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J Am Dent Assoc, Vol 136, No 4, 469-476.
© 2005 American Dental Association
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COVER STORY

CASE REPORT

CASE REPORT
JADA Continuing Education

Trigeminal neuralgia in a patient with multiple sclerosis and chronic inflammatory demyelinating polyneuropathy



ELENI SARLANI, D.D.S., Ph.D., EDWARD G. GRACE, D.D.S., M.A., BIRUTE A. BALCIUNAS, D.D.S., M.S.D. and ANTHONY H. SCHWARTZ, D.D.S.


   ABSTRACT
TOP
 ABSTRACT
CASE REPORT
 DISCUSSION
 TREATMENT
 CONCLUSIONS
 REFERENCES
 
Background. Trigeminal neuralgia (TN) is characterized by unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. Symptomatic or secondary TN involves TN-like pain that develops owing to a central nervous system lesion (benign or malignant) or to multiple sclerosis (MS).

Case Description. The authors present a report of a unique case of a 43-year-old patient with unilateral TN, MS and concomitant chronic inflammatory demyelinating polyneuropathy. The facial pain preceded any other manifestations of the systemic disorders, and only after repeated neurological examinations were these diagnoses established.

Clinical Implications. Magnetic resonance imaging of the brain and repeated neurological evaluations should be implemented in all patients with TN to rule out the presence of underlying disease. The dental practitioner should be familiar with TN to avoid unnecessary dental interventions and ensure prompt initiation of appropriate treatment.

Key Words: Trigeminal neuralgia; multiple sclerosis; neuropathic pain; facial pain

Trigeminal neuralgia (TN) is an uncommon facial pain condition characterized by brief, episodic, lancinating pain in the distribution of one or more divisions of the trigeminal nerve. The pain is severe and typically lasts for seconds. The pain paroxysms often are evoked by trivial stimulation, such as light touch or vibration, to extraoral or intraoral trigger areas. Spontaneous remissions lasting months or years occur in some patients; however, TN usually is progressive, and the pain attacks become more frequent and severe.1 TN may mimic pulpal pain, especially when it is localized in the dentition. Therefore, dental practitioners should increase their awareness and knowledge of this disorder to prevent misdiagnosis and unnecessary dental interventions.

The dental practitioner should be familiar with trigeminal neuralgia to avoid unnecessary dental interventions and ensure prompt initiation of appropriate treatment.

In the majority of cases, TN is an idiopathic disorder. Occasionally, however, TN constitutes manifestation of central nervous system (CNS) lesions (symptomatic TN), such as tumors, cysts, multiple sclerosis (MS) or arteriovenous malformations.2–5 Very rarely has TN been reported in association with peripheral demyelinating disease.6,7 Presented here is a report of a case of TN in a 43-year-old man with MS and concomitant chronic inflammatory demyelinating polyneuropathy. We then provide a review of the literature.


   CASE REPORT
TOP
 ABSTRACT
 CASE REPORT
DISCUSSION
 TREATMENT
 CONCLUSIONS
 REFERENCES
 
The patient was a 43-year-old man who sought treatment for a sharp, right-sided facial pain, localized in the distribution of the mandibular division of the trigeminal nerve, a few months after a motor vehicle accident. The pain was intermittent, lasting a few seconds, and could be triggered by light touch or cold wind. The patient’s medical history was positive for alcoholism. The results of a neurological examination and magnetic resonance imaging (MRI) of the brain were normal. The treating clinician (A.H.S.) diagnosed the patient as having TN and prescribed carbamazepine, which significantly reduced the pain.

Six months later, the patient returned with a complaint of constant facial pain with superimposed paroxysms of stabbing pain lasting for minutes. Moreover, he reported dizziness and blurred vision and developed a painful arthritis in the hands, which the clinician ascribed to carbamazepine. These adverse effects from the medication precluded further treatment with carbamazepine. The clinician prescribed additional medications, including gabapentin and baclofen, in various combinations and dosages, without success (TableGo). A neurosurgeon subsequently performed a percutaneous glycerol rhizotomy on the patient. The procedure had a poor outcome, resulting in significant aggravation of the pain and spread of the pain to include areas subserved by nerves V1, V2, IX and X.


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  		TABLE MEDICATIONS USED IN THE CASE REPORTED FOR THE MANAGEMENT OF FACIAL PAIN.

