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Andrew D Piekarz - One of the best experts on this subject based on the ideXlab platform.
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD) are inherited Pain syndromes predominantly caused by missense mutations in the peripheral neuronal voltage-gated sodium channel (Nav) isoform Nav1.7. While both IEM and PEPD mutations increase neuronal excitability, IEM mutations primarily enhance activation and PEPD mutations impair inactivation. In addition, one PEPD mutation, Nav1.7-I1461T, has been shown to increase resurgent sodium currents in dorsal root ganglion (DRG) neurons. Because resurgent currents have been implicated in increased neuronal excitability, we asked whether (1) additional PEPD mutations located within the putative inactivation gate and docking sites and (2) IEM mutations might also increase these unusual currents. Resurgent currents are generated following open-channel block at positive potentials by an endogenous blocking particle and subsequent expulsion of this blocker upon repolarization to moderately negative potentials. Here we used a mimetic of the putative blocking particle, the Navβ4 peptide, to determine if enhanced resurgent currents are induced by three distinct PEPD mutations and two IEM mutations in stably transfected HEK293 cells. We demonstrate that (1) Nav1.7-mediated resurgent currents are observed in HEK293 cells with the Navβ4 peptide in the recording pipette, (2) while the PEPD mutants M1627K, T1464I and V1299F exhibit enhanced resurgent current amplitudes compared to wild-type, the IEM mutants I848T and L858H do not, and (3) there is a strong correlation between the decay time constant of open-channel fast inactivation and resurgent current amplitude. These data suggest that resurgent currents may play a role in the neuronal hyperexcitability associated with PEPD, but not IEM, mutations.
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Abnormal Pain sensitivity associated with inherited and acquired Pain Disorders occurs through increased excitability of peripheral sensory neurons in part due to changes in the properties of voltage-gated sodium channels (Navs). Resurgent sodium currents (I(NaR)) are atypical currents believed to be associated with increased excitability of neurons and may have implications in Pain. Mutations in Nav1.7 (peripheral Nav isoform) associated with two genetic Pain Disorders, inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD), enhance Nav1.7 function via distinct mechanisms. We show that changes in Nav1.7 function due to mutations associated with PEPD, but not IEM, are important in I(NaR) generation, suggesting that I(NaR) may play a role in Pain associated with PEPD. This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for Pain Disorders associated with I(NaR).
Brian W Jarecki - One of the best experts on this subject based on the ideXlab platform.
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Abnormal Pain sensitivity associated with inherited and acquired Pain Disorders occurs through increased excitability of peripheral sensory neurons in part due to changes in the properties of voltage-gated sodium channels (Navs). Resurgent sodium currents (I(NaR)) are atypical currents believed to be associated with increased excitability of neurons and may have implications in Pain. Mutations in Nav1.7 (peripheral Nav isoform) associated with two genetic Pain Disorders, inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD), enhance Nav1.7 function via distinct mechanisms. We show that changes in Nav1.7 function due to mutations associated with PEPD, but not IEM, are important in I(NaR) generation, suggesting that I(NaR) may play a role in Pain associated with PEPD. This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for Pain Disorders associated with I(NaR).
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD) are inherited Pain syndromes predominantly caused by missense mutations in the peripheral neuronal voltage-gated sodium channel (Nav) isoform Nav1.7. While both IEM and PEPD mutations increase neuronal excitability, IEM mutations primarily enhance activation and PEPD mutations impair inactivation. In addition, one PEPD mutation, Nav1.7-I1461T, has been shown to increase resurgent sodium currents in dorsal root ganglion (DRG) neurons. Because resurgent currents have been implicated in increased neuronal excitability, we asked whether (1) additional PEPD mutations located within the putative inactivation gate and docking sites and (2) IEM mutations might also increase these unusual currents. Resurgent currents are generated following open-channel block at positive potentials by an endogenous blocking particle and subsequent expulsion of this blocker upon repolarization to moderately negative potentials. Here we used a mimetic of the putative blocking particle, the Navβ4 peptide, to determine if enhanced resurgent currents are induced by three distinct PEPD mutations and two IEM mutations in stably transfected HEK293 cells. We demonstrate that (1) Nav1.7-mediated resurgent currents are observed in HEK293 cells with the Navβ4 peptide in the recording pipette, (2) while the PEPD mutants M1627K, T1464I and V1299F exhibit enhanced resurgent current amplitudes compared to wild-type, the IEM mutants I848T and L858H do not, and (3) there is a strong correlation between the decay time constant of open-channel fast inactivation and resurgent current amplitude. These data suggest that resurgent currents may play a role in the neuronal hyperexcitability associated with PEPD, but not IEM, mutations.
