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  • Toothache or Trigeminal Neuralgia: Treatment Dilemmas

    Reposted from TNA Newswire (TNA Headline News) May 21, 2009

    Christopher J. Spencer, John K. Neubert, Henry Gremillion, Joanna M. Zakrzewska,
    and Richard Ohrbach

    Case Review

    A 61-year-old woman presented to her general
    dentist with a complaint of pain associated
    with the maxillary left first premolar. The patient
    described a sharp, lancinating pain that was triggered
    by stimulation of the tooth in question. She also
    reported 2 specific episodes in which she experienced
    severe, shooting electrical shock-like pain followed by a
    hot sensation in the same area. One of these episodes
    was triggered by a cool breeze on her face and the other
    occurred while washing her face. Examination and radiographic
    assessment revealed a periapical osseous lesion
    resulting in a diagnosis of acute apical periodontitis.
    Nonsurgical endodontics was completed with no undue
    Approximately 2 months after the endodontic treatment,
    the patient began to have a recurrence of the
    paroxysmal sharp, shooting pain with a marked increase
    in the frequency of these episodes. The pain was triggered
    by light touch of the left cheek. Each episode
    lasted 1 to 2 seconds; however, she occasionally had 5 to
    10 repetitive bursts. Clinical evaluation resulted in a diagnosis
    of trigeminal neuralgia of the left maxillary division.
    Initial treatment included 100 mg carbamazepine
    bid., which was gradually increased to a maximum dose
    of 600 mg bid. The patient derived modest benefit from
    the medication; unfortunately, cognitive changes necessitated
    a reduction in the dose. Gabapentin was introduced
    in a bedtime dosage regimen of 100 mg. This
    provided a marked reduction in pain for approximately
    1 week. A gradual titration of gabapentin to
    300 mg tid was efficacious for approximately 1 month.
    Neurosurgical consultation and MRI of the brain revealed
    no intracranial pathology and confirmed a diagnosis
    of trigeminal neuralgia. Surgical intervention
    is being considered.

    Christopher J. Spencer, D.D.S.
    Clinical Assistant Professor
    University of Florida College of Dentistry
    Parker E. Mahan Facial Pain Center
    Gainesville, FL

