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Last updated: Sun, Mar 9, 2025
I described earlier the first (sharp and clear) and second (dull and aching) sensations of pain. The two sensations may be separated by an entire second. The separation is explained in part by the different conduction speeds of myelinated and unmyelinated fibers of the sensory neurons and in the new and old ascending tracts. The two sensations are reflected in two separate brain activations that can be captured by EEG or MEG studies.
Painful sensations are detected first in the secondary somatosensory cortex (S2), while non-painful sensations are first detected in the primary somatosensory cortex (S1). Other studies have shown that a brief painful stimulus results in sustained activity in the cortex, which corresponds to sustained perception of pain. While the first pain is associated with activation of the somatosensory cortices, the second pain is more closely associated with activity in the ACC and S2.
A recent fMRI study was able to map the response of brain regions as the pattern of activation changed in response to painful heat stimulation. Parts of the ACC and amygdala activated predictively. The thalamus, basal ganglia, part of the IC, and the supplementary motor area activated next, and were more closely related to the strength of the stimulus. Finally the perception-related part of the IC and parts of the frontal and parietal cortex were activated.
Studies show that pains of different quality activate overlapping sets of brain structures. This may be why we identify all of these types of stimulation as painful.
On the other hand, studies contrasting different types of pain (visceral versus cutaneous) showed that the areas of primary activation within the IC, S1, motor cortex (the area responsible for generating muscle action), and PFC were different for the different pain types. This may point to how we are able to distinguish visceral from cutaneous pain, and why the emotional and motor responses differ for these different types of pain.
Melzack and Wall1 suggest that the brain registers three "psychological dimensions" of pain: sensory-discriminative, motivational-affective, and cognitive-evaluative.
The above descriptions of the ascending pain perception system and the descending pain modulatory system are the merest overviews. What is known about them fills several volumes, and much is still unknown. Many connections have been found, but the roles of many of them are still unknown. Clues have emerged as to the causes of some extremely pernicious conditions, including chronic pain. Much has been learned about the biochemicals that take active roles. Much is left to be known, more is left to be explained, and effective treatments are still lacking. The following describes some of the pain phenomena that are better explained based on knowledge of the brain's role in pain perception. You should keep in mind that the networks that process painful stimulation use the same structures as innocuous sensation, and that the connections between the noxious and innocuous are largely unexplored and unexplained.
Within this section...
"Spinal" Phenomena Also Involve the Brain (Last updated: Sun, Mar 9, 2025)
The Gate-control Circuits (Descending Modulation) (Last updated: Sat, Jul 27, 2024)
Gate Control+ (Last updated: Sun, Mar 9, 2025)
Conditioned Pain Modulation (CPM) or Diffuse Noxious Inhibitory Control (DNIC) (Last updated: Wed, Mar 5, 2025)
Central Pain (Last updated: Sun, Mar 9, 2025)
Phantom Limb Pain and Referred Pain (Last updated: Sun, Mar 9, 2025)
Causalgia (Last updated: Sun, Mar 9, 2025)
Episodic Analgesia (Last updated: Sun, Mar 9, 2025)
Pain Without Injury (Last updated: Sun, Mar 9, 2025)
Disproportionate Pain (This page is incomplete.)
Pain After Healing, a Memory-like Mechanism (This page is incomplete.)
Non-habituation to Pain (Last updated: Sat, Jun 24, 2017)
Affect and Emotion (Last updated: Sun, Mar 9, 2025)
Attention and Priming (Last updated: Sun, Mar 9, 2025)
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Pain Science 4: Partner Systems (Last updated: Fri, Mar 21, 2025)