Mechanism underlying painful radiculopathy in patients with lumbar disc herniation.

BACKGROUND: Painful lumbar radiculopathy is a neuropathic pain condition, commonly attributed to nerve root inflammation/compression by disc herniation. The present exploratory study searched for associations between pain intensity and inflammatory markers, herniated disc size, infection, psychological factors and pain modulation in patients with confirmed painful lumbar radiculopathy scheduled for spine surgery. METHODS: Prior to surgery, 53 patients underwent the following evaluation: pain intensity measured on a 0-10 numeric rating scale (NRS) and the Short-Form McGill Pain Questionnaire; sensory testing (modified DFNS protocol); pain processing including temporal summation and conditioned pain modulation (CPM); neurological examination; psychological assessment including Spielberger's Anxiety Inventory, Pain Sensitivity Questionnaire and the Pain Catastrophizing Scale. Pro-inflammatory cytokine levels (IL-1b, IL-6, IL-8, IL-17, TNFα, IFNg) and microbial infection (ELISA and rt-PCR) in blood and disc samples obtained during surgery. MRI scans assessments for disc herniation size/volume (MSU classification/ three-dimensional volumetric analysis). RESULTS: Complete data were available from 40 (75%) patients (15 female) aged 44.8 ± 16.3 years. Pain intensity (NRS) positively correlated with pain catastrophizing and CPM (r = 0.437, p = 0.006; r = 0.421, p = 0.007; respectively), but not with disc/blood cytokine levels, bacterial infection or MRI measures. CPM (p = 0.001) and gender (p = 0.029) were associated with average pain intensity (adjusted R2  = 0.443). CONCLUSIONS: This exploratory study suggests that pain catastrophizing, CPM and gender, seem to contribute to pain intensity in patients with painful lumbar radiculopathy. The role of mechanical compression and inflammation in determining the intensity of painful radiculopathy remains obscure. SIGNIFICANCE OF STUDY: Pain catastrophizing, CPM and gender rather than objective measures of inflammation and imaging seem to contribute to pain in patients with painful radiculopathy.

Something Must Be Wrong with the Implementation of Cancer-pain Treatment Guidelines. A Lesson from Referrals to a Pain Clinic.

OBJECTIVE: The World Health Organization's (WHO) guidelines for cancer pain management were intentionally made simple in order to be widely implemented by all physicians treating cancer patients. Referrals to pain specialists are advised if pain does not improve within a short time. The present study examined whether or not a reasonable use of the WHO guideline was made by non-pain specialists prior to referral of patients with cancer-related pain to a pain clinic. METHODS: Cancer patients referred to a pain specialist completed several questionnaires including demographics, medical history, and cancer-related pain; the short-form McGill Pain Questionnaire (SF-MPQ); and the Short Form Health Survey SF-12. Data from referral letters and medical records were obtained. Treatments recommended by pain specialists were recorded and categorized as "unjustified" if they were within the WHO ladder framework, or "justified" if they included additional treatments. RESULTS: Seventy-three patients (44 women, 29 men) aged 55 years (range, 25-85) participated in the study. Their pain lasted for a mean of 6 (1-192) months. Mean pain intensity scores on a 0-10 numerical rating scale were 7 (2-10) at rest and 8 (3-10) upon movement. Most patients complied with their referring physician's recommendations and consumed opioids. Adverse events were frequent. No significant correlation was found between the WHO analgesic medication step used and mean pain levels reported. There were 63 patient referrals (85%) categorized as "unjustified," whereas only 11 patients (15%) required "justified" interventions. CONCLUSIONS: These findings imply that analgesic treatment within the WHO framework was not reasonably utilized by non-pain specialists before referring patients to pain clinics.

A Fast Track to Hypoalgesia - The Anaerobic Exercise Effect on Pain Sensitivity.

Maximal anaerobic exercise, is a short high intensity effort, involves activation of the hypothalamus-pituitary-adrenal axis, and may suggest hypoalgesic effects. In addition, this exercise-induced muscle pain may contribute to hypoalgesia via the pain inhibits pain phenomenon, which is related to the diffuse noxious inhibitory control (DNIC) mechanism. We aimed to investigate whether: 1) a single bout of 30 s maximal anaerobic exercise has an analgesic effect on experimental pain sensitivity; 2) DNIC is the underlying mechanism of anaerobic exercise-induced hypoalgesia (EIH). Fifty healthy subjects participated. The experimental group performed the 'Wingate Anaerobic Test' (WAT) and controls set on the bikes without exercising. Psychophysical tests, performed before and after the intervention, in local and remote areas, included: heat (HPT) and pressure pain thresholds (PPT); suprathreshold heat and cold pain stimulation; the conditioned pain modulation (CPM) paradigm testing the DNIC mechanism. Following WAT, PPT and HPT increased (p<0.001) , pain ratings in response to heat and cold stimuli (p<0.001) and CPM (p=0.029) decreased compared with controls. No correlation was found between muscle pain, blood lactate level and EIH. To conclude WAT induces local and remote analgesic effects. The involvement of central pain modulatory processes with DNIC probably not the underline mechanism of EIH.