. The majority of patients fall under the idiopathic category, where the underlying cause is unknown. In symptomaticcases, the neuralgic pain issecondarytoapathological

Kijure 2 ( a d ) Amiws in a-d indicate the lsion. The tumor is compressing major areas of the brain. The compression of rhe trigeminal nerve was considered ihe cause ol" the paroxysmal pain experienced by the patient.

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condition. Examples include meningioma. multiple sclerosis, and cerebellopontine angle (CPA) tumors. Even though the etiology of TN is unclear, the mo.st accepted theory i.s that it is due to a compression of the nerve root by a vessel or tumor. Demyelinization. intrinsic lesions within the nerve root, or at the root entry zone (REZ) have also been reported. There is no specific age category for TN. However, it typically affects patients over age of 50. When it affects younger patients, suspicions of intracranial pathology are raised. This is a case of a cerebellopontine angle tumor. The important message in this case is to consider the atypical and progressive presentation of the patient's pain and his age, which is considered too young for the onset of TN. Usually, if an individual has TN-like features and is under the age of 50, it is necessary to order brain imaging to rule out any possibility of an intracranial lesion. Approximately 0-8% of trigeminal cases are reported to be secondary to a tumor.'-^ There is very limited documentation of the relationship of TN and CPA tumors.-*-^ It has been established that extra-axial lesions in the posterior fossa compressing the nerve root are likely to cause TN. whereas neoplastic compression of the Gasserian ganglion may be associated with atypical facial pain.^ CPA tumors resulting in complaints of TN can originate from a variety of tissue types present in the area. Schwannoma (75%), meningioma (13%), and epidermoid cysts (5%) are the most common tumors. Anatomically the structures are the CPA borders themselves, the internal auditory canal, and compartments of CN VII, and VIII. Due to the anatomic diversity, a small percentage of uncommon tumors have also been

The importance of a thorough history, physical examination, and diagnostic te.sting is illustrated in this case, but can only be successful if the health care provider is aware of the variety of facial pain disorders that may manifest from intracranial lesions and is prepared to perform, order, and interpret these tests accurately. References
Ak.sik I: Mkrcmeural decompression operaiion.s in ihe ircalmenl of some forms of cranial rhizopathy. Acta Neurochir (W\eii) 1993; 125(l-4);(>4-74. Apfelbaum RI: Surgery for tic JouUiureux. Cliti Neurostirg 1983; 3l:3.'il368. Beder.'ion JB, Wilson CB: Evaluation of micro vascular decompression and partial sensory rhizolomy in 252 cases of trigmina! neuralgia. Neurosurg l989;7l(3);3.59-367. Pian JH Jr. Wilkins RH: Treatment of tic douloureux and hemifacial spa.sm by posterior Ibssa exploration: therapeuiic implications of various neurovaseular relationships. A'eiim.iu;-,!' 1984; 14(4);462'471. Puca A. Miglio M. Tamburritii G, Vari R: Trigeminal involvemeni in intracranial tumours. Anatomical atid clinical observations on 73 piitienls. AaaNet<riKlm\WKn) 1993; 125(l-4):47-51. Bullitl E. Tew JM. Boyd J: Intracranial tumors in patients with facial pain. Nettmsurg 19S6 4(61:865-87!.

Dr. Gary Heir isa clinical professor at the Department of Diagnostic Sciences. University of Medicine and Dentistry of New Jersey. Newark. NJ. He is the clinical director of the Orofaciai Pain Clinic at UMDNJ. Dr. Samuel Quek is the program director of the General Practice Residency at the New Jersey Dental School, University of Medicine and Dentistiy of New Jersey. Neivark. NJ.

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