Detrusor-sphincter dyssynergia (DSD) is a lower urinary tract dysfunction syndrome caused by disorders of the neural regulatory pathways for micturition. Its core feature is that the urethral sphincter fails to relax coordinately during detrusor contraction; instead, the persistent abnormal contraction leads to a series of severe complications such as dysuria, elevated intravesical pressure, and upper urinary tract damage.DSD is common in patients with central nervous system lesions, such as spinal cord injury and multiple sclerosis. This paper systematically reviews the latest research progress on the neural mechanisms of DSD, including ① loss of central regulation and excessive excitation of the spinal cord center, i.e., the loss of supraspinal inhibition leading to sacral spinal reflex hyperactivity; ② imbalance of key neurotransmitters and receptors, involving excessive glutamatergic excitation, weakened gamma-aminobutyric acid ergic/glycinergic inhibition, and the involvement of purinergic and endocannabinoid systems; ③ neuroimmunity and inflammatory response, where the activation of microglia and astrocytes after spinal cord injury releases pro-inflammatory factors, exacerbating neuronal excitability and circuit remodeling; ④ peripheral nerve and gut-bladder axis mechanisms, where sphincter structural remodeling and the gut microbiota-neuroimmunity crosstalk form a vicious cycle. The paper focuses on the sacral Onuf's nucleus as the“core hub”and key therapeutic target of DSD, discussing the central role of its dysfunction in the occurrence of synergistic disorders. In terms of therapeutic strategies, the paper summarizes existing traditional methods, such as drugs, botulinum toxin injection and neuromodulation, and envisions the cutting-edge directions of targeted intervention, such as precise strategies including gene therapy and neurotrophic support, as well as the challenges faced in clinical translation. Finally, the paper discusses the application prospects of precision medicine and artificial intelligence in the diagnosis and treatment of DSD, including precise classification based on multi-omics data, artificial intelligence-assisted recommendation of individualized treatment plans, and the development of dynamic closed-loop regulation systems. This paper aims to provide a theoretical basis and research direction for in-depth understanding of the neural mechanisms of DSD, and to promote the precise diagnosis, treatment and neural function remodeling.