Cath Lab Digest

Although commonly present in the patient with diabetes mellitus, motor neuropathy frequently goes undetected. Less dramatic in presentation than sensory neuropathy, the presence of motor deficit secondary to diabetic neuropathy is frequently not evaluated during examination and subsequently goes unrecognized. There is also not a great deal of literature regarding the effects of diabetes on motor function in the lower extremity. As a result, the effects of motor neuropathy on the foot and ankle frequently go unappreciated.
Motor neuropathy in diabetes is common. A recent electrophysiologic study demonstrated that out of 167 consecutive patients with diabetes, sensorimotor neuropathy was present in 59.8 percent of patients while only 18.6 percent of patients demonstrated pure sensory neuropathy without demonstrable motor deficit.¹ In addition, researchers found the presence of compression neuropathy to be common.
The targeting of motor nerves in diabetic neuropathy is well established. Examination of streptozocin-treated mice has demonstrated retraction of the distal motor axon terminals at eight months and delayed motor conduction velocities with no actual motor nerve dropout.² Researchers have also demonstrated that the production of anti-ganglioside antibodies found in diabetic motor neuropathy initiates and perpetuates motor nerve damage.³

What The Literature Reveals About Motor Neuropathy
The initial descriptions of motor neuropathy associated with diabetes primarily involved proximal motor neuropathy, so-called “diabetic amyotrophy.” As elucidated by Garland, proximal motor neuropathy was regarded as “asymmetrical weakness, muscle wasting and areflexia in the legs without objective sensory disturbance in middle-aged patients with diabetes of relatively short duration.”⁴ Researchers generally believe proximal motor neuropathy primarily affects individuals over the age of 50 with leg weakness, which is primarily unilateral to presentation.
Additional descriptions of motor neuropathy in diabetes demonstrated involvement of the quadriceps, iliopsoas and hip adductors as well as the gluteal muscles, hamstrings and gastrocnemius muscles.⁵ The symptoms of motor neuropathy included observable wasting of the involved musculature, knee instability, difficulty with standing and walking, difficulty with stair and step climbing, and patient reports of pain.
With reference to the foot and ankle, early manifestations of motor neuropathy include loss of the Achilles tendon reflex and evolving digital deformities of the toes. Late manifestations include inability of the patient to stand on heels, observable atrophy of the muscles of the arch and of the short extensor muscle belly, gait instability and an increased incidence of falling.
More recent works suggest that motor neuropathy may play a role in the initiation of Charcot’s joint disease as well as ulceration. Dropfoot deformity, as a result of weakness in the anterior compartment muscles, and supination deformity, due to weakness of the pronator muscles, may result in significant functional impairment and gait instability.