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paroxysmal extreme Pain Disorder m1627k mutation in human nav1 7 renders drg neurons hyperexcitable
Molecular Pain, 2008Co-Authors: Sulayman D Dibhajj, Brian W Jarecki, Mark Estacion, Lynda Tyrrell, Tanya Z Fischer, Mark Lawden, Theodore R Cummins, Stephen G WaxmanAbstract:Background Paroxysmal extreme Pain Disorder (PEPD) is an autosomal dominant Painful neuropathy with many, but not all, cases linked to gain-of-function mutations in SCN9A which encodes voltage-gated sodium channel Nav1.7. Severe Pain episodes and skin flushing start in infancy and are induced by perianal probing or bowl movement, and Pain progresses to ocular and mandibular areas with age. Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective.
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paroxysmal extreme Pain Disorder mutations within the d3 s4 s5 linker of nav1 7 cause moderate destabilization of fast inactivation
The Journal of Physiology, 2008Co-Authors: Brian W Jarecki, Patrick L Sheets, James O JacksonAbstract:Single-point missense mutations in the peripheral neuronal voltage-gated sodium channel Nav1.7 are implicated in the Painful inherited neuropathy paroxysmal extreme Pain Disorder (PEPD). The Nav1.7 PEPD mutations are located in regions of the channel suggested to play important roles in fast inactivation. PEPD mutations in the putative inactivation gate have been reported to significantly impair fast inactivation, resulting in pronounced persistent currents. However, PEPD mutations in the S4–S5 linker of domain 3 (D3/S4–S5) had not been characterized and the roles of specific residues in this linker in channel gating are unclear. We functionally characterized two of the D3/S4–S5 PEPD mutations (V1298F and V1299F) and compared their effects on gating to an adjacent non-PEPD mutation (V1300F) and the I1461T PEPD mutation, located in the putative inactivation gate. The primary effect of the V1298F and V1299F mutations is to shift the voltage dependence of fast inactivation by ∼20 mV in the depolarizing direction. We observed a similar effect with the PEPD mutation I1461T. Interestingly, while all three PEPD mutations increased persistent currents, the relative amplitudes (∼6% of peak) were much smaller than previously reported for the I1461T mutation. In contrast, the main effect of the V1300F mutation was a depolarizing shift in the voltage dependence of activation. These data demonstrate that (1) mutations within D3/S4–S5 affect inactivation of Nav1.7 in a residue-specific manner and (2) disruption of the fast-inactivated state by PEPD mutations can be more moderate than previously indicated, which has important implications for the pathophysiology of PEPD.
Jonathan W Theile - One of the best experts on this subject based on the ideXlab platform.
