Spasticity is a common motor disorder that frequently appears following a stroke, characterized by involuntary muscle stiffness or tightness. This stiffness results from an increased resistance to movement in the affected limbs. It is a complex neurological complication that arises from damage to the central nervous system. Understanding spasticity requires examining how a stroke disrupts the brain’s delicate control system over muscle activity.
How the Brain Controls Normal Muscle Tone
Muscle tone, which is the slight, continuous contraction of muscles even at rest, is maintained by a balance between signals that excite muscles and signals that inhibit them. The spinal cord contains local reflex circuits, such as the stretch reflex, which automatically cause a muscle to contract when it is stretched. To prevent these local reflexes from causing uncontrolled movements, the brain sends continuous signals down to the spinal cord. These signals travel through pathways, notably the corticospinal tract, which exerts a dampening influence, regulating the sensitivity of the spinal cord’s reflex arcs. Other descending tracts, such as those from the brainstem (reticulospinal tracts), also modulate muscle tone, resulting in a finely tuned system that maintains posture and allows for smooth, coordinated movement.
The Motor Pathway Damage Caused by Stroke
A stroke occurs when blood flow to a part of the brain is interrupted, leading to cell death. When this damage occurs in the motor cortex or along the major descending nerve tracts, it injures the upper motor neurons. The corticospinal tract, which carries the brain’s regulatory commands, is physically damaged by the lesion. This damage effectively cuts the communication line between the brain and the spinal cord’s reflex machinery, meaning the inhibitory signals are drastically reduced or entirely lost. This physical damage sets the stage for spasticity to develop within the spinal cord.
Spinal Cord Hyperexcitability: The Direct Cause of Spasticity
The central mechanism underlying spasticity is the development of hyperexcitability within the spinal cord’s reflex circuits. When the inhibitory signals from the brain are lost, the spinal cord is no longer under the central damping control, causing the alpha motor neurons that directly control muscle contraction to become overly sensitive. This heightened sensitivity is a form of maladaptive plasticity where the local spinal reflex arcs become unopposed by brain control, meaning even a small stretch of the muscle can trigger a massive, exaggerated reflex response. Scientific evidence also points to changes in the brainstem pathways, specifically the reticulospinal tracts; some excitatory pathways may become hyperexcitable and unopposed by inhibitory descending tracts. Furthermore, the motor neurons themselves can develop denervation hypersensitivity, increasing the sensitivity of their receptors to neurotransmitters, resulting in the exaggerated, involuntary muscle activation known as spasticity.
Characteristics of Spastic Muscle Activity
Spasticity is clinically characterized by muscle overactivity that is dependent on the speed of movement. A quick stretch of the affected muscle will elicit a strong, sudden resistance, distinguishing this velocity-dependent increase in tone from other forms of stiffness. The underlying hyperexcitable stretch reflex also manifests as exaggerated deep tendon reflexes. Another common sign is clonus, which presents as rhythmic, involuntary muscle contractions and relaxations, often seen at the ankle. These physical signs are direct evidence of the overactive, disinhibited spinal cord reflex circuitry. Spasticity often affects specific muscle groups, interfering with voluntary movement, posture, and daily function:
- Shoulder adductors, elbow flexors, and wrist flexors in the upper limbs, leading to a flexed posture.
- Hip adductors and knee extensors in the lower limbs, causing a scissoring gait pattern or toe-walking.