Muscle tone: The neurophysiological basis and pathological changes

The term "muscle tone" was introduced 150 years ago to describe the continu ous contractile tension which was detected in a variety of animal preparati ons. It was suggested by Sherrington that this muscle tone might play an im portant role in the maintenance of posture. For the clinician, the presence of muscle tone is difficult to assess simply by observation under resting conditions. In practice, clinicians test muscle tone by stretching muscles, thus observing the passive resistance to this applied stretch. In normal h uman subjects asked to relax a muscle completely, which is the reference co ndition for the clinician, no motor unit activity is recordable using elect romyography. Even large amplitude stretches of a resting muscle fail to evo ke EMG activity over the entire streching phase. Only transient EMG activit y at the onset of stretch can be recorded. Thus, hypotonicity is difficult to assess under normal clinical testing conditions because the relaxed, nor mal human muscle exhibits no sustained reflex activity during the stretchin g phase. According to Gordon Holmes hypotonia is one of the cardinal sympto ms of acute cerebellar lesions and develops on the side contralateral to th e lesion. It is characterised by loss of postural tone and loss of stretch- dependent resistance in muscles. Since relaxed muscles of healthy subjects do not exhibit reflex activity during the stretching phase, reduced stretch -dependent activity following, acute cerebellar lesions can only be tested in situations in which postural tone or voluntary activation would normally be present. Spastic muscle tone is defined as an exaggerated resistance by relaxed muscles to imposed large amplitude stretches. This enhanced passiv e stretch resistance is easily diagnosed by the investigator, since normal skeletal muscles do not exhibit stretch-evoked activity. This increase in m uscle resistance is accompanied by pathological EMG activity. Therefore, sp asticity as defined by Lance is due to enhanced, dynamic stretch reflex act ivity. However, during voluntary movements of patients with spasticity, no exaggeration of normal EMG-activity can be observed during the stretching p hase of antagonistic muscles. Thus, the slowing of movements of spastic pat ients is not necessarily caused by enhanced stretch reflex activity. Other factors seem to contribute to this slowing of movement, such as paresis joi nt contractures, or changes in muscle fibre properties (stretch activation) . The pathophysiology of increased reflex resistance to stretch of spastic muscles is as yet unclear. After exclusion of hyperactivity of gamma-motone urons and sprouting of afferents as a cause of spasticity, pre- or post-syn aptic changes of the membranes of a-motoneurons have been suggested to prod uce spasticity. The hypertonia of rigidity has a plastic quality, with a wa xy resistance to passive limb displacements, which is in contrast to spasti city independent on the velocity of stretch. Rigidity has been attributed t o an increased excitability of either supraspinal centres in response to ac tivation by primary muscle spindle afferents or spinal motor centres in res ponse to secondary muscle spindle afferents. Alternatively, rigidity has be en attributed to changes in spinal inhibitory mechanisms (autogenic and rec iprocal inhibition). Changes in spinal inhibitory mechanisms might be due t o functional alterations of the reticulo-spinal tract, which receives affer ent input from the nucleus pedunculus pontinuus, which is impaired in Parki nson's disease.