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD) are inherited Pain syndromes predominantly caused by missense mutations in the peripheral neuronal voltage-gated sodium channel (Nav) isoform Nav1.7. While both IEM and PEPD mutations increase neuronal excitability, IEM mutations primarily enhance activation and PEPD mutations impair inactivation. In addition, one PEPD mutation, Nav1.7-I1461T, has been shown to increase resurgent sodium currents in dorsal root ganglion (DRG) neurons. Because resurgent currents have been implicated in increased neuronal excitability, we asked whether (1) additional PEPD mutations located within the putative inactivation gate and docking sites and (2) IEM mutations might also increase these unusual currents. Resurgent currents are generated following open-channel block at positive potentials by an endogenous blocking particle and subsequent expulsion of this blocker upon repolarization to moderately negative potentials. Here we used a mimetic of the putative blocking particle, the Navβ4 peptide, to determine if enhanced resurgent currents are induced by three distinct PEPD mutations and two IEM mutations in stably transfected HEK293 cells. We demonstrate that (1) Nav1.7-mediated resurgent currents are observed in HEK293 cells with the Navβ4 peptide in the recording pipette, (2) while the PEPD mutants M1627K, T1464I and V1299F exhibit enhanced resurgent current amplitudes compared to wild-type, the IEM mutants I848T and L858H do not, and (3) there is a strong correlation between the decay time constant of open-channel fast inactivation and resurgent current amplitude. These data suggest that resurgent currents may play a role in the neuronal hyperexcitability associated with PEPD, but not IEM, mutations.
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nav1 7 mutations associated with paroxysmal extreme Pain Disorder but not erythromelalgia enhance navβ4 peptide mediated resurgent sodium currents
The Journal of Physiology, 2011Co-Authors: Jonathan W Theile, Brian W Jarecki, Andrew D PiekarzAbstract:Abnormal Pain sensitivity associated with inherited and acquired Pain Disorders occurs through increased excitability of peripheral sensory neurons in part due to changes in the properties of voltage-gated sodium channels (Navs). Resurgent sodium currents (I(NaR)) are atypical currents believed to be associated with increased excitability of neurons and may have implications in Pain. Mutations in Nav1.7 (peripheral Nav isoform) associated with two genetic Pain Disorders, inherited erythromelalgia (IEM) and paroxysmal extreme Pain Disorder (PEPD), enhance Nav1.7 function via distinct mechanisms. We show that changes in Nav1.7 function due to mutations associated with PEPD, but not IEM, are important in I(NaR) generation, suggesting that I(NaR) may play a role in Pain associated with PEPD. This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for Pain Disorders associated with I(NaR).
Stephen G Waxman - One of the best experts on this subject based on the ideXlab platform.
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nonlinear effects of hyperpolarizing shifts in activation of mutant nav1 7 channels on resting membrane potential
Journal of Neurophysiology, 2017Co-Authors: Mark Estacion, Stephen G WaxmanAbstract:Inherited erythromelalgia (IEM), the first human Pain Disorder linked to a sodium channel, is widely regarded as a genetic model of neuropathic Pain. IEM is produced by Nav1.7 mutations that hyperp...
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paroxysmal extreme Pain Disorder a molecular lesion of peripheral neurons
Nature Reviews Neurology, 2011Co-Authors: Jinsung Choi, Sulayman D Dibhajj, Rene Te H M Morsche, J P H Drenth, Franck Boralevi, Olivier Brissaud, Jesus Sanchezmartin, Stephen G WaxmanAbstract:BACKGROUND: a 3-month-old male infant presented, beginning on the second day of life, with paroxysmal Painful events that started with tonic contraction of the whole body followed by erythematous harlequin-type color changes. INVESTIGATIONS: screening of the SCN9A gene, which encodes the voltage-gated sodium channel Na(V)1.7, identified a new mutation, Gly1607Arg, located within the domain IV S4 voltage sensor. Whole-cell patch-clamp analysis demonstrated functional effects of the mutant channel that included impaired inactivation-a hallmark of paroxysmal extreme Pain Disorder (PEPD). DIAGNOSIS: the patient was diagnosed as having PEPD, an autosomal dominant Disorder characterized by severe rectal Pain triggered by defecation or perineal stimulation, usually followed by ocular or submaxillary Pain. Erythematous flushing, sometimes in a harlequin pattern, can be a prominent feature of this condition. MANAGEMENT: treatment with carbamazepine (10 mg/kg/day) for approximately 3 months was ineffective in this case, and the parents made a decision to discontinue the drug. The mother was instructed to avoid Painful stimuli that could trigger an episode.
