Recall Bias in Patients with Chronic Low Back Pain: Individual Pain Response Patterns Are More Important Than Pain Itself!

BACKGROUND: Patients' cognitive processing of pain-related information as well as their cognitive, affective and behavioral response pattern when experiencing pain in daily life has been shown to be associated with poorer prognosis in low back pain. However, the relationship between specific cognitive processes such as recall of pain-related material and individual pain responses remains unknown. PURPOSE: The present study sought to investigate recall bias in patients with chronic low back pain (CLBP) compared to healthy controls. Furthermore, it was aimed to investigate the impact of patients' individual pain-related responses on recall bias, comparing fear-avoidance response (FAR), endurance response (ER) and adaptive response (AR) patterns. METHOD: Thirty-one CLBP patients and 31 controls were tested on a free recall task with three word lists comprising pain words and neutral words. Further, the CLBP group was classified into patients with a FAR, ER and AR pattern, using a short screening including the Avoidance-Endurance Questionnaire (AEQ). Group differences with pain status (CLBP vs. healthy) and AEQ responses (FAR, ER, AR) as between-group factors, word type (pain vs. neutral) as within-group factor and free recall as dependent variable were analysed by means of repeated-measures analysis of (co-) variance. RESULTS: Results revealed different pain processing of pain words between FAR and ER patterns, whereas CLBP patients as a whole did not differ from the healthy controls. FAR patients displayed significantly less recall than ER patients. CONCLUSION: Recall biases in CLBP patients are not only a result of experiencing pain but also effected by patients' pain response pattern with respect to fear-avoidance versus endurance.

Associations between fear-avoidance and endurance responses to pain and salivary cortisol in the context of experimental pain induction.

Recent clinical studies in patients with lower back pain indicate that maladaptive fear-avoidance- and endurance-related pain responses (FAR and ER) have an influence on pain-induced physiological stress levels. The aim of the present study was to follow-up these results under well-controlled laboratory conditions. For this purpose, 30 healthy adults were asked to indicate their usual responses to pain, and were then confronted with an experimental pain stimulus (cold pressor test). Cortisol served as a measure of physiological stress. The results reveal positive associations between cortisol and FAR patterns, and negative associations between cortisol and behavioral ER. Conceivably, FAR contribute to long-lasting elevated stress levels in patients with stress-related musculoskeletal pain. In contrast, short-term, stress-lowering effects of ER might even be considered an advantage in coping with pain.

Loss of heterozygosity in malignant rat schwannomas chemically induced in hybrids of inbred rat strains with differential tumor susceptibility.

Rats of the inbred BD strains strongly differ in their susceptibility to the induction of tumors of the central (CNS) and peripheral nervous system (PNS) by N-ethyl-N-nitrosourea (EtNU). Malignant schwannomas induced in (BDIX x BDIV) and (BDIX x BDVI) rat hybrids were analyzed to identify genetic alterations associated with EtNU-induced tumorigenesis in the PNS. EtNU-induced schwannomas exclusively exhibit an A:T T:A transversion mutation of the neu/Erbb-2 gene located on chromosome 10, with subsequent loss of the wild-type neu/Erbb-2 allele at a post-initiation stage. Targeted allelic deletion mapping previously revealed losses of heterozygosity (LOH) at the distal end of chromosome 10 in a large majority of (BDIX x BDIV) schwannomas. The aims of the present study were (i) to scan the whole genome for further LOHs; (ii) to narrow down the consensus regions of frequently occurring allelic deletions using tumors from different crosses of BD rats; and (iii) to determine the sequence of genetic alterations during schwannoma development. A limited number of (BDIX x BDIV) F(1) tumors were initially screened for LOH and microsatellite instability (MI) by amplifying 58 microsatellite markers spanning the whole genome. LOHs on chromosome 5 were detected in 9/17 tumors, with random loss of the parental alleles. Ninety-two schwannomas from different BD rat-crosses were then analyzed to solidify these data and to determine the consensus region of frequent LOHs. The results indicate that LOHs on chromosomes 10 and 5 are required for the development of EtNU-induced malignant schwannomas from immature neu/Erbb-2 mutant glial cells, and that putative tumor suppressor genes are localized on chromosome 10q32.3, corresponding to human chromosome 17q25.3, and the telomeric region of mouse chromosome 11, and on the telomeric quarter of chromosome 5. MI was detected in <0.2% of cases.