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6. General discussion and Summary studied showed a clear stimulus-response to pinprick stimuli, while in the other part a stimulus-response to pinprick stimuli was completely absent. Both types of responses were found within different clinical entities of neuropathic pain indicating that multiple mechanisms e.g. different causes of neuropathic pain, can lead to the same sensory sign e.g. MPS abnormalities. Thus, distinct patterns of sensitisation to pinprick pain are common within different neuropathic pain aetiologies. The identification of somatosensory phenotypes based on a single QST parameter also contributes to the viability of mechanism-based understanding of neuropathic pain. For this purpose, patients of both types of MPS responses could be further investigated using functional magnetic resonance imaging (fMRI). It has been already shown in human brain imaging studies that chronic pain induces structural changes and changes in brain function in different neural regions (Apkarian et al 2011; DaSilva et al 2008; Geha et al 2008; Gustin et al 2011; Schweinhardt & Bushnell 2010; Tracey 2007; 2008; Tracey & Bushnell 2009; Tracey et al 2002). FMRI studies of different MPS responders aimed to investigate potential group-specific changes in the brain might contribute to a mechanistic understanding of these differences. Pharmacological fMRI studies using different classes of drugs known to be efficacious in neuropathic pain should be utilised in this context. Knowledge of specifics in the efficacy of standard drugs for the different MPS responders could be translated into specific requirements for the pharmacokinetics and pharmacodynamics of novel compounds for clinical evaluation. Drug discovery is a very high-risk endeavour, and the time and costs of developing the compounds, as well as the methodologies to translate the research effort into medicines that better meet the needs of pain patients are challenging. QST phenotypic characterization e.g. MPS response pattern, as a tool for patient selection for enrolment into clinical trials could be used to decrease variance and increase the power to detect meaningful drug effects. In addition, knowledge gained in pharmacological intervention studies of this patient population could also help to determine a mechanism-based therapy for neuropathic pain. Implications of QST in non-neuropathic pain diseases Several studies indicate that sensory testing can be used to identify pathophysiological mechanisms and sensory differences across anatomical boundaries in chronic pain diseases. Kleinbohl and colleagues found that responses to phasic and tonic heat pain not only distinguished chronic pain from healthy controls but also discriminated among types of chronic pain (e.g. headache, back pain) with good sensitivity and specificity (Kleinbohl et al 1999). A study in complex regional pain (CRPS) grouped patients based on the spatial extent of sensory deficits showed that patients with more widespread sensory deficits also exhibit greater mechanical hypersensitivity in the affected limb (Rommel et al 2001). Enhancement in the response to painful stimuli was also reported
6. General discussion and Summary in fibromyalgia (Staud et al 2004), temporomandibular disorders (Sarlani & Greenspan 2003), pelvic pain syndromes (Granot et al 2002) and headache disorders (Bendtsen 2000). Thus, somatosensory abnormalities are not limited to neuropathic pain (Cruccu et al 2004; Cruccu et al 2010). These studies indicate that QST can serve to objectify clinical findings and could be used to improve the selection of treatments. In this context, investigating if somatosensory changes contribute to the presence or absence of pain could be also valuable. In an exploratory QST study we showed that patients with chronic patellar tendinopathies had signs of sensitisation e.g. decreased threshold for mechanical pain and an increased vibration disappearance threshold compared to age- and sports activity-matched pain-free controls (van Wilgen et al 2011; chapter 5). Thus, it was hypothesised that sensitisation might contribute to the presence of pain. Currently, little is known whether, or to what degree, somatosensory changes may contribute to the pain in tendinopathies. The pathophysiology of pain in chronic tendinopathy is largely unknown. The presence of sensitisation observed in this study is contradictive to the result of hypesthesia seen in a previous study (Jensen et al 2008). The differences in these studies could be explained by methodological differences. First, it is not known if sensory changes on the contralateral knee as seen in neuropathic pain also take place in tendinopathies. Therefore, in our study reference values were obtained from matched controls rather than using the contralateral side of patients. This could have contributed to a different outcome in the identification of sensory signs between these studies. Secondly, our study was aimed to identify pain contributing abnormalities in somatosensory function. Thus, we have used age- and sports activitymatched pain-free controls for this investigation. Interestingly, overall impaired sensory function for these sport controls compared to healthy controls of our QST database were found (unpublished results). This result would suggest that high intense sports activity might influence sensory function, even if no pain was reported as by these controls. From this study we conclude that sensitisation may play a role in the explanation of pain during and after sports activity in patella tendinopathy patients. Larger QST studies could provide more evidence to what extent somatosensory changes contribute to the pain in tendinopathies. If such studies confirm the diagnosis sensitisation, treatment and medical management of tendinopathies could be adapted. Normative QST values in clinical research Normative QST data are generated by evaluating sensory function in healthy volunteers, a process that generally takes about 30 minutes in which one body area is assessed using the DFNS QST protocol. Ideally, normative data should be collected from different areas of the body since QST data are region specific (Rolke et al 2006a). Also age- and gender-specific differences were observed for some QST parameter (Rolke et al 2006a).
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Quantitative Sensory Testing (QST)
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Promotores: Prof. dr. M.M.R.F. Stru
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Paranimfen Marten Harbers Aribert B
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Contents 3.3.4. Sensory changes at
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0 Contents Chapter 5 Do patients wi
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Chapter 1 General introduction
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1. General introduction stimuli. C-
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1. General introduction Patients re
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Chapter 2 Bilateral sensory abnorma
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