Spasticity and rigidity are two distinct forms of involuntary muscle tone abnormalities that arise following various neurological conditions and injuries. Both can significantly impact affected individuals. Spasticity is characterized by an increase in muscle resistance that depends on the velocity of passive limb movement, frequently associated with alterations involving the pyramidal system. In contrast, rigidity, commonly associated with extrapyramidal lesions—particularly those affecting the basal ganglia, mesencephalon, and spinal cord—remains independent of movement velocity. The rubrospinal and vestibulospinal tracts are implicated in its pathophysiology. Individuals with rigidity struggle with muscle movement through the full range of motion, regardless of speed. It is a hallmark feature of Parkinson’s disease and can also result from severe traumatic brain injury (TBI). Spasticity, on the other hand, often emerges as a secondary consequence of neurological conditions such as spinal cord injury (SCI), stroke, multiple sclerosis (MS), cerebral palsy, amyotrophic lateral sclerosis (ALS), TBI, and metabolic disorders like adrenoleukodystrophy and phenylketonuria. Each year, central nervous system (CNS) disorders leave many individuals with persistent motor impairments, including spasticity and rigidity. However, the absence of a well-defined pathophysiological understanding of these conditions limits the effectiveness of current therapeutic approaches. This entry explores the neurobiological mechanisms underlying spasticity and rigidity, discusses existing experimental and clinical treatments, and highlights recent scientific advancements in this area.