Effects of Spinal Cord Stimulation on Pain Thresholds and Sensory Perceptions in Chronic Pain Patients
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Sensation
Quantitative sensory testing
Sensory threshold
Pain sensation
Pain tolerance
Referred pain
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Abstract The pathophysiology of pain in neuropathy is complex and may be linked to sensory phenotypes. Quantitative sensory testing, a standardized method to evaluate sensory profiles in response to defined stimuli, assesses functional integrity of small and large nerve fiber afferents and central somatosensory pathways. It has revealed detailed insights into mechanisms of neuropathy, yet it remains unclear if pain directly affects sensory profiles. The main objective of this study was to investigate sensory profiles in patients with various neuropathic conditions, including polyneuropathy, mononeuropathy, and lesions to the central nervous system, in relation to self-reported presence or absence of pain and pain sensitivity using the Pain Sensitivity Questionnaire. A total of 443 patients (332 painful and 111 painless) and 112 healthy participants were investigated. Overall, loss of sensation was equally prevalent in patients with and without spontaneous pain. Pain thresholds were equally lowered in both patient groups, demonstrating that hyperalgesia and allodynia are just as present in patients not reporting any pain. Remarkably, this was similar for dynamic mechanical allodynia. Hypoalgesia was more pronounced in painful polyneuropathy, whereas hyperalgesia was more frequent in painful mononeuropathy (compared with painless conditions). Self-reported pain sensitivity was significantly higher in painful than in painless neuropathic conditions. Our results reveal the presence of hyperalgesia and allodynia in patients with central and peripheral lesions of the somatosensory system not reporting spontaneous pain. This shows that symptoms and signs of hypersensitivity may not necessarily coincide and that painful and painless neuropathic conditions may mechanistically blend into one another.
Allodynia
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Abstract The painDETECT Questionnaire (PDQ) is commonly used as a screening tool to discriminate between neuropathic pain (NP) and nociceptive pain, based on the self-report of symptoms, including pain qualities, numbness, and pain to touch, cold, or heat. However, there are minimal data about whether the PDQ is differentially sensitive to different sensory phenotypes in NP. The aim of the study was to analyze whether the overall PDQ score or its items reflect phenotypes of sensory loss in NP as determined by quantitative sensory testing. An exploratory analysis in the Innovative Medicines Initiative Europain and Neuropain database was performed. Data records of 336 patients identified with NP were grouped into sensory profiles characterized by (1) no loss of sensation, (2) loss of thermal sensation, (3) loss of mechanical sensation, and (4) loss of thermal and mechanical sensation. painDETECT Questionnaire profiles were analyzed in a 2-factor analysis of variance. Patients with loss of thermal sensation (2 and 4) significantly more often reported pain evoked by light touch , and patients with loss of mechanical sensation (3 and 4) significantly more often reported numbness and significantly less often burning sensations and pain evoked by light touch . Although the PDQ was not designed to assess sensory loss, single items reflect thermal and/or mechanical sensory loss at group level, but because of substantial variability, the PDQ does not allow for individual allocation of patients into sensory profiles. It will be useful to develop screening tools according to the current definition of NP.
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In patients who experience unilateral chronic pain, abnormal sensory perception at the non-painful side has been reported. Contralateral sensory changes in these patients have been given little attention, possibly because they are regarded as clinically irrelevant. Still, bilateral sensory changes in these patients could become clinically relevant if they challenge the correct identification of their sensory dysfunction in terms of hyperalgesia and allodynia. Therefore, we have used the standardized quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain (DFNS) to investigate somatosensory function at the painful side and the corresponding non-painful side in unilateral neuropathic pain patients using gender- and age-matched healthy volunteers as a reference cohort. Sensory abnormalities were observed across all QST parameters at the painful side, but also, to a lesser extent, at the contralateral, non-painful side. Similar relative distributions regarding sensory loss/gain for non-nociceptive and nociceptive stimuli were found for both sides. Once a sensory abnormality for a QST parameter at the affected side was observed, the prevalence of an abnormality for the same parameter at the non-affected side was as high as 57% (for Pressure Pain Threshold). Our results show that bilateral sensory dysfunction in patients with unilateral neuropathic pain is more rule than exception. Therefore, this phenomenon should be taken into account for appropriate diagnostic evaluation in clinical practice. This is particularly true for mechanical stimuli where the 95% Confidence Interval for the prevalence of sensory abnormalities at the non-painful side ranges between 33% and 50%.
