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Free PDF Download Eur opean Rev iew for Med ical and Pharmacol ogical Sci ences 2013; 17: 3257-3261 Neuropathic pain following spinal cord injury: what we know about mechanisms, assessment and management R. D’ANGELO, A. MORREALE 1, V. DONADIO, S. BORIANI 2, N. MARALDI 2, G. PLAZZI, R. LIGUORI IRCCS Istituto delle Scienze Neurologiche, Dipartimento di Scienze Biomediche e NeuroMotorie, Alma Mater Studiorun, University of Bologna, Bologna, Italy 1Montecatone Rehabilitation Institute, Imola-Bologna, Italy 2IRCCS Istituto Ortopedico Rizzoli, Dipartimento di Scienze Biomediche e NeuroMotorie, Alma Mater Studiorun, University of Bologna, Bologna, Italy Abstract. – BACKGROUND: In biology, it is its physiological response is pain. When pain is easy to understand how a damaged functional caused by non-neural tissues it is called “noci - system may generate wrong signals, but why ceptive pain”, whereas if pain “arises as a direct this should happen when the system is discon - consequence of a lesion or disease affecting the nected is less clear. For this reason, among oth - 1 er pain syndromes, neuropathic pain (NP) follow - somatosensory system” with or without ade - ing spinal cord injury (SCI) leaves most ques - quate stimulation, the term “neuropathic pain” tions unanswered. (NP) has been introduced. AIMS AND METHODS: Our purpose is to re - Spinal cord injury (SCI) directly affects the view current knowledge on NP after SCI, focus - somatosensory system and SCI patients experi - ing on the mechanisms, assessment and man - ence both nociceptive pain and NP, immediately agement of the syndrome. RESULTS: The mechanisms responsible for NP (> 1 month) after the acute injury or developing following SCI are poorly understood: NP is clas - later. Many classifications have been proposed to sically considered a “central pain syndrome” but identify SCI patients’ pain: the accepted taxono - recent evidence from experimental models re - my is based on the ad hoc -formed Task Force of veals a possible “peripheral sensitization”. As - the International Association of the Study of Pain sessment of NP following SCI is well-estab - (IASP) 2. The IASP Task Force divided nocicep - lished: in addition to clinical evaluation and self- tive pain into musculoskeletal (bone/joint/muscle reported scales, many neurophysiological, radio - logical and microscopic investigations may be trauma or inflammation, muscle spasms, sec - performed. The management of NP following SCI ondary overuse syndrome, mechanical instabili - is very difficult: evidence of effective drugs is ty), visceral (renal/bowel/sphincter dysfunction, lacking and alternative new treatment approach - “dysreflexic headache”) and NP on the basis of es yield different outcomes. anatomic involvement referred to SCI level: CONCLUSIONS: Recently clinical and instru - above level (AbL), at level (AtL) or below level mental tools have increased our knowledge on NP, suggesting that the discovery of new treat - (BeL). AbL NP includes compressive mononeu - ment agents will depend on an explanation of ropathies and complex regional pain syndrome, what changes after SCI: future research must AtL NP includes nerve root/cauda equine com - point in this direction. pression, post-traumatic syringomyelia and spinal cord trauma/ischemia, BeL NP includes Key Words: spinal cord trauma/ischemia 3. Moreover, SCI pa - Neuropathic pain, Spinal cord injury, Central sensi - tients with NP typically complain of sensory tization, Peripheral sensitization. phenomena such as allodynia or hyperalgesia in the painful area 4. From the first cohorts examined, pain follow - Introduction ing SCI revealed a high (> 60-80%) overall prevalence 5. Musculoskeletal and AtL pain are The nociceptive system works by processing the most common and earliest experienced types. potentially dangerous internal or external stimuli: BeL and visceral pain occur 2 years after the ini - Corresponding Author: Roberto D’Angelo, MD; e-mail: [email protected] 3257 R. D’Angelo, A. Morreale, V. Donadio, S. Boriani, N. Maraldi, G. Plazzi, R. Liguori tial injury. NP and visceral pain are more likely Brain to be severe and long-lasting, suggesting that SCI leads not only to cord atrophy but also to musculoskeletal pain is more treatable by current cortical atrophy of the primary motor and senso - drugs (non-steroidal anti-inflammatory drugs and ry cortex 19 and, as occurs in other pain syn - opioids). dromes, e.g. phantom limb syndrome 20 , a shift in Thus, NP following SCI is one of the most cortical body representation 21 . Moreover, complex and challenging pain syndromes. This changes in firing and in thalamic neuron mole - paper briefly describes the current main features cules have been found 22 . Thus, functional reorga - of NP, focusing on