Quantitative Pain Assessment Research Articles

Quantitative assessment of neuropathic pain

Quantitative assessment of neuropathic pain

Reliability and validity of a visual analog scale for acute abdominal pain in the ED

The objective of the study was to assess the validity and reliability of the visual analog scale (VAS) in the measurement of acute abdominal pain, and to identify the minimum clinically significant difference in VAS scores among patients with acute abdominal pain. The study was undertaken in preparation for a randomized clinical trial of opioid use in acute abdominal pain. A prospective, observational cohort study of a convenience sample of patients presenting to 2 urban EDs with the chief complaint of acute abdominal pain was conducted. At time 0 and 1 minute later each subject indicated pain severity on a 100mm VAS. This was repeated every 30 minutes for 2 hours. Patients were also asked to contrast their current pain severity with their pain in the preceding 30 minutes using one of 5 graded verbal descriptors: “much less pain,” “little less pain,” “the same pain,” “little more pain,” and “much more pain.” Validity was assessed by performing an analysis of variance for linear trend on the association between the 5 categorical pain descriptors and change in VAS scores. Reliability was assessed using the intra-class correlation coefficient (ICC) between VAS scores taken 1 minute apart, supplemented by a Bland-Altman analysis. The minimum clinically significant difference in pain was defined as the mean difference between sequential VAS scores obtained 30 minutes apart when the patient noted a “little less” or “little more” pain. Differences in VAS scores increased linearly as pain descriptors escalated from “much less” to “much more” pain (P <.001). Reliability was high, ICC = 0.99 [95%CI 0.989 to 0.992] for 0 and 1 minute VAS scores. The minimum clinically significant difference in acute abdominal pain was 16 mm (95% CI 13, 18 mm). VAS measures of acute abdominal pain are valid and reliable. The 95% CI surrounding the minimum clinically significant difference of approximately 16mm overlaps with the 95% CI of minimum clinically significant difference of approximately 13mm reported previously in traumatic and other types of acute pain. We conclude that the VAS is a methodologically sound instrument for quantitative assessment of acute abdominal pain and for detecting clinically important changes in such pain. (Am J Emerg Med 2002;20:287-290. Copyright 2002, Elsevier Science (USA). All rights reserved.)

Quantitative pain assessment in outpatient oncology practice

Quantitative pain assessment in outpatient oncology practice

Quantitative assessment of neuropathic pain.

Quantitative sensory testing (QST) refers to a group of protocols that allows for quantitative measures of somesthetic function. Several protocols evaluate perceptual threshold, whereas others evaluate perception of stimuli above threshold. Each protocol has its own advantages and disadvantages, but one must always weigh a trade-off between accuracy (with longer protocols) and expediency (with shorter protocols). In assessing patients with neuropathic pain, one is interested in both positive and negative sensory symptoms. QST studies, using either neuropathic pain patients or healthy volunteers who have been rendered temporarily hyperalgesic, have demonstrated that pain abnormalities can be modality specific. The fact that various pain abnormalities can exist independently of each other suggests that (at least partially) different neuropathologic processes are responsible for each one. Current research suggests that both peripheral sensitization and central sensitization play a role in these abnormal pain conditions, and identification of precise neuropathologic mechanisms is under active investigation.

Feasibility of quantitative pain assessment in outpatient oncology practice.

Although physicians view failure to assess pain systematically as the most important barrier to outpatient cancer pain management, little is known about pain assessment in this setting. We sought to determine whether pain is routinely assessed and whether routine quantitative pain assessment is feasible in a busy outpatient oncology practice. We conducted a pre- and postintervention chart review of 520 randomly selected medical and radiation oncology patient visits at a community hospital-based private outpatient practice. The intervention consisted of training health assistants (HAs) to measure and document patient pain scores by using a visual analog scale. The main outcome measures included HA documentation of patient pain scores, quantitative and qualitative mention of pain in the physician note, and analgesic treatment before and after the intervention. After the intervention, HA documentation of pain scores increased from 1% to 75.6% (P < .0001). Physician documentation increased from 0% to 4.8% for quantitative documentation (P < .01), and from 60.0% to 68.3% for qualitative documentation (not significant). Of all the patients, 23.1% reported significant pain. Subgroups with greater pain included patients actively receiving radiation treatments and patients with lung cancer. Of patients with significant pain, 28.2% had no mention of pain in the physician note and 47.9% had no documented analgesic treatment. Quantitative pain assessment was virtually absent before our intervention but easily implemented and sustained in a busy outpatient oncology practice. Pain score collection identified a high prevalence of pain, patient subgroups at risk for pain, and a significant proportion of patients with pain that was neither evaluated nor treated by their oncologists.

Chronic pain as an outcome of surgery. A review of predictive factors.

