EN
Pain has been interpreted as a specific sensation in response to potentially or actually noxious agents. Actually, this classical view is supplemented by a distinction between nociception, i.e. the ability to sense noxious stimuli, and emotional appreciation of nociceptive experience. Nociceptive information is targeted mainly to the sensorimotor cortex and the insula, whereas the emotional evaluation occurs in the anterior cingulate cortex. The intensity of pain perception is often disproportional to the nociceptive input. This phenomenon has fundamental adaptive value, whenever sensing more or less pain in some vital situations is important for organism’s survival. Intense or prolonged noxious stimulation causes sensitization of peripheral nociceptors and/or pain centers, leading to hyperalgesia, i.e. sensing more pain to mild noxious stimuli, or to allodynia, as innocuous stimuli become painful. The sensitization involves an activity-driven molecular process, based on heterosynaptic non-Hebbian facilitation. This condition usually subsides along with the progression of the healing process, or transforms into chronic pain. Neuroimaging studies in patients suffering from chronic pain revealed activation of the medial prefrontal cortex and amygdala. Chronic pain, when prolonged, exerts a deleterious action. Repetitive co-occurrence of pain epizodes and incidental environmental cues leads to pathological Pavlovian conditioning of pain. This maladaptive plastic process involves activation of glutamatergic synapses and is based on a Hebbian LTP-like learning mainly in the cingulate and in dorsolateral prefrontal cortex.Apoorly understood problem of the pain story isthe central pain without obvious tissue damage, following brain stroke or other central lesions. Its background may by an imbalance between glutamate and GABA-ergic neurotransmission in thalamocortical pain circuits, or a lack of inhibition from peripheral cold receptors on pain-processing brain areas.