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Neuropathic Pain and Spasticity: Intricate Consequences of Spinal Cord Injury

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Neuropathic Pain and Spasticity: Intricate Consequences of Spinal Cord Injury Spinal Cord (2017) 55, 1046–1050 & 2017 International Spinal Cord Society All rights reserved 1362-4393/17 www.nature.com/sc REVIEW Neuropathic pain and spasticity: intricate consequences of spinal cord injury NB Finnerup Study design: The 2016 International Spinal Cord Society Sir Ludwig Guttmann Lecture. Objectives: The aim of this review is to identify different symptoms and signs of neuropathic pain and spasticity after spinal cord injury (SCI) and to present different methods of assessing them. The objective is to discuss how a careful characterization of different symptoms and signs, and a better translation of preclinical findings may improve our understanding of the complex and entangled mechanisms of neuropathic pain and spasticity. Methods: A MEDLINE search was performed using the following terms: ‘pain’, ‘neuropathic’, ‘spasticity’, ‘spasms’ and ‘spinal cord injury’. Results: This review identified different domains of neuropathic pain and spasticity after SCI and methods to assess them in preclinical and clinical research. Different factors important for pain description include location, onset, pain descriptors and somatosensory function, while muscle tone, spasms, reflexes and clonus are important aspects of spasticity. Similarities and differences between neuropathic pain and spasticity are discussed. Conclusions: Understanding that neuropathic pain and spasticity are multidimensional consequences of SCI, and a careful examination and characterization of the symptoms and signs, are a prerequisite for understanding the relationship between neuropathic pain and spasticity and the intricate underlying mechanisms. Spinal Cord (2017) 55, 1046–1050; doi:10.1038/sc.2017.70; published online 11 July 2017 INTRODUCTION Spasticity is also a multidimensional constellation of phenomenolo- This review discusses the need for a phenotype-based classification of gically diverse symptoms and has been defined as ‘adisordered both neuropathic pain and spasticity in order to understand the sensorimotor control resulting from an upper motor neuron lesion, common and diverse mechanisms of these intertwined consequences presenting as intermittent or sustained involuntary activation of of SCI. muscles’,15 and this broad definition of spasticity is adopted in the Following SCI, neuroplasticity, which involves both neuronal, spinal cord injury musculoskeletal data set.16 This definition includes structural and functional responses, is essential for recovery of the velocity-dependent increase in tonic stretch reflexes (muscle tone) and neurological function, but the dark side of this neuroplasticity can be phasic stretch reflexes (exaggerated tendon jerks) that formed the the development of neuropathic pain and spasticity.1 These common original definition of spasticity,17 as well as flexor- and extensor spasms, disabling conditions negatively affect mood, sleep, quality of life, and flexor reflexes, and altered motor control. Clinically, it is often difficult to participation in activities and active recreation as well as separate spasticity from symptoms and signs caused by structural – employment.2 7 Neuropathic pain is present in 50–60% and spasticity changes in the muscles.18 – in about 70% of individuals living with a SCI.5,8 11 The aim of this review is to present different domains of neuropathic Neuropathic pain is a multidimensional constellation of phenomen- pain and spasticity with possible different underlying mechanisms and ologically different symptoms and is defined as ‘pain caused by a lesion to discuss the assessment of these in preclinical and clinical research. or disease of the somatosensory nervous system’.12,13 Neuropathic pain The hope is that a more elaborate classification will improve the following SCI includes at- and below-level SCI neuropathic pain, where translation of preclinical studies to the clinic and understanding of the at-level pain may consist of both peripheral and central neuropathic complex and entangled mechanisms of neuropathic pain and spasticity. pain, while below-level pain is a central neuropathic pain condition.14 The pain may be spontaneous and described as burning, squeezing, NEUROPATHIC PAIN AND SPASTICITY: TWO SIDES OF THE shooting or pricking pain, and/or evoked (allodynia and hyperalgesia), SAME COIN? which is most commonly evoked by touch and cold stimuli. Clinically, Central neuropathic pain shares many features with spasticity and has it may be difficult to distinguish neuropathic pain from other types of even been termed ‘sensory spasticity’.19 Both pain and spasticity can pain such as musculoskeletal pain, which is common after SCI, due to, have a late onset and develop