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Florin Allmendinger,1 Paulina Simonne Scheuren,1– 4 Iara De Schoenmacker,1 Florian Brunner,5 Jan Rosner,1,2,6 Armin Curt,1 Michèle Hubli1 1Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland; 2Department of Neurology, University Hospital Bern, Inselspital, University of Bern, Bern, Switzerland; 3International Collaboration on Repair Discoveries, Vancouver, BC, Canada; 4Department of Anesthesiology, Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada; 5Department of Physical Medicine and Rheumatology, Balgrist University Hospital, University of Zurich, Zurich, Switzerland; 6Danish Pain Research Center, Department of Clinical Medicine, Aarhus University, Aarhus, DenmarkCorrespondence: Florin Allmendinger, Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Forchstrasse 340, Zurich, CH-8008, Switzerland, Tel +41 44 510 72 11, Email florin.allmendinger@balgrist.chPurpose: The pathophysiological mechanisms underlying the development of chronic pain in complex regional pain syndrome (CRPS) are diverse and involve both peripheral and central changes in pain processing, such as sensitization of the nociceptive system. The aim of this study was to objectively distinguish the specific changes occurring at both peripheral and central levels in nociceptive processing in individuals with chronic CRPS type I.Patients and Methods: Nineteen individuals with chronic CRPS type I and 16 age- and sex-matched healthy controls (HC) were recruited. All individuals underwent a clinical examination and pain assessment in the most painful limb, the contralateral limb, and a pain-free control area to distinguish between peripheral and central mechanisms. Contact-heat evoked potentials (CHEPs) were recorded after heat stimulation of the three different areas and amplitudes and latencies were analyzed. Additionally, quantitative sensory testing (QST) was performed

PURPOSE: The pathophysiological mechanisms underlying the development of chronic pain in complex regional pain syndrome (CRPS) are diverse and involve both peripheral and central changes in pain processing, such as sensitization of the nociceptive system. The aim of this study was to objectively distinguish the specific changes occurring at both peripheral and central levels in nociceptive processing in individuals with chronic CRPS type I. PATIENTS AND METHODS: Nineteen individuals with chronic CRPS type I and 16 age- and sex-matched healthy controls (HC) were recruited. All individuals underwent a clinical examination and pain assessment in the most painful limb, the contralateral limb, and a pain-free control area to distinguish between peripheral and central mechanisms. Contact-heat evoked potentials (CHEPs) were recorded after heat stimulation of the three different areas and amplitudes and latencies were analyzed. Additionally, quantitative sensory testing (QST) was performed in all three areas. RESULTS: Compared to HC, CHEP amplitudes in CRPS were only increased after stimulation of the painful area (p=0.025), while no increases were observed for the pain-free control area (p=0.14). None of the CHEP latencies were different between the two cohorts (all p>0.23). Furthermore, individuals with CRPS showed higher pain ratings after stimulation of the painful limb compared to their contralateral limb (p=0.013). Lastly, compared to HC, mechanical (p=0.012) and thermal (p=0.046) sensitivity was higher in the painful area of the CRPS cohort. CONCLUSION: This study provides neurophysiological evidence supporting an intact thermo-nociceptive pathway with signs of peripheral sensitization, such as hyperexcitable primary afferent nociceptors, in individuals with CRPS type I. This is further supported by the observation of mechanical and thermal gain of sensation only in the painful limb. Additionally, the increased CHEP amplitudes might be related to fear-induced alterat

Squatting is a common daily activity and fundamental exercise in resistance training and closed kinetic chain programs. The aim of the present study was to investigate the effects of an experimentally induced weakness of the gluteal muscles on joint kinematics, reactions forces (JRFs), and dynamic balance performance during deep bilateral squats in healthy young adults. Ten healthy adults received sequential blocks of 1) branch of the superior gluteal nerve to the tensor fasciae latae (SGNtfl) muscle, 2) superior gluteal nerve (SGN), and 3) inferior gluteal nerve (IGN) on the dominant right leg. At the control condition and following each block, the participants were instructed to perform deep bilateral squats standing on two force plates. Hip, knee, ankle, and pelvis kinematics did not differ significantly following iatrogenic weakness of gluteal muscles. The most important finding was the significant differences in JRFs following SGN and IGN block, with the affected hip, patellofemoral, and ankle joint demonstrating lower JRFs, whereas the contralateral joints demonstrated significantly higher JRFs, especially the patellofemoral joint which demonstrated an average maximum difference of 1.43 x body weight compared to the control condition. When performing a deep bilateral leg squat under SGN and IGN block, the subjects demonstrated an increased center of pressure (CoP) range and standard deviation (SD) in mediolateral compared to the control condition. These results imply that squat performance changes significantly following weakness of gluteal muscles and should be considered when assessing and training athletes or patients with these injuries. This article is protected by copyright. All rights reserved.

