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<br>Background: Motor cortex stimulation (MCS) is a potentially efficient remedy for chronic neuropathic ache. The neural mechanisms underlying the discount of hyperalgesia and allodynia after MCS usually are not utterly understood. Objective: To analyze the neural mechanisms chargeable for analgesic results after MCS. We take a look at the speculation that MCS attenuates evoked blood oxygen-degree dependent signals in cortical areas involved in nociceptive processing in an animal model of chronic neuropathic pain. 10) that acquired unilateral electrolytic lesions of the proper spinal cord at the extent of C6 (SCL animals). In these animals, we performed magnetic resonance imaging (fMRI) experiments to review the analgesic results of MCS. On the day of fMRI experiment, 14 days after spinal cord lesion, the animals have been anesthetized and epidural bipolar platinum electrodes have been positioned above the left primary motor cortex. Two 10-min periods of fMRI were performed before and after a session of MCS (50 μA, 50 Hz, 300 μs, for 30 min). During every fMRI session, the right hindpaw was electrically stimulated (noxious stimulation: 5 mA, 5 Hz, 3 ms) utilizing a block design of 20 s stimulation off and 20 s stimulation on. A normal linear mannequin-based statistical parametric evaluation was used to analyze whole mind activation maps. Region of curiosity (ROI) evaluation and [BloodVitals SPO2](https://trlittlegit.func.tairongkj.com/isaac438719995) paired t-test have been used to match modifications in activation before and after MCS in these ROI.<br>
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