Current Concepts In Diagnosing And Treating Drop Foot

Author(s): 
Nicholas Romansky, DPM, Kelly Scollon-Grieve, MD, and James G. McGinness, CPO

Drop foot can have a complex etiology and the effects of the condition can affect quality of life for patients. These authors provide insights on the workup and diagnosis of drop foot, and discuss treatments ranging from medical therapies and surgery to AFOs and functional electrical stimulation.

Drop foot is a weakness of ankle dorsiflexion and is frequently accompanied by weakness of the extensor hallucis longus and extensor digitorum longus muscles, causing difficulty with dorsiflexion of the toes. This results from a deep fibular (peroneal) nerve compromise. Physical examination findings consistent with a drop foot are difficulty clearing the foot during the swing phase of the gait cycle, a steppage gait, an equinovarus deformity of the foot and ankle, and an uncontrolled foot slap.1

   Motor symptoms present with drop foot as well as weakness of other muscles that the common peroneal nerve supplies. An essential component of drop foot is paresthesias that accompany the distribution of the common peroneal nerve.
Radiculopathy at the L4/5 level is the most commonly recognized cause of drop foot. It is usually the result of a disc herniation or foraminal stenosis at that level compressing the L4 and/or L5 nerve roots.2

   After radiculopathy, the second most common cause of drop foot is a common fibular (peroneal) neuropathy. The common fibular nerve originates in the popliteal fossa as one of two terminal divisions of the sciatic nerve and then divides at the fibular neck into the deep and superficial peroneal nerves.

   The fibular nerve is most often injured as it traverses around the fibular neck. The most common cause of nerve injury is external compression, which can happen in hospitalized patients due to rapid weight loss and compression from the bed rails, from casting or pneumatic compression devices. In addition, individuals with habitual leg crossing are subject to external compression. Common or deep fibular nerve injury can occur during surgical procedures such as a total knee arthroplasty, in which the nerve may be injured due to traction or compression.

   Other causes of common fibular nerve injury include: trauma; traction of the common fibular nerve with an inversion and plantarflexion ankle injury; prolonged squatting (strawberry picker’s knee); compression by an intraneural or extraneural mass lesion; diabetic neuropathy; inflammatory neuropathy; and vascular pathology.1

   Direct trauma to the tibialis anterior muscle that causes rupture or compartment syndrome may also lead to drop foot. Drop foot can also be a complication of rapid weight loss for two reasons. A decreased fat pad surrounding the fibular nerve at the fibular head can subject the area to increased compression from external sources. Alternately, a patient may have micronutrient deficiencies (i.e. vitamin B12) after bariatric surgery.3

   Peripheral nerve injuries can also arise from lumbosacral plexopathy and injury of the common fibular division of the sciatic nerve. Upper motor neuron causes are rare but one must consider them. These causes include: cerebrovascular accident, motor neuron disease, amyotrophic lateral sclerosis, multiple sclerosis, brain tumor and spinal cord injury.2

   The lumbosacral spine origin of drop foot is more common than one would think. Podiatrists need to look above the foot and ankle, and listen to the patient. One should first ask the patient if he or she has any history of lumbosacral spine symptoms or origin in the past. Ask the patient if there is any other joint pain. This may help find or localize the origin and cause of symptoms.

   Drop foot can occur prior to lumbosacral spine surgical nerve decompression as a result of nerve decompression or because of an intraoperative complication of decompression. The etiology in these cases revolves around acute and chronic lumbar degeneration.4 Typically, the result of surgical nerve decompression depends on the acute or chronic nature as well as magnitude and duration of compression of the L-S spine. If surgery occurs, most improvement occurs six weeks postoperatively.

   Drop foot can occur following hip and knee replacement with damage and localized hematoma to the sciatic nerve and its branches. This is especially the case if bleeding occurs at the operative site.

   For a full list of drop foot etiologies, see “A Guide To Common Drop Foot Etiologies” at right).4-9

Pertinent Pearls On The Workup And Diagnosis Of Drop Foot

The workup of a drop foot should include a thorough neurologic exam to rule out any more serious central or primary causes of the drop foot. This includes motor strength testing and sensation and reflex examination of all limbs, including assessment for pathologic reflexes such as Babinski, Hoffmann’s and clonus reflexes.

