Conditioned Pain Modulation in Patients With Acute and Chronic Low Back Pain

Abstract

Objectives: Disturbed endogenous pain modulation is likely one of the mechanisms underlying central hypersensitivity and might be a contributing factor for the development and maintenance of chronic pain. To our knowledge, no study has investigated endogenous pain modulation in both acute and chronic low back pain (LBP). We tested the hypothesis that endogenous pain inhibition is impaired in patients with acute and chronic LBP. Materials and Methods:We evaluated 40 patients with acute LBP, 34 patients with chronic LBP and 30 pain-free controls for their conditioned pain modulation (CPM), with pressure pain tolerance and cold pressor as test and conditioning stimulus, respectively. Measurements were repeated up to 10 minutes after cold pressor test.Results: There was no difference in CPM among the groups immediately after cold pressor test. However, the decline in CPM effect was significantly faster in chronic and acute LBP patients than in controls, with no evidence for differences between pain groups.Discussion: The present study provides evidence for some alterations of endogenous modulation in both acute and chronic LBP. CPM was still detected in both patient groups, indicating that endogenous modulation, although effective for a shorter duration, is partially functioning in patients with LBP.Key Words: conditioned pain modulation, acute low back pain, chronic low back pain (Clin J Pain 2016;32:116-121) T he central nervous system is capable to modulate signals coming from peripheral tissues, leading to either amplification or attenuation of the nociceptive input. 1 One important aspect of central pain modulation is endogenous inhibition, as its impaired efficiency may be a determinant of symptoms in pain patients. In humans, 1-test paradigm to evaluate the endogenous pain modulatory system is conditioned pain modulation (CPM), which occurs when the response to a painful test stimulus is inhibited by an additional conditioning painful stimulus. 2 Disturbed CPM is likely one of the mechanisms underlying central hypersensitivity and might be 1 contributing factor for the development and maintenance of chronic pain. Patients with chronic low back pain (LBP) display decreased pain thresholds after stimulation of nonpainful tissues and enlargement of the areas of referred pain, 3-5 which is strongly suggestive for widespread central hypersensitivity. Although hypersensitivity has been documented, the mechanisms underlying exaggerated pain responses in acute and chronic LBP are unclear. One of these mechanisms may be deficient endogenous pain modulation. Most studies have focused on chronic pain conditions, but deficient pain modulation could also be present in the acute phase. Furthermore, most studies have assessed CPM at 1 time-point, and information on its time course after cessation of the conditioning stimulus is sparse.The hypothesis of this study was that endogenous pain inhibition is impaired in patients with acute and chronic LBP. We evaluated the inhibitory effect not only immediately after the condit...

Pain Modulation: From Conditioned Pain Modulation to Placebo and Nocebo Effects in Experimental and Clinical Pain

“…In patients with acute and chronic low back pain, CPM effect is triggered following counter-irritation, but its duration is significantly reduced compared to healthy individuals (Mlekusch et al, 2016). Moreover, CPM efficacy may predict the analgesic effect of pregabalin treatment for painful chronic pancreatitis (Olesen et al, 2013).…”

Assessment and manifestation of central sensitisation across different chronic pain conditions

“…Evidence has been provided that endogenous modulation is also impaired in acute LBP (Mlekusch et al, 2016) raising the question for how long the LBP should be present in order to have an impact on CPM.…”

“…myofascial temporomandibular joint pain (Bragdon et al, 2002), chronic LBP (Peters et al, 1992;Mlekusch et al, 2016), whiplash (Daenen et al, 2013(Daenen et al, , 2014De Kooning et al, 2015), long-standing patellofemoral pain (Rathleff et al, 2016), myofascial pain (Hilgenberg-Sydney et al, 2016), fibromyalgia (Kosek and Hansson, 1997;Staud, 2009), painful knee OA (Arendt- , chronic LBP (Correa et al, 2015), frequent episodic tension-type headache (Drummond and Knudsen, 2011), chronic tension-type headaches (Sandrini et al, 2006), chronic daily headache (Hilgenberg-Sydney et al, 2016), endotoxemia (Karshikoff et al, 2015), interstitial cystitis (Ness et al, 2014), irritable bowel syndrome (Wilder-Smith and Robert-Yap, 2007;Williams et al, 2013), and chronic pancreatitis (Olesen et al, 2010).…”

Temporal aspects of endogenous pain modulation during a noxious stimulus prolonged for 1 day

“…While the prolonged noxious stimulus produced by capsaicin resulted in less efficient CPM in young healthy adults, the temporal effects of CPM in patient populations are less clear. Patients with acute or chronic low back pain have similar CPM as healthy adults immediately after a conditioning stimulus, although the magnitude of CPM declined more rapidly in the patient groups than the controls (Mlekusch et al, ). Additionally, over a span of 4 months, CPM declined in a linear fashion in healthy adults (Marcuzzi, Wrigley, Dean, Adams, & Hush, ).…”