Background: Persistent somatoform paindisorder (SPD) is a condition in which the patient suffers from persistent, severe and distressing pain; and from associated physical and psychological distress. While presence of restless leg syndrome (RLS) in SPD is understudied, their association might have an impact on general well‑being and quality of life (QoL) in SPD. Aims and Objectives: Present study aimed at evaluating the prevalence of RLS in SPD patients attending outpatient department services at a tertiary care institute in eastern India. Materials and Methods: Two hundred and forty consecutive patients with SPD were screened initially and after applying appropriate inclusion and exclusion criteria, 192 subjects (male = 85, female = 107) were included in the study. Severity of RLS was assessed using a questionnaire of the International Restless Legs Syndrome Study Group and QoL was measured on QoL Enjoyment and Satisfaction Questionnaire‑Short Form (Q‑LES‑Q‑SF). Results: Revealed a 28% prevalence of RLS is in patients with SPD, which is much higher than its estimated population prevalence. A larger proportion of those with RLS had continuous course of SPD, longer duration of SPD, and higher daytime sleepiness. They also had poorer scores on Q‑LES‑Q‑SF, indicating a poorer QoL overall. Discussion and Conclusion: This is the first report, to the best of our knowledge, on this aspect from India. While this association between RLS and SPD may have biological explanation based on abnormal monoaminergic neurotransmission system, the findings call for more vigilant approach to SPD patients in order to improve their QoL and add to their well‑being.
The actual treatment of the incriminating chronic paindisorder marks an enormous problem and needs more attention in public health. The treatment does not result in a reduction of symptoms. It is just consuming time, hope and energy of these patients (Gada, 2007). The endless and unsatisfactory searching has a negative effect on their quality of life (Sullivan, Thorn, Haythornthwaite, Keefe, Martin, Bradley & Lefebvre 2001). Furthermore, it is expected that more than 61% of people with a chronic paindisorder will not perceive any higher levels of positive well-being. But why is it important to think about positive well-being if the people affected by a chronic paindisorder have greater problems? The answer is given by the meaning of the word ‘chronic’: a chronic paindisorder is believed to have no cure, so these people have no hope of full recovery (Gaskin & Richard, 2012). The actual focus in treatment on trying to heal the pain symptoms is misleading and needs to be changed. What is possible instead? It is more successful to strengthen the fighter, save their energy and increase quality of life. But how could this work? The answer is given by Keyes (2007) with the two continua model for positive well-being.
Researchers have shown increasing interest in sponta- neous and low-frequency neural activities in PSPD patients using resting-state fMRI or electroencephalogra- phy (EEG). For instance, it was found that somatoform paindisorder patients exhibited higher regional homoge- neity (ReHo) in the left precentral gyrus, the prefrontal cortex and default-mode network, but decreased ReHo in the bilateral primary somatosensory cortex, the posterior cerebellum, and the occipital lobe comparing with healthy controls. 8,9 Further, using independent component analysis to isolate intrinsic connectivity networks (ICNs) and to calculate the functional network connectivity (FNC) such as intra- and inter-ICNs, Zhao and his colleagues found altered FNCs between the sensorimotor network, the audio network, the visual network, the default-mode network, the executive control network, the salience network, the right-frontoparietal network, the left-frontoparietal net- work, and the cerebellum network in PSPD patients. 10 A resting-state EEG study revealed that somatoform paindisorder patients exhibited hyperexcitability resting-state cortical oscillations at the parietal region. 11 The evidence above suggests that PSPD patients manifest large-scale brain functional reorganization at different levels.
The Physical Component Summary (PCS) measure  in our patient group had to be 1 standard deviation or more below the population norm (≤ 40), as measured with the SF-36 (see below). A score less than 40 also meets the DSM-IV criterion B for “significant distress or psycho- social impairment due to the somatoform pain” in patients with paindisorder . As a second precondition, sum scores on the 15-item Patient Health-Questionnaire (PHQ-15) had to be above 10, representing at least medium somatic symptom severity (see below). The German version of the Brief Pain Inventory (BPI)  was used to estimate the intensity of each participant’s pain. We reviewed patients’ medical charts and contacted the treating physicians to rule out possible or unclear organic explanations for the symptoms of our chronic pain pa- tients. Patients with insufficient cognitive abilities, severe and chronic somatic or nervous diseases, unambiguous nociceptive pain, hypochondriasis, a severe comorbid mental disorder causing major impairment in social func- tioning (e.g., schizophrenia or severe substance abuse) or insufficient German language skills were excluded. All participants were white, of Caucasian origin, and right handed, as assessed by the Edinburgh handedness inven- tory . Additional file 1: Table S6 lists all medications that patients were currently taking.
