[Neuropathic pain and neuroplasticity in functional imaging studies]

Abstract

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. However, the cerebral processing of hyperalgesia and allodynia is still controversially discussed. In recent years, neuroimaging methods (functional magnetic resonance imaging, fMRI; magnetoencephalography, MEG; positron emission tomography, PET) have provided new insights into the aberrant cerebral processing of neuropathic pain. The present paper reviews different cerebral mechanisms contributing to chronicity processes in neuropathic pain syndromes. 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.