Whereas studies of somatotopic representation of touch have been useful to distinguish multiple somatosensory areas within primary (SI) and secondary (SII) somatosensory cortex regions, no such analysis exists for the representation of pain across nociceptive modalities. Here we investigated somatotopy in the operculo-insular cortex with noxious heat and pinprick stimuli in 11 healthy subjects using high-resolution (2 × 2 × 4 mm) 3T functional magnetic resonance imaging (fMRI). Heat stimuli (delivered using a laser) and pinprick stimuli (delivered using a punctate probe) were directed to the dorsum of the right hand and foot in a balanced design. Locations of the peak fMRI responses were compared between stimulation sites (hand vs. foot) and modalities (heat vs. pinprick) within four bilateral regions of interest: anterior and posterior insula and frontal and parietal operculum. Importantly, all analyses were performed on individual, non-normalized fMRI images. For heat stimuli, we found hand-foot somatotopy in the contralateral anterior and posterior insula [hand, 9 ± 10 (SD) mm anterior to foot, P < 0.05] and in the contralateral parietal operculum (SII; hand, 7 ± 10 mm lateral to foot, P < 0.05). For pinprick stimuli, we also found somatotopy in the contralateral posterior insula (hand, 9 ± 10 mm anterior to foot, P < 0.05). Furthermore, the response to heat stimulation of the hand was 11 ± 12 mm anterior to the response to pinprick stimulation of the hand in the contralateral (left) anterior insula (P < 0.05). These results indicate the existence of multiple somatotopic representations for pain within the operculo-insular region in humans, possibly reflecting its importance as a sensory-integration site that directs emotional responses and behavior appropriately depending on the body site being injured.
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http://dx.doi.org/10.1152/jn.00253.2010 | DOI Listing |
Brain
January 2025
Institute of Neurological Sciences and Psychiatry, Hacettepe University, 06100, Ankara, Turkey.
Cortical spreading depolarization (CSD), the neurophysiological event believed to underlie aura, may trigger migraine headaches through inflammatory signaling that originates in neurons and spreads to the meninges via astrocytes. Increasing evidence from studies on rodents and migraine patients supports this hypothesis. The transition from pro-inflammatory to anti-inflammatory mechanisms is crucial for resolving inflammation.
View Article and Find Full Text PDFEur J Pain
January 2025
Institute of Neuroscience (IoNS), UCLouvain, Brussels, Belgium.
Background: Identifying the subset of patients at risk for developing persistent pain after surgery is clinically important as they could benefit from targeted prevention measures. In this prospective study, we investigated if the preoperative assessment of the individual susceptibility to developing experimentally induced secondary hyperalgesia is associated with post-thoracotomy pain at 2 months.
Methods: Forty-one patients scheduled to undergo a posterolateral thoracotomy were recruited before surgery and followed prospectively for 2 months.
Int Rev Neurobiol
November 2024
Department of Human Neuroscience, Sapienza University, Rome, Italy. Electronic address:
Timely and accurate diagnosis of neuropathic pain is critical for optimizing therapeutic outcomes and minimizing treatment delays. According to current standards, the diagnosis of definite neuropathic pain requires objective confirmation of a lesion or disease affecting the somatosensory nervous system. This can be provided by specialized neurophysiological techniques as conventional methods like nerve conduction studies and somatosensory evoked potentials may not be sufficient as they do not assess pain pathways.
View Article and Find Full Text PDFEur J Pain
March 2025
Institute of Neuroscience, Université Catholique de Louvain, Brussels, Belgium.
Eur J Pain
March 2025
Department of Clinical Medicine, Danish Pain Research Center, Aarhus University, Aarhus, Denmark.
Background: Neuropathic pain is pain due to a disease or lesion of the somatosensory system, and can be either spontaneous, evoked or both. Hyperpathia is a type of evoked pain defined by IASP as 'a painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold'. The literature is sparse, and definitions are unclear and inconsistent.
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