From “mechanical” to “neuropathic” back pain concept in FBSS patients. A systematic review based on factors leading to the chronification of pain (part C)

Abstract

IntroductionBeyond 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”. MethodsLiterature searches included an exhaustive review of 643 references and 74 book chapters updated by searching the major electronic databases from 1930 to August 2013. ResultsInflammatory 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. ConclusionA 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.