The journal of pain : official journal of the American Pain Society
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The firing rate of low threshold motor units is decreased in constant force contractions during experimental pain. However, as firing rate is a determinant of force, it is unclear how force is maintained. Increased synergist muscle activity may compensate. This was investigated by evaluation of motor unit firing rate in synergist ankle plantar flexor muscles (triceps surae). Single motor unit action potentials were recorded in medial gastrocnemius and soleus muscles with fine wire electrodes in 10 subjects. Gross muscle activity was estimated from surface electromyographic (EMG) recordings. Bolus injections of 5% hypertonic saline were injected into lateral gastrocnemius to induce pain (low intensity, 0.5 mL; high intensity, 1.5 mL). Subjects gently plantar-flexed the ankle to recruit 1 to 4 motor units and performed 3 20-second contractions to this target before, during, and after pain. Firing rate decreased approximately 12% in synergist heads of triceps surae during pain and recovered after pain. Despite reduced firing rate, root-mean-square surface EMG amplitude did not change. The effect of nociceptor stimulation is not restricted to painful muscles but reduces motor unit firing in synergist muscles. Changes in synergist muscles cannot explain the maintenance of muscle force. Maintenance of surface EMG amplitude suggests recruitment of additional motor units. ⋯ This study showed that activity of synergist muscles can be affected by muscle pain. However, the changes in activity of synergist muscles may not compensate for changes in the painful muscle. This finding provides evidence of more widespread effects of pain on muscle control.
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We sought to examine whether the presence of a noncancer pain condition is independently associated with an increased risk for suicidal ideation, plan, or attempt after adjusting for sociodemographic and psychiatric risk factors for suicide and whether risk differs by specific type of pain. We analyzed data from the National Comorbidity Survey Replication, a household survey of U.S. civilian adults age 18 years and older (n = 5692 respondents). Pain conditions, nonpain medical conditions, and suicidal history were obtained by self-report. DSM-IV mood, anxiety, and substance use disorders were assessed using the World Health Organization's Composite International Diagnostic Interview. Antisocial and borderline personality traits were assessed with the International Personality Disorder Examination screening questionnaire. In unadjusted logistic regression analyses, the presence of any pain condition was associated with lifetime and 12-month suicidal ideation, plan, and attempt. After controlling for demographic, medical, and mental health covariates, the presence of any pain condition remained significantly associated with lifetime suicidal ideation (odds ratio, 1.4; 95% confidence interval, 1.1-1.8) and plan. Among pain subtypes, severe or frequent headaches and "other" chronic pain remained significantly associated with lifetime suicidal ideation and plan; "other" chronic pain was also associated with attempt. ⋯ The risk for suicidal thoughts and behaviors that may accompany back, neck, and joint pain can be accounted for by comorbid mental health disorders. There may be additional risk accompanying frequent headaches and "other" chronic pain that is secondary to psychosocial processes not captured by the mental disorders assessed.
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Clinical Trial
A study of clinical, magnetic resonance imaging, and somatosensory-evoked potential in central post-stroke pain.
This study evaluates the clinical spectrum of central post-stroke pain (CPSP) and correlates it with magnetic resonance imaging (MRI) and somatosensory-evoked potential (SEP) changes. Thirty-one consecutive CPSP patients whose median age was 51 years were evaluated and subjected to quantitative sensory testing and median and tibial SEPs. Cranial MRI abnormalities were noted and correlated with clinical and SEP abnormalities. The majority of patients (n = 21) developed CPSP within 3 months of stroke, and CPSP was the presenting symptom in 7 patients. Five patients had focal symptoms and 26 had hemibody symptoms with or without facial involvement. Pain threshold was reduced in 12, and 3 did not have pain perception. Allodynia was present in 11, static in 4, dynamic in 5, and cold in 7 patients. Temporal summation was present in 14, punctate hyperalgesia in 11, and cold hyperalgesia in 3 patients. Cranial MRI revealed infarction in 23 and intracerebral hemorrhage in 8 patients; 16 had thalamic and 15 extrathalamic lesions. SEP was abnormal in 15 of 22 (68.2%) patients. There was no difference in symptoms and severity of CPSP, quantitative sensory testing, and SEP abnormalities in thalamic and extrathalamic stroke. ⋯ CPSP is a poorly recognized entity that can interfere with rehabilitation, reduce the quality of life, and interfere with the activities of daily living and recreational activities. This report concludes that the symptoms and severity of CPSP in thalamic and extrathalamic stroke do not differ significantly.
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Neuropeptides released from axons of primary afferent nociceptive neurons are the key elements for the incidence of neurogenic inflammation and their release is associated with dorsal root reflexes (DRRs). However, whether the release is due to the triggering of DRRs and plays a role in inflammation-induced pain still remain to be determined. The present study assessed the role of calcitonin gene-related peptide (CGRP) in sensitization of primary afferent nociceptors induced by activation of transient receptor potential vanilloid-1 (TRPV(1)) after intradermal injection of capsaicin and determined if this release is due to activation of primary afferent neurons antidromically by triggering of DRRs. Under dorsal root intact conditions, primary afferent nociceptive fibers recorded in anesthetized rats could be sensitized by capsaicin injection, as shown by an increase in afferent responses and lowering of the response threshold to mechanical stimuli. After DRRs were removed by dorsal rhizotomy, the capsaicin-evoked sensitization was significantly reduced. In dorsal root intact rats, peripheral pretreatment with a CGRP receptor antagonist could dose-dependently reduce the capsaicin-induced sensitization. Peripheral post-treatment with CGRP could dose-dependently restore the capsaicin-induced sensitization under dorsal rhizotomized conditions. Capsaicin injection evoked increases in numbers of single and double labeled TRPV(1) and CGRP neurons in ipsilateral dorsal root ganglia (DRG). After dorsal rhizotomy, these evoked expressions were significantly inhibited. ⋯ These data indicate that the DRR-mediated neurogenic inflammation enhances sensitization of primary afferent nociceptors induced by capsaicin injection. The underlying mechanism involves antidromic activation of DRG neurons via upregulation of TRPV(1) receptors whereby CGRP is released peripherally.
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In recent years, the National Institutes of Health (NIH) has experienced unprecedented reductions in its customary annual budget increases. Consequently, researchers, health care policy planners and others have a pressing need for accurate information on NIH funding patterns. We created a unique and objective system for compiling, classifying, and analyzing data on NIH grant awards and funding for research on pain, nausea, and dyspnea using naïve observers, cross-validation by multiple raters, and face validation by experts. We present results of our method and analyses for the period from 2003 to 2007. Following a 12% increase from 2003 to 2004, funding for pain research fell by 9.4% per year on average over the next 3 years. The percent of the total NIH budget going to support pain research increased to 0.78% in 2004 but fell to 0.61% in 2007. A piecewise regression model confirmed the declining trend represented a significant fit to the data (R(2)=0.98, p=0.024). Separate breakdowns by Institutes showed similar patterns. Analyses of nausea and dyspnea research support revealed small but steady increases over the same period. Declining support for pain research disproportionate to decreases in the NIH budget signals a need for measures to promote funding for meritorious applications. ⋯ Results of 5 year trends in numbers of grants and funding for research in pain, nausea, and dyspnea by the NIH show overall declines for pain but slight increases for nausea and dyspnea. Declining support for pain research that exceeds the reductions in the total NIH budget signals a need for measures to increase pain research funding.