Many studies have focused on defining the network of brain structures involved in normal physiological pain. The different dimensions of pain perception (i.e., sensory discriminative, affective/emotional, cognitive/evaluative) have been shown to depend on different areas of the brain. In contrast, much less is known about the neural basis of pathological chronic pain. In particular, it is unclear whether such pain results from changes to the physiological "pain matrix". We review here studies on changes in brain activity associated with neuropathic pain syndromes-a specific category of chronic pain associated with peripheral or central neurological lesions. Patients may report combinations of spontaneous pain and allodynia/hyperalgesia-abnormal pain evoked by stimuli that normally induce no/little sensation of pain. Modern neuroimaging methods (positron emission tomography (PET) and functional MRI (fMRI)) have been used to determine whether different neuropathic pain symptoms involve similar brain structures and whether these structures are related to the physiological "pain matrix". PET studies have suggested that spontaneous neuropathic pain is associated principally with changes in thalamic activity and the medial pain system, which is preferentially involved in the emotional dimension of pain. Both PET and fMRI have been used to investigate the basis of allodynia. The results obtained have been very variable, probably reflecting the heterogeneity of patients in terms of etiology, lesion topography, symptoms and stimulation procedures. Overall, these studies indicated that acute physiological pain and neuropathic pain have distinct although overlapping brain activation pattern, but that there is no unique "pain matrix" or "allodynia network".