   Physicians must access the entire clinical picture through the use of laboratory studies and other diagnostic modalities. Nerve conduction and electromyographic studies are an important extension of the neurologic examination as they can help zero in on the local site of injury, establish the degree of damage and predict the degree of recovery. Laboratory studies to evaluate for a metabolic or toxic cause may be indicated if there is no trauma or obvious cause for the drop foot. The following tests are useful: fasting blood sugar, hemoglobin A1c, erythrocyte sedimentation rate, C-reactive protein, serum protein electrophoresis, blood urea nitrogen, creatinine and vitamin B12 levels.1

   Imaging is also important in establishing the cause of drop foot. If there is trauma to the area, plain films of the tibia and fibula are indicated to determine if there is any bony injury. One may employ magnetic resonance imaging (MRI) to help evaluate for local tibia/fibula injury, brain injury, spinal cord pathology or nerve root impingement. Ultrasound evaluation of the peroneal nerve may be useful in assessing for a focal entrapment around the fibular head.1

   One must take numerous factors into account when deciding on the treatment approach for the individual with drop foot. The etiology, chronicity, prognosis, distribution, location, severity and medical comorbidities are critical factors. Treatment modalities can consist of nonsurgical, surgical and brace assistance, or any combination of the above.

How Effective Are AFOs And Bracing?

Bracing with an AFO and physical therapy is useful in all causes of drop foot to assist in ambulation and prevent contracture of the ankle plantar flexors. Clinicians may use conventional AFOs for those who would benefit from minimal skin contact. These patients would include those who have lower limb swelling, circulation concerns, and/or insensitivity.

   The primary purpose of the AFO is to increase dorsiflexion during swing phase, provide medial and lateral stability at stance, and possibly increase pushoff stimulation at the late phase of stance. An equinus contracture can decrease the maximum success of the AFO. Generally if the AFO is constructed for anterior use to the malleoli, it requires rigid immobilization, which one would employ in patients with upper motor neuron lesions or diseases, or post-cerebrovascular accident victims. If an AFO fits posterior to the malleoli and plantarflexes at heel strike, push off occurs to neutral during swing phase, providing dorsiflexion assistance. This results in a more natural, functional gait.

   The Foot Up Device (Innovative Technologies) is a simple AFO that works surprisingly well for partial drop foot.

   Years ago, the profession considered short leg braces, conventional or metal bracing attached to the shoes as the main solution for this gait dysfunction. A simple leg tracing, accurate measurements and a skilled orthotist are all that is necessary to construct this type of brace. Providing enough dorsiflexory assistance often required the use of a Klenzak ankle system in which dual spring mechanisms supply assistive forces that would overcome the resistance of the foot and ankle with no active dorsiflexion. One can modify all the patient’s shoes for removal of the brace, which allows easy shoe interchange.

   The advent of plastic bracing has been an especially significant addition for the treatment of drop foot. This process involves the orthotist taking a cast of the lower limb and carefully crafting a custom made orthosis. Various modifications, such as the addition of joint systems with these thermoplastic braces, can further customize the treatment of the individual patient’s condition. Tamerac joints simulate spring action and assist the foot and ankle in moving through a normal range of motion. Controlled ankle motion joints can limit joint motion to a specific degree range of motion. In treating drop foot and other mechanical problems of a weakened foot and ankle, another axiom is to brace only what the deficit demonstrates. Over-bracing, while well intended, may weaken other critically needed support systems of the ankle complex. If patients are always in the brace, then the leg muscles go unused and the muscles weaken.

   However, there are certain contraindications for bracing. Do not recommend plastic bracing if the patient has swelling of the lower extremities, insensate feet or compromised circulation. In our opinion, the condition of diabetes is also a valid reason for not prescribing a total contact plastic orthoses. Skin breakdown problems can be daunting and may ultimately lead to additional complications.

   The adaptation of new materials has provided us with a new option for the treatment of drop foot. Carbon fiber AFOs are very light and offer very good cosmesis. Although it may come in different designs, the single carbon upright extends from the foot plate and up the posterior portion of the leg. Using the stored potential energy principle at heel strike, the brace allows the foot to plantarflex as normal. When the foot is flat and subsequent to initiation of toe off, the brace coils and picks up the toe in time to offer clearance for swing through.

   The advantages of this brace are that it has minimal skin contact and is very comfortable for the patient to wear. The disadvantages include patient weight limitations as well as the need to avoid aggressive bending while hyperflexing, which may lead to brace failure.

