Spasticity is a common and challenging complication that can follow a stroke, manifesting as muscle stiffness and involuntary spasms. This condition is defined as a velocity-dependent increase in muscle tone, meaning the faster a muscle is stretched, the more resistance it exhibits. Post-stroke spasticity affects a significant portion of stroke survivors, with estimates suggesting that between 20% and 43% of patients experience it within the first year.
The Role of Upper Motor Neurons
The root cause of spasticity lies in damage to the central nervous system, specifically to the pathways known as the Upper Motor Neurons (UMNs). These neurons originate in the motor cortex of the brain and travel down to the brainstem and spinal cord, acting as the primary system for voluntary movement control. A major function of the UMN pathways is to provide inhibitory regulation over the reflex circuits that reside in the spinal cord.
When a stroke, whether ischemic or hemorrhagic, occurs in areas of the brain that house these UMNs, the transmission of this regulatory signal is disrupted. The resulting effect is an interruption of the delicate balance between excitatory and inhibitory signals that normally regulate muscle tone. The spinal circuits below the level of the injury are no longer kept in check by the brain, setting the stage for their hyperexcitability.
The Physiological Mechanism of Hyperexcitability
The interruption of the UMN pathway leads to an immediate state of disinhibition, causing the spinal cord’s reflex arcs to become hypersensitive. Without the brain’s regulatory control, the Lower Motor Neurons (LMNs) within the spinal cord begin to fire excessively in response to minimal stimuli. The primary mechanism involves the over-amplification of the stretch reflex, which is the body’s natural, protective response to prevent a muscle from being overstretched.
Normally, when a muscle is rapidly stretched, sensory receptors called muscle spindles send a signal back to the spinal cord, causing the muscle to contract briefly. In spasticity, the loss of descending inhibition means the spinal neurons that process this stretch signal become hyper-responsive. This results in an exaggerated and sustained contraction of the muscle in response to even a gentle movement, which is the characteristic velocity-dependent resistance of spasticity.
Specific brainstem pathways, such as the reticulospinal tract, are thought to become hyperexcitable following UMN damage, providing an increased excitatory drive to the LMNs. Furthermore, at the cellular level, the LMNs themselves undergo changes, becoming more excitable due to alterations in their intrinsic properties and neurotransmitter balance.
Over time, the chronic over-contraction and lack of movement initiate secondary, non-neural changes within the muscle tissue itself. Muscles held in a shortened position can lose sarcomeres, which are the basic contractile units of muscle fibers. This structural remodeling physically increases the stiffness of the muscle and surrounding connective tissue, creating a fixed contracture that further contributes to the perceived tightness and resistance.
Common Exacerbating Factors
While the stroke-induced UMN damage is the underlying cause, various external and internal factors can significantly worsen the frequency and severity of existing spasticity. Identifying and managing these factors can often provide immediate relief from severe spasms.
Physical discomfort, such as pain from pressure sores, an ingrown toenail, or tight-fitting clothing, can act as a peripheral irritant that increases the muscle’s involuntary response. Similarly, internal physiological issues like a full bladder or bowel, or the presence of a urinary tract infection (UTI), send heightened sensory signals to the spinal cord. These signals can easily overwhelm the disinhibited motor pathways, triggering a spasm.
Environmental and emotional factors also play a substantial role in exacerbating spasticity. Emotional stress, anxiety, or even sudden loud noises can activate the autonomic nervous system, leading to an increase in muscle tone. Changes in temperature, particularly exposure to cold or dampness, are frequently reported by survivors as triggers that intensify their muscle stiffness and spasms.