Quantitative Sensory Testing (QST) - Does assessing ... - TI Pharma

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1. General introduction ongoing pain, hyperalgesia and / or allodynia which are frequently reported by patients with neuropathic pain. Primary afferent fibres (Aβ-, Aδ-, and C-fibres) transmit impulses fromthe periphery, through the the dorsal dorsal root ganglion root ganglion (DRG) and (DRG) into the and dorsal into horn the dorsal of the spinal horn cord. of the Nociceptive spinal specific cord. Nociceptive (NS) cells are specific mainly found (NS) in the cells superficial are mainly dorsal horn found (laminae in the I–II), superficial whereas most dorsal wide dynamic horn ranges (laminae (WDRs) I–II), are whereas located deeper most (lamina wide dynamic V). Projection ranges neurones (WDRs) from are lamina located I innervate deeper areas (lamina such as the V). parabrachial Projection area neurones (PB) and periaqueductal from lamina grey I innervate (PAG) and areas such pathways such as the are parabrachial affected by limbic area areas. (PB) and From periaqueductal here descending grey pathways (PAG) (yellow and arrows) such pathways from brainstem are affected nuclei such by as limbic the rostral areas. ventromedial From here medulla descending (RVM) are pathways activated (yellow and modulate arrows) spinal from processing. brainstem Lamina nuclei V neurones such as mainly the rostral project to ventromedial the thalamus (spinothalamic medulla (RVM) tract), Figure 1-2: Pain pathways from periphery are and activated from here the and various modulate cortical spinal regions processing. forming the to brain Lamina ‘pain matrix’ V neurones (primary and mainly secondary project somatosensory, to the thalamus insular, anterior (spinothalamic cingulate, and prefrontal tract), and cortices) from are here activated. the various cortical regions forming the ‘pain From: matrix’ D’Mello R., (primary Dickenson and A. secondary H., Br. J. Anaesth. somatosensory, 2008;101:8-16 insular, (with permission). anterior cingulate, and prefrontal cortices) are activated. 1.1. Neuropathic pain The International Association for the Study of Pain (IASP) defined pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Most pain resolves quickly but sometimes pain becomes chronic despite removal of the stimulus and apparent healing of the body. Chronic pain is defined as pain lasting more than three months (Woolf & Mannion 1999). A specific subclass of chronic pain is neuropathic pain. The IASP defined neuropathic pain as a direct consequence of a lesion or disease affecting the somatosensory system (Treede et al 2008). The prevalence of neuropathic pain is estimated to be as much as 7–8% of the general population in Europe (Bouhassira et al 2008; Torrance et al 2006). Clinical entities of neuropathic pain include diabetic polyneuropathies, postherpetic neuralgia, trigeminal neuralgia, central post stroke pain and spinal cord injury pain. But also traumatic / postsurgical neuropathies and painful radiculopathies represent common conditions (Torrance et al 2006).
1. General introduction Patients report that their neuropathic pain symptoms often have a burning, lancinating, or shooting quality with unusual tingling, crawling, or electrical sensations (Bennett et al 2007), which can be persistent or paroxysmal pain that is independent of a stimulus (Woolf & Mannion 1999). Patients with neuropathic pain may also experience evoked pain (i.e., stimulus-induced pain and hypersensitivity), mostly reported as mechanical and/or thermal hypersensitivity. Table 1-1 shows a summary of terms to describe symptoms and sensory signs commonly seen in neuropathic pain patients. Neuropathic pain can be very disabling, severe and intractable for patients. The understanding of the underlying neurobiological processes in neuropathic pain is still evolving (Haanpaa et al 2009). The Joint Commission on Accreditation of Healthcare Organizations, USA, acknowledged the lack of understanding in the field of pain and declared the ten-years beginning 2001 as the “Decade of Pain Control and Research”. Since the beginning of the new millennium pain is also regarded as the fifth vital sign. Table 1-1: Common symptoms and signs in neuropathic pain TERMS DEFINI<strong>TI</strong>ON Symptoms Paresthesias Non-painful positive sensations (“ant-crawling”, “tingling”) Burning pain Frequent quality of spontaneous pain sensations Shooting pain Spontaneous or evoked intense pain sensations of several Signs seconds duration Hypesthesia Impaired sensitivity to a stimulus Tactile hypesthesia Impaired sensitivity to tactile stimuli Cold hypesthesia Impaired sensitivity to cold Hypoalgesia Impaired sensitivity to a normally painful stimulus Hyperalgesia Increased pain sensitivity (may include a decrease in threshold and an increase in suprathreshold response) Punctate hyperalgesia Hyperalgesia to punctuate stimuli such as pinprick Static hyperalgesia Hyperalgesia to blunt pressure Heat hyperalgesia Hyperalgesia to heat stimuli Cold hyperalgesia Hyperalgesia to cold stimuli Allodynia Pain due to a non-nociceptive tactile stimulus Adapted from Haanpää, M.L. et al., 2009; Am J Med , 2009; 122:S13-21
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References Abate M, Silbernagel KG,
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de la Llave-Rincon AI, Fernandez-de
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Kehlet H, Jensen TS, Woolf CJ. 2006
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Robinson JM, Cook JL, Purdam C, Vis
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Visentini PJ, Khan KM, Cook JL, Kis
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Nederlandse samenvatting Met de ont
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Acknowledgement To produce a work s
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