Edward G. Grace

Sex differences in temporal summation of pain and aftersensations following repetitive noxious mechanical stimulation

&NA; Several studies demonstrate that women are more sensitive to experimental pain than men. In addition, women exhibit greater temporal summation of heat and mechanically evoked pain. Since temporal summation of pain is centrally mediated, its greater expression in women suggests a central nociceptive hyperexcitability relative to men. The purpose of this study was to pursue this theory, by further assessing sex differences in (1) temporal summation of mechanically evoked pain, and (2) aftersensations following repetitive noxious stimulation. Sixteen series of 10 repetitive, mildly noxious, mechanical stimuli were applied to the fingers of 25 women and 25 age‐matched men. The subjects rated the pain intensity and unpleasantness caused by the first, fifth and tenth stimulus in the series, as well as their aftersensations 15 s and 1 min following the end of stimulation. Data were analyzed by three‐way repeated‐measures analysis of variance. Pain and unpleasantness ratings increased with repetition of stimulation (P<0.0001). Temporal summation of pain intensity and unpleasantness ratings were more pronounced in women than men (P<0.0001). In addition, significant temporal summation occurred only with 2 s interstimulus interval for men (P<0.0005), but with 2 and 5 s interstimulus interval for women (P<0.0001). Moreover, women provided greater ratings for the intensity and the unpleasantness of aftersensations (P<0.0005), and reported painful aftersensations at greater frequency (P<0.05). Greater temporal summation of pain and aftersensations in women suggests that their central processing of nociceptive input may be more easily upregulated into pathological hyperexcitability, possibly accounting for the higher prevalence of various chronic pain conditions among women.

Evidence for indirect effects of pain catastrophizing on clinical pain among myofascial temporomandibular disorder participants: the mediating role of sleep disturbance.

Summary Pain catastrophizing was associated with greater sleep disturbance, and both pain catastrophizing and pain‐related rumination indirectly affected clinical pain and pain‐related interference through alterations in sleep. ABSTRACT Sleep disturbance and pain catastrophizing are important mediators of the chronic pain experience. To date, these factors have not been considered concurrently despite compelling theoretical rationale to do so. In the present study, we examined whether pain catastrophizing not only has direct effects on clinical pain and pain‐related interference, but also indirect effects through its association with sleep disturbance. We evaluated this hypothesis using a cohort (n = 214) of myofascial temporomandibular disorder participants using a statistical bootstrapping technique recommended for tests of indirect effects. Results suggested that pain catastrophizing was associated with greater sleep disturbance, and that a significant portion of variance in clinical pain severity and pain‐related interference attributable to pain catastrophizing was mediated by sleep disturbance. Supplementary analyses revealed that the rumination component of catastrophizing seemed to be indirectly related to clinical outcomes through sleep disturbance. No evidence for indirect effects was observed for helplessness and magnification components. These results suggest that rumination about pain may contribute to clinical pain indirectly through alterations in sleep. Prospective studies are needed to examine lagged associations between these constructs. These findings have important theoretical and clinical implications. Critically, interventions that reduce pain catastrophizing may concurrently improve sleep and clinical pain.

Naturalistic changes in insomnia symptoms and pain in temporomandibular joint disorder: a cross-lagged panel analysis.

&NA; An increasing number of prospective studies suggest a bi‐directional association between the pain and sleep quality. Few of these investigations have controlled for synchronous correlations, an important source of extraneous variance in lagged associations, which may have confounded conclusions of prior investigations. Despite high rates of insomnia in temporomandibular joint disorders (TMD), no studies have examined temporal associations between naturalistic fluctuations in insomnia and pain in TMD. We conducted cross‐lagged panel analysis to examine reciprocal temporal associations between 1‐month changes in insomnia symptom severity and self‐reported pain over 3 months among 53 TMD patients. This rigorous analytic strategy represents a comprehensive method to explore possible reciprocal temporal associations between insomnia and pain that controls for both auto‐ and synchronous correlations. Analyses revealed that initial‐month increases in insomnia were associated with next‐month increases in average daily pain, but not vice versa. The direction of the effect was such that initial‐month increases in insomnia symptom severity were associated with next‐month increases in average daily pain. These data suggest that naturally occurring fluctuations in insomnia symptom severity are prospectively associated with fluctuations in daily pain experience for persons with TMD. Potential mechanisms by which insomnia might influence pain in TMD and therapeutic implications of these findings are discussed.

Orofacial pain--Part I: Assessment and management of musculoskeletal and neuropathic causes.

