Neuropathic Pain Syndrome Displayed by Malingerers

The Oregon Nerve Center, Good Samaritan Medical Center, 1040 NW 22nd Ave., Suite 600, Portland, OR 97210, USA.
The Journal of Neuropsychiatry and Clinical Neurosciences (Impact Factor: 2.82). 07/2010; 22(3):278-86. DOI: 10.1176/appi.neuropsych.22.3.278
Source: PubMed


Among 237 patients communicating chronic pain, associated with sensory-motor and "autonomic" displays, qualifying taxonomically for neuropathic pain, there were 16 shown through surveillance to be malingerers. When analyzed through neurological methods, their profile was characteristically atypical. There were no objective equivalents of peripheral or central processes impairing nerve impulse transmission. In absence of medical explanation, all 16 had been adjudicated, by default, the label complex regional pain syndrome (CRPS). The authors emphasize that CRPS patients may not only harbor unrecognized pathology ("lesion") of the nervous system (CRPS II), hypothetical central neuronal "dysfunction" (CRPS I), or conversion disorder, but may display a recognizable simulated illness without neuropsychiatric pathology.

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    • "Besides, the enhanced autonomic sympathetic activity was found facilitating nociceptive fibers to develop CRPS, but no direct evidence of activation of nociceptors related to sympathetic discharge was found [4]. Therefore, central nerve system (CNS) was concentrated on for its involvement in the pathogenesis of CRPS, especially when nerve injury existed [2,5]. In general, pain signal produced from the distal area due to various reasons needs to be transmitted along afferent fibers to dorsal root ganglia (DRG), the first relay station for pain signaling into the CNS. "
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    ABSTRACT: Abstract DRG is of importance in relaying painful stimulation to the higher pain centers and therefore could be a crucial target for early intervention aimed at suppressing primary afferent stimulation. Complex regional pain syndrome (CRPS) is a common pain condition with an unknown etiology. Recently added new information enriches our understanding of CRPS pathophysiology. Researches on genetics, biogenic amines, neurotransmitters, and mechanisms of pain modulation, central sensitization, and autonomic functions in CRPS revealed various abnormalities indicating that multiple factors and mechanisms are involved in the pathogenesis of CRPS. Epigenetics refers to mitotically and meiotically heritable changes in gene expression that do not affect the DNA sequence. As epigenetic modifications potentially play an important role in inflammatory cytokine metabolism, neurotransmitter responsiveness, and analgesic sensitivity, they are likely key factors in the development of chronic pain. In this dyad review series, we systematically examine the nerve injury-related changes in the neurological system and their contribution to CRPS. In this part, we first reviewed and summarized the role of neural sensitization in DRG neurons in performing function in the context of pain processing. Particular emphasis is placed on the cellular and molecular changes after nerve injury as well as different models of inflammatory and neuropathic pain. These were considered as the potential molecular bases that underlie nerve injury-associated pathogenesis of CRPS.
    Full-text · Article · Jun 2014 · Medical science monitor: international medical journal of experimental and clinical research
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    • "Personal injury insurers require a means to assess the physical and psychological status of their insured, as occurrences of unconscious symptom exaggeration (Dersh, Polatin, Leeman and Gatchel, 2004; Howard, Kishino, Johnston, Worzer and Gatchel, 2010), frank malingering (Greve, Ord, Bianchini and Curtis, 2007; Ochoa and Verdugo, 2010), and over-provision of services (Eisendrath, Rand and Feldman, 1996; Green 2011) exist in personal injury cases. Without independent medical examinations (IMEs), insurers' costs would escalate to a level that would potentially make the provision of coverage unrealistic. "
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    Full-text · Article · Jun 2014 · Psychological Injury and Law
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