Analysis of gait
Figure 3.2 shows a quantitative gait analysis in a normal subject for the timing and amplitude of elec-tromyographic (EMG) activation of muscle groups (3.2a), the ground reaction forces elicited (3.2b), and the joint angles at the hip, knee, and ankle (3.2c) during the step cycle (Dobkin, 2003a). Surface and wire electrodes are used for EMG data. Electrogoniometers, computerized video analysis with joint markers, and electromagnetic field motion analysis will reveal the kinematics in two or three dimensions. Kinetics are measured by a force plate in the ground or embedded in a treadmill, as well as by a load cell embedded in a shoe. Energy cost is also measurable by oxygen consumption studies. These procedures take considerable expertise, time, and equipment to perform and analyze. The numerous variables collected and their interactions demand special statistical and modeling approaches. Of clinical importance, walking velocity correlates with many of the measured temporal parameters of the gait cycle. Formal gait studies are best reserved for a research laboratory and for presurgical evaluations of orthopedic and neurosurgical procedures. Knowledge of the typical patterns revealed by analyses in normal, hemi-paretic, and paraparetic subjects does help inform an observational analysis of a new patient.
The gait cycle can be assessed by educated observational skills and knowledge of the disease and its resulting symptoms and impairments. By combining a visual assessment of the stance (initial heel contact, foot flat, midstance, heel off) and swing phases (toe off, midswing, and end of swing heel contact), the clinician can look for temporal as well as kinematic asymmetries between the phase components for each leg. For example, a hemiparetic gait often reveals temporal differences - a shorter step length for the unaffected leg because the affected leg is impaired as it supports single-limb stance; greater double-limb support time compared to healthy persons, mostly from less time spent in single-limb stance on the affected leg; and shorter duration of swing for each leg. Kinematic differences include excessive flexion at the hip during midstance which, by moving the center of gravity forward, increases the knee extensor moment; decreased lateral shift to the paretic side during single-limb stance; less knee flexion and ankle dorsiflexion during swing, which may lead to circumduction of the affected leg or vaulting off the unaffected one to clear the affected foot; and initial contact with the whole foot or forefoot rather than heel contact followed by a rocker motion onto the forefoot that provides forward momentum. Using cluster analysis, formal gait studies characterized differences among patients based on walking velocity, knee extension in terminal stance, and peak dorsiflexion in swing during inpatient rehabilitation for stroke (Mulroy et al., 2003). At 6 months, explanatory variables of impairment were velocity, knee extension in terminal
(a) Stance phase Swing phase
(a) Stance phase Swing phase
stance, and knee flexion in pre-swing. Treatment approaches could address each of these patterns.
Paraparetic gait (Chapter 30 ofVolume II) during the stance phase may include absent heel strike, excessive hip and knee flexion and plantar flexion, pelvic drop with compensatory lateral shift of the trunk to the stance leg, and poor plantar flexor force for push off. During the swing phase, excessive plantar flexion and insufficient hip or knee flexion may impair foot clearance. The pelvis may drop on the swing side from weakness and overactive hip adductors may narrow the base of support. As in children with spastic diplegia from cerebral palsy, motor control of paraparetic gait is complicated by variations in residual selective strength, use of synergistic movements, loss of coordination of muscle firing patterns, hypertonicity that is state dependent, limitations in range of motion, tissue changes in muscles and across joints, and truncal and multi-joint interactions during stance and swing phases.
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