effects of laser treatment. Clinical examiner and statistician were blinded to the group allocation. Group-A patients received 500 mg naproxen (a product of Parsdarou co., Tehran, Iran) every 12 hour for 2 weeks and placebo laser. Group-B patients were exposed to diode He-Ga-Ar laser irradiation (LMPT200, 890 nm wavelength, 10 pulse, E 50 mW power) for 5 minutes for 2 days a week and for 2 weeks plus a placebo drug has been given to them too. Pain intensity, degree of mouth opening in mm and masticatory muscle tenderness were evaluated in patients before and 2 weeks after both types of treatment and recorded in the questionnaires. The amount of mouth opening was assessed by measuring the distance between the upper and lower incisors using a ruler. This distance was measured 2 times and the mean value was calculated and recorded. The amount of mouth opening was measured before and 2 weeks after the treatment.
(a). Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) are useful for pain and inflammation. In mild cases, they may be the only drugs required for analgesia. There are several classes of NSAIDs and the response of the individual injured worker to a specific medication is unpredictable. For this reason a range of NSAIDs may be tried in each case with the most effective preparation being continued. Patients should be closely monitored for adverse reactions. The US Food and Drug Administration advises all NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. Naproxen sodium does not appear to be associated with increased risk of vascular events. Administration of proton pump inhibitors, histamine 2 blockers, or prostaglandin analog misoprostol along with these NSAIDs may reduce the risk of duodenal and gastric ulceration but do not impact possible cardiovascular complications. Due to the cross-reactivity between aspirin and NSAIDs, NSAIDs should not be used in aspirin-sensitive patients, and should be used with caution in all asthma patients. NSAIDs are associated with abnormal renal function, including renal failure, as well as, abnormal liver function. Certain NSAIDs may have interactions with various other medications. Individuals may have adverse events not listed above. Intervals for metabolic screening are dependent upon the patient’s age, general health status and should be within parameters listed for each specific medication. Complete blood count (CBC), liver and renal function should be monitored at least every six months in patients on chronic NSAIDs and initially when indicated.
Overdiagnosis could also be considered which may contribute to the inclusion of subclinical OCD. However, subclinical OCD prevalence was considered separately in our study (25.8%), which had even a different gender correlation (male) than OCD itself. The high prevalence of OCD symptoms has been reported previously. In a general population study, in 1037 individuals in New Zealand, it was reported that 21-23% of the general population (13%-17% of healthy population) have endorsed obsession-compulsion as defined in DSM-IV, but only 2-3% met the full criteria (37). Overdiagnosis of OCD by the lay interviewers compared to the experienced personnel (3.1% dropped to 0.6%) was postulated to be due to labeling of worries or concerns as obsessions and overestimating the degree of functional impairment or distress attributable to obsessive-compulsive symptoms (30). Although, in our study, most patients were diagnosed to have compulsive feature of OCD and the interviews were done by a psychologist, estimation of functional impairment or distress was difficult because of comorbid paindisorder.
The main data in support of a trauma-genetic model of dissociation are derived from cross-sectional studies in which both self-reports of traumatic experiences and dissociation have been collected in clinical as well as non-clinical samples . Moreover, the results of a limited amount of prospective and longitudinal studies also suggest that overwhelming events have the potential to induce dissociative phenomena [7, 8]. Empirical studies of the link between trauma and dissociation in patients with somatoform disorder, however, are relatively scarce. This is striking, given the fact that some bodily dysfunctions of patients with particular somatoform disorders can be regarded as manifestations of somatoform disso- ciation and as related to traumatic experiences . Among the group of somato- form disorders, the few studies on trauma (in particular childhood, sexual abuse) and dissociation are mainly confined to conversion disorder and chronic pelvic paindisorder. The current article will elaborate upon our current knowledge of these two disorders.
and .94. With regard to convergent validity, scores on all subscales of the OMMP except social distancing were significantly correlated with anxious and depressive cog- nitions (r’s between .26 and .64 for depression and .27 and .50 for anxiety) . OMMP factors were found to be positively associated with coping strategies such as emotion-focused coping, and negatively associated with others, such as problem-focused coping. Orbach and colleagues  reported that these associations were moderate, suggesting the scale assesses a subjective experience of mental pain. Thus, it can be significantly differentiated from other measures of distress including the concepts of anxiety and of depression. Another study  reported that, among a sample of thirty five individ- uals who made medically serious suicide attempts and with 67 not serious suicide attempters as well as 71 healthy controls, cronbach alpha coefficients for the fac- tors of OMMP scale ranged between .72 and .89., with the exception of the social distancing factor, which was found to be .42.
