Neuropathic pain

Abstract

Pain usually results from activation of nociceptive afferents by actually or potentially tissue-damaging stimuli. Pain may also arise by activity generated within the nervous system without adequate stimulation of its peripheral sensory endings. For this type of pain, the International Association for the Study of Pain introduced the term neuropathic pain, defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system." While this definition has been useful in distinguishing some characteristics of neuropathic and nociceptive types of pain, it lacks defined boundaries. Since the sensitivity of the nociceptive system is modulated by its adequate activation (e.g., by central sensitization), it has been difficult to distinguish neuropathic dysfunction from physiologic neuroplasticity. We present a more precise definition developed by a group of experts from the neurologic and pain community: pain arising as a direct consequence of a lesion or disease affecting the somatosensory system. This revised definition fits into the nosology of neurologic disorders. The reference to the somatosensory system was derived from a wide range of neuropathic pain conditions ranging from painful neuropathy to central poststroke pain. Because of the lack of a specific diagnostic tool for neuropathic pain, a grading system of definite, probable, and possible neuropathic pain is proposed. The grade possible can only be regarded as a working hypothesis, which does not exclude but does not diagnose neuropathic pain. The grades probable and definite require confirmatory evidence from a neurologic examination. This grading system is proposed for clinical and research purposes.

Capsaicin 8% patch versus oral pregabalin in patients with peripheral neuropathic pain

“…In this study (ELEVATE), patients were between 18 and 80 years of age and had a documented diagnosis of probable or definite PNP using the currently recognized grading system (Treede et al., 2008). Patients had PNP due to post‐herpetic neuralgia (PHN) (pain persisting for at least 6 months since shingles vesicle crusting), post‐traumatic nerve injury (PNI) (minimum of 3 months) or non‐diabetic painful peripheral polyneuropathy (minimum of 3 months), and had an average numeric pain rating scale (NPRS) (Farrar et al., 2001) score ≥4 over a period of at least 4 consecutive days.…”

“…Painful neuropathy or peripheral neuropathic pain (PNP) is a common neurological condition according to the revised International Association for the Study of Pain (IASP) definition (Treede et al., 2008), and is estimated to affect ~7–8% of the general population in Europe (Torrance et al., 2006; Bouhassira et al., 2008). Managing patients with PNP is challenging (Dworkin et al., 2007, 2010; Finnerup et al., 2010; Finnerup, Attal et al ., 2015); it often becomes chronic, with marked long‐term reductions in health‐related quality of life (HRQOL) (O'Connor, 2009), decreased individual productivity and increased patient and healthcare expenditure (Rodríguez et al., 2007; Navarro et al., 2011).…”

Nanoparticle-encapsulated emodin decreases diabetic neuropathic pain probably via a mechanism involving P2X3 receptor in the dorsal root ganglia

“…Diabetic neuropathic pain (DNP) is the most common complication of T2DM. DNP leads to dysfunction in the dorsal root ganglia (DRG) [2][3][4]. Toxicity of hyperglycaemia is associated with local metabolic changes in T2DM [3,5].…”

Enhanced c‐Fos expression in the central amygdala correlates with increased thigmotaxis in rats with peripheral nerve injury

“…Pain involves sensory, emotional and cognitive aspects, with neuropathic pain representing a particularly complex condition arising as a direct consequence of lesion or disease of the somatosensory system (Treede et al., 2008). Evidence suggests a reciprocal relationship exists between affective disturbances and somatic symptoms (Haythornthwaite et al., 1991; Wilson et al., 2001).…”