ONE potential adverse outcome from surgery is chronic pain. Analysis of predictive and pathologic factors is important to develop rational strategies to prevent this problem. Additionally, the natural history of patients with and without persistent pain after surgery provides an opportunity to improve the understanding of the physiology and psychology of chronic pain. Ideally, studies of chronic postoperative pain should include (1) sufficient preoperative data (assessment of pain, physiologic and psychologic risk factors for chronic pain); (2) detailed descriptions of the operative approaches used (location and length of incisions, handling of nerves and muscles); (3) the intensity and character of acute postoperative pain and its management; and (4) follow-up at intervals to 1 yr or more. In addition, there would be information about postoperative interventions that may influence pain, such as radiation therapy or chemotherapy. At long-term follow-up visits, patient function, physical signs, and symptoms would be evaluated using a standardized algorithm, including quantitative and descriptive pain assessments. We found no studies that contain all of these data. For this review, we specifically sought population data that reflect the incidence of chronic postoperative pain or predictors (medical, physiologic, and psychologic) of chronic pain. We selected five groups of surgeries (limb amputations, breast surgery, gallbladder surgery, lung surgery, and inguinal hernia surgery). These surgeries were selected because the incidence of pain is known to be high, thus improving the probability of detecting predictive factors. They also represent a range of major surgical procedures.

The effect of peripheral glycerol on trigeminal neuropathic pain examined by quantitative assessment of abnormal pain and sensory perception.

In nine patients with trigeminal neuropathic pain after nerve injury, we examined prospectively the effect of peripheral glycerol neurolysis on abnormal pain and sensory perception. In the painful facial skin area of these patients, we found increased temperature and tactile thresholds and the presence of abnormal temporal summation of pain. In seven patients, neuropathic pain was peripheral and disappeared after application of local anaesthesia at or proximal to the site of nerve injury. Neuropathic pain was central in two patients, and unresponsive to local anaesthesia applied proximal to the site of nerve injury. Six weeks after injection of glycerol proximal to the site of nerve injury, no or marginal pain relief was found in 8 patients with peripheral or central trigeminal neuropathic pain. On the other hand, in one of the patients with peripheral trigeminal neuropathic pain, glycerol was given at the site of nerve injury, and produced total pain relief for the whole observation period of 7 months. In this patient, pain relief was associated with normalisation of abnormal temporal summation of pain, which was not observed in the 8 patients with no or marginal pain relief. No further changes in temperature or tactile thresholds were found in any of the 9 patients after a single injection of absolute glycerol. Total pain relief in one of the patients probably is related to the ability of glycerol to inhibit ongoing ectopic impulse generation at the site of nerve injury. We suggest that glycerol-induced reduction of primary afferent hyperactivity may secondarily result in down-regulation of central neuronal hyperexcitability. The efficacy of application of glycerol at the site of nerve injury in patients with peripheral trigeminal neuropathic pain may warrant further investigation. However, this prospective study does not provide evidence that application of glycerol proximal to the site of nerve injury has a place in the treatment of trigeminal neuropathic pain.

Trigeminal neuropathic pain: pathophysiological mechanisms examined by quantitative assessment of abnormal pain and sensory perception.

This study was undertaken to examine the pathophysiological characteristics of trigeminal neuropathic pain. The study included 23 consecutive patients with trigeminal neuropathic pain (15 patients with pain after nerve injury and 8 patients with pain of spontaneous origin). For each patient, quantitative examination of sensory and pain perception was performed in the painful facial skin area, and results were compared with the findings for the contralateral nonpainful facial skin area. In the painful facial skin area of patients with neuropathic pain after nerve injury, we demonstrated increased temperature and tactile thresholds, as well as abnormal temporal summation of pain (i.e., repetitive nonpainful skin stimulation produced an abnormal progressive increase of pain intensity, with abnormal radiation of pain and aftersensation). In the painful skin area of patients with pain of spontaneous origin, temperature and tactile thresholds were not increased, but heat pain and cold pain thresholds were significantly reduced, indicating heat and cold hyperalgesia. The characteristics of temporal summation of pain were not significantly altered in the painful facial skin area in this group of patients. This clinical study provides evidence that the pathophysiological mechanisms of trigeminal neuropathic pain after nerve injury involve impaired function of both small unmyelinated fibers and large myelinated fibers. An explanation for the finding of abnormal temporal summation of pain may involve hyperexcitability of central wide-dynamic range neurons. The results suggest that other mechanisms are involved in trigeminal neuropathic pain of spontaneous origin. Reduced heat and cold pain thresholds indicate heat and cold hyperalgesia, which possibly may be explained by sensitization of peripheral C nociceptors.

A QUANTITATIVE TOOL TO ASSESS CHANGES IN ABDOMINAL PAIN IN CHILDREN

Background: Abdominal Pain in children is very common but very difficult to assess objectively. We are developing a scoring system for objectively measuring abdominal pain before and after treatment. Methods: To begin to assess the validity of our approach we studied twenty-two children treated with H2 antagonists for acid-peptic disease. An abdominal pain score (APS) was calculated from three component indices: pain frequency (PF), pain severity (PS), and peptic index (PI). Scoring for PF was: 2 =multiple daily episodes of pain; 1.5=one episodes of pain per day; 1=3-4 episodes per week; and 0.5 = 2-3 episodes per month. PS was scored 0 to 10 according to a previously validated affective facial scale **. PI was scored by assigning 1 point to each of the following symptoms: nausea, vomiting, loss of appetite or weight loss, chest pain, epigastric pain, relationship to meals, waking at night with pain and pain on awakening in the morning. Results: Of the 22 children treated for 23 ± 6 days, 11 reported improvement (Responders) and 11 reported no improvement (Nonresponders). Table Conclusion: Initial quantitative assessment of pain (APS) could not predict outcome. However, there was a clear quantitative distinction between those reporting improvement from those reporting no change. This distinction was evident in all three components of the APS. We conclude the demonstrated ability of the APS to quantitate improvement in patients responding to H2 antagonists may be useful in quantitating abdominal pain in groups of children with vague recurrent abdominal pain.

