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Query: UMLS:C0184567 (acute pain)
3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most orofacial pain originates in the oral cavity and the surrounding structures. However, advances in the understanding of pain neurophysiology have shown that convergent afferent nociceptive transmissions from non-trigeminal, extraoral sources can enter the trigeminal system. This may confuse the diagnosis by presenting as (or contributing to) dental, sinus, temporomandibular and other head and neck pains. Incorrect diagnoses may lead to inappropriate and/or invasive procedures, creating further problems. Professor Richard Kroening (former Director of the UCLA Pain Management Center) repeatedly emphasised the maxim that "without correct diagnosis, there can be no prognosis". My own areas of special interest have included acute pain management (anaesthesia and conscious sedation) and chronic orofacial pain. I have seen many dental patients who have been referred to multidisciplinary pain management clinics, often after years of failed treatment attempts. More recent experience as a member of a hospital team evaluating long term ACC patients with many types of persistent pain problems again confirms the premise that accurate diagnosis is critical if management is to be successful.
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PMID:Chronic orofacial pain: a clinical challenge. 1867 28

The evidence that action shapes perception has become widely accepted, for example, in the domain of vision. However, the manner in which action-relevant factors might influence the neural dynamics of acute pain processing has remained underexplored, particularly the functional roles of anterior insula (AI) and midanterior cingulate cortex (mid-ACC), which are frequently implicated in acute pain. To address this, we examined a unique group of heterozygous carriers of the rare R221W mutation on the nerve growth factor (NGF) gene. R221W carriers show a congenitally reduced density of C-nociceptor afferent nerves in the periphery, but can nonetheless distinguish between painful and nonpainful stimulations. Despite this, carriers display a tendency to underreact to acute pain behaviorally, thus exposing a potential functional gap in the pain-action relationship and allowing closer investigation of how the brain integrates pain and action information. Heterozygous R221W carriers and matched controls performed a functional magnetic resonance imaging (fMRI) task designed to dissociate stimulus type (painful or innocuous) from current behavioral relevance (relevant or irrelevant), by instructing participants to either press or refrain from pressing a button during thermal stimulation. Carriers' subjective pain thresholds did not differ from controls', but the carrier group showed decreased task accuracy. Hemodynamic activation in AI covaried with task performance, revealing a functional role in pain-action integration with increased responses for task-relevant painful stimulation ("signal," requiring button-press execution) over task-irrelevant stimulation ("noise," requiring button-press suppression). As predicted, mid-ACC activation was associated with action execution regardless of pain. Functional connectivity between AI and mid-ACC increased as a function of reported urge to withdraw from the stimulus, suggesting a joint role for these regions in motivated action during pain. The carrier group showed greater activation of primary sensorimotor cortices-but not the AI and mid-ACC regions-during pain and action, suggesting compensatory processing. These findings indicate a critical role for the AI-mid-ACC axis in supporting a flexible, adaptive action selection during pain, alongside the accompanying subjective experience of an urge to escape the pain.
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PMID:Mutation Carriers with Reduced C-Afferent Density Reveal Cortical Dynamics of Pain-Action Relationship during Acute Pain. 3236 82