    Orofacial Pain: Unknown Etiology

    Many acute, chronic, and recurrent painful maladies
    occur in the orofacial region. Lipton et al11 reported that
    22% of the U.S. population have orofacial pain on more
    than 1 occasion in a 6-month period. However, the etiology
    of pain for countless patients who have chronic orofacial
    pain disorders is unknown. In many instances,
    these patients may not recognize an injury or serendipitously
    report having a relatively minor dental procedure
    (eg, restoration or root canal) completed at the time of
    pain onset. Although pain involving the teeth and the periodontium
    is the mostcommonpresenting concern in dental
    practice, other nonodontogenic causes of orofacial pain
    must be considered in the differential diagnostic process.
    Neuropathic orofacial pain, which is pain initiated or
    caused by a primary lesion or dysfunction in the nervous
    system, is relatively common. It is diagnosed in approximately
    25% to 30% of patients presenting in a tertiary
    care University-based Facial Pain Center.19 Conditions
    representative of neuropathic orofacial pain are postherpetic
    neuralgia, trigeminal neuralgia, traumainduced
    neuropathy, atypical odontalgia/nonodontogenic
    toothache, idiopathic oral burning, and Complex Regional
    Pain Syndrome (CRPS). In some instances, diagnosis
    can be difficult, as neuropathic orofacial pain is associated
    with significant interpatient variability regarding
    presentation and response to treatment. Additionally,
    neuropathic pain conditions are frequently associated
    with qualities that the patient is not familiar, thus making
    it difficult for the patient to communicate their pain
    experience. Typical descriptors used by patients include
    stabbing, burning, electric-like, and/or sharp, with
    numbness or tingling projected to a cutaneous area.15,16
    However, aching pain does not preclude the possibility
    of a neuropathic basis for the patient’s pain.
    The present case illustrates an interesting conundrum
    whereby the practicing clinician must decide whether the 2 pain complaints (tooth vs neuropathic pain) are
    related or are merely coincidental. Such comorbid conditions
    may result in diagnostic confusion and a perpetuation
    of the patient’s pain condition. Although the etiology
    and pathophysiology of odontogenic pain is well
    known (ie, bacteria-induced destruction of tooth structure
    and subsequent activation of tooth nociceptors),
    mechanisms underlying trigeminal neuralgia are less understood.
    It is possible that coexistent sources of pain in
    this patient are indeed playing an additive role in the
    overall pain complaint. As such, this provides an interesting
    scenario whereby a persistent peripheral noxious
    stimulus (ie, tooth pain) can sensitize trigeminal ganglion
    neurons in the brainstem (ie, central sensitization)
    that may in turn influence the trigeminal neuropathic
    pain. Central sensitization involves an activity-dependent
    increase in the excitability of neurons in the dorsal
    horn of the spinal cord.4,17,21,22 and its trigeminal homolog
    in the brainstem.3,13 Central sensitization is reflected
    in the reduced threshold of activation and increased
    responsiveness of central neurons associated
    with an increase in receptive field size of the neurons.22
    The increased excitability of central neurons, which receive
    convergent input from other, usually nearby tissues,
    typically results in expanded areas of referred pain
    as well as sensitivity to previously non-noxious stimuli (ie,
    allodynia). Importantly, these symptoms can persist beyond
    the initial noxious stimulus,21 which, if maintained,
    can continue to drive central sensitization.8
    This case also highlights that trigeminal neuropathic
    pain may exist in many forms and may easily be mistaken
    to represent an odontogenic source. The pitfall for the
    practicing dentist is to focus on the odontogenic pain
    component while the physician focuses on the trigeminal
    neuropathic pain component. Failure to identify the
    source of the patient’s entire problem may lead to erroneous
    and ineffective treatment. Therefore, it is important
    to consider all sources of pain in trying to delineate
    the etiology and ultimately recommend treatment. Optimum
    management can only be achieved by determining
    an accurate and complete diagnosis and identifying
    all of the factors associated with the underlying pathology
    on a case-specific basis.
    John K. Neubert, DDS, PhD
    Assistant Professor
    Departments of Orthodontics and Neuroscience
    University of Florida
    Gainesville, FL
    Henry Gremillion, DDS, MAGD
    Associate Professor
    College of Dentistry
    University of Florida
    Parker E Mahan Facial Pain Center
    Gainesville, FL