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nav1 7 gain of function mutations as a continuum a1632e displays physiological changes associated with erythromelalgia and paroxysmal extreme Pain Disorder mutations and produces symptoms of both Disorders
The Journal of Neuroscience, 2008Co-Authors: Mark Estacion, Sulayman D Dibhajj, Paul J Benke, Rene Te H M Morsche, Emmanuella M Eastman, Lawrence J Macala, J P H Drenth, Stephen G WaxmanAbstract:Gain-of-function mutations of Na(V)1.7 have been shown to produce two distinct Disorders: Na(V)1.7 mutations that enhance activation produce inherited erythromelalgia (IEM), characterized by burning Pain in the extremities; Na(V)1.7 mutations that impair inactivation produce a different, nonoverlapping syndrome, paroxysmal extreme Pain Disorder (PEPD), characterized by rectal, periocular, and perimandibular Pain. Here we report a novel Na(V)1.7 mutation associated with a mixed clinical phenotype with characteristics of IEM and PEPD, with an alanine 1632 substitution by glutamate (A1632E) in domain IV S4-S5 linker. Patch-clamp analysis shows that A1632E produces changes in channel function seen in both IEM and PEPD mutations: A1632E hyperpolarizes (-7 mV) the voltage dependence of activation, slows deactivation, and enhances ramp responses, as observed in Na(V)1.7 mutations that produce IEM. A1632E depolarizes (+17mV) the voltage dependence of fast inactivation, slows fast inactivation, and prevents full inactivation, resulting in persistent inward currents similar to PEPD mutations. Using current clamp, we show that A1632E renders dorsal root ganglion (DRG) and trigeminal ganglion neurons hyperexcitable. These results demonstrate a Na(V)1.7 mutant with biophysical characteristics common to PEPD (impaired fast inactivation) and IEM (hyperpolarized activation, slow deactivation, and enhanced ramp currents) associated with a clinical phenotype with characteristics of both IEM and PEPD and show that this mutation renders DRG and trigeminal ganglion neurons hyperexcitable. These observations indicate that IEM and PEPD mutants are part of a physiological continuum that can produce a continuum of clinical phenotypes.
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paroxysmal extreme Pain Disorder m1627k mutation in human nav1 7 renders drg neurons hyperexcitable
Molecular Pain, 2008Co-Authors: Sulayman D Dibhajj, Brian W Jarecki, Mark Estacion, Lynda Tyrrell, Tanya Z Fischer, Mark Lawden, Theodore R Cummins, Stephen G WaxmanAbstract:Background Paroxysmal extreme Pain Disorder (PEPD) is an autosomal dominant Painful neuropathy with many, but not all, cases linked to gain-of-function mutations in SCN9A which encodes voltage-gated sodium channel Nav1.7. Severe Pain episodes and skin flushing start in infancy and are induced by perianal probing or bowl movement, and Pain progresses to ocular and mandibular areas with age. Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective.
Robert J Gatchel - One of the best experts on this subject based on the ideXlab platform.
