Der Schmerz
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Neuropathic pain syndromes are characterised by the occurrence of spontaneous ongoing and stimulus-induced pain. Stimulus-induced pain (hyperalgesia and allodynia) may result from sensitisation processes in the peripheral (primary hyperalgesia) or central (secondary hyperalgesia) nervous system. The underlying pathophysiological mechanisms at the nociceptor itself and at spinal synapses have become better understood. ⋯ These mechanisms include reorganisation of cortical somatotopic maps in sensory or motor areas (highly relevant for phantom limb pain and CRPS), increased activity in primary nociceptive areas, recruitment of new cortical areas usually not activated by nociceptive stimuli and aberrant activity in brain areas normally involved in descending inhibitory pain networks. Moreover, there is evidence from PET studies for changes of excitatory and inhibitory transmitter systems. Finally, advanced methods of structural brain imaging (voxel-based morphometry, VBM) show significant structural changes suggesting that chronic pain syndromes may be associated with neurodegeneration.
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Neuroplasticity is the ability of the central nervous system to induce functional and microstructural changes in order to adapt to a new environment. However, so-called maladaptive neuroplasticity can also bring disadvantages, such as reduced inhibition of input signals, one of the suspected causes of chronic pain. With the method of repetitive transcranial magnetic stimulation (rTMS) a technique has been developed that makes it possible to study cortical excitability changes in the human brain non-invasively over a long time. ⋯ In phase II trials its efficacy has been demonstrated. Ongoing studies are focusing on management of the placebo effect; however, it is easier to control this effect in tDCS compared to rTMS. Phase III trials are currently in preparation.
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Functional neuroimaging methods such as positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) provide fascinating insights into the cerebral processing of pain. Neuroimaging studies have shown that no clearly defined "pain centre" exists. ⋯ Sophisticated study designs nowadays permit the characterisation of different components of pain processing. In this review, we summarise neuroimaging studies, which contributed to the characterisation of these different aspects of cerebral pain processing, such as somatosensory (discrimination of different stimulus modalities, noxious vs non-noxious, summation), emotional, cognitive (attention, anticipation, distraction), vegetative (homeostasis) and motor aspects.
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In order to transform a nociceptive stimulus into a painful perception, a highly specialized chain of structural and functional elements is necessary. This system comprises nociceptors in the periphery with specific molecular properties for differential coding of noxious submodalities, ascending and descending tracts that can control the input into the dorsal horn of the spinal cord as well as supraspinal processing that regulates the integration of nociceptive information with other sensory modalities and autonomic function. In this article, structures involved in nociceptive signal processing starting from the periphery up to spinal and cerebral structures are discussed in the order of their spatio-temporal activation sequence - as far as these are known. ⋯ Different input to the dorsal horn of the spinal cord by different nerve fiber populations to superficial and deep layers is explained, ascending tracts as well as descending systems capable of either facilitating or inhibiting the upstream flow of nociceptive information, together with their known transmitters. Finally, thalamic relay nuclei for sensory and nociceptive signals, as well as subcortical and cortical projection targets are discussed. To complete the current view of the nociceptive system, information from molecular biology and anatomic tracing studies as well as data from functional electrophysiologic cell recordings in animals and imaging studies in humans are assembled.
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Nociceptive information processing and related pain perception are subject to substantial pro- and antinociceptive modulation. Research on the involved circuitry and the implemented mechanisms is a major focus of contemporary neuroscientific studies in the field of pain and will provide new insights into the prevention and treatment of chronic pain states. Placebo analgesia is a powerful clinical example of the cognitive modulation of pain perception. ⋯ This cognitively triggered endogenous modulation of pain involves, at least in part, the endogenous opioid system. Most recently, functional magnetic resonance imaging data of the human spinal cord revealed that these mechanisms involve the inhibition of nociceptive processing at the level of the dorsal horn of the spinal cord. Here we discuss recent advances in pain imaging research focusing on cognitively triggered endogenous pain control mechanisms and respective implications for future research strategies.