    Surgical Strategies for Pain Relief

    There continue to be a variety of surgical treatments
    for patients with trigeminal neuralgia in whom efficacy
    and tolerability of medications is reduced. Surgical treatments
    are broadly divided into 2 groups. The first group,
    ablative or destructive techniques, damage the trigeminal
    nerve. The tissue disruption resulting from the intervention
    can be partial or complete and/or selective or
    indiscriminate. The second surgical treatment, termed
    microvascular decompression (MVD), is a nondestructive
    procedure that attempts to relieve pressure on the trigeminal
    Of the ablative procedures, percutaneous radiofrequency
    thermocoagulation/rhizotomy (RFT) is one example.
    This procedure involves the insertion of a needle
    under radiographic control through the foramen ovale
    into the trigeminal cistern. Once the needle is accurately
    located and checked by the use of radiology, then a lesion
    can be made. An electrical stimulus is passed
    through the needle tip which generates a temperature
    between 60°C and 80°C. This is maintained for 60 to 300
    seconds. The position of the needle and the area of the
    lesion can, to some extent, be predicted by waking the
    patient at the start of the procedure to test the area that
    has been affected. For the majority of patients, only an
    overnight hospital stay is required as the procedure does
    not require a full general anesthetic but very heavy sedation.
    A recent randomized, controlled trial showed
    that pulsed radiofrequency (at lower temperatures than
    described above) did not give pain relief of sufficient
    quality and the trial was stopped early.7
    A review of all the literature of surgical management
    of trigeminal neuralgia25 showed that there were no
    randomized, controlled trials of treatments using RFT.
    The studies that have been conducted include independent
    observers to evaluate the outcomes.1 A systematic
    review of all ablative procedures12 suggests that RFT provides
    the longest-term and most complete pain relief,
    which at 5 years is just over 50%. The majority of patients
    will report sensory numbness, which may be confined to
    only 1 branch of the trigeminal nerve but can extend to
    all 3 branches. The extent of sensory loss can vary from
    mild paresthesia to the rare (2%) but extremely debilitating
    anesthesia dolorosa. If the first trigeminal nerve
    division is involved, corneal anesthesia may occur in up to
    10% of cases, and this must be identified before the
    patient leaves the hospital, so that protective eyewear
    can be issued. This numbness can lead to corneal damage
    and subsequent loss of sight in 1% of patients. There is a
    12% risk of masticatory weakness, resulting in difficulties
    with eating, but these tend to resolve over time. The
    risk of these side effects can be reduced by using lower
    temperatures, but this results in a shorter pain relief period.
    The second treatment strategy, MVD, appears to offer
    the best long-term outcome, but not all patients can be
    offered this form of major surgery due to coagulopathies,
    infection, or general frailty. RFT, therefore, offers
    an alternative in patients who are not medically fit for
    surgery or who are fearful of a major operation and its
    risk of serious complications. Although mortality has
    been reported after RFT, this is very low in comparison to
    MVD. Patients must be aware that RFT may need to be
    repeated for them to remain free of pain. The major risk is the sensory loss, which can affect the quality of life of
    more than 65% of patients.24
    In summary, the advantages of RFT include (1) safe in
    medically compromised patients, (2) highly specific for
    the targeted trigeminal nerve branch, (3) immediate
    pain relief, (4) low mortality rate, (5) relatively low recurrence
    rate, and (6) few complications outside the trigeminal
    nerve branch territory.23 The disadvantages of RFT
    include (1) patients with coagulopathies are not suitable
    candidates, (2) a cooperative patient is necessary, (3) the
    equipment is expensive, (4) it is tedious to do because of
    the need to continuously request patient feedback, (5)
    sensory loss is inevitable, (6) risk of anesthesia dolorosa,
    (7) risk of corneal damage, (8) need to wear safety
    glasses, and (9) risk of masseteric dysfunction. Patients
    taking part in a hypothetical decision-making process on
    management of trigeminal neuralgia opted for surgery
    compared with continued medication, and MVD was
    only marginally more frequently chosen that other procedures.
    Prof Joanna M. Zakrzewska
    Consultant Oral Medicine
    Eastman Dental Hospital
    UCLH Foundation NHS Trust
    London, UK

