Dynamic Changes in Nociception and Pain Perception After Spinal Cord Stimulation in Chronic Neuropathic Pain Patients :

We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.

Experimental determination of pain sensitivity has received increasing attention because of emerging clinical applications (including prediction of postoperative pain and treatment response) and scientific implications (e.g. it has been proposed that above-average pain sensitivity is a risk factor for the development of chronic pain disorders). However, the use of experimental pain sensitivity assessment on a broad scale is hampered by its requirements on time, equipment and human resources and the fact that it is painful for the tested subject. Alternatives to experimental pain testing are currently lacking. Here we developed a self-rating instrument for the assessment of pain sensitivity, the Pain Sensitivity Questionnaire (PSQ) that is based on pain intensity ratings of daily life situations and takes 5-10min to complete. Adequate reliability of the PSQ was confirmed in 354 subjects. In a validation study comprising 47 healthy subjects, the results of comprehensive experimental pain testing, including different modalities (heat, cold, pressure, and pinprick) and different measures (pain thresholds, pain intensity ratings), were compared to the results of the PSQ. PSQ scores were significantly correlated to experimental pain intensity ratings (r = 0.56, p < 0.001) but not to pain thresholds (r = 0.03). Prediction of experimental pain intensity ratings by the PSQ was better than by pain-associated psychological factors (pain catastrophizing, depression, anxiety). This shows that the PSQ may be a simple alternative to experimental pain intensity rating procedures in healthy subjects and makes the PSQ a highly promising tool for clinical and experimental pain research.

The present study examined catastrophizing in rheumatoid arthritis (RA) patients. Subjects were 223 RA patients who were participants in a longitudinal study. Each patient completed the Catastrophizing scale of the Coping Strategies Questionnaire (CSQ) on 2 occasions separated by 6 months (time 1, time 2). The Catastrophizing scale is designed to measure negative self-statements, castastrophizing thoughts and ideation (sample items = 'I worry all the time about whether it will end,' 'It is awful and I feel that it overwhelms me'). Data analysis revealed that the Catastrophizing scale was internally reliable (alpha = 0.91) and had high test-retest reliability (r = 0.81) over a 6 month period. Correlational analyses revealed that catastrophizing recorded at time 1 was related to pain intensity ratings, functional impairment on the Arthritis Impact Measurement scale (AIMS), and depression at time 2. Predictive findings regarding catastrophizing while modest were obtained after controlling for initial scores on the dependent variables, demographic variables (age, sex, socioeconomic status), duration of pain, and disability support status. Taken together, these findings suggest that catastrophizing is a maladaptive coping strategy in RA patients. Further research is needed to determine whether cognitive-behavioral interventions designed to decrease catastrophizing can reduce pain and improve the physical and psychological functioning of RA patients.