• R J Verdugo, L A Bell, M Campero, F Salvat, B Tripplett, J Sonnad, and J L Ochoa.
• Oregon Nerve Center at Legacy Good Samaritan Medical Center, Departments of Neurology and Neurosurgery, Oregon Health and Science University, Portland, OR 97210, USA.
• Acta Neurol. Scand. 2004 Dec 1; 110 (6): 368-76.

ObjectivesThe aim of this study was to discern the pathophysio-logical bases for neuropathic hyperalgesias.MethodsIn this study, neurological and neurophysiological evaluation of 132 consecutive hyperalgesia patients using rigorous clinical and laboratory protocols were carried out.ResultsTwo discrete semeiologic entities emerged: classic neurological vs atypical, fulfilling taxonomically complex regional pain syndrome (CRPS) II and I, respectively. The classic group (34.9%) exhibited sensorimotor patterns restricted to nerve distribution and documented nerve fiber dysfunction. Among them four (3.03%) had sensitization of C-nociceptors, seven (5.3%) had central release of nociceptive input, and 35 (26.52%) probable ectopic nerve impulse generation. The atypical group (65.1%) displayed weakness with interrupted effort; non-anatomical hypoesthesia and hyperalgesia; hypoesthesia or paresis reversed by placebo, or atypical abnormal movements, and physiological normality of motor and sensory pathways.ConclusionsSpatiotemporal features of neuropathic hyperalgesia constitute key criteria for differential diagnosis between CRPS II and I and, together with other behavioral sensorimotor features, signal psychogenic pseudoneurological dysfunction vs structural neuropathology. 'Neuropathic' hyperalgesias may reflect neuropathological or psychopathological disorders.

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