   Negative aspects of conventional bracing include heaviness of the orthoses and the possible stigma of wearing braces. In general, patients quickly become accustomed to wearing this brace and find that the benefits outweigh the negatives.

A Closer Look At Medical Therapy Options

Alternative and adjunctive treatments may include oral antidepressants such as amitriptyline (Elavil, Merck), nortriptyline, gabapentin (Neurontin, Pfizer) and pregabalin (Lyrica, Pfizer). Other options are oral and topical non-steroidal anti-inflammatory drugs (NSAIDs) such as capsaicin, diclofenac, nabumetone (Relafen, GlaxoSmithKline), meloxicam (Mobic, Boehringer Ingelheim), a Flector patch (Pfizer) or a Lidoderm patch (Endo Pharmaceuticals).

   There are companies and local pharmacies that “compound” topicals to meet the specific needs of the patient. For example, one can also use customized topical components with ketoprofen, amitriptyline or gabapentin. Oral or transdermal narcotics are options but one should use them in a limited fashion. Optimizing the control of other comorbidities such as diabetes, hypothyroidism and vitamin deficiencies of B1, B6 and B12 can also be useful.

   One may also consider chemodenervation and nerve blocks in combination with AFOs.10 In the last few decades, chemodenervation has emerged as a treatment option, especially for intramuscular hyperactivity in upper motor neuron syndromes. This process helps clinicians to manage focal muscle or muscle activities through the use of agents such as botulinum toxin (Botox, Allergan), Myobloc (Solstice) or Dysport (Medicis). One can use phenol alone or phenol and alcohol combined and injected. These modalities have been in use in the last four decades.

   The agent one uses depends on the patient’s clinical entity and the strengths and weaknesses of the individual agents. One can use these agents for short-term or for sustained effort. Nerve blocks and regional anesthesia can be useful for both diagnostic and long-term therapeutic motor and sensory treatment.

   In addition to conventional therapy, more proximal involvement should occur on the contralateral side. Patients should perform proximal core strengthening and stability exercises including those for the gluteus medius and piriformis, and hamstring stretches in addition to Pilates and yoga.

Can Functional Electrical Stimulation Have An Impact?

Functional electrical stimulation can be beneficial for patients diagnosed with drop foot. Patients with intact peripheral nerves who have suffered from central nervous system disorders such as stroke, traumatic brain injury, multiple sclerosis, spinal cord injury or cerebral palsy are the most appropriate candidates for functional electrical stimulation.11 Also, if the patient has a history of poor adherence with AFOs or has rejected them in the past due to bulk, weight, heat or limitations in shoewear, functional electrical stimulation is an excellent alternative.

   Functional electrical stimulation systems such as the WalkAide® (Innovative Neurotronics) apply low-level electrical currents directly to the common peroneal nerve to help restore functional dorsiflexion during walking. The unit fits in a cuff that attaches to the proximal calf region just below the knee. The system has the ability to measure the position and speed of the lower limb through inclinometers and accelerometers, and the electrical current flows through self-adhesive electrodes that attach inside the cuff. A unique feature of the WalkAide system is the tilt sensor, which analyzes angular velocity during the gait cycle to know when to send the appropriate stimulus to the muscle. Other systems use a heel switch, which can complicate the triggering of the system and make for a more inefficient gait pattern.11

   After the initial training on donning and doffing of the self-contained cuff system, most patients are able to do this themselves. Placement of the electrodes within the cuff on the limb may require an initial marking on the skin for the patient to assist in placement but with time, patients can become proficient at knowing exactly where their “sites” are and how the electrodes must be aligned.

   When it comes to using electrical stimulation versus an AFO, there are several advantages. First, with functional electrical stimulation, patients have the ability to produce an active contraction that will help to prevent muscle atrophy. Additionally, motor learning and neuroplastic changes in the central nervous system are enhanced by the repetitive active movement that occurs with gait facilitated by functional electrical stimulation.12

   A recent study conducted at the National Institutes of Health further supports the evidence base for using functional electrical stimulation to improve gait.13 The study looked at 19 children with the diagnosis of cerebral palsy ranging in age from 7 to 20. The investigators documented the children’s gait pattern initially after a four-week “training” period and after a three-month treatment period with the WalkAide functional electrical stimulation system.

