Pathophysiology of Spasticity: Implications for Neurorehabilitation

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.

Big conductance calcium‐activated potassium channel openers control spasticity without sedation

“…This study indicates that potassium‐induced hyperpolarization following opening of the α pore in BK Ca channels is a novel central mechanism of action of these anti‐spastic drugs and, in neural membranes, will act to limit excessive action potential generation. Such membrane hyperpolarization is the common mechanism of action of many anti‐spastic agents, which counter excitatory depolarizing signals that can lead to spasticity (Toda et al, ; Trompetto et al, ). This pathway is mediated directly through the opening of BK Ca potassium channels, as shown here, and via calcium channel inhibition and notably activation of inwardly rectifying potassium channels after G protein signalling with CB 1 receptor and GABA B agonists, and through chloride ion influx following stimulation of GABA A receptors (Isomoto et al, ; Howlett et al, ; Pertwee et al, ).…”

Electromyographic assessment of paratonia

“…Parkinsonian rigidity is typically described as velocity-independent and sensitive to dopaminergic treatment (Meara and Cody 1992). Spasticity is defined as a velocitydependent increase in muscle tone due to the exaggeration of the stretch reflex (Lance 1980;Trompetto et al 2014). Oppositional paratonia appears during passive muscle elongation and can be difficult to distinguish from spasticity and rigidity.…”

Unilateral dorsiflexor strengthening with mirror therapy to improve motor function after stroke: A pilot randomized study

“…Although the most widely reported assessment of spasticity in the stroke population (Thibaut et al, ), the MAS assesses the resistance to passive movement, not just stretch‐reflex hyperexcitibility. Spastic cocontraction is another component of muscle overactivity influencing MAS scores (Vattanasilp, Ada, & Crosbie, ), brought on by abnormal reflex activity, causing simultaneous activity in the agonist and antagonist muscles (Gracies, ; Trompetto et al, ). The reduced MAS scores for both groups in this study may be attributed to an improved motor output or firing pattern to the untrained limb, too minimal to be detected in strength measures, potentially reducing spastic cocontraction.…”