Posttraumatic stress disorder (PTSD) is a known risk factor for the development of chronic pain conditions, and almost 1 in 5 individuals with chronic pain fulfills the criteria for PTSD. However, the relationship between PTSD and pain is poorly understood and studies on pain perception in patients with PTSD show inconsistent results suggesting that different sensory profiles exist among individuals with PTSD. Here, we (1) systematically summarize the current literature on experimentally evoked pain perception in patients with PTSD compared to subjects without PTSD, and (2) assess whether the nature of the traumatic event is associated with different patterns in pain perception. The main outcome measures were pain threshold, pain tolerance, and pain intensity ratings as well as measures of temporal summation of pain and conditioned pain modulation. A systematic search of MEDLINE, EMBASE, Web of Science, PsycINFO, and CINAHL identified 21 studies for the meta-analysis, including 422 individuals with PTSD and 496 PTSD-free controls. No main effect of PTSD on any outcome measure was found. However, stratification according to the nature of trauma revealed significant differences of small to medium effect sizes. Combat-related PTSD was associated with increased pain thresholds, whereas accident-related PTSD was associated with decreased pain thresholds. No clear relationship between PTSD and experimentally evoked pain perception exists. The type of trauma may affect pain thresholds differently indicating the presence of different subgroups with qualitative differences in pain processing.

BACKGROUND: Beyond initial lesions, any form of spinal (re)operation can cause direct potential aggression to the nervous system by contact with neural tissue or by imprinting a morphological change on the neural tissue. The potential consequences of nerve root injury affect both peripheral and axial dermatomal distribution. The hypothesis of a possible neuropathic aspect associated with the back pain component of failed back surgery syndrome (FBSS) therefore appears to be reasonable. Its pathophysiology remains unclear due to the permanent interplay between nociceptive and neuropathic pain components, resulting in the coexistence of physiological and pathological pain at the same anatomical site. This paper is designed to extensively review the fundamental mechanisms leading to chronification of pain and to suggest considering the emerging concept of \"neuropathic back pain\".
METHODS: Literature searches included an exhaustive review of 643 references and 74 book chapters updated by searching the major electronic databases from 1930 to August 2013.
RESULTS: Inflammatory and neuropathic back pain could be distinguished from pure nociceptive pain as a result of an increased activity and responsiveness of sensitized receptors at the peripheral nervous system and also as a consequence of increased afferent inflow to the central nervous system, moving to a new, more excitable \"wind-up\" state. This can be clinically translated to an amplified response to a moderate/intense stimulus (primary hyperalgesia) or an aversive sensation provoked by the activation of low-threshold mechanoreceptors through non-noxious stimuli, which defines allodynia. Activated non-neuronal cells including microglia have been found to be cellular intermediaries in mechanical allodynia. Major changes in the spinal cord are the loss of inhibitory mechanisms, resulting in an increased activity of interneurons or projection neurons and a structural reorganization of the central projection pattern. This abnormal excitability of sensory neurons is coupled to changes in the neurotransmitter phenotype, which could induce a resistance to conventional analgesic treatments.
CONCLUSIONS: A clear understanding of the factors leading to the chronification of back pain should help us to move to the choice of mechanism related pain treatments to improve outcomes in FBSS chronic condition.