In the eighteenth century, the investigation of movement was based on the premise that upright stance and gait and also differentiation of hand movements represented a basic requirement for human cultural development. This necessitates that the nervous system must function to automatically balance the body's center of mass over the feet during all motor activities. In other words, every movement must begin and end with a postural adjustment. Nevertheless, basic neuronal mechanisms underlying quadrupedal locomotion remain preserved during human gait.
Analysis of human gait first became possible toward the end of the nineteenth century with the development of photographic recordings of running movements. Later, the technique for recording electrophysiological responses during locomotion was developed and was first demonstrated in cats.
The relative significance of reflexes on central rhythms and programming in locomotion has been addressed. The central mechanisms involved in locomotion are reflected in a reciprocal mode of leg muscle activation and a di- or triphasic pattern of antagonistic leg muscle activity following displacement of the feet that is thought to be programmed in its basic structure. This electromyographic (EMG) pattern is assumed be evoked by a multisensory afferent input and generated by spinal interneuronal circuits that are closely connected with spinal locomotor centers. The extent to which the timing of the pattern can be modified by afferent input has not yet been fully explored. A basic requirement of bipedal locomotion is that both legs act in a cooperative manner; each limb affects the strength of muscle activation and the time-space behavior of the other. There exists some evidence that this interlimb coordination is mediated by spinal interneuronal circuits, which are themselves under supraspinal (e.g., cerebral and cerebellar) control.
In regard to the reflex mechanisms, short latency stretch reflexes in leg extensor muscles are profoundly modulated during gait mainly by presynaptic inhibition group IA input and less by fusimotor influences. During large transla-tional perturbations a significant contribution of this reflex has not yet been demonstrated. However, they may be involved in the compensation of the small ground irregularities at distinct phases of gait. Compensation for larger displacements during gait is provided by polysynaptic spinal reflexes. This includes an activation of synergistic muscle groups of both legs. These EMG responses are thought to be mediated predominantly by peripheral information from group II (and probably III) afferents, converging with different peripheral and supraspinal inputs onto common in-terneurons on a spinal level. These reflexes modulate the basic motor pattern of spinal interneuronal circuits underlying the respective motor task.
During recent years, increasing evidence has come up for the crucial importance of load receptor input in the control of bipedal stance and gait in quadrupeds and bipeds. Yet we are still at the beginning of an understanding of its nature and its interaction with other afferent inputs and control mechanisms. Vestibular and visual functions are mainly context dependent and are essential when afferent input from other sources is reduced.
one of the first symptoms of a lesion within the central motor system represents movement disorder, which is most characteristic during locomotion in patients with spasticity, cerebellar lesions, or Parkinson's disease. The clinical examination reveals typical changes in tendon tap reflexes and muscle tone typical for one of the movement disorders. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms in operation during an active movement. By the recording and analysis of electro-physiological and biomechanical parameters during a functional movement such as locomotion, the significance of, for example, impaired reflex behavior or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and significance of the mechanisms underlying the disorder of functional movement that impairs the patient.
University Hospital Balgrist
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