mechanisms, assessment and nization of the brain caused by sensory denerva - management . tion is due to double-speed mechanisms. The first, faster mechanism results from unmasking Mechanisms of NP Following SCI dormant synapses, while the second, slower but The spinal cord close to the site of injury is stronger mechanism reflects thickening of the probably where most anatomic and functional deafferented cortex with growth of lateral, closer changes occur after injury. Thus, the first stud - regions. ies 6 considered it the “site of origin of the distal burning”. However, the recent development of Periphery simulating animal models 7,8 has disclosed a Except for mechanical root/nerve insults, NP broader range of sites responsible for NP fol - following SCI is classically considered a “central lowing SCI. We first describe what happens in pain syndrome” and few reports have investigat - the spinal cord, then in the brain and peripheral ed the morphological and functional evolution of structures. cutaneous structures after SCI 23-25 . Peripheral pain generators may be stimulated in SCI pa - Spinal Cord tients with residual spinothalamic tract pathways, Acute ischemic or traumatic damage triggers a mimicking exacerbation of NP 26 . Animal models series of mutually-related and self-sustained of AbL NP 27 revealed increased responsiveness events in the spinal cord 9,10 . Pathogenic insult in - of uninjured primary afferent fibers suggesting cludes anatomical, neurochemical, excitotoxic there is a permanent change in the fibers and /or and inflammatory alterations. These components in the chemical environment in the skin named lead to a change in spinal neuron function and “peripheral sensitization” 27,28 . Lowering of the then to pain. threshold to mechanical and heat stimuli in the The cascade does not occur in a programmed overlying SCI segments may be considered a hu - sequential fashion but evidence of an influence of man equivalent 29 . sex, strain and gonadal hormones 11 and of selec - tive neuroprotective agents 12 suggests that molecu - Assessment of NP Following SCI lar events are prevalent in the first stage. In partic - International Consensus recurrently review ular, inflammation (cytokines, prostaglandins, re - general recommendations for NP assessment 30,31 . active oxygen species) and neuromodulator (gluta - NP after SCI overall adopts the same 32 . mate, GABA, opioid, serotonergic, noradrenergic) The first step is to identify pain as possible NP agents change expression and function 9,13 produc - by definition 1, rejecting any other possible somatic ing 3 main effects: cause. Screening tools, like self-reported scales, in particular DN4 33 , are available and useful. • Activation of microglia 14 and astrocytes from a The second step is clinical examination to as - resting state; sess pain intensity, using a visual analogue scale • Different neuronal firing: increased neuron re - (VAS) or numeric rating scale (NRS): even if it is cruitment after stimulation, enhanced irregular a subjective estimation of pain, these scales read - background activity, and alterations in sodium ily provide information on pain evolution over currents 15,16 are present and modulated by in time and the effect of treatment. Clinical evalua - situ administration of local anesthetics 6; tion should include an assessment of sleep, • Long-term synaptic plasticity 17 , including mood, and quality of life 34 . modified synaptic connection and regulatory The third step is to perform laboratory tests proteins, apoptosis or rescuing of neurons, and is mostly confined to research trials. Elec - modified regulation of gene transcription/ troneuromyography is sensitive in assessing any translation 18 . associated damage of the peripheral motor path - 3258 Neuropathic pain following spinal cord injury ways 35,36 . Although expensive, laser-evoked po - elucidate causative mechanisms and much tentials (LEP) are useful for assessing the func - progress has been achieved in recent years. In tion of the A-delta fiber subcortical pathways and particular, peripheral sensitization may explain can localize the lesion with precision 37 . MRI is why NP occurs with or without a complete loss useful to quantify spinal cord damage and its of spinothalamic tract function 47 or in other dis - consequences (post-traumatic syringomyelia). eases with theoretical pure motor CNS involve - Activation brain imaging (PET-fMRI) is an inter - ment, e.g. locked-in syndrome 48,49 . Further inves - esting research tool, investigating synaptic tigations must focus on pathogenesis: discover - changes. Skin biopsy is not much used in SCI pa - ing targets we may improve our current limited tients in contrast with other pain syndromes. therapeutic weapons. Management of NP Following
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