• A change in muscle length, becoming lengthened or shortened

• Muscle atrophy, whereby muscle proteins (actin and myosin myofilaments) are lost. Locally there is a loss of sarcomeres in the muscle fibre and globally a reduction in muscle mass (Ryan et al. 2002) and cross-sectional area.

Weakness in neurological conditions

Disorders affecting the peripheral nervous system such as Guillain–Barré syndrome and motor neuron disease often present with weakness as a primary symptom. Damage to the alpha motor neurons interferes with the nerve conduction, which ultimately means that insufficient motor units are recruited and muscle weakness presents. Secondary to this, further weakness may occur as a result of disuse, leading to a loss of sarcomeres and therefore muscle mass (atrophy) (Ryan et al. 2002). Following damage to the peripheral nervous system, motor units can be re-innervated via regeneration of the damaged neuron. However, if the nerve lesion is a long distance from a completely denervated motor unit it may be re-innervated as a result of axonal sprouting from adjacent alpha motor neurons. If this sprouting is heterotypic (not from the same muscle fibre type) the patient may present with dysfunctional incoordinated movement (Lieber 2002). This is a consequence of a disruption in the order of recruitment of motor units (the size principle). The recruitment of small units (type I) followed by the larger units (type IIx) ensures that the force of contraction is built up slowly and smoothly. However, if sprouting occurs from a neuron innervating a type I motor unit to re-innervate a type IIx motor unit the outcome will be large increases in force production too early in the sequence of recruitment and hence an incoordinated movement.

In disorders of the central nervous system (CNS) such as cerebrovascular accident (CVA), Parkinson’s disease and multiple sclerosis, the mechanism underlying muscle weakness is a consequence of damage to higher centres or the pathways involved in motor control. This results in altered signalling down the descending tracts to the alpha motor neuron pool in the spinal cord, the outcome of which is a dysfunction in the timing or pattern of motor unit recruitment or the number of units being recruited. However, ultimately these factors may lead to insufficient or inappropriate recruitment of motor units in a given context and consequently insufficient force to overcome the resistance of the task, or weakness (paresis). Over time, the reduced force production will also be contributed to by a loss of sarcomeres and therefore muscle mass (atrophy) as a consequence of disuse (Ryan et al. 2002). This secondary onset muscle weakness is a common symptom in neurologically impaired patients and may present in any circumstance which leads to movement dysfunction and disuse, e.g. motor impairments but also sensory impairment (S3.23) and cognitive/perceptual deficits (S3.33).

In CNS lesions, muscle weakness is evident in association with both hypotonia (reduced muscle tone) and hypertonia (increased muscle tone; S3.21). The relationship between these concepts is complex but it appears likely that both altered tone states are contributory factors that negatively influence force production (weakness). The pathophysiology which defines alterations in muscle tone also leads to a dysfunction in the timing or pattern of motor unit recruitment or the number of units able to be recruited. Therefore, muscle weakness during movement may be apparent. In terms of assessment a comparison of the conceptual definitions of tone and weakness gives the therapist a simplified tool by which to differentiate. Muscle tone is defined as the resistance to passive movement, representing the background level of tension or stiffness in a muscle (Moore and Kowalske 2000). Therefore it should be assessed in a muscle at rest. Muscle weakness on the other hand is defined as the inability to generate sufficient force to overcome the resistance of a task and therefore by definition should be assessed during movement activities.