The present study was conducted to examine the influence of PTSD on pain experience in subjects on opioid (methadone or buprenorphine)
maintenance therapy for the treatment of opioid addiction. Both experimental pain testing and subject’s self-reported pain experience were used to test two major hypotheses: 1) subjects with PTSD would have either increased or decreased sensitivity to experimental pain testing as compared to control subjects (No PTSD); and 2) subjects with PTSD would self-report exacerbated pain (higher pain severity and pain interference) as compared to control subjects (No PTSD). Collectively, the results indicate that the presence of PTSD did not exacerbate responses to experimental pain testing as administered by a cold pressor test or mechanical pinprick test. The data also indicate that subjects with PTSD demonstrated more personal distress as reflected by a significantly higher pain interference score, and a trend toward greater pain severity, though not quite meeting level of significance possibly related to our sample size limitations. These results are independent of factors of age, gender, race (White vs. Non- White), disability status (yes or no), depression (mean PHQ-9 score), anxiety (mean State Trait score) and years on opioid agonist therapy (OAT).
To date, relatively little research on the sensitivity to pain- ful stimuli, or the expression of pain, in infants, children or adults with ASD has been conducted. Accurate pain assess- ment, in order to provide appropriate and timely care, can be a challenging task especially in children with ASD . However, pain assessment strategies for children with ASD are poorly understood  and relatively little is written about the relationship between pain and ASD in the pain literature . Due to communication and assessment difficulties, there is a greater likelihood that their pain may go unrecognised and untreated (e.g., [34, 35]). Another potential barrier to assessing pain in children with ASD is the prevailing belief, frequently based on anecdotal observation or clinical impres- sion, that pain insensitivity is a common feature in children with ASD (e.g., [2, 36–40]). Parents, caregivers, and mental health professionals have reported that some children with ASD appear to withstand painful stimuli (bumps, cuts, etc.) show absence of nociceptive reflexes (e.g., absence of hand withdrawal reflex when burning oneself), or lack of protective body position in cases of broken legs or arms . However, nearly all of the support for this notion of pain insensi- tivity is derived from anecdotal reports and limited clinical observations [24–29, 42–44]. Despite the lack of systematic studies of pain sensitivity and reactivity in ASD, the pres- ence of pain insensitivity in ASD has been given further validation because of its inclusion as an associated feature in standard diagnostic texts. In DSM-IV and DSM-IV-TR “a high threshold for pain” is described [2, 45] while in DSM- III the “ignoring of pain” is described (APA, 1987). Not only are children with ASD considered to have “reduced pain sen- sitivity,” but they have also been described as “not feeling pain as intensely as others” , having an “indifference to pain”  and having a “high threshold for pain” . The belief that children with ASD are insensitive to pain may bias observers’ judgements of pain in these children .
The prevalence of TMD found in this study is similar to that observed by other studies that used the FAI to identify TMD signs and symptoms among the university population (Pinto et al., 2017; Bezerra et al., 2012; Goyatá et al., 2010). However, other studies with undergraduate students using the same index found discrepancies in prevalence, ranging from 42 to 92% (Minghelli et al., 2014; Wahid et al., 2015; Habib et al., 2015; Lemos et al., 2015; Sousa et al., 2016; Al Moaleem et al., 2017). These differences can be explained by different data collection methodologies, gender distribution or differences in the sample, where cultural, economic and dietary habits are considered (Al Moaleem et al., 2017). According to Sousa et al. (2016), because it is easy to apply and interpret, the use of indexes, especially when validated and widely disseminated in the literature, are effective to identify possible TMD signs and symptoms for early diagnosis of this disorder. They affirm that, regarding risk groups, young undergraduate students represent the object of studies, mainly due to the level of demand for academic performance as one of the fundamental factors for future professional perspectives. In addition, several Brazilian and international studies have used the FAI to classify patients according to TMD signs and symptoms (Minghelli et al., 2014; Habib et al., 2015; Lemos et al., 2015; Al Moaleem et al., 2017; Berni et al., 2015; Dantas et al., 2015). Research data from Bortoleto et al. (2013) show that 40 to 60% of individuals in the general population have some type of TMD. This may be a conservative estimate, as many patients have no complaints of any TMD-associated symptoms. The possible explanation for this fact is the presence of subclinical signs that are not reported as symptoms. Gender is considered a predisposing factor in the occurrence of TMD. The data obtained through the application of the IAF in this study showed that women were more affected (63.8%) compared to men (36.2%), corroborating the results of other studies (Parente and Cerdeira, 2013; Minghelli et al., 2014; Pinto et al., 2017; Correia et al., 2015; Goyatá et al., 2010; Dantas et al., 2015; Medeiros et al., 2011; Ferreira et al., 2016). However, two studiesfound a higher prevalence of TMD among men (Mello et al., 2014; Bezerra et al., 2012).
