Spasticity
Pathophysiology
Although the pathophysiology of spasticity is not clearly understood, several theories have been proposed to explain this change in muscle tone, which comprises one component of the upper motor neuron syndrome. In general, spasticity develops when an imbalance occurs in the excitatory and inhibitory input to α motor neurons, leading to hyperexcitability.
| Possible mechanisms of spasticity |
| Increased neuronal excitability |
| Enhanced excitatory synaptic input |
| Segmental afferents |
| Regional excitatory interneurons |
| Descending pathways, i.e., lateral vestibulospinal tract |
| Reduced inhibitory synaptic input |
| Renshaw cell recurrent inhibition |
| Ia inhibitory interneurons |
| Ib afferent fibers |
| Change in intrinsic electrical properties of the neuron |
| Change in passive membrane electrical properties |
| Change in voltage sensitive membrane conductance |
| Enhanced stretch-evoked synaptic excitation of neurons |
| γ efferent hyperactivity |
| Excitatory interneurons more sensitive to muscle afferent |
Lesion of the upper motor neuron
An upper motor neuron lesion, such as occurs with a CP, stroke, TBI, or SCI, disrupts not only the pyramidal tract, but also the corticospinal tract that is involved in voluntary movement. The same damage to the higher centers provokes an imbalance in spinal reactivity through a modification of the descending input received by spinal neurons.
After a variable period of time, spinal circuits undergo plastic rearrangements that lead to abnormal muscle contractions and abnormal reflex responses, some of which meet the classic definition of spasticity. A reciprocal potentiation is then likely to occur between spasticity and muscle shortening.
Pathophysiology of Impairment After a Central Nervous System Lesion
Spinal versus Cerebral Models of Spasticity
The spinal model of spasticity posits that removal of inhibition on segmental polysynaptic pathways leads to a slow progressive rise of the excitatory state through cumulative excitation. What follows is afferent activity from one segment leading to muscle response many segments away and an overexcitation of flexors and extensors. In the cerebral model, enhanced excitability of monosynaptic pathways causes a rapid build-up of reflex activity, subsequently leading to a bias toward overactivity in the antigravity muscles and the development of hemiplegic posture.
Spasticity may cause pain (which may also affect sleep and, subsequently, affect), joint deformity, macerated skin, difficulty performing activities of daily living or ambulating, muscle tightness or stiffness (particularly when the patient attempts to use fine-motor skills), muscle spasms, or fatigue. Spasticity also manifests in typical patterns, although they may not always be as readily apparent as those shown below.
