I. Pain characteristics: shortened standing phase time of the affected lower limb, shortened stride length and decreased gait speed.
1. Hip pain: compensatory movements such as lowering of the shoulder joint on the affected side, elevation of the shoulder joint on the opposite side and excessive tilting of the trunk to the opposite side allow the body weight to cross over the painful joint to reduce the mechanical pressure on the joint surface to reduce pain.
2.Knee pain: mild flexion of the knee joint can reduce the tension of the joint capsule, and toe landing instead of foot following the ground.
3. Anterior foot pain: reduced plantarflexion of the ankle joint and loss of toe-off motion.
4.Ankle or posterior foot pain: when landing for the first time, the foot follows the ground and is replaced by the tip of the foot or the medial or lateral side of the foot.
II. Muscle weakness
(A) Gluteus maximus muscle weakness
1, the role of the gluteus maximus: hip extension and spinal stabilizer muscle (to prevent the body’s center of gravity from falling too far forward when the foot touches the ground.)
2, muscle strength decline in performance: the trunk in the entire standing phase always remain backward, the bilateral shoulder joints retracted, thus forming a thoracic convex abdominal gluteus maximus gait.
3.Mechanism: When the gluteus maximus muscle strength is weakened, its role is compensated by the paraspinatus muscle, resulting in the contraction of the paraspinatus muscle to pull the hip joint backward after the foot follows the ground in order to prevent falling, so that the body’s line of gravity falls behind the hip joint and locks the hip joint in the extended position.
4.Compensation: The simple weakness of the gluteus maximus muscle can be compensated by the contraction of the N cord muscle and make the gait close to normal. Clinically, if the S1 nerve root is damaged, the N cord muscle and the gluteus maximus muscle are damaged at the same time.
(B) gluteus medius muscle weakness
1.The role of gluteus medius muscle: hip joint abduction, play a role in stabilizing and supporting the pelvis.
2, muscle strength decreases when the performance of.
Unilateral: Trendelenberg gait, that is, when the affected side is in the standing phase, the pelvis on the healthy side declines, the pelvis on the affected side protrudes to the lateral side, the trunk tilts compensatingly to the affected side, the shoulder joint on the affected side is downward, the hip and knee flexion increases, and the ankle dorsiflexion increases.
Bilateral: swaying up and down and left and right, so called duck walk.
(C) Hip flexor muscle weakness
The hip flexor is the main accelerator muscle in the swing phase, and its muscle strength is reduced, resulting in the lack of power for limb travel in the swing phase, which can only be compensated by the trunk swinging backward at the end of the support phase and suddenly swinging forward at the early stage of the swing phase.
(D) Quadriceps palsy
1, three periods of quadriceps muscle involvement: the end of the striding phase DD extension of the lower leg standing phase DD eccentric contraction, control of knee flexion degree toes off the ground after DD initiation of the lower limb forward stride.
2, quadriceps paralysis, mainly manifested as the impact on the foot following the ground phase.
At this time, the gluteus maximus contraction maintains the proximal femur position and the triceps calf contraction maintains the distal femur position, thus locking the knee joint in the hyperextension position.
3. If there is also hip extensor weakness, some patients lean over and press the thigh with their hands to help extend the knee during the heel first landing phase and the standing phase.
4. Repeated knee hyperextension will greatly increase the load on the knee ligaments and joint capsule, leading to injury and pain.
(E) Anterior tibial muscle weakness
1. Role of anterior tibial muscle: dorsiflexion of ankle joint.
2. Performance
① When the anterior tibial muscle is weak, after the foot touches the ground, the support phase is shortened early and rapidly enters the middle of the support phase because the ankle joint cannot control plantarflexion. In anterior tibial muscle palsy, the patient develops foot drop in the swing phase, resulting in functional hyperextension of the lower extremity, often compensated by excessive hip flexion and knee flexion (cross-threshold gait), while the early phase of the support phase is preceded by full-foot or toe-to-toe contact with the ground, mostly in patients with common peroneal nerve palsy.
② Simultaneous and combined hip flexor weakness or lower extremity spasticity is manifested as toe dragging walking, accompanied by hip abduction and external rotation.
(F) gastrocnemius muscle weakness
1, gastrocnemius muscle role: stirrups away from the action at the end of the standing phase, prompting the leg to swing forward.