    Why Now? Biobehavioral Factors

    This case illustrates the complex task of the clinician in
    determining which factors are important to consider at
    each stage of the progression of a pain disorder. The
    field of orofacial pain tends to be focused on the nociceptive
    and neuropathic aspects of the pain; this commentary
    addresses additional possibilities.
    At the outset, the patient reported idiopathic onset
    (61-year-old individual with presumably no significant
    history of problems with the affected teeth or region)
    and clinical characteristics with overlapping diagnostic
    possibilities (sharp pain episodes triggered by tooth stimulation;
    sharp pain episodes triggered by stimulation to
    the face), coupled with a pathology (periapical tooth
    lesion, signifying pulpal death) from which nociception
    sufficient to explain the complaint could be reasonably
    inferred. Given these specific facts, focusing at that stage
    on only the somatic characteristics of the problem would
    be sensible. We learn that several months after somatic
    intervention for the obvious pathology, the pain episodes
    associated with the previously identified allodynia
    have recurred and escalated. A somatic diagnosis (trigeminal
    neuralgia) emerged, and medication appropriate
    to that diagnosis was implemented. It appears that
    the response to medication was variable over time, and
    an intervention was considered.
    At the time of recurrence, the clinician’s task became
    more difficult: A decision point emerged with respect to
    what additional evaluation and therapeutic possibilities
    should be considered. Although the first intervention
    (for the tooth pulp) indicated the clinician’s reasonable
    belief that the allodynia suggestive of neuroplastic
    changes would resolve once the source of the nociception
    was removed, the recurrence of the allodynia suggested
    that the initial presentation might not have been
    simply an acute disorder but rather possibly the acute
    presentation of a chronic process. The clear identification
    of additional somatic symptoms (eg, the neuropathic
    pain symptoms in this case) that point to a particular
    physiological process at the time of recurrence in
    any disorder can be seductive in that it overshadows consideration
    of possible chronicity as well as making the
    question of “Why now?” for the emergence of the initial
    complaint more salient. That is, the retrospective view at
    the time of recurrence opens the door to reconsidering
    what other factors might be contributing to the pain
    symptoms that may represent a chronic process.
    Although the evidence for the role of biobehavioral
    factors affecting musculoskeletal pain and chronic pain
    in general is very good,2 there is very little known about
    how such factors might affect neuropathic pain. Yet, the
    available evidence does suggest that neuropathic pain is
    no different than other chronic pain conditions with respect
    to the potential importance of biobehavioral factors.
    10 Because of the evident pathology (periapical lesion)
    appropriate to the pain complaint at the time of
    initial presentation, it is understandable that the clinician
    focuses on further pathological contributions to the
    nociceptive pain (eg, trigeminal nerve impingement),
    and indeed the somatic contributions must be considered.
    However, because pain is clearly affected by multiple
    levels of processing in the brain,14 the suggestion of
    chronicity, coupled with uncertainty about how the symptom
    course will unfold in time after yet another somatic
    intervention, leads to the question of when should other
    possible contributions to pain experience and symptom expression
    be considered? So, we return to the question of
    “Why now?” Why, indeed, does pain expression suddenly
    unfold given the evidence of ongoing pathology heretofore
    not reaching into consciousness? Is it because of a
    change in the pathology (eg, pulpal status? degree of impingement
    upon the trigeminal nerve?) or perhaps because
    of a change in central processing independent of any
    ongoing nociceptive process?9
    We have straightforward biobehavioral assessment
    methods for use in temporomandibular disorders that
    would appear to be as useful and relevant for other orofacial
    pain conditions.5,6 As is true for any pain condition,
    these methods assess the cognitive and behavioral processes
    associated with central changes that may be
    caused by persistent pain or that may affect the expression
    and course of pain. These assessment methods, however,
    are not used currently in any systematic way in most
    clinical settings; moreover, we as yet do not have the
    data demonstrating the clear relevance for their routine
    application for orofacial pain disorders as compared with
    use in temporomandibular disorders. The use of such
    methods will lead to that data, however, and certainly,
    for the given patient, to assess factors perhaps relevant
    to the question of “Why now?” might lead to insights
    leading to additional treatments (eg, cognitive behavioral
    therapy for catastrophizing, relaxation skills for
    stress-related anxiety responses) that might facilitate better response to analgesics20 and even perhaps to neuroleptic
    medications (though that is not yet been demonstrated),
    or perhaps augmenting the effects of interventional
    procedures, for example, and reduce risk of
    recurrence of the pain—which is known to occur in a
    substantial number of cases.
    These are questions for which we do not as yet have
    answers. And yet, we do know enough about biobehavioral
    factors in general to at least move them around on
    our clinical decision board and utilize them, recognizing
    that we are still largely probing in the dark with respect
    to the best way to operationalize those processes. Better
    to assess for the presence of cognitive and behavioral
    factors relevant to pain before significant intervention
    rather than after, as it allows such treatments to have at
    least a reasonable chance of success. Resorting to such
    treatments after failure of all somatic interventions puts
    too much of a burden on the treatment, the practitioner,
    and the patient.
    Richard Ohrbach, DDS, PhD
    Associate Professor
    Department of Oral Diagnostic Sciences
    University at Buffalo
    Buffalo, NY


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    The Journal of Pain, Vol 9, No 9 (September), 2008: pp 767-770
    Available online at www.sciencedirect.com

    Address correspondence to Judith A Paice, PhD, RN, Editor, Case Reviews
    in Pain; Director, Cancer Pain Program, Northwestern University, Feinberg
    School of Medicine, Chicago, IL 60611-2927. E-mail: j-paice@northwestern.edu
    © 2008 by the American Pain Society

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