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What is Pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
International Association for the Study of Pain1
Chronic pain
Pain lasting beyond expected recovery period and identifiable pathology insufficient to explain the pain state Disrupts sleep and normal activities of living Does not serve a protective, adaptive function
Neuropathic pain
Abnormal nociceptive signaling caused by an impairment of the nervous system Serves no functional or adaptive purpose Causes and examples
Visceral pain: originates in internal organs Somatic pain: originates in skin, muscle, skeletal structures
Pain Transduction2
Nociceptor = pain receptor: specialized receptor for detecting tissue injury/damage Two classes of nociceptive afferent fibers
Drawing of A-delta axon
Type Caliber A-delta Small diameter, thinly myelinated Thermal & high-threshold mechanical
Drawing of C axon
C Small diameter, unmyelinated Polymodal: high-intensity mechanical, chemical, heat, cold 0.5-2 More prolonged sensation of dull pain
5-30
Ion channels in nerve terminal open in response to noxious stimuli, initiating an action potential, the pain signal2 Peripheral sensitization: local tissue injury with release of inflammatory mediators can enhance nociceptor response2,3
Pain Transmission
Nociceptors (primary sensory afferents) have cell body in dorsal root ganglia; synapse to second-order neurons in dorsal horn of spinal cord Pain impulses can trigger a withdrawal reflex via connections to motor neurons in the spinal cord3 Impulses ascend to brain via various ascending tracts1,3
Spinothalamic tract > thalamus Spinohypothalamic tract > hypothalamus Spinomesencephalic tract > mesencephalon Spinoreticular tract > reticular formation of brainstem
Pain Perception
Perception of and reaction to pain are influenced by social and environmental cues, as well as by cultural norms and personal experience1
Both cortical and limbic systems are involved in conscious awareness (perception) of pain1
Recognition of location, intensity, and quality of pain is mediated by processing of signals from the spinothalamic tract > thalamus > somatosensory cortex1 Pain information processing in the brainstem, midbrain, and limbic system appear to mediate affective, motivational, and behavioral responses to painful stimuli3
Pain Modulation
Gate control theory advanced by Melzack and Wall in 1965 focused on descending pathways from the brain to the spinal cord that inhibit pain signaling4 Current view: signals originating in the brain can both inhibit and facilitate pain signal transmission3 Neurotransmitters involved in these pathways include
Endogenous opiates (enkephalins, dynorphins, beta-endorphins)2 Serotonin Norepinephrine
References
1. National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: National Pharmaceutical Council; 2001. Carver A. Pain. In: Dale DC, Federman DD, eds. ACP Medicine. New York, NY: WebMD; 2005:1-18. Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150(3699):971-979.
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