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use of the central sensitization inventory csi as a treatment outcome measure for patients with chronic spinal Pain Disorder in a functional restoration program
The Spine Journal, 2017Co-Authors: Randy Neblett, Meredith M Hartzell, Tom G Mayer, Mark A Williams, Kelley Bevers, Robert J GatchelAbstract:Abstract Background Context The Central Sensitization Inventory (CSI) is a valid and reliable patient-reported instrument designed to identify patients whose presenting symptoms may be related to central sensitization (CS). Part A of the CSI measures a full array of 25 somatic and emotional symptoms associated with CS, and Part B asks if patients have previously been diagnosed with one or more specific central sensitivity syndromes (CSSs) and related Disorders. The CSI has previously been validated in a group of patients with chronic Pain who were screened by a trained psychiatrist for specific CSS diagnoses. It is currently unknown if the CSI can be a useful treatment-outcome assessment tool for patients with chronic spinal Pain Disorder (CSPD) who are not screened for comorbid CSSs. It is known, however, that previous studies have identified CS-related symptoms, and comorbid CSSs, in subsets of patients with CSPDs. Studies have also shown that CS-related symptoms can be influenced by cognitive and psychosocial factors, including abuse history in both childhood and adulthood, sleep disturbance, catastrophic and fear-avoidant cognitions, and symptoms of depression and anxiety. Purpose This study aimed to evaluate CSI scores, and their associations with other clinically relevant psychosocial variables, in a cohort of patients with CSPD who entered and completed a functional restoration program. Study Design/Setting A retrospective study of prospectively collected data from a cohort study of patients with CSPD, who completed the CSI at admission to, and discharge from, an interdisciplinary function restoration program (FRP) was carried out. Patient Sample A cohort of 763 patients with CSPD comprised the study sample. Outcome Measures Clinical interviews evaluated mood Disorders and abuse history. A series of self-reported measures evaluated comorbid psychosocial symptoms, including Pain intensity, Pain-related anxiety, depressive symptoms, somatization symptoms, perceived disability, and sleep disturbance, at FRP admission and discharge. Methods Patients were grouped into five severity level groups, from mild to extreme, based on total CSI scores, at FRP admission, and then again at discharge. The FRP included a quantitatively directed and medically supervised exercise process, as well as a multimodal psychosocial disability management component. Results The CSI severity groups were strongly associated with Major Depressive Disorder and previous abuse history (p Conclusions In the present study, admission CSI scores were highly associated with previous CSS diagnoses, CS-related symptoms, and clinically relevant patient-reported psychosocial variables. All psychosocial variables, as well as scores on the CSI, were significantly improved at FRP discharge. The CSI may have important clinical utility, as a screener and as a treatment outcome measure, for patients with CSPD participating in an interdisciplinary FRP.
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use of the central sensitization inventory csi as a treatment outcome measure for chronic spinal Pain Disorder patients in a functional restoration program
The Spine Journal, 2017Co-Authors: Randy Neblett, Meredith M Hartzell, Tom G Mayer, Mark A Williams, Kelley Bevers, Robert J GatchelAbstract:Background Context The Central Sensitization Inventory (CSI) is a valid and reliable patient-reported instrument designed to identify patients whose presenting symptoms may be related to Central Sensitization (CS). Part A of the CSI measures a full array of 25 somatic and emotional symptoms associated with CS, and Part B asks if patients have previously been diagnosed with one or more specific Central Sensitivity Syndromes (CSSs) and related Disorders. The CSI has previously been validated in a group of chronic Pain patients who were screened by a trained psychiatrist for specific CSS diagnoses. It is currently unknown if the CSI can be a useful treatment-outcome assessment tool for chronic spinal Pain Disorder (CSPD) patients who are not screened for comorbid CSSs. It is known, however, that previous studies have identified CS-related symptoms, and comorbid CSSs, in subsets of patients with CSPDs. Studies have also shown that CS-related symptoms can be influenced by cognitive and psychosocial factors, including abuse history in both childhood and adulthood, sleep disturbance, catastrophic and fear-avoidant cognitions, and symptoms of depression and anxiety. Purpose To evaluate CSI scores, and their associations with other clinically-relevant psychosocial variables, in a cohort of CSPD patients who entered and completed a functional restoration program. Study Design/Setting A retrospective study of prospectively-collected data from a cohort study of CSPD patients who completed the CSI at admission to, and discharge from, an interdisciplinary function restoration program (FRP). Patient Sample A cohort of 763 CSPD patients Outcome Measures Clinical interviews evaluated mood Disorders and abuse history. A series of self-reported measures evaluated comorbid psychosocial symptoms, including Pain intensity, Pain-related anxiety, depressive symptoms, somatization symptoms, perceived disability, and sleep disturbance, at FRP admission and discharge. Methods Patients were grouped into five severity level groups, from Mild-to-Extreme, based on total CSI scores, at FRP admission, and then again at discharge. The FRP included a quantitatively-directed and medically-supervised exercise process, as well as a multimodal psychosocial disability management component. Results The CSI severity groups were strongly associated with Major Depressive Disorder and previous abuse history (p < .01), which are known risk factors for CS-related symptoms and diagnoses. CSI scores were also strongly associated with patient-reported CSS diagnoses on CSI Part B. The percentage of patients who reported a comorbid CSS diagnosis increased in each higher CSI-severity group, from 11% in the Subclinical group, to 56% in the Extreme group. The CSI severity groups were significantly related to other CS-related patient-reported symptoms, including Pain intensity, Pain-related anxiety, depressive symptoms, somatization symptoms, perceived disability, and sleep disturbance (ps < .001). CSI scores, along with all other psychosocial measures, decreased at treatment discharge. Conclusions In the present study, admission CSI scores were highly associated with previous CSS diagnoses, CS-related symptoms, and clinically relevant patient-reported psychosocial variables. All psychosocial variables, as well as scores on the CSI, were significantly improved at FRP discharge. The CSI may be have important clinical utility, as a screener and as a treatment outcome measure, for CSPD patients participating in an interdisciplinary FRP.
