A 55-yr-old male with ankylosing spondylitis complained of progressive pain and difficulty with ambulation for the previous 8 mos. Despite having required multiple disease-modifying regimens for more than 20 yrs, he had remained independent with activities of daily living, and he was ambulatory without any assistive device. Eight months before presentation, he began to develop increasingly severe “crunching” pain in his hips and gluteal area, which forced him to lean forward with ambulation, such that he had required the use of a standard walker for the previous 6 mos.
On physical examination, he demonstrated an antalgic gait, forward flexion (35 degrees) at the hips, and a short stride length with a brief left-heel strike, but then an immediate transition to a left-forefoot stance and sagging at the knees into mild flexion. Left-leg midstance to toe-off was notable for toe walking throughout (Fig. 1). Examination of the hips revealed painful, limited hip range of motion, particularly in internal rotation and extension, with no loss of range of motion at the knees, feet, or ankles. Plain films of the hips showed severe, circumferential narrowing bilaterally, and fusion of the SI joints. Spine films showed significant ankylosis.
Why does this patient walk on his toes on the left foot immediately after an abnormally shortened heel strike? We suggest that the patient’s progressive, painful, degenerative loss of hip extension and rotation, combined with an ankylosed/fused spine (thus an inability to compensate with lordosis), leads to anterior migration of his weight line during ambulation. After heel strike, he transitions quickly into a left-forefoot stance, sagging at the knee into mild flexion to avoid the painful terminal knee and hip extension required for left-leg stance. He thereby maintains his center of gravity vertically and his sightline level by rising to his toes with flexed hip and knee during stance.
This is analogous to the more familiar case of toe walking in Duchenne muscular dystrophy, the progression of which has been described as follows1: weakness in gluteus maximus leads to lumbar lordosis, with all hip extension generated by the hamstrings. Tightness develops in the iliotibial band and tensor fascia lata, causing a wide-based gait. The quadriceps weaken, and to maintain passive stabilization of the weight line in front of knee and behind the hip, the patient rises up on his toes. Lastly, the neck is brought into mild flexion.
1. Johnson E. Pathokinesiology of Duchenne muscular dystrophy: implications for management. Arch Phys Med Rehabil