Biomedical subjects
Publications and source records attributed to J J Marbach.
This study investigated the records from one insurance company's reimbursed claims for any TMD-related treatment. Females were disproportionately represented among those treated by surgical means.
A stepwise method for treating TMPDS is presented. Step 1-start patient on a regimen of chloroethane or chlorofluorocarbon spray and exercise. Step 1A--if a clicking joint is the chief complaint, start with click exercise. Step 1B--if restricted mouth opening is the chief complaint, start with range of motion exercise; employ exercises sequentially, not simultaneously. Step 2--if pain is moderate to severe, start with amitriptyline 10 mg at bedtime, increasing the dose in 10-mg increments to 40 mg. Step 3--for nonresponders, add injections of tender points with lidocaine and consider a trial of a different tricyclic. Step 4--for nonresponders, consider a trial of tender point injections combining dexamethasone with local anesthetic. Start by injecting the three most painful tender points with 0.5 mL of a solution of 1 mg of dexamethasone combined with two thirds bupivacaine and one third lidocaine to reach the desired volume. Repeat injections, varying the sites as required. Do this once weekly for 4 to 6 weeks for an adequate trial. This regimen can be continued for an extended period of time with appropriate precautions in place. The value of judgment-free psychosocial support cannot be overemphasized. Patients with TMPDS are faced with long-term problems of pain management. An understanding clinician can provide the sustained support required to prevent the cycle of ever more invasive treatments with their potential for harm.
Developing a treatment strategy for patients who are in chronic pain can be challenging for any health care professional, particularly when traditional measures to relieve pain are ineffective. Pain treatment can be further complicated by phenomena known as phantom pain--most often associated with limb amputation. The author describes three phantom syndromes experienced in the orofacial region: phantom tooth pain, phantom bite syndrome and intraoral stump pain.
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In this study, 110 female myofascial face pain patients were assessed monthly for 10 months on measures of pain, distress, and stressful life events. D. A. Kenny and A. J. Zautra's (1995) structural equation model for examining the separate trait, state, and error components of the variables was used to analyze the data. Both pain and distress had sizable trait variance, and the trait components were correlated. The 2 variables also showed sizable state variance, and the states of pain covaried with states of distress. A significant time-lagged relationship between the 2 variables was found: Increases in distress led to elevations in pain 1 month later. Stressful life events arising from major social roles were also associated with greater distress, but not pain. Illness events unrelated to the pain syndrome were associated with both pain and distress.
It is widely accepted that abnormal personality factors play an important role in the etiology and maintenance of myofascial-type temporomandibular disorder, or M/TMD. However, the foundation on which this belief rests is based largely on clinical lore, rather than on any evidence. The continued belief in the stress theory has important implications. Clinicians continue to be trained in unproven but traditionally sanctioned treatments. Such approaches not only may lead to problems of patient care, they may forge an unstable foundation for future research. Two theories are examined in this article: the psychosomatic and psychophysiological models. The findings show that both theories lack evidence, and further research is warranted because definitive studies are unavailable. The data from this study do not support the contention that M/TMD cases are characterized by a specific premorbid personality.
The symptoms of phantom tooth pain are often considered to be of psychological origin by those unfamiliar with its clinical characteristics. Part of the problem is that phantom tooth pain is often confused with atypical facial pain. Extensive literature exists for the latter that suggests a psychological cause. Many studies of atypical facial pain, however, suffer from one or more of four methodologic problems. In the present study, 115 phantom tooth pain cases are compared with a contrast group of 151 facial pain cases and 137 nonpain controls on a variety of personality characteristics. Only one trait personality factor, locus of control, statistically differentiates the three groups. The chief psychological difference of the phantom tooth pain sample compared with the control and contrast groups was higher scores on a measure of demoralization. Demoralization can be interpreted as a consequence as well as an antecedent of the chronic pain state. Evidence for each opinion is presented. Suggestions for obtaining informed consent of prospective endodontic patients are suggested. This study has not demonstrated that phantom tooth pain cases are characterized by a specific premorbid personality.
