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Figure 4: Alteration of brain circuitry in cLBP. Light blue boxes: anatomical structures, purple boxes: physiological events, yellow boxes: end result of the pathways. Peripheral afferent pain sensation reaches the spinal cord via the dorsal root ganglion. It travels through the spinothalamic tract and reaches the somatosensory cortex. In the somatosensory cortex, the GABAergic neurons produce desynchronized ɣ band oscillation. This can also be produced in the case of allodynia. The net result is nociception. On the other hand, the amygdala is activated via nociceptive stimuli (via the parabrachial nucleus) and stress. The net output of the central amygdala is the affective component of pain. The CeA also induces prefrontal deactivation (by reciprocal modulation) and facilitation of nociception in the PAG (by the CeA–PAG output pathway). Activation of the basolateral amygdala produces GABAergic feed forward inhibition of the prefrontal cortex. Prefrontal deactivation reduces rewards. On the other hand, desynchronized ɣ band oscillation in the somatosensory cortex increases activity in the rACC, which increases aversion. This circuitry is mainly GABAergic and acts through cortical and subcortical areas. The sensory and affective component of pain is the main target of this pathway. The fine-tuning balance between descending facilitation and inhibition in this circuit is altered, and the descending pain modulation system (PAG and RMV) is inhibited. CeA = central amygdala, cLBP = chronic nonspecific low back pain, GABA = gamma aminobutyric acid, PAG = periaqueductal gray, rACC = rostral anterior cingulate cortex, RVM = rostral ventral medullary area

Figure 4: Alteration of brain circuitry in cLBP. Light blue boxes: anatomical structures, purple boxes: physiological events, yellow boxes: end result of the pathways. Peripheral afferent pain sensation reaches the spinal cord via the dorsal root ganglion. It travels through the spinothalamic tract and reaches the somatosensory cortex. In the somatosensory cortex, the GABAergic neurons produce desynchronized ɣ band oscillation. This can also be produced in the case of allodynia. The net result is nociception. On the other hand, the amygdala is activated via nociceptive stimuli (via the parabrachial nucleus) and stress. The net output of the central amygdala is the affective component of pain. The CeA also induces prefrontal deactivation (by reciprocal modulation) and facilitation of nociception in the PAG (by the CeA–PAG output pathway). Activation of the basolateral amygdala produces GABAergic feed forward inhibition of the prefrontal cortex. Prefrontal deactivation reduces rewards. On the other hand, desynchronized ɣ band oscillation in the somatosensory cortex increases activity in the rACC, which increases aversion. This circuitry is mainly GABAergic and acts through cortical and subcortical areas. The sensory and affective component of pain is the main target of this pathway. The fine-tuning balance between descending facilitation and inhibition in this circuit is altered, and the descending pain modulation system (PAG and RMV) is inhibited. CeA = central amygdala, cLBP = chronic nonspecific low back pain, GABA = gamma aminobutyric acid, PAG = periaqueductal gray, rACC = rostral anterior cingulate cortex, RVM = rostral ventral medullary area