The homeostatic set point, norepinephrine (NE), and obsessive-compulsive disorder (OCD) are closely related

Results: 1) The motivations behind all human behaviors (reflex movements, rhythmic movements, voluntary movements) can be divided into two categories: pursuing the upward regulation of homeostatic set points and avoiding the downward regulation of homeostatic set points. 2) Behaviors are not directly triggered by cognition but are mediated through a valuation system that converts cognitive information into interoceptive signals, which subsequently drive action. 3) There are five main cognitive activities in the human brain: perceptual inference, cognitive reasoning, adjusting expected needs (adjusting homeostatic set points), planning motor sequences, and planning compensatory motor sequences. These cognitive activities form the neural basis of cognitive flexibility. 4) The subgenual anterior cingulate cortex（sgACC） and ventromedial prefrontal cortex(vmPFC) mediate the storage of homeostatic set points. Dense connections from the hippocampus to the sgACC and vmPFC mediate the retrieval of homeostatic set points. 5) The anterior midcingulate cortex (aMCC, also known as the dorsal anterior cingulate cortex, dACC) mediates the planning and storage of compensatory motor sequences. 6) The anterior insula (AI), periaqueductal gray (PAG), rostral anterior cingulate cortex (rACC), von Economo neurons (VENs), and fork cells mediate the real-time adjustment of homeostatic set points. 7) Neural mechanism of mindfulness: Downregulation of homeostatic set points mediated by the rostral anterior cingulate cortex (rACC). 8) The norepinephrine (NE)-mediated neurophysiological responses in the cerebral cortex demonstrate marked consistency with OCD symptomatology, leading us to hypothesize that this mechanism constitutes the primary underlying mechanism responsible for cognitive inflexibility in OCD patients.