Brain mechanisms of social touch-induced analgesia in females Can self-reported pain characteristics and bedside test be used for the assessment of pain mechanisms? An analysis of results of May - Volume - Supplement 1. Published May Other Supplements.
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What’s Causing Your Abdominal Pain and How to Treat It
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Please try after some time. Wheeler, Claire H. In Brief. In Brief: Spinal lamina X neurons integrate direct and indirect inputs from several types of thin primary afferent fibers, thus playing an important role in nociception.
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In Brief: Self-reported symptoms show only little or moderate association with findings on quantitative sensory testing. Both methods should be used complementary for pain assessment and optimizing treatment. Banerjee, Geetanjoli; Edelman, E. Jennifer; Barry, Declan T. Pain After Surgery presents the current knowledge and expertise of top global researchers on changes in central nervous system function accompanying and following surgery, as a model of chronic pain development.
In this unique title, international experts focus on unexpected pain as a consequence of indicated medical or surgical treatment. Acute pain is frequently associated with anxiety and hyperactivity of the sympathetic nervous system eg, tachycardia, increased respiratory rate and BP, diaphoresis, dilated pupils.
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Chronic pain does not involve sympathetic hyperactivity but may be associated with vegetative signs eg, fatigue, loss of libido, loss of appetite and depressed mood. People vary considerably in their tolerance for pain. Acute pain , which usually occurs in response to tissue injury, results from activation of peripheral pain receptors and their specific A delta and C sensory nerve fibers nociceptors.
Chronic pain related to ongoing tissue injury is presumably caused by persistent activation of these fibers.
Overview of Pain
However, the severity of tissue injury does not always predict the severity of chronic or acute pain. Chronic pain may also result from ongoing damage to or dysfunction of the peripheral or central nervous system which causes neuropathic pain. Nociceptive pain may be somatic or visceral. Somatic pain receptors are located in skin, subcutaneous tissues, fascia, other connective tissues, periosteum, endosteum, and joint capsules.
Stimulation of these receptors usually produces sharp or dull localized pain, but burning is not uncommon if the skin or subcutaneous tissues are involved. Visceral pain receptors are located in most viscera and the surrounding connective tissue. Visceral pain due to obstruction of a hollow organ is poorly localized, deep, and cramping and may be referred to remote cutaneous sites.
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Visceral pain due to injury of organ capsules or other deep connective tissues may be more localized and sharp. Psychologic factors modulate pain intensity to a highly variable degree.
Thoughts and emotions have an important role in the perception of pain. Many patients who have chronic pain also have psychologic distress, especially depression and anxiety. Because certain syndromes characterized as psychiatric disorders eg, some somatic symptom disorders are defined by self-reported pain, patients with poorly explained pain are often mischaracterized as having a psychiatric disorder and are thus deprived of appropriate care.
Pain impairs multiple cognitive domains including attention, memory, concentration, and content of thought, possibly by demanding cognitive resources. Many pain syndromes are multifactorial. For example, chronic low back pain and most cancer pain syndromes have a prominent nociceptive component but may also involve neuropathic pain due to nerve damage. Pain fibers enter the spinal cord at the dorsal root ganglia and synapse in the dorsal horn. From there, fibers cross to the other side and travel up the lateral columns to the thalamus and then to the cerebral cortex.
Repetitive stimulation eg, from a prolonged painful condition can sensitize neurons in the dorsal horn of the spinal cord so that a lesser peripheral stimulus causes pain wind-up phenomenon. Peripheral nerves and nerves at other levels of the CNS may also be sensitized, producing long-term synaptic changes in cortical receptive fields remodeling that maintain exaggerated pain perception.
This process of chronic afferent input causing increased sensitivity lower thresholds and remodeling of central nociceptive pathways and receptors is termed central sensitization. It explains why the following occur:. Substances released when tissue is injured, including those involved in the inflammatory cascade, can sensitize peripheral nociceptors.