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Related Concept Videos

Somatosensation01:33

Somatosensation

The somatosensory system relays sensory information from the skin, mucous membranes, limbs, and joints. Somatosensation is more familiarly known as the sense of touch. A typical somatosensory pathway includes three types of long neurons: primary, secondary, and tertiary. Primary neurons have cell bodies located near the spinal cord in groups of neurons called dorsal root ganglia. The sensory neurons of ganglia innervate designated areas of skin called dermatomes.

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Assessment of Knee Hyperalgesia in Mice using Pressure Application Measurement
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Cortical processing of mechanical hyperalgesia: a MEG study.

Christian Maihöfner1, Florian Jesberger, Frank Seifert

  • 1Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany. christian.maihoefner@uk-erlangen.de

European Journal of Pain (London, England)
|April 7, 2009
PubMed
Summary
This summary is machine-generated.

Secondary mechanical hyperalgesia involves brain processing. The secondary somatosensory cortex (S2) shows increased activation correlated with pain intensity, suggesting its role in processing this type of pain.

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Determining heat and mechanical pain threshold in inflamed skin of human subjects
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Last Updated: Jun 24, 2026

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Determining heat and mechanical pain threshold in inflamed skin of human subjects
13:21

Determining heat and mechanical pain threshold in inflamed skin of human subjects

Published on: January 14, 2009

Area of Science:

  • Neuroscience
  • Pain Research
  • Somatosensory Processing

Background:

  • Mechanical hyperalgesia, characterized by heightened pain sensitivity, can arise from tissue inflammation or nerve injury.
  • Peripheral sensitization causes primary hyperalgesia at the injury site, while central sensitization leads to secondary hyperalgesia in surrounding areas.
  • The cerebral processing of secondary mechanical hyperalgesia, particularly involving the somatosensory cortices (S1, S2) and posterior parietal cortex (PPC), requires further investigation.

Purpose of the Study:

  • To investigate the cortical processing of secondary mechanical hyperalgesia using magnetoencephalography (MEG).
  • To elucidate the response patterns of S1, S2, and PPC during secondary mechanical hyperalgesia.

Main Methods:

  • Induced secondary mechanical hyperalgesia in 12 healthy subjects via repetitive electrical stimulation of mechanoinsensitive c-nociceptors.
  • Applied pin-prick stimuli inside and outside the hyperalgesic area.
  • Quantified cortical activations using MEG to detect and analyze responses in S1, S2, and PPC.

Main Results:

  • Identified sequential activation of contralateral S1, PPC, and S2, along with ipsilateral S2 activation, during both hyperalgesia and normal pain.
  • Observed significantly higher activation in contralateral PPC and bilateral S2 during hyperalgesia compared to normal pain; S1 showed no significant difference.
  • Found a significant correlation between increased magnetic field strength in bilateral S2 and higher pain ratings during hyperalgesia.

Conclusions:

  • The secondary somatosensory cortex (S2) appears to be involved in processing secondary mechanical hyperalgesia in the human brain.
  • Posterior parietal cortex (PPC) activation may be associated with increased attentional processing during mechanical hyperalgesia.