   The outcomes showed that 95 percent of the kids chose the functional electrical stimulation as the preferred treatment over wearing a brace or not wearing anything.13 The participants wore the unit for an average of 5.7 hours per day and demonstrated improved kinematics including improved dorsiflexion during the swing phase of gait as well as at initial contact. In addition, the use of functional electrical stimulation allowed plantarflexion at toe off during gait, which an AFO typically blocks.

   While functional electrical stimulation is continuing to demonstrate a viable alternative to AFO use for many patients with drop foot, it is not for everyone. Patients with peripheral nerve pathologies such as poliomyelitis, lumbar spinal stenosis, Guillain-Barré syndrome or spinal disc injury are not candidates. In addition, functional electrical stimulation is contraindicated for individuals with pacemakers, defibrillators, fixed plantarflexion contractures or if they have a history of seizure disorder.

   Functional electrical stimulation does little to control knee or ankle stability so one must consider this when evaluating a patient for his or her appropriate needs. One can also consider incorporating the use of a supramalleolar orthosis, a University of California Biomechanics Lab device or custom foot orthoses with the use of functional electrical stimulation. Managing patients with the right combination of treatments typically results in greater success and more patient satisfaction.

   While there are notable contraindications for the use of functional electrical stimulation to improve gait, it can be a viable alternative for many individuals with drop foot. A recent patient who suffered an incomplete T5-T6 spinal cord injury is thrilled to be able to go without the use of a traditional style AFO. She wears her functional electrical stimulation unit 12 to 14 hours a day and is able to independently don and doff the unit. She is also able to wear almost any shoe she wants. When she travels to Florida in the winter, it does not present her with issues of bulk or heat.

   Additionally, we have seen improved gait characteristics such as increased dorsiflexion during swing and at initial contact with functional electrical stimulation.

Key Insights On Surgical Solutions For Drop Foot

The surgical goal is to achieve a stable, well-aligned foot and ankle to leg relationship. Removal of the source of compression is usually necessary if it is a focal compression of the fibular nerve, sciatic nerve, nerve root, or spinal cord or brain tumor.

   Surgical options in the lower extremity include ankle arthrodesis and tendon transfer. Arthrodesis may occur at the ankle joint, Lisfranc’s joint or with a triple/pantalar arthrodesis with or without Achilles tendon lengthening. For symptomatic relief of pain, consider analgesics, neuropathic pain medications and nerve blocks.1,14

   Drop foot due to direct trauma to the dorsiflexors generally requires surgical repair. When nerve injury is the cause of drop foot, treatment focuses on restoring the nerve continuity by nerve grafting (transfer of functional fascicles, nerve repair or removal of the nerve insult). Many surgical techniques are available. These techniques typically involve modification of the Bridle procedure with and without the Achilles tendon lengthening to achieve adequate dorsiflexion. In patients with drop foot due to residual neurological or anatomical factors such as polio or upper motor neuron lesions or Charcot foot, arthrodesis may be the preferred surgical option.

In Conclusion

The podiatrist must determine a complete clinical diagnosis, including the performance of a comprehensive clinical neurologic exam. The podiatrist should involve other healthcare providers such as a physical medicine rehabilitation professional or interventional spine MD or DO. A team approach of individuals including an orthotist and prosthetist is absolutely imperative for successful outcomes and a maximally functioning patient. The single use of one treatment option is strongly discouraged as a combination of treatments in linear fashion should maximize the function of the patient.

   There are specific tests and modalities available. These include electrical stimulation guidance, MRI of the L-S spine to further delineate local or more proximal causes, electromyography, electromyography signal amplifiers, computed tomography scan, fluoroscopy and ultrasound. All of these modalities can aid in the diagnosis and treatment of drop foot.

   Dr. Romansky is a Fellow of the American College of Foot and Ankle Surgeons. He is in private practice at Healthmark Foot and Ankle Associates in Media and Phoenixville, Pa.

   Dr. Scollon-Grieve is in private practice at Premier Orthopaedic Sports and Spine Rehabilitation Division in Havertown, Pa.

   Mr. McGinness is affiliated with JG McGinness Prosthetics & Orthotics in Norristown, Pa.