 
During the two years after the procedure, the patient developed mild numbness and tingling in his hands, forearms and feet; bilateral arm weakness; and progressive vision and gait difficulties. Hematologic assessment for Lyme titers and rheumatic disease was negative. The results of MRI and auditory evoked potential studies were normal. However, the results of visual evoked potential studies were consistent with decreased bilateral visual acuity. A neurologist diagnosed MS on the basis of the results of the positive visual evoked potential studies and the clinical course of the disease. The neurologist initiated a regimen of physical therapy as well as glatiramer acetate injections. The patient tolerated these well, and they resulted in slight amelioration of the symptoms. The patient also was taking tizanidine, lamotrigine, baclofen and zolpidem (TableGo); these medications controlled his facial pain poorly.

In the following three years, the patient had three cerebrovascular accidents, which resulted in acute, short-term left hemisensory symptoms and hemiparesis. The vascular lesions did not involve the vicinity of the trigeminal nociceptive pathway; the patient reported no change in the facial pain characteristics after the cerebrovascular accidents.

Five years after undergoing the glycerol rhizotomy procedure, the patient developed significant left foot drop and diffuse bilateral pain in the lower extremities. In addition, neurological examination revealed decreased sensation in response to pinprick and vibration in a patchy manner in the bilateral upper and lower extremities. The neurologist ordered electrophysiological studies to assess involvement of motor fibers, sensory fibers or both, as well as primary axonal or demyelinative pathology.8 Electrophysiological studies showed significantly decreased nerve conduction velocities with temporal dispersion as well as increased F-wave latency, consistent with demyelination in the upper and lower extremities. The neurologist diagnosed the patient with chronic inflammatory demyelinating polyneuropathy. Intravenous immunoglobulin therapy was prescribed but was not tolerated well, as the patient developed a rash and headache.

Currently, the patient takes multiple medications, including tizanidine, lamotrigine, oxcarbazepine, baclofen and methadone (TableGo); these medications only poorly control his facial pain.


   DISCUSSION
TOP
 ABSTRACT
 CASE REPORT
 DISCUSSION
TREATMENT
 CONCLUSIONS
 REFERENCES
 
Epidemiology. TN has an incidence of 4.5 per 100,000 population. The disorder is more prevalent among females (F:M sex ratio of 1.74:1) and affects primarily older people; the average age of onset is between the fifth and seventh decades. The majority of cases are unilateral; approximately 4 percent of cases are bilateral. TN most commonly involves either the maxillary or mandibular division of the trigeminal nerve alone, while the ophthalmic division rarely is affected alone. Involvement of more than one division of the trigeminal nerve is not uncommon.

Trigeminal neuralgia is characterized by spontaneous remissions that may last months or even years. Nevertheless, with time, pain attacks become more frequent, while remissions occur less often.

Clinical characteristics. TN is characterized by severe, stabbing pain that may be accompanied by a contraction of the facial musculature (hence the term "tic douloureux"). Pain attacks are episodic, last only seconds to a few minutes and may recur in clusters. The pain is characterized by sudden onset and cessation, and the patient is completely asymptomatic between attacks. Pain paroxysms may be provoked by innocuous sensory stimulation of trigger zones in the receptive field of the affected branch.9 Common daily activities such as talking, eating, drinking, swallowing, exposure to cold air, shaving, brushing the teeth or washing the face can trigger the pain, significantly compromising the patient’s quality of life. The trigger zone always is ipsilateral to the pain; however, it may not coincide with the area of pain. Common extraoral trigger zones occur above the supraorbital foramen, the inner canthus of the eye, lateral to the ala nasi and over the mental foramen. Typically, immediately after a jab of pain, there is a refractory period during which further pain attacks cannot be evoked.

TN is characterized by spontaneous remissions that may last months or even years. Nevertheless, with time, pain attacks become more frequent, while remissions occur less often and last for a shorter period.1 In prolonged cases, patients may develop atypical features, such as persistent pain between episodes.1 Continuous pain is more common in symptomatic TN, as in the case discussed here.

Pathophysiology. Most idiopathic TN cases are thought to be induced by vascular compression of the trigeminal root-entry zone, which results in demyelination of trigeminal sensory fibers.10–13 Histopathologic examination of trigeminal nerve roots from patients with compression of the nerve root by a blood vessel reveals focal loss of myelin, close apposition of the demyelinated axons and lack of intervening astrocytic processes.11,12 Demyelination may result in ectopic generation of action potentials, presenting clinically as spontaneous pain.14 Moreover, demyelination promotes ephaptic neural transmission—namely, development of abnormal contacts between adjacent nerve axons, which results in inappropriate spread of action potentials and activation of one nerve on activity in another. Such inappropriate spread of action potentials may underlie the generation of pain by innocuous stimulation.14 In the course of time, excessive afferent input of nerve impulses may produce central sensitization, resulting in atypical TN features, such as constant pain.1,15

Differential diagnosis. The clinician should consider a number of other conditions when making the diagnosis of TN.