Phantom tooth pain is a syndrome of persistent pain or paresthesia in teeth and other oral tissues that may follow dental or surgical procedures such as pulp extirpation, apicoectomy, tooth extractions, or exenteration of the contents of the maxillary antrum. It can also occur when nerves are injured after trauma to the face or even after routine inferior alveolar nerve blocks if the needle pierces the nerve sheath. In the case of tooth extraction, the pain is found in the edentate area. After periodontal surgery, pain or paresthesia is located in the gingiva. The incidence of phantom tooth pain after extirpation may be as high as 3% of cases. Clinically, phantom tooth pain is similar in many essential characteristics to deafferentation pain syndromes also known as phantom pain syndromes. A limitation to this taxonomy is the lack of definitive information with respect to the pathophysiology of deafferentation pain in the trigeminal nerve. This article amplifies previous clinical descriptions of phantom tooth pain. Current concepts in the pathophysiology of neuropathic pain are reviewed as they pertain to phantom tooth pain. Treatments are described that use three routes of drug administration: oral, nerve blocks by injections, and intranasal applications. Reasons are discussed for the high rates of morbidity after dental and neurosurgery in attempts to treat phantom tooth pain.
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The choice of an appropriate control group has been recognized as one of the most difficult problems in the methodology of case/control studies, both in theory and in practice. In the study of chronic pain, a "well control group" has frequently been employed. Although this design has intuitive appeal, it contains the potential for bias and error. In order to obtain the proper control group, the same exclusion criteria should be applied to cases and controls. Second, controls should be selected independently of exposure to the putative risk factors under investigation. To illustrate the nature of this problem we present two numerical examples, using a chronic pain disorder.
It is widely accepted that abnormal personality traits are important factors in the aetiology and maintenance of the temporomandibular pain and dysfunction syndrome (TMPDS). However, the foundation upon which this paradigm rests is largely based on clinical lore rather than evidence. The continued belief in the stress theory has onerous implications. First of all, clinicians could be lulled into a false sense of security about the efficacy of traditionally sanctioned treatments. Second, and potentially more important is the chilling effect on research that results from the premature and unsupported conclusions voiced by many, that certain issues regarding the diagnosis and treatment of TMPDS are solved. Such conclusions will lead not only to problems of patient care but may forge an unstable foundation for future research. Three theories are examined for convergent evidence in support of the putative relationship between personality and TMPDS. They are the 1) psychosomatic 2) coping and 3) psychophysiological theories. Currently evidence lacks for all three theories although there is partial support for the latter. It has not been demonstrated that TMPDS cases are characterized by a specific premorbid personality.
In 136 women with TMPDS observed for one year, pain was highly variable. No respondent had a consistent pattern of pain increase or decrease.
Pain intensity among 136 women with TMPDS was compared with the signs and symptoms of TMPDS. Most masticatory muscle pain was related to TMPDS pain intensity. Clicking, restricted mandibular range and evidence of tooth grinding were not related to pain intensity.
It is widely accepted that abnormal personality traits and psychological stress are important factors in the etiology and maintenance of the temporomandibular pain and dysfunction syndrome (TMPDS). However, this assumption is based largely on clinical lore rather than research evidence. Continued belief in the stress theory has onerous implications. Such conclusions will lead not only to problems of patient care, but may also forge an unstable foundation for future research. Three theories have been advanced that support a relationship between personality and TMPDS. They are the psychosomatic, coping and psychophysiological theories. But evidence in support of all three theories is currently lacking. It has not been shown that TMPDS cases are characterized by a specific premorbid personality or an exaggerated vulnerability to psychological stress.
There is a lack of information about the precise strength of the relationship between chronic pain and depression. In a prior study, women with temporomandibular pain and dysfunction syndrome (TMPDS) had much higher scores than did controls on a measure of nonspecific psychological distress. The question arose as to whether rates of clinical depression are also unusually high in TMPDS patients. Their former treating clinician rates cases for likely lifetime presence or absence of depression. A subset of those rated as likely depressed then had their diagnoses verified independently through a structured clinical interview by a psychiatrist and clinical psychologist. Results revealed a minimum lifetime prevalence rate for major depression of 41%. A rate of this magnitude in TMPDS cases is clearly much higher than would be found for women of similar background in the general population.