musculoskeletal pain population (DeGood & Tait, 2001; Potter & Jones, 1992). Coping flexibility refers to the number of coping strategies that an individual utilizes on a regular basis to cope with their pain (DeGood & Tait, 2001). In a chronic pain sample that was seeking treatment for their pain; higher levels of coping flexibility were found to predict greater self-perception of control regarding the pain condition, and potentially greater use of effective coping strategies. However, coping flexibility did not predict ratings of pain severity (Haythornthwaite, Menefee, Heinberg, & Clark, 1998). Research that has focused on diverting attention away from the pain condition has been correlated with positive adjustment to pain; however, this relationship has often been found to be moderated by additional variables (e.g., pain intensity; Affleck, Urrows, Tennen, & Higgins, 1992; DeGood & Tait, 2001). Conflicting results have been found regarding the use of reinterpreting pain, coping self-statements, and ignoring pain (DeGood & Tait, 2001). Coping strategies such as praying or hoping have been found to be associated with poor adjustment to pain. Subsequently, it has been hypothesized that this
In the diagnosis and treatment of patients with GPP/PD, exploring comorbid psychiatric conditions is as important as eliminating organic causes. One of these conditions is childhood psychogenic trauma. Especially if cases that are positive with history are examined in terms of somatoform dissociation, perhaps additional attempts in the treatment of treatment-resistant patients may increase treatment response rates. Along with our results, supporting the idea that at least one group of GPP/PD can be considered as a trauma-based disorder, it can be said that a wider sample study is needed on this subject.
Although much has been written about GPPPD and SPD as separate entities, there is a paucity of literature describing the potential co-existence of these two condi- tions. The study results could be used to assist in plan- ning healthcare services for women with GPPPD and to develop hypotheses for future research . Since a multidisciplinary and multidimensional approach is already recommended for treating GPPPD, describing the sensory processing patterns of women with GPPPD may have important implications for future treatment of GPPPD. Sensory processing intervention has not been evaluated as a possible option for managing GPPPD, despite evidence suggesting that SPD intervention assists with pain management . Current conventional, multi- disciplinary treatment methods for female sexual dys- function, e.g. sensate focus, may be rendered ineffective or actually worsen the condition in persons with SPD, thus necessitating identifying the sensory processing patterns of women with GPPPD prior to commencing treatment.