Orofacial pain is a common complaint, affecting the lives of millions of people around the world. Chronic orofacial pain often constitutes a challenging diagnostic problem that can be complicated by psychosocial factors and typically requires multidisciplinary treatment approaches. The fundamental prerequisite for successful management of orofacial pain is an accurate diagnosis. Generating a differential diagnosis, which will ultimately lead to a definite diagnosis, requires thorough knowledge of the diagnostic range of orofacial pain. There is a vast array of orofacial pain categories including: (1) musculoskeletal, (2) neuropathic, (3) vascular, (4) neurovascular, (5) idiopathic, (6) pain caused by local, distant, or systemic pathology, and (7) psychogenic. This article presents the salient clinical features and the therapeutic approaches for the various subtypes of musculoskeletal and neuropathic pain. Musculoskeletal pain is the most prevalent orofacial pain, with temporomandibular disorders and tension-type headache being the main examples. Neuropathic pain develops secondary to neural injury and/or irritation and can be distinguished into episodic, including trigeminal neuralgia and glossopharyngeal neuralgia, as well as continuous, such as herpetic and postherpetic neuralgia, traumatic neuralgia, and Eagles syndrome.

The use of an oral exercise device in the treatment of muscular TMD.

ABSTRACT Forty-five patients with a primary diagnosis of muscular MD were evaluated and treated in a university based facial pain center. The patients were equally and randomly assigned to one of three treatment groups. Group 1 patients were treated with traditional therapies appropriate for the particular patient. Group two patients used similar therapies that were appropriate for the patient but also had an oral vertical exercise device integrated into their therapy. Patients in the third group were instructed in home care, educated about TMD, and instructed in the use of the oral exercise device. Results indicated that all three groups demonstrated significant overall patient clinical and subjective improvement. The three groups did not differ significantly from each other in degree of patient improvement.

Orofacial Pain--Part II: Assessment and management of vascular, neurovascular, idiopathic, secondary, and psychogenic causes.

Chronic orofacial pain is a common health complaint faced by health practitioners today and constitutes a challenging diagnostic problem that often requires a multidisciplinary approach to diagnosis and treatment. The previous article by the same authors in this issue discussed the major clinical characteristics and the treatment of various musculoskeletal and neuropathic orofacial pain conditions. This second article presents aspects of vascular, neurovascular, and idiopathic orofacial pain, as well as orofacial pain due to various local, distant, or systemic diseases and psychogenic orofacial pain. The emphasis in this article is on the general differential diagnosis and various therapeutic regimens of each of these conditions. An accurate diagnosis is the key to successful treatment of chronic orofacial pain. Given that for many of the entities discussed in this article no curative treatment is available, current standards of management are emphasized. A comprehensive reference section has been included for those who wish to gain further information on a particular entity.

Chronic Temporomandibular Disorders Are Not Necessarily Associated with a Compromised Endogenous Analgesic System

AIMS To test whether temporomandibular disorders (TMD) case-control differences in conditioned pain modulation (CPM) exist, using a mechanically evoked temporal summation (TS) model. METHODS A series of 10 repetitive, mildly noxious, mechanical stimuli were applied to the fingers of 30 women with TMD, who had a primary diagnosis of masticatory myofascial pain, and 30 age-matched healthy women. The subjects rated the pain intensity caused by the 1st, 5th, and 10th stimuli in the series. To evaluate CPM, the same series of mechanical stimulations were applied with concomitant exposure of the other hand to a painfully cold water bath. Statistical inferences were based on t tests, chi-square tests, or analysis of variance (ANOVA), as appropriate. RESULTS Pain ratings increased significantly with stimulus repetition (P < .01) and CPM significantly reduced TS of pain (P < .01). Of particular note, both groups showed very similar degrees of CPM, with no significant group difference. CONCLUSION Painful TMD is not necessarily associated with a compromised ability to engage the endogenous analgesic system in an experimental setting.

Facial pain and monosymptomatic hypochondriasis

ported that the transfusion of fresh plasma from hemophilia A had no significant effect on a patient’s factor VIII level. Including our case, there is no report of a case where the transfusion of normal fresh plasma led to a delayed rise of both factors by newly synthesizing factors V and VIII from a common precursor. This necessitates further studies as to the existence of a common precursor. No further transfusions were required when local hemostatic treatment was used after the transfusion of fresh plasma. We therefore believe that replacement therapy is necessary only to permit local hemostatic treatment to be effective and that no further blood replacement is necessary after that point.