This chapter presents a comprehensive examination of the neuroanatomical foundations underlying spasticity in upper motor neuron lesions, integrating classical understanding with contemporary research findings. The discussion begins with Lance’s foundational definition of spasticity as a velocity-dependent increase in tonic stretch reflexes and traces its evolution to current conceptualizations that recognize broader sensorimotor control aspects. The text thoroughly analyzes the anatomical components involved in spasticity, including a detailed exploration of spinal cord structures, brainstem pathways, and peripheral mechanisms. Special attention is given to the organization and function of alpha motor neurons, primary afferents, and spinal interneurons, along with their roles in reflex pathway modulation. This chapter extensively covers the structure and function of muscle spindles and Golgi tendon organs, emphasizing their crucial roles in proprioception and motor control. A significant portion examines the complex organization of descending motor pathways, particularly the corticospinal system and brainstem motor control mechanisms, including the rubrospinal, vestibulospinal, and reticulospinal systems. The text also analyzes the pathophysiological mechanisms underlying exaggerated stretch reflexes, clonus, and spasms in upper motor neuron syndrome. The final section provides a detailed anatomical analysis of characteristic spastic posture patterns in both upper and lower extremities, examining specific joint involvement and the biomechanical principles underlying these patterns. Throughout this chapter, clinical correlations are integrated with basic science concepts, offering a bridge between theoretical understanding and practical application in rehabilitation medicine and spinal cord medicine. This comprehensive approach provides clinicians with a thorough understanding of the complex mechanisms underlying spasticity and their implications for therapeutic intervention.