Secondary hyperalgesia i CNS? Dependent on central sensitization + convergence. = Decreased threshold for sensitization --> projection neurons more ready

Empirical evidence supports increased sensitivity to experimental pain in can be conceptualized as a latent hyperalgesia secondary to long-term opioid exposure. Both hyperalgesia and opioid tolerance involve neuroplastic changes Amitriptyline potentiates morphine analgesia by a direct action on the central

For example, through a process of central sensitization, the firing of dorsal horn nociceptors can change dramatically in the setting of injury (produced by either tissue or nerve damage). Secondary are hyperalgesias occurring outside such an area. (2) According to another definition, a hyperalgesia is primary when the reason is sensitization of nociceptors and secondary when it is due to alterations of central synaptic transmission. When central sensitization and referred pain co-occur, secondary hyperalgesia may take a different form: silent nociceptors can mediate new regions of cutaneous or deep muscle hypersensitivity (64 These early QST studies typically noted the same findings of secondary hyperalgesia or allodynia seen in animal models of central sensitization, and this was used to infer that these same underlying processes may be playing a role in humans with these chronic pain conditions. Lack of secondary hyperalgesia and central sensitization in an acute sheep model. Mather LE(1), Cousins MJ, Huang YF, Pryor ME, Barratt SM. Author information: (1)Department of Anaesthesia and Pain Management, University of Sydney at Royal North Shore Hospital, St Leonards, NSW, Australia. lmather@med.usyd.edu.au Secondary hyperalgesia is due to central neuron sensitization and requires continuous nociceptor input from the zone of primary hyperalgesia for its maintenance.

Secondary hyperalgesia central sensitization

Peripheral sensitization is an increased sensitivity to an afferent nerve stimuli. This occurs after there has been an injury or cell damage to the area, and produces a flare response due to nociceptors producing lots of neuropeptides. Background and Objectives We aimed to determine the following in an experimental acute pain model in sheep: (1) whether multimodal analgesia with intravenous fentanyl and ketorolac was more effective than fentanyl alone; (2) whether secondary hyperalgesia (central sensitization) occurred in adjacent (foreleg) dermatomes after thoracic surgery; (3) whether ketorolac used preemptively influenced (TKA) feel postoperative hyperalgesia in the second operated knee compared with the first knee. Ketamine is an important drug for central temporal summation and inhibition of secondary mechanical hyperalgesia. This study investigated whether central sensitization has a significant effect on hyperalgesia after consecutive operations. that the development of secondary hyperalgesia to punc-tate mechanical stimuli following a standardised injury is caused by central changes in response to a conditioning stimulus and transmitted by A-delta fibers [1, 9–11].

“allodynia“ and “pin prick“. Thermal hyperalgesia does not occur in the secondary zone.

secondary hyperalgesia rather than central sensitization. 3. History taking in order to recognize central sensitization. Simply listening to the story of the patient

Some researchers speculate central sensitization to be the explanatory 2016-05-11 Fingerprint Dive into the research topics of 'Secondary hyperalgesia to punctate mechanical stimuli. Central sensitization to A-fibre nociceptor input'. Together they form a unique fingerprint.

1999-07-06

Secondary hyperalgesia central sensitization

Because central sensitization is considered to … that the development of secondary hyperalgesia to punc-tate mechanical stimuli following a standardised injury is caused by central changes in response to a conditioning stimulus and transmitted by A-delta fibers [1, 9–11].

The focus of spatial attention during the induction of central sensitization can modulate the subsequent development of secondary hyperalgesia. 572.0KB. Public.
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Secondary hyperalgesia is inducible in most individuals and is attributed to central neuronal sensitization. Some individuals develop large areas of secondary hyperalgesia (high-sensitization responders), while others develop small areas (low-sensitization responders). HFS‐induced hyperalgesia is suitable to discriminate or compare individuals but it may not be sensitive to changes due to an intervention.

This study formally establishes the reliability of secondary hyperalgesia induced by electrical high‐frequency stimulation. Discussion: The area of secondary hyperalgesia may serve as a quantitative measure of the central sensitization induced by cutaneous heat stimulation, and thus may be a biomarker of an individual’s pain sensitivity.
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Analgesia · Analgesics · Hyperalgesia · Pain Insensitivity, Congenital congenital absence of pain = PAIN SENSITIVITY, CONGENITAL; differentiate from PAIN

Human experimental and clinical pain models [8, 9] can be used to study central sensitization. One feature of central sensitization is secondary hyperalgesia, where sensory stimulation of normal tissue adjacent to an in-jury is perceived as painful. Secondary Secondary hyperalgesia is indicative of central sensitization.

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Primary hyperalgesia refers to pain sensitivity at the site of an injury, while secondary hyperalgesia refers to enhanced sensation in surrounding undamaged tissues, sometimes in remote sites distant from the injury.

572.0KB. Public. 0 … Woolf 2011 Central sensitization. scott Coulson. Download PDF. Download Full PDF Package.

Secondary hyperalgesia, or central sensitization, involves spinal neuroplasticity and facilitation of supraspinal noxious transmission. The stimulus response

Some individuals develop large areas of secondary hyperalgesia Secondary hyperalgesia to punctate mechanical stimuli. Central sensitization to A-fibre nociceptor input. Brain 1999; 122: 2245 –2257.

Secondary hyperalgesia shares clinical characteristics with neurogenic hyperalgesia in patients with neuropathic pain. Abnormal brain responses to somatosensory stimuli have been found in patients with hyperalgesia as well as in normal subjects during experimental central sensitization. The aim of this study was to assess the effects of input (viscero-somatic sensitization) (2,30). Especially increased sensitivity at asymptomatic remote areas, referred to as secondary hyperalgesia, rather than pri-mary hyperalgesia (at asymptomatic places), is sugges-tive for CS (31). In addition, CS entails much more than generalized hypersensitivity to pain: It is characterized Background and Objectives We aimed to determine the following in an experimental acute pain model in sheep: (1) whether multimodal analgesia with intravenous fentanyl and ketorolac was more effective than fentanyl alone; (2) whether secondary hyperalgesia (central sensitization) occurred in adjacent (foreleg) dermatomes after thoracic surgery; (3) whether ketorolac used preemptively influenced The focus of spatial attention during the induction of central sensitization can modulate the subsequent development of secondary hyperalgesia. 572.0KB.