• Elena Enax-Krumova, Nadine Attal, Didier Bouhassira, Rainer Freynhagen, Janne Gierthmühlen, Per Hansson, Bianca M Kuehler, Christoph Maier, Juliane Sachau, Märta Segerdahl, Thomas Tölle, Rolf-Detlef Treede, Lise Ventzel, Ralf Baron, and Jan Vollert.
• From the Department of Neurology (E.E.-K.), BG University Hospital Bergmannsheil GmbH, Ruhr-University Bochum, Germany; INSERM U-987 (N.A., D.B.), Centre D'Evaluation et de Traitement de La Douleur, CHU Ambroise Paré, Boulogne-Billancourt; Université Versailles-Saint-Quentin (N.A., D.B.), Versailles, France; Department of Anaesthesiology (R.F.), Critical Care Medicine, Pain Therapy & Palliative Care, Pain Center Lake Starnberg, Benedictus Hospital Feldafing; Department of Anaesthesiology (R.F.), Klinikum rechts der Isar, Technische Universität München, Munich; Division of Neurological Pain Research and Therapy (J.G., J.S., R.B.), Department of Neurology, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Germany; Department of Pain Management and Research (P.H.), Norwegian National Advisory Unit on Neuropathic Pain, Division of Emergencies and Critical Care, Oslo University Hospital, Norway; Department of Molecular Medicine and Surgery (P.H.), Karolinska Institutet, Stockholm, Sweden; Pain Medicine (B.K., J.V.), Chelsea and Westminster Hospital NHS Foundation Trust; Pain Research (B.K.), Department Surgery and Cancer, Faculty of Medicine, Imperial College, Chelsea and Westminster Campus, London, UK; University Hospital of Pediatrics and Adolescent Medicine (C.M.), Ruhr-University Bochum, Germany; MS Medical Consulting (M.S.); Karolinska Institute (M.S.), Department of Physiology and Pharmacology, Stockholm, Sweden; Department of Neurology (T.T.), Klinikum rechts der Isar, Technische Universität München, Munich; Department of Neurophysiology (R.-D.T., J.V.), Mannheim Center for Translational Neuroscience MCTN, Medical Faculty Mannheim, Heidelberg University, Germany; Danish Pain Research Center (L.V.), Department of Clinical Medicine, and Department of Oncology (L.V.), Aarhus University Hospital, Denmark. Elena.Krumova@rub.de.
• Neurology. 2021 Jul 27; 97 (4): e389-e402.

ObjectiveTo test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms.MethodsWe analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area.ResultsAmong 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function.ConclusionMechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.© 2021 American Academy of Neurology.

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