INTRODUCTION Degenerative cervical myelopathy (DCM) is the most common cause of non-traumatic incomplete spinal cord injury, but its pathophysiology is poorly understood. As spinal cord compression observed in standard MRI often fails to explain a patient's status, new diagnostic techniques to assess DCM are one of the research priorities. Minor cardiac-related cranio-caudal oscillations of the cervical spinal cord are observed by phase-contrast MRI (PC-MRI) in healthy controls (HCs), while they become pathologically increased in patients suffering from degenerative cervical myelopathy. Whether transversal oscillations (i.e., anterior-posterior and right-left) also change in DCM patients is not known. METHODS We assessed spinal cord motion simultaneously in all three spatial directions (i.e., cranio-caudal, anterior-posterior, and right-left) using sagittal PC-MRI and compared physiological oscillations in 18 HCs to pathological changes in 72 DCM patients with spinal canal stenosis. The parameter of interest was the amplitude of the velocity signal (i.e., maximum positive to maximum negative peak) during the cardiac cycle. RESULTS Most patients suffered from mild DCM (mJOA score 16 (14-18) points), and the majority (68.1%) presented with multisegmental stenosis. The spinal canal was considerably constricted in DCM patients in all segments compared to HCs. Under physiological conditions in HCs, the cervical spinal cord oscillates in the cranio-caudal and anterior-posterior directions, while right-left motion was marginal [e.g., segment C5 amplitudes: cranio-caudal: 0.40 (0.27-0.48) cm/s; anterior-posterior: 0.18 (0.16-0.29) cm/s; right-left: 0.10 (0.08-0.13) cm/s]. Compared to HCs, DCM patients presented with considerably increased cranio-caudal oscillations due to the cardinal pathophysiologic change in non-stenotic [e.g., segment C5 amplitudes: 0.79 (0.49-1.32) cm/s] and stenotic segments [.g., segment C5 amplitudes: 0.99 (0.69-1.42) cm/s]). In contrast, right-left

INTRODUCTION First-line pain treatment is unsatisfactory in more than 50% of chronic pain patients, likely because of the heterogeneity of mechanisms underlying pain chronification. OBJECTIVES This cross-sectional study aimed to better understand pathomechanisms across different chronic pain cohorts, regardless of their diagnoses, by identifying distinct sensory phenotypes through a cluster analysis. METHODS We recruited 81 chronic pain patients and 63 age-matched and sex-matched healthy controls (HC). Two distinct chronic pain cohorts were recruited, ie, complex regional pain syndrome (N = 20) and low back pain (N = 61). Quantitative sensory testing (QST) was performed in the most painful body area to investigate somatosensory changes related to clinical pain. Furthermore, QST was conducted in a pain-free area to identify remote sensory alterations, indicating more widespread changes in somatosensory processing. RESULTS Two clusters were identified based on the QST measures in the painful area, which did not represent the 2 distinct pain diagnoses but contained patients from both cohorts. Cluster 1 showed increased pain sensitivities in the painful and control area, indicating central sensitization as a potential pathomechanism. Cluster 2 showed a similar sensory profile as HC in both tested areas. Hence, either QST was not sensitive enough and more objective measures are needed to detect sensitization within the nociceptive neuraxis or cluster 2 may not have pain primarily because of sensitization, but other factors such as psychosocial ones are involved. CONCLUSION These findings support the notion of shared pathomechanisms irrespective of the pain diagnosis. Conversely, different mechanisms might contribute to the pain of patients with the same diagnosis.

Modulated autonomic responses to noxious stimulation have been reported in experimental and clinical pain. These effects are likely mediated by nociceptive sensitization, but may also, more simply reflect increased stimulus-associated arousal. To disentangle between sensitization- and arousal-mediated effects on autonomic responses to noxious input, we recorded sympathetic skin responses (SSRs) in response to 10 pinprick and heat stimuli before (PRE) and after (POST) an experimental heat pain model to induce secondary hyperalgesia (EXP) and a control model (CTRL) in 20 healthy females. Pinprick and heat stimuli were individually adapted for pain perception (4/10) across all assessments. Heart rate, heart rate variability, and skin conductance level (SCL) were assessed before, during, and after the experimental heat pain model. Both pinprick- and heat-induced SSRs habituated from PRE to POST in CTRL, but not EXP (P = 0.033). Background SCL (during stimuli application) was heightened in EXP compared with CTRL condition during pinprick and heat stimuli (P = 0.009). Our findings indicate that enhanced SSRs after an experimental pain model are neither fully related to subjective pain, as SSRs dissociated from perceptual responses, nor to nociceptive sensitization, as SSRs were enhanced for both modalities. Our findings can, however, be explained by priming of the autonomic nervous system during the experimental pain model, which makes the autonomic nervous system more susceptible to noxious input. Taken together, autonomic readouts have the potential to objectively assess not only nociceptive sensitization but also priming of the autonomic nervous system, which may be involved in the generation of distinct clinical pain phenotypes.NEW & NOTEWORTHY The facilitation of pain-induced sympathetic skin responses observed after experimentally induced central sensitization is unspecific to the stimulation modality and thereby unlikely solely driven by nociceptive sensitization.