Tumors. Occasionally, TN develops secondary to posterior fossa compressive lesions, such as cysts and tumors.2–4 Cheng and colleagues2 reported that tumors are detected in 2 percent of patients who have typical TN.

Multiple sclerosis. TN also may be caused by demyelinating plaques of MS involving the trigeminal nociceptive pathway.5,16 MS is diagnosed in 2 to 4 percent of patients with TN.15 Typically, patients with TN and MS are younger than those with idiopathic TN and are more likely to have bilateral facial pain.5 In the vast majority of cases, TN develops later in the course of MS; occasionally, however, TN may appear first.5 TN’s development in patients younger than 50 years of age may be the first manifestation of MS, as was the case in our patient. A demyelinating plaque extending into the root entry zone of the trigeminal nerve is a common finding among patients with TN and MS, while plaques in other CNS regions do not seem to be associated with TN.11,17 Meaney and colleagues18 reported that vascular compression may be the underlying cause of TN, even in patients with MS. The authors demonstrated vascular compression of the root entry zone in a subset of these patients, with subsequent elimination of the TN pain after decompression of the nerve root.18 TN in association with demyelinating peripheral neuropathy secondary to Charcot-Marie-Tooth disease6,7 or with infarction of the root entry zone19 has been reported.

The case presented here is unique, being the first reported case of TN in association with both MS and chronic inflammatory demyelinating polyneuropathy. The patient also had experienced multiple infarctions; however, these did not precede the development of pain, did not involve the trigeminal nociceptive pathway and did not alter the facial pain characteristics.

MS is a chronic CNS disease, characterized by discrete areas of demyelination, axon damage and associated inflammation.20–22 MS lesions are disseminated in time and space (that is, occur in different parts of the CNS at least three months apart) and can result in a wide variety of symptoms and signs, including numbness, paresthesias, pain, weakness, spasticity, fatigue, vertigo, visual difficulties, gait dysfunction, bladder disturbances and cognitive changes.20,23,24 The disease appears typically between the ages of 18 and 45 years. Approximately 80 to 85 percent of patients have relapsing-remitting MS, characterized by acute attacks interspersed with recovery periods, while 10 to 15 percent of patients have primary progressive MS, characterized by steady progressive deterioration of neurological function. Significant disability develops over a course of 10 to 20 years, and approximately 50 percent of patients eventually die as a result of complications of the disease.20

Greater risk of MS in first-degree relatives of patients with MS and high concordance rates between monozygotic twins suggest a genetic susceptibility to the disease.24,25 Environmental factors are believed to play an important role, while an infectious trigger also has been hypothesized.20 Even though the mechanisms underlying the genesis of the disease still are unclear, an autoimmune pathogenesis is favored.26 Glucocorticoids are effective in reducing the severity and duration of acute exacerbations, but they do not affect the course of MS over time.27 In contrast, disease-modifying therapies, such as glatiramer acetate and interferon beta, reduce the number of relapses, improve recovery from attacks and delay disease progression and development of disability.27–29 The patient presented here experienced alleviation of symptoms after receiving glatiramer acetate therapy. Glatiramer acetate exerts anti-inflammatory effects by binding to major histocompatibility complex molecules and inhibiting myelin-reactive T cells.30,31 In addition, glatiramer acetate induces anti-inflammatory Th2 cells, which may exert their protective action by crossing the blood-brain barrier and by producing anti-inflammatory cytokines in response to cross-recognition of myelin antigens.31 Inhibition of brain inflammation, which has been associated with irreversible brain tissue injury, is thought to delay the occurrence of irreversible CNS lesions.32

Chronic inflammatory demyelinating polyneuropathy. Chronic inflammatory demyelinating polyneuropathy is an acquired peripheral neuropathy, characterized by multifocal demyelination of spinal roots, major plexuses and proximal nerve trunks.33 The exact etiology is unknown, but autoimmune mechanisms have been implicated.33–35 The disease has a chronic course that may be either progressive or relapsing-remitting. The clinical manifestations are variable but include motor and sensory symptoms, such as spontaneous pain, paresthesia, numbness and muscle weakness of the upper and lower extremities.33 Occasionally, cranial nerves and respiratory muscles also are involved.34 Treatment consists of intravenous immunoglobulin therapy, plasma exchange, corticosteroid therapy and immunosuppressive drug therapy.35