Figure 1 Discovery of a CLTCL1 mutation in individuals with lack of pain or touch sensing and severe intellectual disability. (A) Image of an affected child aged 5 years, noting corneal opacity secondary to lack of a corneal reflex. (B) Family pedigree with parents being double first cousins and the filled in symbols indicating their affected children (two female and one male). (C) The affected individuals were concordant and homozygous for consecutive variants in five autosomal regions. The candidate mutation was localized to one of these regions on chromosome 22. This contained the gene CLTCL1 for which a cartoon of the exon/intron structure is shown. In exon 7 we identified the c.988G4A mutation in CLTCL1, for which electrophoretograms of the Sanger sequencing results are shown for an affected child homozygous for the mutant A allele, an unaffected carrier parent heterozygous for the wild-type G and mutant A alleles, and a typical control wild-type G allele. The gene mutation resulted in the alteration of an invariant negatively charged glutamic acid 330 to a basic charged lysine in the encoded protein CHC22. The amino acid at position 330 in CHC22 is the first of an invariant pair of acidic amino acids present in all clathrin heavy chain proteins, which is evolutionarily conserved through vertebrates (with two clathrin heavy chains, CHC17 and CHC22, termed 1 and 2, respectively in this figure), insects and amoeba (with a single CHC17 like clathrin heavy chain). Protein sequence data are for human as a representative mammal (CHC22 is NP_009029.3; CHC17 is NP_004850.1), Xenopus tropicalis for amphibians (XP_002931934.2; NP_001011039.1), Danio rerio for fish
Complex regional pain syndrome (CRPS) is among the sequelae of actual or potential tissue injury after surgery or trauma; symptoms include severe pain, hyperalgesia, allody- nia, changes in skin color/temperature, and abnormal motor or trophic symptoms. 9 There are two subtypes of CRPS; type 1 develops in the absence of de ﬁ nable nerve injury, and type 2 is accompanied by a nerve lesion. The etio – pathological pro- cesses of CRPS are also poorly understood, and there have been contrasting results regarding the role of psychological factors. Previous studies have suggested that there is no asso- ciation between psychological factors and CRPS. 10 However, other recent research has suggested that central mechanisms are also involved in the pathophysiology of CRPS and have demonstrated associations between psychological factors and pain outcomes in patients with CRPS. 11,12 Regardless, these results are not conclusive and few studies have speci ﬁ cally investigated this topic. 13 – 15 Several studies that have examined psychological traits in patients with chronic pain using the Minnesota Multiphasic Personality Inventory (MMPI-2) 16,17 and reported that psychological factors modulate pain sensiti- zation by mediating physiological responses to psychological stressors. 18 The MMPI-2 assesses personality traits and psy- chopathologies from various perspectives 19 and previous research has demonstrated that the validity indicators of this tool are capable of detecting intentional exaggeration. 20 However, a recent review noted the dearth of research on CRPS, despite accumulating evidence of the usefulness of the MMPI for patients with other types of pain in relation to the different aspects of personality traits, patterns of psychopathology for differential diagnostic groupings, and malingering. 21 Indeed, patients with pain may exhibit exagger- ated or feigned pain behaviors when they are involved in medico-legal situations. 22
Anticonvulsant drugs are prescribed to treat a range of medical conditions in addition to seizure disorders, like epilepsy. Among those are bipolar disorder, fibromyalgia, and pain caused by nerve injuries (neuralgia) or other disorders.
Overall, study results showing how well anticonvulsants work in treating those three conditions are mixed, and varies by both specific drug and disorder. Other treatment options might work as well as or better than anti- convulsants. That said, some anticonvulsants have been linked to clear clinical benefits, and several have been approved by the Food and Drug Administration for treating bipolar disorder, nerve pain, or fibromyalgia. Anticonvulsants can cause serious side effects, including an increased risk of suicide and life-threatening skin rashes. They can also cause dangerous interactions with other medications. Newer anticonvulsants marketed since the late 1990s have sometimes been touted as safer and posing less risk of adverse effects than older ones. No large, good quality studies have tested this directly, but small, short-term studies that compared the drugs don't support such a conclusion.
The first aim of this paper is to translate and adapt the MPI to Spanish achieving the maximum degree of equivalency between the versions. This adaptation requires a study of the structural properties of the instrument. Thus, a second objective involves executing confirmatory factor analysis of the MPI to test if the original structure proposed by the authors reproduces the same in our temporomandibular sample patients. We expect that the original structure of the authors is confirmed on the basis of two fundamen- tals: a) to carefully obtain the highest equivalence possi- ble between the Spanish version and the original, b) the existence of adaptations to other languages in the Euro- pean context basically confirming the original structure of the instrument in other heterogeneous samples of patients with chronic pain. Finally, a third objective corre- sponds to the evaluation of the internal consistency of the MPI scales in this sample.
essentially on the description of the observed found ones, that appear in closed groups, rather than etiology mechanisms, allowing to set the standards for methods of gathering indispensable data and make possible comparison of the found ones among several investigators (Schiffman, 2014 and Santos, 2004). Then, already having the diagnosis of each case at hand, arouses a necessity of searching studies to elucidate the agents related to the TMD’s etiology in patients using prosthesis, warranting a new patient´s recovering aiming the goal of assuring them an adequate stomatognathic function (Santos, 2004). This present work purposed to stipulate the predominance of temporomandibular disorder in patients using full dental prosthesis attended at University of West of the Santa Catarina odontological clinics, observing the connection within: age, period using full prosthesis, temporomandibular disorder and the carriage of chronicle pain.