The normal gait cycle, defined as the period between successive points at which the heel of the same foot strikes the ground, is illustrated in Fig. 6-1, based on the studies of Murray and coworkers, and of Olsson. In this figure, the cycle is initiated by the heel strike of the right foot. The stance phase, during which one foot is in contact with the ground, occupies 60 to 65 percent of the cycle. The swing phase begins when the left toes leave the ground. For 20 to 25 percent of the walking cycle, both feet are in contact with the ground (double-limb support). In later life, when the steps shorten and the cadence (the rhythm and number of steps per minute) decreases, the proportion of double-limb support increases (see further on). Surface electromyograms show an alternating pattern of activity in the legs, predominating in the flexors during the swing phase and in the extensors during the stance phase.
When analyzed in greater detail, the requirements for locomotion in an upright, bipedal position may be reduced to the following elements: (1) antigravity support of the body, (2) stepping, (3) the maintenance of equilibrium, and (4) a means of propulsion. Locomotion is impaired in the course of neurologic disease when one or more of these mechanical principles are prevented from operating normally.
The muscles of greatest importance in maintaining the erect posture are the erector spinae and the extensors of the hips and knees. The upright support of the body is provided by righting and antigravity reflexes, which allow a person to arise from a lying or sitting position to an upright bipedal stance and to maintain firm extension of the knees, hips, and back, modifiable by the position of the head and neck. These postural reflexes depend on the afferent vestibular, somatosensory (proprioceptive and tactile), and visual impulses, which are integrated in the spinal cord, brainstem, and basal ganglia. Transection of the neuraxis between the red and vestibular nuclei leads to exaggeration of these antigravity reflexes—decerebrate rigidity.
Stepping, the second element of the gait cycle, is a basic movement pattern present at birth and integrated at the spinal, midbrain, and diencephalic levels. It is elicited by contact of the sole with a flat surface and a shifting of the center of gravity—first laterally onto one foot, allowing the other to be raised, and then forward, allowing the body to move onto the advancing foot. Rhythmic stepping movements can be initiated and sustained in decerebrate or “spinal” cats and dogs. This is accomplished in animals through the activity of interneurons that are organized as rhythmic “locomotor generators,” akin to the pattern generators that permit the rhythmic movement of wings or fins. There is no clear evidence for a similar system of locomotor control in monkeys or humans. There are poorly localized spinal mechanisms for walking in man but they cannot produce the act of walking and they require descending control from vaguely defined higher centers. These higher areas are located in the caudal midbrain tegmentum and pontine reticular formation (in or near the pediculopontine nucleus); they control the spinal gait mechanisms through the reticulospinal, vestibulospinal, and tectospinal pathways in the ventral cord (see Eidelberg and colleagues and Lawrence and Kuypers).
Moreover, these brainstem locomotor regions are activated by frontal cortical areas that are absolutely integral to initiating and engaging the gait cycle. Although a discrete “gait center” cannot be found in the cerebrum, frontal lesions can devastate gait as discussed further on. Often, the supplementary motor areas relating to the legs (superior frontal gyri on both sides) or periventricular white matter are implicated. In all likelihood, the medial frontal lobes embody automatic programs for walking that are intimately tied to adjacent networks in the striatum.