VA Title: Research Scientist UM Title: Associate Professor Contact Information Location: 1: Research Service VAMC (151), Room 807, 1201 NW 16th street, Miami FL 33125 2: Miami Project to Cure Paralysis
Lois Pope Life Center (R-48)
(6-34) 1095 NW 14th Terrace
Miami, FL 33136 Office Phone: 305-575-6992 or 305-243-7125 Email: Eva.Widerstrom-Noga@va.gov ewiderstrom-noga @miami.edu Affiliations VA Miami VA Research Service UM Miami Project to Cure Paralysis, Department of Neurological Surgery Department of Rehabilitation Medicine Neuroscience Program Education
Doctor of Dental Surgery 1986, University of Goteborg, Sweden PhD 1993, Physiology, University of Goteborg, Sweden Description of Research Expertise Research Interests: - Chronic pain after neurotrauma - Multidimensional pain assessment - Quantitative sensory testing - Magnetic resonance spectroscopy of the brain Key Words Neuropathic pain, spinal cord injury, pain measurement, psychosocial factors, biomarkers Research description In Brief Chronic pain is one of the most frequently reported reasons for reduced quality of life following SCI. The neuropathic pains experienced after SCI are heterogeneous with differing mechanistic origins that are influenced by genetic background. Despite the growing knowledge base regarding the pathophysiological mechanisms at the spinal, thalamic, and cortical levels involved in causing, exacerbating, and sustaining SCI-related neuropathic pain, current treatments are generally unsuccessful. Extensive basic research suggests that a multitude of pathophysiological mechanisms either alone, or in combination, may cause specific patterns of sensory signs and symptoms such as burning pain, thermal or mechanical hyperalgesia. Unfortunately, the translation of basic research findings regarding neuropathic pain mechanisms to clinical settings has been hampered because conclusive studies regarding their clinical presentation are lacking. Due to the complexity of numerous interrelated genetic, cellular, and molecular origins of neuropathic pain, clinical pain assessment needs to incorporate multiple dimensions of the pain phenotype to guide identification of underlying mechanisms and to develop assessment tools that can predict the likelihood of response to treatment. My main areas of interest are: 1. Evaluation of sensory dysfunction: Sensory dysfunction following SCI is clinically manifested as both spontaneous and evoked sensations. These abnormalities can, for example, be quantitative, such as threshold changes, i.e., hypo- or hyperesthesia or qualitative, such as allodynia, dysesthesia or paresthesia. However, spontaneous neuropathic pain, evoked pain and motor excitability may share common mechanisms, such as neuronal hyperexcitability due to loss of input to certain populations of neurons or lack of inhibition. In order to better elucidate such mechanisms, we perform quantitative sensory testing (QST) in the evaluation of these pain conditions. 2. Evaluation of psychosocial impact: The refractory nature of the painful conditions following SCI suggests that personal characteristics related to adaptation and coping skills are critical determinants for quality of life. Despite seemingly similar pain conditions, clinical observation suggests that there is wide variability in how people respond to treatment interventions and adapt to SCI-related pain. For this purpose, we are developing and psychometrically testing various methods for the evaluation of the psychosocial impact of pain. 3. Determining cortical pain-generating mechanisms: Neuroimaging studies strongly suggest that pain perception is dependent on a network of sensory cortical areas (primary and secondary somatosensory cortices, insular cortex), limbic areas (anterior cingulate), associative cortex (prefrontal cortex) and subcortical structures, such as the thalamus. Dysfunction in these networks may underlie the generation and maintenance of chronic pain and associated conditions. The extent to which these basic mechanisms translate into clinical signs and symptoms in people with chronic neuropathic pain associated with SCI is largely unknown. In my lab, we are conducting imaging studies to assess neuronal function in the thalamus and areas of the cingulate cortex in individuals with neuropathic pain and SCI. Representative Publication: (5 max) Widerström-Noga EG, Cruz-Almeida Y, Martinez-Arizala A, Turk DC. Internal consistency, stability, and validity of the spinal cord injury version of the multidimensional pain inventory. Arch Phys Med Rehabil 2006;87:516-23. Widerström-Noga E, Biering-Sørensen F, Bryce T, Cardenas DD, Finnerup NB, Jensen MP, Richards JS. The international spinal cord injury pain basic dataset. Spinal Cord. 2008;46:818-23. Felix ER, Widerström-Noga E. Reliability and Validity of Quantitative Sensory Testing in Persons with Spinal Cord Injury and Chronic Neuropathic Pain. In press. Journal of Rehabilitation Research and Development. 2009;46(1):69-84. Cruz-Almeida Y, Felix ER, Martinez-Arizala A, Widerström-Noga EG. Pain Symptom Profiles in Persons with Spinal Cord Injury. Pain Medicine. 2009; 10:1246-59. Widerström-Noga EG, Cruz-Almeida Y, Felix ER, Adcock JP. Relationship between pain characteristics and pain adaptation type in persons with SCI. Journal of Rehabilitation Research and Development. 2009;46(1):1-12. |