slowly over time after SCI, and once for example, spasms, contractures and overuse. developed, they often become chronic. In addition, both conditions Department of Clinical Medicine, Danish Pain Research Center, Aarhus University, Aarhus, Denmark Correspondence: Professor NB Finnerup, Department of Clinical Medicine, Danish Pain Research Center, Aarhus University Hospital, Noerrebrogade 44, Building 1A, Aarhus C, DK-8000 Denmark. E-mail: fi[email protected] This is a review in relation to The 2016 Sir Ludwig Guttmann Lecture at the 55th ISCoS Annual Scientific Meeting, Vienna, Austria. Received 27 February 2017; revised 17 May 2017; accepted 18 May 2017; published online 11 July 2017 Pain and spasticity after SCI NB Finnerup 1047 Table 1 Different domains in neuropathic pain and their assessment phenotypes of pain and spasticity may prevent us from identifying in human and animal research similarities. In a questionnaire study based solely on patient-reported outcomes, the presence of pain was related to the presence of spasticity Domain Clinical assessment Preclinical assessment and a higher intensity rating of muscle stiffness, while only pain with Ongoing pain Numeric rating scale Conditioned place- typical neuropathic pain descriptors was related to the frequency of Visual analog scale preference paradigms spasms.5 This suggests that different subtypes of pain and spasticity may be related. The multidimensional nature of pain and spasticity Evoked pain Pain intensity to: Supraspinal responses to: calls for the use of different scales to measure various aspects of Thermal gain Thermal stimulation Thermal stimulation 27,28 29,30 (for example, thermal (e.g. cold plate, spasticity and pain, and these will be discussed in the following Mechanical gain rollers, acetone droplet, acetone droplet, sections. thermal testing) radiant heat) Mechanical stimulation Mechanical stimulation MULTIDIMENSIONAL ASSESSMENT OF PAIN fi (for example (e.g. mono laments, For neuropathic pain, there is now good evidence from clinical monofilaments, cotton, cotton, brush) brush) research to suggest that at-level and below-level pain are two different pain types. Below-level pain often develops months later than at-level Somatosensory function Sensory testing to Supraspinal responses to pain, and sensory hypersensitivity is a predictor of below-level but not Thermal loss thermal and thermal and mechanical at-level pain.8,31 However, hypersensitivity is not always present early Mechanical loss mechanical stimuli stimuli on in patients who develop below-level pain,31,32 and within both Onset of pain Early (within weeks) Early (within days) below-level and at-level pain, there likely are different pain phenotypes Late (within months) Late (within weeks) with different constellations of sensory descriptors and sensory signs that may reflect different underlying mechanisms and possible Location Location of pain and Location of sensory different responses to treatment. For example, within both central sensory loss and gain loss and gain fi At-level At-level and peripheral neuropathic pain, ve distinct dimensions have been Below-level Below-level identified based on neuropathic pain descriptors, that is, burning pain, squeezing pain, paroxysmal pain, evoked pain, and pins and needles Pain quality Pain questionnaires, NA sensations.33 Using cluster analysis of the results of quantitative for example: fi Burning pain Neuropathic pain sensory testing, three different clusters have also been identi ed based Pressing/squeezing symptom inventory on sensory profiles, which are as follows: (1) a cluster characterized by Paroxysmal pain Pain Quality loss of small and large fiber function; (2) a cluster characterized by Pricking pain/pins Assessment relatively preserved large and small fiber sensory functions in and needles Scale combination with thermal hyperalgesia and (3) a cluster characterized Evoked pain by thermal sensory loss and mechanical allodynia and hyperalgesia.34 Other domains Questionnaires or Behavioral tests, for Psychological factors such as anxiety and depression, pain catastro- interview example, phizing, and adaptive pain coping are also important factors in the Anxiety/depression Thigmotaxis paradigm 35,36 multidimensional neuropathic pain description. Evidence is now Pain impact Elevated-plus maze fi Pain catastrophizing Burrowing beginning to emerge supporting that such phenotype-based classi ca- Participation tions are related to pain mechanisms and that they may have treatment implications.29,37 Sodium channel blockers are, for example, suggested to be more effective in patients with preserved pain and may be elicited by touch and other non-painful stimulation. thermal sensation than in patients who have mainly sensory loss.38,39 Gabapentin and pregabalin, which are classic drugs used in the Some of the factors relevant for characterizing
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