Muscle tone
What is normal muscle tone?
Muscle tone is often referred to as a state of readiness in a muscle at rest (resting tone) which provides us with a background level of tone from which we can function efficiently. It is defined by the resistance to passive movement, which is an expression of the stiffness of the muscle fibres (Brodal 2004). Normal tone should be high enough to keep you up against gravity but low enough to allow movement.
Caution• The individual will ‘follow’ the movement (i.e. the muscles are active but allowing the movement to occur)
• The limb can be ‘placed’ at any point in the movement and will remain in its designated position.
Muscle tone is considered to depend physiologically on two factors:
Non-neural factors
This is a consequence of the mechanical-elastic properties of the soft tissues (compliance or stiffness of soft tissue structures) and incorporates the thixotropic properties (viscosity) of the muscle and the muscle length. These factors contribute a significant component to the normal resting tone of a muscle which explains how we are able to stand still with only minimal corrective bursts of postural muscle activity (Simons and Mense 1998). These non-neural factors can be influenced by age, temperature and exercise.
Neural factors
The neural factors relate to the degree of activation of the contractile apparatus of the muscle. Our muscles are constantly contracting or active and it is the nervous system that controls the appropriate level of this background activity. The level of muscle contraction is a result of the output from the alpha motor neuron (AMN) in the ventral horn of the spinal cord (S2.13) which innervates the muscle itself. The AMN output is dictated by the final outcome of competing inhibitory and excitatory synapses from various inputs related to both the peripheral and central nervous systems. These include:
• Muscle spindles (tonic component of the stretch reflex) (TSR) (S2.13)
• Golgi tendon organ (GTO) (S2.13)
• Somatosensory receptors in the body (skin, joints, connective tissue, muscles) (S3.23)
• Sensory systems such as visual, auditory, vestibular (S2.10)
• Limbic system related to our emotional state (S2.9)
• Interneurons within the spinal cord
• Various higher centres via the descending tracts (Reticular formation S2.10) (Nielsen et al. 2007).
What is abnormal muscle tone?
Individuals who have a neurological lesions affecting the central nervous system (CNS) may lose the ability to control the level of muscle tone and may present with resting tone that is either too low (hypotonia) or too high (hypertonia) (Brodal 2004). It is also common to see both these characteristics present in an individual patient.
In CNS lesions, muscle weakness (S3.30) is evident in association with both hypotonia (reduced muscle tone) and hypertonia (increased muscle tone). The relationship between these concepts is complex but it appears likely that both altered tone states directly contribute to a reduction in force production (weakness) of the muscle. The pathophysiology which defines alterations in muscle tone will also lead to a dysfunction in the timing or pattern of motor unit recruitment or the number of units able to be recruited. This will lead to a presentation of muscle weakness during certain movements. It should also be noted that when altered tone exists over a prolonged period, the outcome may be disuse of the part, and further muscle weakness may occur as a consequence of sarcomere loss and reduction in cross-sectional area (S3.30).
In terms of assessment, a comparison of the conceptual definitions gives the therapist a simplified tool by which to differentiate muscle tone and weakness. 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.
Hypotonia
Pathophysiology of hypotonia
Hypotonia presents in many pathologies involving the central nervous system, e.g. multiple sclerosis, traumatic brain injury and cerebrovascular accident (CVA). Where an acute insult occurs, the nervous system may go into a state of neural shock (Kwakkel et al. 2003). The shock results in reduced neuronal conduction (S2.6) and a breakdown in communication within the nervous system. If the motor systems are affected, an insufficient number of alpha motor neurons can be recruited and hypotonia presents. Over time, as the nervous system recovers the neural shock subsides, neural transmission is resumed and muscle tone begins to return. However, there is no guarantee that it will return to normal.
If the patient still presents with hypotonia after a 4-week period, the presentation is sometimes termed ‘prolonged muscular flaccidity’ (Kwakkel et al. 2003). In CVA, the prognosis for the final outcome is poor if this state remains beyond 3 months (Formisano et al. 2005). The definitive cause of prolonged muscular flaccidity is unclear in the current literature. It has been hypothesized to result from a reduction in the levels of arousal and central drive leading to insufficient excitation at the alpha motor neuron. However, the cortical loops associated with the basal ganglia and cerebellum are also found to be severely affected in patients with prolonged muscular flaccidity (Pantano et al. 1995).
Hypertonia
Rigidity defined
Traditionally, rigidity is defined as an increased resistance to passive movement which is constant throughout the range of movement. The resistance occurs throughout the full range of a passive movement and will be present in all muscles (including the face). The resistance is described as ‘lead-pipe’ (constant through range) or ‘cogwheel’ (resistance followed by a period of ‘give’) (Fung and Thompson 2002; Xia and Rymer 2004). As a result of rigidity affecting all muscle groups, patients often present with a lack of rotation, especially in the trunk (Wright et al. 2007). Recent studies have shown that rigidity is also velocity dependent (Mak et al. 2007; Xia et al. 2009). Voluntary movement is difficult both to initiate and arrest. Tendon reflexes are usually normal.
Pathophysiology of rigidity
Neural factors
The neural factors are a result of damage to the basal ganglia (S2.11) and particularly, the dopamine-producing cells of the substantia nigra (SN). The dopaminergic neurons of the SN project to the striatum and normally modulate the activity of both the direct and indirect pathways within the basal ganglia (S2.11), having the opposite effect on each. The direct pathway facilitates the initiation and selection of the correct voluntary movement programmes to achieve a task, while the indirect pathway helps to prevent any unwanted movement programmes. In PD, the loss of dopaminergic cells in the SN means that the ability to modulate motor programme selection is lost and there is inappropriate competition between the correct and incorrect movement programmes being sent to the cortex. At a muscular level, this presents as inappropriate co-contraction (Xia and Rymer 2004; Xia et al. 2009) attributed to inadequate reciprocal inhibition (Meunier et al. 2000). Consequently, a hypokinetic movement disorder presents, or in simple terms a lack of movement.