Cluster headache and chronic paroxysmal hemicrania. The excruciating intensity of TN pain and its intermittent temporal pattern may result in a misdiagnosis of cluster headache or chronic paroxysmal hemicrania.36 However, both cluster headache and chronic paroxysmal hemicrania typically affect younger adults.37,38 In addition, these neurovascular headaches are characterized by attacks of longer duration (minutes to hours), which typically occur around the clock and interrupt the patient’s sleep.39,40 In contrast to TN, these attacks cannot be triggered by innocuous cutaneous stimulation.36,40 Moreover, a unique feature of cluster headache and chronic paroxysmal hemicrania is that autonomic phenomena—such as conjunctival injection, lacrimation, nasal congestion and rhinorrhea—accompany the pain.41

Lyme disease. Lyme disease also should included in the differential diagnosis of TN. Lyme disease or Lyme borreliosis is an infectious, tick-transmitted disease, caused by spirochetes of the Borrelia burgdorferi species complex. Lyme disease can manifest with an array of symptoms involving multiple organs and systems, such as skin, heart, eye, joints and the peripheral nervous system and the CNS.42 Neurological manifestations of the disease may include meningitis, single or multiple cranial neuropathies, painful radiculopathies and diffuse polyneuropathies.43,44 On rare occasions, patients with Lyme disease may have neurogenic pain similar to that of TN.45,46 This possibility should be ruled out via hematologic assessment for Lyme titers.

Failure of dental treatment to provide long-term pain relief should raise the suspicion of trigeminal neuralgia.

Dental pain. When the sharp, paroxysmal pain of TN is localized in the dentition or the surrounding structures, it may be misdiagnosed as dental pain.16,36 Frequently, patients with TN undergo numerous dental procedures until the diagnosis of TN is made. These procedures may offer temporary pain relief for a few weeks; however, the pain always recurs and often is even worse. Failure of dental treatment to provide long-term pain relief should raise the suspicion of TN. An important feature that distinguishes TN from dental pain is that TN typically does not interrupt the patient’s sleep. Moreover, pain originating from dental pathology usually is progressive, and its character changes with time. Tooth vitality tests and radiographic examination also will serve to exclude dental pathology.

Awareness of underlying conditions. Thorough medical examination and imaging should be undertaken in all patients with TN to rule out underlying conditions. Occasionally, neurological signs indicative of secondary causes of TN become apparent only later in the course of the disease, resulting in a delayed diagnosis.2,5 In the case presented here, both the neurological examination and the MRI of the brain were normal initially. However, even though the MRI failed to depict any demyelinating plaques even later in the disease process, subsequent neurological assessments led to the diagnosis of MS and chronic inflammatory demyelinating polyneuropathy, thus emphasizing the importance of repeating neurological examinations in patients with TN.16


   TREATMENT
TOP
 ABSTRACT
 CASE REPORT
 DISCUSSION
 TREATMENT
CONCLUSIONS
 REFERENCES
 
Pharmacological approaches. Pharmacological therapy is the first line of treatment for TN. The goal of the medical management is the reduction of neuronal hyperexcitability in the peripheral nervous system, the CNS or both.47–49 Various antiepileptic drugs are used, including carbamazepine, oxcarbazepine, lamotrigine, phenytoin and gabapentin.47–52 Other potentially effective medications include antispasmolytic agents, such as baclofen, a {gamma}-aminobutyric acid receptor agonist, and tizanidine, an {alpha}2-adrenergic agonist.50

Carbamazepine has been found effective in several controlled trials and is the mainstay of pharmacotherapy for TN.51 The most common adverse effects include sedation, fatigue, dizziness, blurred vision, nausea, vomiting and allergic skin reactions. Periodic complete blood cell count and liver function monitoring tests are essential, since agranulocytosis and aplastic anemia, as well as hepatocellular and cholestatic jaundice, can occur rarely.47 Oxcarbazepine, a daughter drug of carbamazepine, is a safer alternative to carbamazepine and does not require routine monitoring of hematologic and hepatic profiles during treatment.52

Often, drug combinations are used to maximize effectiveness and minimize adverse effects.53 The clinician should attempt gradual withdrawal of the medications once complete pain control is achieved, because remission periods are common. Patients with TN and with MS may respond initially to pharmacological treatment; however, relapse is frequent. The patient in this report was responsive to carbamazepine, but use of the drug was discontinued owing to adverse effects.

