Supraspinal nociceptive networks in neuropathic pain after spinal cord injury

• Published in: Human brain mapping Vol. 42; no. 12; pp. 3733 - 3749
• Main Authors: Huynh, Vincent, Lütolf, Robin, Rosner, Jan, Luechinger, Roger, Curt, Armin, Kollias, Spyridon, Hubli, Michèle, Michels, Lars
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 15.08.2021
• Subjects: Adult; Aged; Cerebral Cortex - diagnostic imaging; Cerebral Cortex - physiopathology; Chronic Disease; Connectome; contact heat evoked potentials; Cortex (insular); Cortex (somatosensory); Diabetic neuropathy; Evoked Potentials - physiology; Female; Fibromyalgia; Humans; Information processing; Magnetic Resonance Imaging; Male; Medical imaging; Middle Aged; Nerve Net - diagnostic imaging; Nerve Net - physiopathology; Neural networks; Neuralgia; Neuralgia - diagnostic imaging; Neuralgia - physiopathology; Neuroimaging; neuropathic pain; Nociception - physiology; Pain; pain extent; Pain perception; Paralysis; Paraplegia - diagnostic imaging; Paraplegia - etiology; Paraplegia - physiopathology; Paraplegics; Phenotypes; Plasticity; quantitative sensory testing; resting‐state functional connectivity; Sensory integration; Spinal cord injuries; Spinal Cord Injuries - complications; Spinal Cord Injuries - diagnostic imaging; Spinal Cord Injuries - physiopathology; spinal cord injury; Substantia grisea; Thalamus; Thalamus - diagnostic imaging; Thalamus - physiopathology; voxel‐based morphometry; spinal cord injury; neuropathic pain; pain extent; contact heat evoked potentials; resting-state functional connectivity; voxel-based morphometry; quantitative sensory testing
• ISSN: 1065-9471; 1097-0193; 1097-0193
• DOI: 10.1002/hbm.25401

Neuropathic pain following spinal cord injury involves plastic changes along the whole neuroaxis. Current neuroimaging studies have identified grey matter volume (GMV) and resting‐state functional connectivity changes of pain processing regions related to neuropathic pain intensity in spinal cord injury subjects. However, the relationship between the underlying neural processes and pain extent, a complementary characteristic of neuropathic pain, is unknown. We therefore aimed to reveal the neural markers of widespread neuropathic pain in spinal cord injury subjects and hypothesized that those with greater pain extent will show higher GMV and stronger connectivity within pain related regions. Thus, 29 chronic paraplegic subjects and 25 healthy controls underwent clinical and electrophysiological examinations combined with neuroimaging. Paraplegics were demarcated based on neuropathic pain and were thoroughly matched demographically. Our findings indicate that (a) spinal cord injury subjects with neuropathic pain display stronger connectivity between prefrontal cortices and regions involved with sensory integration and multimodal processing, (b) greater neuropathic pain extent, is associated with stronger connectivity between the posterior insular cortex and thalamic sub‐regions which partake in the lateral pain system and (c) greater intensity of neuropathic pain is related to stronger connectivity of regions involved with multimodal integration and the affective‐motivational component of pain. Overall, this study provides neuroimaging evidence that the pain phenotype of spinal cord injury subjects is related to the underlying function of their resting brain. Neuropathic pain after spinal cord injury is related to neuroplastic changes of brain areas involved with lateral and medial pain processing and pain modulation. This study shows novel neuroimaging evidence of the accompanying neuroplastic changes that relate to certain neuropathic pain characteristics after spinal cord injury.