Post-stroke spasticity is a common and disabling complication of upper motor neuron injury following cerebrovascular events. It is characterized by velocity-dependent increase in muscle tone, exaggerated tendon reflexes, and abnormal posturing due to loss of inhibitory control over spinal reflexes. Spasticity typically develops weeks to months after stroke and contributes significantly to long-term disability.

Clinically, post-stroke spasticity affects the limbs in predictable patterns, commonly involving flexor muscles of the upper limb and extensor muscles of the lower limb. Patients experience muscle stiffness, involuntary spasms, pain, joint contractures, and impaired voluntary movement. These features interfere with mobility, self-care, and rehabilitation progress.

Neurological assessment of spasticity involves evaluation of tone, reflexes, range of motion, functional impact, and associated pain. Differentiating spasticity from rigidity or weakness is essential for targeted management. Severity varies widely and may fluctuate with posture, emotional stress, or intercurrent illness.

Management focuses on reducing excessive muscle tone, preventing secondary complications, and improving functional ability. Early identification and intervention are critical to preventing contractures and irreversible musculoskeletal changes. Treatment strategies are individualized and often require ongoing adjustment.

Spasticity management is an integral component of post-stroke neurological care and rehabilitation. Neurologists coordinate long-term strategies that align tone reduction with functional goals, ensuring that treatment enhances rather than compromises voluntary movement.

Post-stroke spasticity represents a chronic neurological sequela requiring structured assessment, multidisciplinary collaboration, and sustained follow-up to optimize recovery and quality of life.