Phases in human walking (gait cycle), with diagrams

The gait cycle is the sequence of events between one event of one limb and the recurrence of the same event in the same limb. It has two phases: stance phase and swing phase.

Stance phase — the period when the foot is in contact with the ground. During double stance the weight is transferred from one foot to the other.

Swing phase — during single stance the centre of mass of the body passes over the supporting foot in preparation for shifting to the other limb, while the opposite limb swings forward.

Step is the period from initial contact of one limb to the initial contact of the contralateral limb.

Stride is the period from the initial contact of a particular limb to the point of initial contact of the same limb. A stride equals one gait cycle, and there are two steps in each stride. Figure 1. The walking gait cycle (one stride = one gait cycle)

Stance phase (approximately 60% of the cycle) has five sub-phases: initial contact (heel strike, 0–2%), loading response (0–10%), mid-stance (10–30%), terminal stance (heel off, 30–50%) and pre-swing (toe off, 50–60%).

Swing phase (approximately 40% of the cycle) has three sub-phases: initial swing (acceleration, 60–73%), mid-swing (73–87%) and terminal swing (deceleration, 87–100%).

Double support occupies about 20% of the cycle and occurs twice, at the beginning and end of stance. Double support disappears in running — this is the defining difference between walking and running.

Functional tasks: weight acceptance (initial contact and loading response), single limb support (mid-stance and terminal stance), and limb advancement (pre-swing to terminal swing).

Human locomotion depends on higher command and control centres in the brainstem and forebrain, and the pathway used depends on whether the stimulus is internal or external.

In normal, internally cued walking, the supplementary motor area (SMA) of the frontal cortex fires significantly just before gait initiation, and this preparatory activity is sent to the primary motor cortex (M1).

SMA activity is then switched off by phasic activity from the basal ganglia (BG), which provides a non-specific cue that both triggers the sub-movement and instructs the SMA to prepare the next signal. This BG–SMA interaction ensures smooth running of predictable, well-learned, automatic movement sequences.

When movement is externally cued, the BG–SMA pathway is bypassed and sensory information feeds directly into the pre-motor area (PMA) through visual, auditory and proprioceptive pathways.

The motor cortex, basal ganglia and cerebellum then pass input to the pedunculopontine nucleus (PPN), which projects to the brainstem reticular nuclei, from which instructions for gait pass along non-pyramidal pathways into the ventral spinal cord.

Clinical correlation — Parkinson’s disease: disordered cueing from the basal ganglia disturbs internal rhythm formation and impairs feedback to the SMA, producing bradykinesia, gait initiation failure and freezing. PD patients therefore rely on intact PMA (external cue) pathways — gait improves with external cues such as stepping over coloured patterns on the ground. Vascular dementia and stroke show a similar compensatory dependence on PMA pathways.

Gait speed declines 12–16% per decade, and maximum gait speed by up to 20%.

Step length is reduced and time spent in double limb support is increased — the body’s way of buying stability at the cost of speed.

Gait becomes slower, more uncertain and uncoordinated, and lacks a full range of motion, from stiffer joint capsules and ligaments and loss of muscle mass.

Feet are not picked up as high, increasing the tendency to trip. Older men develop a wide-based, short-stepped gait; older women a narrow-based, waddling gait. These changes correlate with white matter changes on MRI and with subsequent cognitive impairment.

After acute stroke, patients may show decreased hip and knee flexion during the swing phase, causing foot drag and tripping.