Abstract
Spasticity is the velocity-dependent increase in muscle tone due to the exaggeration of stretch reflex. It is only one of the several components of the upper motor neuron syndrome (UMNS). The central lesion causing the UMNS disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. However, the delay between the acute neurological insult (trauma or stroke) and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain. An important plastic change in the spinal cord could be the progressive reduction of postactivation depression due to limb immobilization. As well as hyperexcitable stretch reflexes, secondary soft tissue changes in the paretic limbs enhance muscle resistance to passive displacements. Therefore, in patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia. Compelling evidences state that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.
Highlights
Spasticity is a stretch reflex disorder, manifested clinically as an increase in muscle tone that becomes more apparent with more rapid stretching movement
The central lesion causing the upper motor neuron syndrome (UMNS) disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex
In patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia
Summary
Spasticity is a stretch reflex disorder, manifested clinically as an increase in muscle tone that becomes more apparent with more rapid stretching movement. It is a common consequence of lesions that damage upper motor neurons causing upper motor neuron syndrome (UMNS). The main objectives of this paper are (1) to describe the clinical features of spasticity as one component of UMNS; (2) to describe the mechanisms of muscle tone in normal subjects; (3) to show that spasticity is due to an exaggeration of stretch reflexes caused by an abnormal processing of sensory inputs in the spinal cord; (4) to show that muscle hypertonia in patients with UMNS is caused by muscle shortening and fibrosis (intrinsic hypertonia); (5) to show that lesions damaging upper motor neurons disturb the balance of supraspinal inhibitory and excitatory inputs controlling the stretch reflex; (6) to describe changes of stretch reflex excitability in the spinal cord triggered by the upper motor neurons dysfunction; and (7) to underline that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia
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