BACKGROUND Allodynia and hyperalgesia are common signs in individuals with complex regional pain syndrome (CRPS), mainly attributed to sensitization of the nociceptive system. Appropriate diagnostic tools for the objective assessment of such hypersensitivities are still lacking, which are essential for the development of mechanism-based treatment strategies. OBJECTIVES This study investigated the use of pain-autonomic readouts to objectively detect sensitization processes in CRPS. METHODS Twenty individuals with chronic CRPS were recruited for the study alongside 16 age- and sex-matched healthy controls (HC). All individuals underwent quantitative sensory testing and neurophysiological assessments. Sympathetic skin responses (SSRs) were recorded in response to 15 pinprick and 15 noxious heat stimuli of the affected (CRPS hand/foot) and a control area (contralateral shoulder/hand). RESULTS Individuals with CRPS showed increased mechanical pain sensitivity and increased SSR amplitudes compared with HC in response to pinprick and heat stimulation of the affected (p < 0.001), but not in the control area (p > 0.05). Habituation of pinprick-induced SSRs was reduced in CRPS compared to HC in both the affected (p = 0.018) and slightly in the control area (p = 0.048). Habituation of heat-induced SSR was reduced in CRPS in the affected (p = 0.008), but not the control area (p = 0.053). CONCLUSIONS This is the first study demonstrating clinical evidence that pain-related autonomic responses may represent objective tools to quantify sensitization processes along the nociceptive neuraxis in CRPS (e.g. widespread hyperexcitability). Pain-autonomic readouts could help scrutinize mechanisms underlying the development and maintenance of chronic pain in CRPS and provide valuable metrics to detect mechanism-based treatment responses in clinical trials. SIGNIFICANCE This study provides clinical evidence that autonomic measures to noxious stimuli can objectively detect sensitization pro

Study design Expert opinion, feedback, revisions, and final consensus. Objectives To update the International Spinal Cord Injury Pain Basic Data Set (ISCIPBDS version 2.0) and incorporate suggestions from the SCI pain clinical and research community with respect to overall utility. Setting International. Methods The ISCIPBDS working group evaluated these suggestions and made modifications. The revised ISCIPBDS (Version 3.0) was then reviewed by members of the International SCI Data Sets Committee, the American Spinal Injury Association (ASIA) Board, the International Spinal Cord Society (ISCoS) Executive and Scientific Committees, individual reviewers and societies, and posted on the ASIA and ISCoS websites for 1 month to elicit comments before final approval by ASIA and ISCoS. Results The ISCIPBDS (Version 3.0) was updated to make the dataset more flexible and useful: 1. The assessment can be based on the patient’s perception of several of his/her “worst” pain(s) or based on the International SCI Pain (ISCIP) Classification-defined or other pain types, depending on the specific research questions or clinical needs. 2. Pain interference should usually be rated for overall pain but may also be used for specific pain problems if needed. 3. An optional pain drawing was added to complement the check box documentation of pain location. 4. Data categories consistent with the Extended Pain Dataset list of current treatments were added. 5. Several new training cases were added., Study design: Expert opinion, feedback, revisions, and final consensus. Objectives: To update the International Spinal Cord Injury Pain Basic Data Set (ISCIPBDS version 2.0) and incorporate suggestions from the SCI pain clinical and research community with respect to overall utility. Setting: International. Methods: The ISCIPBDS working group evaluated these suggestions and made modifications. The revised ISCIPBDS (Version 3.0) was then reviewed by members of the International SCI Data Sets Committee, the American Spinal Injury Association (ASIA) Board, the International Spinal Cord Society (ISCoS) Executive and Scientific Committees, individual reviewers and societies, and posted on the ASIA and ISCoS websites for 1 month to elicit comments before final approval by ASIA and ISCoS. Results: The ISCIPBDS (Version 3.0) was updated to make the dataset more flexible and useful: 1. The assessment can be based on the patient’s perception of several of his/her “worst” pain(s) or based on the International SCI Pain (ISCIP) Classification-defined or other pain types, depending on the specific research questions or clinical needs. 2. Pain interference should usually be rated for overall pain but may also be used for specific pain problems if needed. 3. An optional pain drawing was added to complement the check box documentation of pain location. 4. Data categories consistent with the Extended Pain Dataset list of current treatments were added. 5. Several new training cases were added.