2, gastrocnemius muscle weakness: the explosiveness of the stirrup action is weakened, the body forward movement force is reduced, the movement is slowed down, slowing down the lower limbs forward, which leads to a shortened stride length, walking speed decreased.
III. Deformity
1, hip flexion deformity in the middle and late support phase: if the deformity is unilateral, the contralateral lower limb presents functional overgrowth, using hip lift marching or trunk tilt to compensate for the contouring function of the swing phase, and the stride length is shortened.
2.Knee flexion
It is less common and is usually caused by osteoarthritic deformities or lesions. Patients maintain a flexed knee position in both the support and swing phases. Patients must use compensatory mechanisms to stabilize the knee joint during the brace phase. The patient is unable to extend the knee at the end of the swing phase, resulting in a shortened stride length.
3. Knee stiffness has a joint flexion angle of <40 degrees (normal is 60 degrees) in the late brace phase and early swing phase, as well as delayed hip flexion in both the hip and swing phases. Knee flexion in the swing phase is driven by hip flexion, and a decrease in hip flexion will reduce knee flexion, resulting in foot dragging. Patients often use circle gait, try to lift the hip or tiptoe on the opposite lower limb to compensate in the swing phase.
4.If the ankle joint is plantar flexion deformed, the toe or forefoot is on the ground when walking, the trunk is leaning forward, the body weight is shifting forward, and the hip flexion and knee flexion increase when stepping phase.
IV. Sensory impairment
The proprioception provides joint position and movement information in joint activities, and has an important role in muscle tone regulation and muscle control; at the same time, the feedback mechanism of proprioception is important for maintaining the stability of joint function.
V. Central nervous system injury
(A) Hemiplegic gait
Typical hemiplegic gait performance: 1.
1.When the upper limb is swinging: shoulder, elbow, wrist and finger joints are flexed and internalized.
2. Lower extremity extensor synergy pattern: hip extension, inversion and internal rotation, knee extension, ankle plantarflexion and inversion.
3.Walking speed is slowed down, the stride length of the healthy side is shortened, the foot follows the ground when landing for the first time, and the knee is reversed.
4. The standing phase of the affected side is shortened, and the knee flexion angle is significantly reduced or disappeared due to the spasm of quadriceps muscle during the swing phase.
(C) scissor gait (scissorgait)
Causes: Spasm of the hip internal retractor muscle group, commonly found in patients with spastic cerebral palsy or traumatic brain injury.
Performance: When stepping phase, the lower limb steps forward medially, accompanied by N cord muscle spasm and knee flexion; ankle plantar flexor spasm appears with the front of the foot on the ground, and the toes drag the ground when the lower limb swings forward; the hip and knee are excessively flexed, the standing phase time is prolonged, the stepping phase time is shortened, the step base (support surface) is reduced, the stride length is reduced, and the step speed is slowed down.
(D) Parkinson’s disease gait (Parkinson’sgait)
Lesion site: basal ganglia.
Performance characteristics: bilateral motor control disorders and dysfunction, characterized by lack of movement and stiffness of the muscles of the face, trunk, upper and lower extremities.
Gait performance: difficulty in starting walking, prolonged double support phase, forward tilt of trunk during walking, mild hip and knee flexion, reduced joint range of motion, no plantar flexion of ankle joint during striding phase, shortened stride length and stride stride length, thin stride, almost disappearance of upper limb swing, easy to fall.
Panic gait: Patients walk rapidly forward with small steps, although it is difficult to start walking, and once started and difficult to stop, can not stop or turn at will, showing a forward or panic gait.
(E) ataxia gait (ataxicgait)
Causes: damage to the cerebellum or its conduction pathways; impaired sensation in the lower extremities.
Typical features: walking with two upper limbs abducted to maintain body balance, step base widening, high leg lift, foot landing heavy; can not walk in a straight line, but in a curve or in a “Z” shape; because walking is not easy to control, so walking swaying instability, like a drunkard, so also known as Moet gait or drunkard gait.
Lower extremity sensory impairment: manifested as a widening of the step base, rapid stride frequency (stumbling); at the same time, due to the lack of proprioceptive feedback, patients often need to look down at their feet when walking, and thus find it difficult to walk in the dark.