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.
Sayer, et al., demonstrated a progressive loss of measurable grip strength associated with glucose intolerance and diabetes.6 They noted an increasing loss of motor strength with chronicity of diabetes. They also found that an increasing loss of motor strength was associated with increasing levels of glucose intolerance even when a diagnosis of diabetes had not occurred.6
Anderson and colleagues demonstrated decreased strength of the ankle joint dorsiflexors in patients with diabetes.7 Decreased ankle joint dorsiflexion and plantarflexion strength were present in all patients with diabetes, were more profound in patients with asymptomatic neuropathy, and expressed even further in patients with symptomatic neuropathy. These authors concluded that all patients with diabetes have ankle and knee muscle weakness as a result of motor neuropathy associated with diabetes, and that the degree of weakness was related to the degree of neuropathy.
Understanding The Potential Impact Of Motor Neuropathy
The clinical manifestations of diabetic motor neuropathy include accelerated neurodegeneration and difficulty with walking and stopping, resulting in gait instability and an increased propensity to falling.8
In addition, researchers have suggested that diabetic motor neuropathy may represent a sentinel event in the evolution of Charcot’s joint disease. Jeffcoate, et al., have proposed that motor neuropathy results in joint instability and subluxation with altered force distribution within the joints of the foot.9 In the presence of vascular calcification and osteopenia, the altered force distribution results in microfracture inducing bone cytokine activity. In the presence of continued weightbearing, this results in bone resorption and breakdown in part due to increased blood flow secondary to the loss of sympathetic innervation.
Motor neuropathy significantly affects the intrinsic muscles of the foot, resulting in atrophy and weakness of the digital stabilizers. As a result of instability at the metatarsophalangeal joints due to weakness of muscles such as the lumbricales and interosseous muscles, hammertoes develop with secondary metatarsal head prolapse and increased forefoot plantar pressures.
In addition, instability of the midtarsal joint and midfoot joints occur due to loss of intrinsic muscle strength. Subluxation of the digits results not only in retrograde plantarflexion of the metatarsals and increased plantar pressure but also results in anterior fat pad displacement, which further increases the likelihood of ulceration. A recent study of 318 patients with plantar forefoot ulcerations revealed that the most common associated factors were male gender, mononeuropathies and motor neuropathies.10
Magnetic resonance imaging and volumetric studies have demonstrated atrophy of the intrinsic muscles of the foot associated with diabetic motor neuropathy. Anderson and colleagues demonstrated the total volume of intrinsic muscles in the feet of patients with diabetic neuropathy to be half of normal when studied by MRI.11 These authors further demonstrated that the degree of muscle atrophy is related to the severity of diabetic neuropathy.
Greenman, et al., recently demonstrated a small muscle atrophy not infrequently occurs prior to the clinical detection of neuropathy in a patient with diabetes. They also found that atrophy of the intrinsic muscles of the foot is common and that a strong association exists between diabetic peripheral neuropathy and the presence of intrinsic foot muscle atrophy.12
As a result of motor neuropathy and intrinsic muscle atrophy, hammertoe deformities develop in the patient with diabetes mellitus. Hammertoes are known to increase plantar pressure below the metatarsal heads and increase the risk of plantar ulceration.13 Researchers have also similarly demonstrated that the associated resultant plantar fat pad displacement increases focal plantar pressures and the risk of ulceration in the patient with diabetes.14
What You Should Know About Posterior Tibial Nerve Compression
Researchers have advocated decompression of the tarsal tunnel for the management of anesthesia, paresthesia and dysesthesia in the patient with diabetes mellitus.15 Not infrequently, patients with diabetes undergo posterior tibial nerve decompression in association with decompression of the common peroneal nerve and its branches as well as the deep peroneal nerve. Although such surgery is typically for relief of sensory associated signs and symptoms, it is intriguing to postulate whether this surgery might be indicated in order to help thwart the progression of motor neuropathy.
