European journal of pain : EJP
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One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves the central nervous system (CNS) so that incoming impulses in low-threshold mechanoreceptors from the area of secondary hyperalgesia can evoke painful sensations instead of touch. ⋯ Here we review the evidence gathered in support of this model in the intervening years with special reference to experimental studies of antidromic activity (Dorsal Root Reflexes--DRRs) in nociceptive afferents and on the acquisition of low-threshold inputs by nociceptor-specific neurons in the spinal dorsal horn. We also discuss and identify potential molecular mechanisms that may underlie the presynaptic interaction model and therefore that could be responsible for the development of secondary hyperalgesia.
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Awareness that SCI pain is common emerged during the past decade. However, there are a number of unresolved issues. There is a need for variety of experimental models to reflect diversity of SCI pains. ⋯ More attention should be given to a condition of the spinal cord below and above the SCI lesion. A consensus for what is an optimal SCI functional assessment for patients with sensory complaints and pain should be developed. Further extensive SCI pain research is needed prior to spinal cord regeneration trials in order to be able to cope with a potential for newly developed pains that may appear during incomplete spinal cord regenerative attempts.
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Neuropathic pain is part of the neurological disease spectrum and may be an expression of severe medical pathology. Painful neuropathies have multiple disguises and may to a certain extent be mimicked by non-neurological pain conditions. Painful neuropathic conditions express themselves with spontaneous and/or abnormal stimulus-evoked pain. ⋯ This is a sound approach and should be pursued. It is mandatory, however, to retain the traditional organ-based diagnostic workup, which should precede further in-depth characterization of specific pain mechanisms. Extensive preparatory work is needed on how to link certain symptoms and signs to specific mechanisms, as elucidated from animal studies, before we can introduce mechanism-coupled treatment strategies.
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"He slept less and less; they gave him opium and began to inject morphine. But this did not relieve him. The dull pain he experienced in the half asleep condition at first only relieved him as a change, but then it became as bad, or even more agonizing, than the open pain."--Tolstoy, The Death of Ivan Ilyitch. ⋯ Those who work in chronic pain are unfortunately only too aware of the problems that such pains can cause. One of the hallmarks of neuropathic pain is poor or incomplete relief with opioids. As with so many things in medicine, there is nothing novel in this realization, as the Tolstoy quotation shows.
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The overarching reason that pain patients seek medical attention is because their pain interferes with some or all aspects of their quality of life (QOL). Interventions are considered successful by the patient if QOL is improved. Simple pain scores, although providing important information, do not capture the patient's total pain experience, which includes the effect on QOL. A focus on patient QOL should be adopted by all clinicians treating patients with neuropathic pain to work toward successful outcomes.