Abnormal joint powers before and after the onset of claudication symptoms

Abstract

Objective: Claudication is the most common manifestation of peripheral arterial disease, producing significant ambulatory compromise. Our study evaluated patients with bilateral lower limb claudication and characterized their gait abnormality based on advanced biomechanical analysis using joint torques and powers.

Methods: Twenty patients with bilateral claudication (10 with isolated aortoiliac disease and 10 with combined aortoiliac and femoropopliteal disease) and 16 matched controls ambulated on a walkway while 3-dimensional biomechanical data were collected. Patients walked before and after onset of claudication pain. Joint torques and powers at early, mid, and late stance for the hip, knee, and ankle joints were calculated for claudicating patients before and after the onset of claudication pain and were compared to controls.

Results: Claudicating patients exhibited significantly reduced hip and knee power at early stance (weight-acceptance phase) due to decreased torques produced by the hip and knee extensors. In mid stance (single-limb support phase), patients had significantly reduced knee and hip power due to the decreased torques produced by the knee extensors and the hip flexors. In late stance (propulsion phase), reduced propulsion was noted with significant reduction in ankle plantar flexor torques and power. These differences were present before and after the onset of pain, with certain parameters worsening in association with pain.

Conclusions: The gait of claudication is characterized by failure of specific and identifiable muscle groups needed to perform normal walking (weight acceptance, single-limb support, and propulsion). Parameters of gait are abnormal with the first steps taken, in the absence of pain, and certain of these parameters worsen after the onset of claudication pain.

Figure 1

An illustration of the three phases of walking with the dominant flexor and extensor muscle groups that are involved in each phase based on the joint torques generated. The dominant muscle groups are identified in black if they contract concentrically (muscle shortens as it contracts) and in grey if they contract eccentrically (muscle lengthens as it contracts). A) Weight acceptance phase. It is also known as early stance, initial contact and heel strike phase and lasts from ipsilateral heel strike to contralateral toe off thus covering the first double support phase (initial 20% of stance). The right leg is accepting most of the weight of the body as it descents from previously being in single support on the left leg. In this phase the right hip extensors concentrically contract to extend the hip (reflected in the HET torque and H1 power in Tables 3 and 4), the knee extensors eccentrically contract to allow the knee to bend (reflected in the KET torque and K1 power in Tables 3 and 4) and the ankle dorsiflexors eccentrically contract to maintain the ankle dorsi-flexed (reflected in the ADT torque and A1 power in Tables 3 and 4). B) Single limb support phase. It is also known as the mid-stance phase and lasts from contralateral (here left) toe off until contralateral heel strike. During single support the center of mass of the body is at its highest point and over the extended ipsilateral (here right) leg. The body has maximum potential energy getting ready to fall forward for the next double support. Limited muscular contractions are needed during this phase except its early part where the knee extensors contract concentrically to extend the knee and straighten the leg (reflected in the KET torque and K2 power in Tables 3 and 4) and the late part where the hip flexors contract eccentrically to control the movement of the pelvis (reflected in the HFT torque and H2 power in Tables 3 and 4). C) Propulsion phase. It is also known as the late stance or toe-off phase and lasts from contralateral heel strike to ipsilateral toe off. It is the last 20% of stance and it is the second double support phase. In this phase the body is propelled forward onto the extended left leg mainly by the action of the right ankle plantarflexors (posterior calf compartment muscles, the most important of which are the gastrocnemius and soleus). Functionally, these muscles contract concentrically (reflected in the APT torque and A3 power in Tables 3 and 4) and accelerate the trunk forward and upward over the left leg (i.e., providing forward progression and weight support). In this phase the knee flexors eccentrically contract, controlling the knee movement (reflected in the KFT torque and K3 power in Tables 3 and 4) and the hip flexors concentrically contract (reflected in the HFT torque and H3 power in Tables 3 and 4) to assist the ankle plantar flexors to accelerate the trunk forward and lift the leg over the ground into the swing phase.

Figure 2

Proposed pathway for the pathogenesis of gait impairment in patients with Peripheral Arterial Disease (PAD). The primary problem in claudicating patients is the presence of atherosclerotic blockages in the arteries supplying their legs. At rest, claudicating patients have adequate leg perfusion and experience no symptoms. During walking, however, the increased metabolic needs of the limb cannot be met and as the exercise continues the limb becomes progressively ischemic and painful, eventually forcing the patient to stop and rest. During rest, the metabolic demands of the limb return to baseline and the leg is reperfused. Repeated cycles of ischemia/reperfusion, occurring with basic daily activities, as simple as walking, initiate a combination of mitochondrial dysfunction, oxidative damage and inflammation which eventually produces a myopathy and axonal polyneuropathy in the claudicating limbs. We propose that the gait impairments we have identified at baseline (in the first few steps taken and prior to the onset of muscle pain) reflect the effects of this myopathy and neuropathy in the function of the PAD limbs. Several of these biomechanic impairments get worse after onset of claudication symptoms when exercise induced ischemia and increasing workload produce progressively worsening ischemic muscle pain and restriction of the lower extremity bioenergetics.