![]() ![]() In contrast to this general notion, Bernstein highlighted the fact that muscle tone may actually reflect a state of preparedness to a movement and thus it may not be possible to estimate muscle tone when the person is asked to relax and not to make any movement. ![]() However, all these definitions have a common fallacy of assuming that the person is in completely relaxed state, which is often impossible to achieve unless using muscle relaxants. In a relaxed state, resistance to an external motion (R TOT) depends on inertia (R IN), apparent stiffness (resistance to stretch/R ST) and damping (resistance to velocity/R DA): R TOT = R IN + R DA + R ST. Mathematically, muscle tone can be interpreted as the change in resistance or force per unit change in length (Δ force/Δ displacement of the tissue). The viscoelastic component in turn depends upon multiple factors like the sarcomeric actin-myosin cross-bridges, the viscosity, elasticity, and extensibility of the contractile filaments, filamentous connection of the sarcomeric non-contractile proteins (e.g., desmin, titin), osmotic pressure of the cells, and also on the surrounding connective tissues. However, apart from the active or contractile component resulting from the activation of motor unit and detectable by EMG, muscle tone also has a passive or viscoelastic component, independent of neural activity that can’t be detected by EMG. Studies with electromyographic (EMG) assessment often equate muscle tone with baseline EMG level in a relaxed state. This definition of tone has some ambiguities such as, what does the ‘resistance to passive stretch’ mean is not clear and ‘felt by the examiner’ opens the door to subjective variation during clinical examination and interrater variability of the assessment. ![]() Muscle tone is traditionally defined as ‘the tension in the relaxed muscle’ or ‘the resistance, felt by the examiner during passive stretching of a joint when the muscles are at rest’. The mechanisms underlying these have been discussed thereafter because they are important both clinically and pathophysiologically from a movement disorder perspective. Dystonia and paratonia have altered tone secondary to network disruption in the basal ganglia, the thalamocortical circuits, and their connections. In the motor control system, spasticity and rigidity are predominantly an output system problem, while dystonia is a system level processing problem. The other two disorders of altered tone, namely dystonia and paratonia, are not exactly related to the physiological dysfunction of the tone pathways. Spasticity and rigidity, the two types of hypertonia, have been elaborated in the context of the dysfunction in the supraspinal pathways and the interaction between spinal cord and muscle spindle. In this review, we have discussed the controversies regarding the definition of muscle tone and its classification, followed by the mechanisms and pathways responsible for maintaining tone. This hierarchy of motor control includes cortex (extensive processing capability with highest degree of freedom), basal ganglia (learning and teaching of context dependent tasks with less degrees of freedom), cerebellum (fine-tuning), brainstem reticular system (common pathway for ascending and descending tracts), spinal cord (the main pathway for ascending and descending tracts), and muscle spindle (final common pathway with least degree of freedom). Tone is basically a construct of motor control, upon which power is intrinsically balanced. It is regulated by its input and output systems and has critical interplay with power and task performance requirements. Muscle tone is a complex and dynamic state, resulting from hierarchical and reciprocal anatomical connectivity. ![]()
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