Hemiplegic CVA gait deviations and patterns

One of the major goals of rehabilitation for a patient recovering from a CVA is to

restore normal ambulation. Motor deficits of patients who suffered from CVA are characterized by muscle paralysis (hemiplegia) or weakness (hemiparesis) on the side of the body opposite to the site of the brain lesion (O’Sullivan, et al., 2001). This hemiplegia or hemipraresis may compromise the patients ability to generate adequate strength or control for voluntary movements. The major problems of gait of hemiplegic CVA patients can be described into two aspects on the gait deviations of: (1)

the stance phase and (2) the swing phase.

During the early stance phase, the gait deviations in ankle/ foot complex include equinovarus foot which resulting in initial contact of the forefoot, an unequal step length, a lack of dorsiflexion range on the involved side, and an instability of ankle joint in mid stance. At the end of the stance phase in normal gait, the body is forward progressing by the push-off power. However, for patients recovering from a CVA, such push off is difficult to be generated when the ankle is paralyzed. At the knee joint, weak knee extensors will either cause excessive flexion or hyperextension during forward progression. While normal gait producing small amount (about 20 degrees) of knee flexion during forward progression, an excessive flexed knee during forward progression is a result of a knee flexion contracture or delayed contraction of knee extensors. This causes an excessive ankle dorsiflexion of more than neutral combined with weak hip and knee extension weakness or poor propioception at knee and ankle.

In this situation, the knee joint remains an abnormal degree of 20 to 30 degrees during forward progression.

On the other hand, knee recurvatum during forward progression can be a result from weak knee extensors. As a stabilizing force to prevent the knee from buckling during mid-stance, the patient with CVA compensates by locking knee in hyperextension. This knee recurvaturm continues and delays forward progession. In

addition knee recuravatum during forward progression can result from an ankle plantarflexion contracture greater than 90 degrees or severe spasticity in quadriceps.

With impaired propioception, the knee is instable or snaps back into recurvatum.

Last, in gait deviations at hip joint, poor propioception or positioning (typically in hip adduction or flexion) is one of the gait abnormalities during stance phase. Also weak abductors at hip joint result in Trendelenburg limp during this phase.

While the swing phase, the ankle joint shows deviations on several aspects.

Ankle plantarflexors contracture or spasticity, dorsiflexors weakness, and delayed contraction of dorsiflexors cause the foot-drop pattern. This deviation causes toes dragging during mid-swing. Weak or spastic quadriceps causes inadequate knee flexion which induces insufficient foot clearance. And weak knee extensors or propioception causes inadequate foot positioning at the end of swing phase.

Gait analysis studies report reduced walking speed, lower stride length, lower cadence, and longer stance phases on paretic side are reported (Olney, 1996). A linear relationship between the decreased stride length and cadence with walking speed has been found (Nakamura et al, 1988). In addition, the relationship between cadence and walking speed are linear up to a speed of about 0.33 m/s and a cadence of about 90 step/

min. Furthermore, they found that further increase on waling speed primarily attribute to increases in stride length. Hsu determined that the walking speed of patients with

CVA ranged from 0.18 to 1.03 m/s depending on the level of severity (Hsu, 2003).

The changes in the proportion of stance and swing phase phase for the patients with a CVA are described as follow (Olney, 1996): first, the stance phase of both the paretic and non paretic side is longer in duration and occupies a greater proportion of the full gait cycle in subjects with CVA than in able-bodied walking at normal speeds; second, the stance phase is longer and occupies a greater proportion on paretic side than on non paretic side; third, a greater proportion of gait cycle is spent in double support than that of able-bodied walking at normal speeds.

Furthermore, joint motion is very different between normal and CVA hemiplegic gait. Comparing the results reported by Burdett et al with normal gait, hemiplegic gait was characterized by the following differences: (1) decreased hip flexion at heel-strike, increased hip flexion at toe-off, and decreased hip flexion during mid-swing; (2) more knee flexion at heel-strike and less knee flexion at toe-off as well as mid-swing, and (3) reduced ankle dorsiflexion at heel-strike as well as mid-swing and less ankle plantarflexion at toe-off (Burdett, 1988). Other evidence of kinematic and kinetic gait patterns is identified in three planes across patients with CVA in a study of Kim and Eng (2004). They found that in the frontal plane, a gait pattern different from that found in a normal person’s gait is identified at the hip joint on the paretic side. It displayed an additional hip abductor moment associated with a positive power burst at

toe-off into swing which resulted in a second abduction angle peak. Two common patterns are also identified at the knee in the frontal plane. The first pattern is an valgus moment throughout stance. This valgus moment was associated with a knee power generation phase resulting in knee valgus in early stance and a knee power absorption phase resulting in knee valrus during propulsion. In addition, a second pattern of knee varus moment just prior to toe-off is found in some of their subjects on their paretic and non-paretic limbs, respectively, which is associated with a power generation phase during propulsion.

In the transverse plane, except for the hip joint, Kim and Eng also noted that gait patterns on the paretic side are highly variable across those subjects. At the knee, at least two distinct moment patterns are identified. One pattern consisted of an external rotator moment for the first half of stance followed by an internal rotator moment in the latter half of stance on the involved side. Another pattern consisted of an internal rotator moment throughout stance. The knee power phases are very low and highly variable with only one consistent characteristic: a generation burst during push-off.

Several patterns are also identified at the ankle joint. The most predominant pattern is the pronation moment at the subtalar joint through most of stance. This moment pattern is associated with a consistent absorption burst during push-off resulting in subtalar supination as the heel lifted off from the floor and moved laterally on the

forefoot in contact with the ground.

Last, Kim and Eng identified in the sagittal plane, more than one type of gait pattern should be noted. On the paretic side, in addition to the typical knee extensor-flexor-extensor moment pattern found in normal gait, half of the subjects recovering from a CVA displayed a knee flexor moment pattern. This flexor moment pattern is associated with a kinematic knee extension thrust pattern in eight of those subjects. These subjects showed knee extended (or hyperextended) at weight acceptance which is not normally seen in normal gait. This corresponding knee power phase represented the negative work done by the knee flexors and other soft tissues eccentrically controlling the abrupt knee extension. In healthy gait, there is a phase that is commonly seen which occurred later in stance which produces positive work to flex the extended knee in preparation for swing phase. At the ankle joint, sagittal kinetic patterns differed between the paretic and non-paretic sides in that there was an absence of dorsiflexor moment at initial contact on the paretic side. The absence of the normal eccentric dorsiflexor moment resulted in a lack of plantarflexion after initial contact in those subjects (Kim and Eng, 2004).