Surgical procedures. For patients with TN who become refractory to pharmacological treatment or cannot tolerate its adverse effects, surgical intervention is recommended. Surgical techniques used for TN treatment are peripheral surgery, percutaneous ablative procedures, stereotactic radiosurgery and microvascular decompression (MVD).

Peripheral surgery. Peripheral surgery entails lesioning of peripheral branches of the trigeminal nerve, and using cryotherapy, neurectomy, alcohol block or radiofrequency. Peripheral techniques are the least invasive of all surgical procedures but are characterized by low effectiveness and a high recurrence rate.15,54,55

Percutaneous ablative techniques. Percutaneous ablative procedures involve nerve lesioning at the level of the gasserian ganglion by percutaneous radiofrequency thermocoagulation, balloon compression, injection of glycerol or a combination of these.56–59 These neurodestructive procedures have good initial results and carry less risk than MVD; however, they are associated with a higher incidence of pain recurrence. Potential complications include loss of touch sensation, dysesthesias, corneal damage, anesthesia dolorosa and temporary masseteric weakness.

Dentists should be competent in the differential diagnosis of trigeminal neuralgia from other facial pain causes, including dental pathology.

The patient described in this case report underwent percutaneous glycerol rhizotomy. During this procedure, a needle is advanced, with the aid of fluoroscopy, through the foramen ovale into the trigeminal cistern, where glycerol is injected in close proximity with the pregaglionic trigeminal rootlets.51,60 The sensory fibers of the trigeminal nerve are affected, resulting in termination or reduction of the TN attacks.61 Percutaneous glycerol rhizolysis causes sensory loss and masseteric weakness less frequently than do the two alternative percutaneous procedures, but it has higher recurrence rates.51,58,59

Stereotactic radiosurgery. Stereotactic radiosurgery, also known as gamma knife surgery, involves lesioning of the trigeminal nerve at the root entry zone using stereotactic techniques and radiation between 70 and 90 grays.62,63 This procedure is less invasive and thus is suitable for medically compromised patients. Outcomes are similar to those of other ablative procedures.64,65 However, there may be a latency period of three to six months, after which maximum pain relief is obtained.62,64 This technique’s highest success rates are observed when it is used as primary treatment in patients with typical symptoms.64,66,67 Facial sensory loss, paresthesias and dysesthesias are the most common complications.58,62,66 A positive correlation between development of trigeminal dysfunction and pain relief after gamma knife surgery has been reported.62

Microvascular decompression. MVD of vessels compressing the nerve root is effective and has a low incidence of recurrence of TN.68,69 However, it entails posterior fossa craniotomy and involves serious risks, including hearing impairment, ataxia, brainstem infarction, cerebellar injury and death.69 Magnetic resonance tomographic angiography can depict vascular compression of the nerve and is useful in identifying patients who are good candidates for MVD.10,70


   CONCLUSIONS
TOP
 ABSTRACT
 CASE REPORT
 DISCUSSION
 TREATMENT
 CONCLUSIONS
REFERENCES
 
Dentists should be competent in the differential diagnosis of TN from other facial pain causes, including dental pathology. A correct diagnosis will lead to appropriate management and preclude unsuccessful attempts to treat the pain with irreversible dental procedures.

This case report illustrates that TN occasionally is associated with a serious systemic disease. Appropriate diagnostic tests are indicated for all patients with TN, since early diagnosis and treatment of an underlying systemic disease will have a significant impact on the prognosis. Anticonvulsant medications constitute the first line of TN treatment; however, many patients eventually require surgical intervention, owing to diminished response to pharmacological therapy or to the development of intolerable adverse effects. Surgical procedures that can reduce the frequency and severity of TN attacks include peripheral surgery, percutaneous ablative procedures, stereotactic radiosurgery and MVD.


   FOOTNOTES
 

Dr. Sarlani is an assistant professor, Department of Diagnostic Sciences and Pathology and Department of Biomedical Sciences, and co-director, Brotman Facial Pain Center, Dental School, University of Maryland, Baltimore, 666 W. Baltimore St., Room 2-A-15, Baltimore, Md. 21201-1586, e-mail "ens002{at}dental.umaryland.edu". Address reprint requests to Dr. Sarlani.


Dr. Grace is an associate professor, Department of Health Promotion and Policy, and director, Brotman Facial Pain Center, Dental School, University of Maryland, Baltimore.


Dr. Balciunas is an associate professor, Department of Diagnostic Sciences and Pathology, Dental School, University of Maryland, Baltimore.


Dr. Schwartz is a clinical assistant professor, Department of Health Promotion and Policy, Dental School, University of Maryland, Baltimore.


   REFERENCES
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