Chapter 2 Quantitative experimental assessment of pain and hyperalgesia in animals and underlying neural mechanisms

The primary aim of this chapter is to critically examine the use of acute noxious stimuli to assess pain in normal animals and in animal models of persistent pain. The new strategies are suggested to examine nomifensine behavior evoked by controlled stimuli over a wide range of stimulus intensities in assessing underlying neural mechanisms and treatments. As pain is normally a conscious perception, a more realistic animal model might incorporate a cognitive-evaluative component associated with nocifensive behavior. For this reason, this chapter develops the operant response model that requires the rat to perceive and respond to a noxious stimulus with a bar-press. It is interesting that rats respond over a higher range of stimulus intensities in this paradigm compared to the measure of tail flick reflex force. One might speculate that the operant response is a measure of the motivation of the animal working to avoid the noxious stimuli or of the probability that the animal will or will not tolerate it. On the other hand, in human studies using identical noxious radiant heat stimuli, the threshold for reflexive limb withdrawal was higher compared to that for pain sensation. However, the fact that subjects knew the stimuli would not cause tissue damage may have influenced their withdrawal threshold. These observations further underscore the need for caution in extrapolating from measures.

Efficacy of Laparoscopic Pelvic Denervation in Central-Type Chronic Pelvic Pain: A Multicenter Study

ABSTRACT Our aim was to evaluate the efficacy of laparoscopic pelvic denervation (uterosacral resection or presacral neurectomy) for the treatment of chronic pelvic pain with a predominant central-type localization in women with endometriosis or with no visible pathology. In a retrospective analysis performed in six centers, we evaluated the data relative to 58 patients with midline pelvic pain laparoscopically treated, with a follow-up of at least 6 months including a quantitative pain assessment. The distribution of types of pain (dysmenorrhea, deep dyspareunia, and pelvic pain not related to menses or coitus) was not different among stage I–II endometriosis, stage III–IV endometriosis, and no visible pathology, except that deep dyspareunia was significantly (p < 0.05) less frequent in the absence of visible pathology than in moderate to severe endometriosis. Both types of laparoscopic denervations significantly (p < 0.001) reduced after 6 months the intensity of midline dysmenorrhea, pelvic pain, and d...

Pain response to perineuromal injection of normal saline, epinephrine, and lidocaine in humans

In animal neuroma models the application of alpha-adrenergic agonists causes a burst of spontaneous afferent activity. The increased activity has been hypothesized to generate nociceptive input. Corroborative work in humans, however, has not been done. Nine subjects with chronic nerve end neuromas received prineuromal injections of normal saline, epinephrine (5 μg), and lidocaine in a blinded manner. Qualitative and quantitative pain assessments were performed with each injection. Epinephrine, but not saline, caused an intense increase in reported pain with subjects often commenting that the appendage was “on fire”. Lidocaine significantly reduced but did not completely abolish the reported pain. The chemosensitivity of the neuroma to epinephrine may explain some of the clinical responses noted after sympathetic system manipulation. It is likely that alpha-adrenergic sensitivity is only one of many components sustaining or exacerbating pain after nerve injury.

Prevalence of the Shoulder-Hand Pain Syndrome in an Inpatient Stroke Rehabilitation Population: A Quantitative Cross-Sectional Study

Of 41 patients with hemiparesis and associated functional deficits requiring inpatient rehabilitation a mean of 8 weeks post unilateral hemispheric stroke, 17 (41%) had evidence of pain, edema, and vasomotor changes in the affected upper extremity. These 17 patients met criteria for stage I of the shoulder-hand syndrome (SHS). The prevalence of SHS in patients with hemiplegia without proprioceptive deficit or visual neglect was 7%, whereas it was present in 61% of patients with hemiplegia plus impaired proprioception and visual neglect. The prevalence of SHS in our population is considerably higher than that reported from previous retrospective studies. Such studies have not used quantitative assessment of pain, edema, and vasomotor dysfunction to establish the diagnosis. We conclude that SHS is a common rehabilitation problem during the subacute phase post stroke. It occurs despite currently available techniques for supporting and exercising the affected limb. From our data it is apparent that weakness is a necessary but not sufficient cause of SHS post stroke. Impaired hemispatial awareness or cognitive impairment must also be present affecting the patient's ability to position, protect, and exercise the affected limb. Reproducible measures of pain, edema and vasomotor dysfunction exist and should be used to develop more effective techniques for SHS prophylaxis and treatment.