References

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3. Weyns FJ, Beckers F, Vanormelingen L, et al. Drop foot as a complication of weightloss after bariatric surgery: is it preventable? Obes Surgery. 2007; 17(9):1209-12.
4. Ghahreman A, Ferch RD, Rao P, Chandran N, Shadbolt B. Recovery of ankle dorsiflexion weakness following lumbar decompressive surgery. J Clin Neurosci. 2009; 16(8):1024-1027.
5. Ramanan M, Chandran N. Common peroneal nerve decompression. ANZ J Surgery. 2011; 81(10):707-712.
6. Shultz SP, Sitler MR, Tierney RT, Hillstrom HJ, Song J. Consequences of pediatric obesity on the foot and ankle complex. J Am Podiatr Med Assoc. 2012; 102(1):5-12.
7. Da Cunha-Bang SA, Crone C, Christensen T. Non-Hodgkin’s lymphoma presenting drop foot. Clinical Neurol Neurosurg. 2012; epub March 22.
8. Kelly JJ, Karcher DS. Lymphoma and peripheral neuropathy: a clinical review. Muscle Nerve. 2005; 31(3):301-13.
9. Koffman BM, Greenfield LJ, Ali II, Pirzada NA. Neurologic complications after surgery for obesity. Muscle Nerve. 2006; 33(2):166-76.
10. Elovic EP, Esquenazi A, Alter KE, et al. Chemodenervation and nerve blocks in the diagnosis and management of spasticity and muscle over activity. Am Acad Phys Med Rehab. 2009; 1(9):842-851.
11. Cameron MH. The WalkAide functional electrical stimulation system – a novel therapeutic approach for drop foot in central nervous system disorders. European Neurological Review. 2010; 5(2):18-20
12. Everaert DG, Thompson AK, Chong SL, Stein RB. Does functional electrical stimulation for drop foot strengthen corticospinal connections? Neurorehabil Neural Repair. 2010; 24(2):168-77.
13. Prosser L, et al. Effectiveness of a novel functional electrical stimulation device to improve unilateral drop foot in cerebral palsy. Abstracts of the American Academy of Cerebral Palsy and Developmental Medicine 65th Annual Meeting. October 2011.
14. Ring H, Tregar I, GruendingerL, Hausdorff JM. Neuroprosthesis for footdop compared with an ankle-foot orthosis: effects on postural control during walking. J Stroke Cerebrovasc Dis. 2009;18(1):41-7.

Additional References

15. Doug O, Apaydin D, Sevim S, Talas DU, Aral M. Ultrasound-guided versus ‘blind’ injection of botulinum toxin-A for treatment of sialorrhoea in patients with Parkinson’s Disease. Clin Neurol Neurosurg. 2004; 106:93-96.
16. Yang EJ, Rha D, Yoo JK, Park ES. Accuracy of manual needle placement for gastrocnemius muscle in children with cerebral palsy checked against ultrasonography. Arch Phys Med Rehabil. 2009:90:741-744.
17. Sabut SK, Sikdar C, Kumar R, Mahadeveppa M. Improvement of gait and muscle strength with functional electrical stimulation in subacute and chronic stroke patients. 33rd Annual International Conference of IEEE EMBS. Boston, Massachusetts, August 30-September 3, 2011.
18. Bale M, Strand LI. Does functional strength training of the leg in subacute stroke improve physical performance? A pilot randomized controlled trial. Clin Rehabil. 2008; 22(10-11):911-921.
19. Gritsenko V, Prochazka A. A functional electric stimulation assisted exercise therapy system for hemiplegic hand function. Arch Phys Med Rehabil. 2004; 85(6):881-5.
20. Fullerton B, Erler A, Phlmann B, Gerlach FM. Predictors of dropout in German disease management program for type 2 diabetes. BMC Health Services Research 2012; 10:8.
21. Stewart JD. Drop foot: where, why and what to do? Pract Neurol 2008; 8(3):158-69.
22. Kuntz C 4th, Blake L, Britz G. Magnetic resonance neurography of peripheral nerve lesions in the lower extremity. Neurosurgery. 1996; 39(4):750-6; discussion 756-7.
23. Elfar JC, Jacobson JA, Puzas JE, Rosier RN, Zuscik MJ. Erythropoietin accelerates functional recovery after. J Bone Joint Surg Am. 2008; 90(8):1644-53.

   For further reading, see “Key Insights On Tendon Transfers For Drop Foot” in the May 2009 issue of Podiatry Today. To access the archives, visit www.podiatrytoday.com.

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