A significant number of patients with diabetes are known to have entrapment neuropathies.16 As noted earlier, the most common electrophysiologic findings are that of sensory and motor neuropathy, and not pure sensory neuropathy. Researchers have recently elucidated the use of diagnostic ultrasound for the diagnosis of tarsal tunnel syndrome in a patient with diabetes mellitus. Diffuse enlargement of the posterior tibial nerve, evidence of focal compression, venous encroachment and synovitis of the flexor hallucis longus represented the most common etiologic factors.14,17
Although the signs and symptoms of tarsal tunnel syndrome are typically sensory in nature, intrinsic muscle atrophy and weakness may occur. Electrodiagnostic studies demonstrating motor dysfunction may represent an indication for decompression of the posterior tibial nerve. Such changes would be present on electromyography and are consistent with denervation. In addition, progressive motor weakness of the anterior or lateral musculature of the leg may benefit from decompression of the common peroneal nerve and its branches.
Essential Keys To Detection And Treatment
The recognition of motor neuropathy in the patient with diabetes provides the podiatric physician with the opportunity to intercede and hopefully prevent or minimize many of the complications associated with motor neuropathy. In addition, the presence of motor neuropathy may alter surgical decision making in the patient with diabetes.
For example, recognition that the intrinsic muscles of the foot are no longer acting to stabilize the digits might suggest that, in certain patients, arthrodesis or flexor tendon transfer might represent more appropriate corrections for hammertoe deformity than standard resection arthroplasty. Similarly, the presence of motor neuropathy may be associated with a higher risk of complications following commonly performed procedures such as lengthening of the Achilles tendon or gastrocnemius recession as adjunctive procedures in the management of diabetes and associated foot pathology.
The treatment of motor neuropathy begins with recognition. In addition to the usual examination of the patient with diabetes for sensory deficit, the podiatric physician should devote equal effort to the detection of motor neuropathy. Elicitation of reflexes, manual muscle testing and observation for the presence of atrophy involving the plantar musculature or short extensor muscle belly should proceed in all cases.
Recognizing that motor neuropathy results in gait instability, deformities, ulceration and possibly the inciting of Charcot’s joint disease, one should consider appropriate intervention. Such interventions would include increased utilization of physical therapy for muscle strengthening. Consider the use of appropriate braces or orthotic therapy when indicated. Additionally, when electrodiagnostic studies demonstrate the presence of evolving motor deficit, one should consider decompression of the appropriate nerves.
Pharmacologic management of motor neuropathy requires remittive therapy. When it comes to the treatment of symptomatic sensory neuropathy, agents such as pregabalin (Lyrica, Pfizer) or tricyclic anti-depressants are antinociceptive in nature, and would not be expected to play a role in the management of motor neuropathy. Remind patients that proper management of diabetes is required in order to prevent the progression of motor neuropathy.
In addition, agents that are helpful in restoration of nerve function would be of potential benefit in reducing the progression of motor neuropathy. For example, researchers have demonstrated that the antioxidant alpha lipoic acid improves motor nerve conduction velocities.21
The use of methylcobalamin has demonstrated reversal of the progression of motor neuropathy symptoms and signs.22 More recently, Walker has demonstrated restoration and normalization of nerve function utilizing L-methyl folate, methylcobalamin, and pyridoxal 5’-phosphate (Metanx, Pamlab).23
Motor neuropathy in the patient with diabetes mellitus is responsible for significant pathology. The presence of motor neuropathy is frequently undetected because the average practitioner does not seek it in examination. Motor neuropathy plays a role in the development of gait instability and falls, Charcot’s joint disease, plantar ulceration and foot deformity. In addition, the presence of motor neuropathy may adversely affect the outcome of common surgical interventions.
When one has diagnosed motor neuropathy, control of diabetes and utilization of remittive agents helpful in restoration of nerve function represent cornerstones of management. Increased utilization of orthotics and braces may mitigate the effects of motor neuropathy on the foot and ankle. The potential role of decompression surgery to delay or reverse the effects of motor neuropathy is intriguing although speculative at this time.
Dr. Jacobs is a Fellow of the American College of Foot and Ankle Surgeons and a Fellow of the American Professional Wound Care Association. He is in private practice in St. Louis.
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