Inhibition of cortical somatosensory processing during and after low frequency peripheral nerve stimulation in humans.

OBJECTIVE: Transcutaneous low-frequency stimulation (LFS) elicits long-term depression-like effects on human pain perception. However, the neural mechanisms underlying LFS are poorly understood. We investigated cortical activation changes occurring during LFS and if changes were associated with reduced nociceptive processing and increased amplitude of spontaneous cortical oscillations post-treatment. METHODS: LFS was applied to the radial nerve of 25 healthy volunteers over two sessions using active (1 Hz) or sham (0.02 Hz) frequencies. Changes in resting electroencephalography (EEG) and laser-evoked potentials (LEPs) were investigated before and after LFS. Somatosensory-evoked potentials were recorded during LFS and source analysis was carried out. RESULTS: Ipsilateral midcingulate and operculo-insular cortex source activity declined linearly during LFS. Active LFS was associated with attenuated long-latency LEP amplitude in ipsilateral frontocentral electrodes and increased resting alpha (8-12 Hz) and beta (16-24 Hz) band power in electrodes overlying operculo-insular, sensorimotor and frontal cortical regions. Reduced ipsilateral operculo-insular cortex source activity during LFS correlated with a smaller post-treatment alpha-band power increase. CONCLUSIONS: LFS attenuated somatosensory processing both during and after stimulation. SIGNIFICANCE: Results further our understanding of the attenuation of somatosensory processing both during and after LFS.

Differential effects of hunger and satiety on insular cortex and hypothalamic functional connectivity.

The insula cortex and hypothalamus are implicated in eating behaviour, and contain receptor sites for peptides and hormones controlling energy balance. The insula encompasses multi-functional subregions, which display differential anatomical and functional connectivities with the rest of the brain. This study aimed to analyse the effect of fasting and satiation on the functional connectivity profiles of left and right anterior, middle, and posterior insula, and left and right hypothalamus. It was hypothesized that the profiles would be altered alongside changes in homeostatic energy balance. Nineteen healthy participants underwent two 7-min resting state functional magnetic resonance imaging scans, one when fasted and one when satiated. Functional connectivity between the left posterior insula and cerebellum/superior frontal gyrus, and between left hypothalamus and inferior frontal gyrus was stronger during fasting. Functional connectivity between the right middle insula and default mode structures (left and right posterior parietal cortex, cingulate cortex), and between right hypothalamus and superior parietal cortex was stronger during satiation. Differences in blood glucose levels between the scans accounted for several of the altered functional connectivities. The insula and hypothalamus appear to form a homeostatic energy balance network related to cognitive control of eating; prompting eating and preventing overeating when energy is depleted, and ending feeding or transferring attention away from food upon satiation. This study provides evidence of a lateralized dissociation of neural responses to energy modulations.

Functional magnetic resonance imaging of cerebral activation during spinal cord stimulation in failed back surgery syndrome patients.

Spinal cord stimulation (SCS) consisting of electrical stimulation of the dorsal spinal cord using epidural electrodes has been shown to relieve chronic neuropathic pain. To analyze the cerebral activation patterns related to SCS, and to evaluate the effects of SCS on the processing of acute experimental pain, we performed functional magnetic resonance imaging (fMRI) on eight patients suffering from failed back surgery syndrome who were also being treated with SCS for severe pain in their legs and lower back. Three types of stimulation were used, each lasting 36s: (i) SCS, (ii) heat pain (HP) applied to the leg affected by neuropathic pain, and (iii) simultaneous HP and SCS. During SCS, we found increased activation of the medial primary sensorimotor cortex somatotopically corresponding to the foot and/or perineal region, contralateral posterior insula, and the ipsilateral secondary somatosensory cortex (S2). Decreased activation was seen in the bilateral primary motor cortices and the ipsilateral primary somatosensory cortex corresponding to the shoulder, elbow and hand. Compared to separately presented HP and SCS, simultaneous HP and SCS showed statistically significant activation of the bilateral inferior temporal cortex and the ipsilateral cerebellar cortex. The activation of the primary motor cortex, insula and S2 during SCS may directly interfere with the processing of neuropathic pain. When SCS is associated with heat pain, the paralimbic association cortex and cerebellum show activation exceeding the sum of activations resulting from separate SCS and heat pain stimulation. The explanation of this could possibly rest with the continuous comparisons of simultaneous pain and somatosensory sensations occurring in a single dermatome.

Effects of spinal cord stimulation on the cortical somatosensory evoked potentials in failed back surgery syndrome patients.

OBJECTIVE: To evaluate the functional activation of the somatosensory cortical regions in neuropathic pain patients during therapeutic spinal cord stimulation (SCS). METHODS: In nine failed back surgery syndrome patients, the left tibial and the left sural nerves were stimulated in two sessions with intensities at motor and pain thresholds, respectively. The cortical somatosensory evoked potentials were analyzed using source dipole analysis based on 111 EEG signals. RESULTS: The short-latency components of the source located in the right primary somatosensory cortex (SI: 43, 54 and 65ms) after tibial nerve stimulation, the mid-latency SI component (87ms) after sural nerve stimulation, and the mid-latency components in the right (approximately 161ms) and left (approximately 168ms) secondary somatosensory cortices (SII) were smaller in the presence of SCS than in absence of SCS. The long-latency source component arising from the mid-cingulate cortex (approximately 313ms) was smaller for tibial and larger for sural nerve stimuli during SCS periods compared to periods without SCS. CONCLUSIONS: SCS attenuates the somatosensory processing in the SI and SII. In the mid-cingulate cortex, the effect of SCS depends on the type of stimulation and nerve fibers involved. SIGNIFICANCE: Results suggest that the effects of SCS on cortical somatosensory processing may contribute to a reduction of allodynia during SCS.