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the fear avoidance components scale facs responsiveness to functional restoration treatment in a chronic musculoskeletal Pain Disorder cmpd population
The Clinical Journal of Pain, 2017Co-Authors: Randy Neblett, Meredith M Hartzell, Tom G Mayer, Mark J Williams, Sali Rahadi Asih, Antonio Cuestavargas, Robert J GatchelAbstract:OBJECTIVES To assess the clinical validity and factor structure of the Fear-Avoidance Components Scale (FACS), a new fear-avoidance measure. MATERIALS AND METHODS In this study, 426 chronic musculoskeletal Pain Disorder patients were admitted to a Functional Restoration Program (FRP). They were categorized into 5 FACS severity levels, from subclinical to extreme, at admission, and again at discharge. Associations with objective lifting performance and other patient-reported psychosocial measures were determined at admission and discharge, and objective work outcomes for this predominantly disabled cohort, were assessed 1 year later. RESULTS Those patients in the severe and extreme FACS severity groups at admission were more likely to "drop out" of treatment than those in the lower severity groups (P=0.05). At both admission and discharge, the FACS severity groups were highly and inversely correlated with objective lifting performance and patient-reported fear-avoidance-related psychosocial variables, including kinesiophobia, Pain intensity, depressive symptoms, perceived disability, perceived injustice, and insomnia (Ps<0.001). All variables showed improvement at FRP discharge. Patients in the extreme FACS severity group at discharge were less likely to return to, or retain, work 1 year later (P≤0.02). A factor analysis identified a 2-factor solution. DISCUSSION Strong associations were found among FACS scores and other patient-reported psychosocial and objective lifting performance variables at both admission and discharge. High discharge-FACS scores were associated with worse work outcomes 1 year after discharge. The FACS seems to be a valid and clinically useful measure for predicting attendance, physical performance, distress, and relevant work outcomes in FRP treatment of chronic musculoskeletal Pain Disorder patients.
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somatization as a predictor of outcomes following functional restoration of chronic disabling occupational musculoskeletal Pain Disorder patients
Journal of Applied Biobehavioral Research, 2013Co-Authors: Meredith M Hartzell, Yunhee Choi, Randy Neblett, Mark V Williams, Tom G Mayer, Robert J GatchelAbstract:Chronic disabling occupational musculoskeletal Pain Disorder (CDOMPD) patients often have high levels of somatization, a phenomenon in which somatic symptoms are medically unexplainable. Examination of 1,458 CDOMPD patients, who completed the patient health questionnaire (PHQ) somatization module from 2003 to 2010 and underwent functional restoration treatment, were divided into low, moderate, and high somatization at pretreatment. Somatization was highly responsive to treatment, and those with high somatization reported the highest depressive symptoms, disability, and Pain intensity, and the lowest health-related quality of life at pre- and post-treatment. Somatization levels significantly predicted 1-year socioeconomic outcomes of work return, work retention, and healthcare utilization. High somatization may act as a “red flag” for clinicians, indicating patients may be at risk for poor treatment outcomes.