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It is still unclear whether the quality of painful thermal sensation is determined only by conduction in specific, dedicated nociceptive channels (i.e. C or Adelta nociceptors) or whether it is a result of integrated activity in both nociceptive and non-nociceptive systems. To evaluate this question, we conducted quantitative and qualitative somatosensory testing in spinal cord injury subjects who suffered from partial or complete loss of thermal sensibility. Testing was performed in skin areas, below the level of the lesion, which were either lacking any thermal sensibility, lacking only one thermal sensation (either heat or cold) or having normal thermal sensations. We found that, in areas lacking any thermal sensibility, warm and cold stimuli produced a sensation of pricking pain, which had no thermal quality and was detected at significantly higher thresholds than in normal controls (48.5 +/- 1.8 and 9.7 +/- 5.1 degrees C for noxious heat- and noxious cold-induced pricking pain, respectively). Normal thermal pain sensations, consisting of normal perception of thermal quality and normal mean pain thresholds, were present both in normal skin areas (42.1 +/- 1.9 and 27.6 +/- 2.25 degrees C for heat and cold pain, respectively) and in areas in which only one thermal modality remained intact, when tested for that modality. Thus, testing for heat pain in areas in which only warm sensation was intact, or cold pain when only cold was intact produced normal qualities and thresholds of pain (42.8 +/- 3.4 and 24.4 +/- 6.2 degrees C for heat and cold pain, respectively). No spatial summation of pricking pain was observed, in contrast to the marked summation of heat pain in normal areas. In areas with only a single intact thermal modality, the quality of the perceived non-painful sensation was not determined by the thermal stimulus but by the intact modality (paradoxical sensation). Cold stimuli were perceived as warm in areas in which only warm sensation was preserved, and vice versa. A similar pattern was also seen for pain perception in areas with intact warm sensation. In these areas, both noxious heat and cold elicited a sensation of heat pain. No consistent pattern of heat-elicited pain was observed in areas in which only cold sensation was intact. These data suggest that the integrity of non-noxious thermal systems is essential for the normal perception of thermal pain, and that the subjective sensation of pain depends on the integration of information from nociceptive and non-nociceptive channels.
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Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions. Sodium channel Nav1.7 is essential for acute human pain but its role in chronic neuropathic pain is unclear. Minett and colleagues show that Nav1.7 expression specifically in sympathetic neurons, rather than sensory neurons, is required for the development of chronic neuropathic pain after injury.
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Quantitative sensory testing methods are now standard in the evaluation of sensory function in man, while few normal equine values have been reported.The aim of this experimental study was (a) to define the tactile sensory, mechanical nociceptive and thermal nociceptive thresholds of the equine face; (b) to assess the effect of age, sex, stimulation site and shaving; (c) to evaluate the reliability of the methods and (d) to provide reference facial quantitative sensory testing values.Method description.Thirty-four healthy Warmblood horses were used in the study. Six (tactile sensory threshold) and five (mechanical nociceptive and thermal nociceptive thresholds) areas of the left side of the face with clear anatomical landmarks were evaluated. Ten horses had two (mechanical nociceptive threshold) or three (tactile sensory and thermal nociceptive thresholds) of these areas shaved for another study. A linear Mixed model was used for data analysis.All thresholds increased with age (tactile sensory threshold: by 0.90 g/y (CI = [0.12 g; 0.36 g]) P = .001; mechanical nociceptive threshold: by 0.25 N/y (CI = [0.13-0.36 N]) P = .000; thermal nociceptive threshold: by 0.2°C/y (CI = [0.055-0.361]) P = .008). Sex had no effect on thresholds (tactile sensory threshold: P = .1; mechanical nociceptive threshold: P = .09; thermal nociceptive threshold: P = .2). Stimulation site affected tactile sensory and mechanical nociceptive thresholds (P = .001 and P = .008), but not thermal nociceptive threshold (P = .9). Shaving had no significant effect on any of the thresholds (tactile sensory threshold: P = .06; mechanical nociceptive threshold: P = .08; thermal nociceptive threshold: P = .09).Only the left side was investigated and measurements were obtained on a single occasion.Handheld quantitative sensory testing does not require shaving or clipping to provide reliable measurements. Stimulation over the nostril (tactile sensory threshold), temporomandibular joint (mechanical nociceptive threshold) and supraorbital foramen (thermal nociceptive threshold) resulted in the most consistent thresholds.
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Psychophysical experiments were carried out on 16 human subjects to determine how low intensity mechanical and thermal skin stimuli interfere with the sensation of pain. Moderate or intense pain was induced by low frequency (2 Hz) electrical stimulation within cutaneous fascicles of the median nerve at wrist level, and vibration, pressure, cooling or warming were applied for short periods (usually 20–60 sec) within or outside the skin area to which the pain was projected. Vibration within the area of projected pain reduced the sensation of pain more efficiently than vibration outside that area. Moderate pain was sometimes completely inhibited but intense pain was only moderately reduced. Pressure and cooling produced some pain relief whereas mild warming had an ambiguous effect. Since the painful input derived from stimulation of fibres in the nerve trunk, and not from peripheral nociceptors, the pain suppressing effects of vibration and cooling are not explicable in terms of lowered excitability of the nociceptive nerve endings in the skin. Instead, the results indicate that activity in low threshold mechanoreceptive and cold sensitive units suppresses pain at central (probably segmental) levels.
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Elderly individuals and patients with polyneuropathy often feel heat pain or burning sensation on quantitative sensory testing (QST) of warm perception distally in the lower limbs. We therefore studied heat pain threshold (HPT), warm perception threshold (WPT) and the difference between heat pain and warm perception thresholds in 48 patients with symptoms and signs of polyneuropathy matched according to age and gender with 48 healthy persons.QST (using method of limits) was performed on the distal calf and the dorsal foot.Particularly in the neuropathy group several individuals (58%) had an unpleasant feeling, often burning, when the thresholds according to the WPT algorithm were recorded. Difference between heat pain and warm perception thresholds in the lower calf of the patients was 3.9 +/- 3.5 and 5.8 +/- 3.4 degrees C in the controls (P = 0.012), and on the foot 3.8 +/- 2.8 vs 5.3 +/- 3.6 degrees C (P = 0.02).When performing QST it is important to assess also quality features of warm perception, such as burning and heat pain sensation.
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