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Key Insights On Nerve Testing
Are peripheral nerve pathologies the root cause of a patient’s lower extremity pain? These authors discuss entrapment neuropathies, large fiber neuropathy and lumbosacral radiculopathy, among other conditions, and share their insights on helpful diagnostic tools. In the podiatric profession, we are frequently faced with chronic painful musculoskeletal processes that get labeled as arthritis, chronic plantar fasciitis, neuroma, etc. Perhaps it would behoove us to start thinking of an underlying neurological pathology that may be responsible for foot or ankle pain. In the senior author’s opinion, there is more neurological pathology causing foot and ankle pain than is being diagnosed. This may explain the cases in which patients have chronic musculoskeletal conditions and undergo surgery, but their pain never improves. Accordingly, let us take a closer look at peripheral nerve pathologies that are common in the lower extremity and their physical examination findings along with appropriate diagnostic tools that may be useful. Polyneuropathies, both axonal and demyelinating, are peripheral neuropathies that are generalized and symmetrical. They are often described as a “stocking and glove” distribution that preferentially affects lower extremities before upper extremities. The symptoms of polyneuropathy can be divided into positive and negative ones. Positive symptoms include pain, paresthesias and fasciculations. Negative symptoms of polyneuropathy may include numbness, weakness, imbalance and gait instability. The loss of peripheral nerve function almost always involves axonal loss, which may occur uniformly in all types of axons or may predominantly affect one fiber type or size. There are five major function classes of axons that may be assessed by neurophysiologic techniques. These classes include: large myelinated motor axons (skeletal muscle control and reflexes); large myelinated sensory axons (vibration and proprioception); small myelinated sensory axons (cold and warmth sensation); unmyelinated sensory axons (pain); and autonomic axons (cardiac rate, blood pressure, sweating). In order to effectively diagnose neuropathy, one must ask subjective questions of patients as to whether they are experiencing positive or negative symptoms, and pursue an appropriate detailed neurologic examination of all the potentially affected nerve fibers. In regard to the neurologic exam, this would involve reliable testing procedures that are standardized, reproducible, simple, noninvasive and not time consuming. When You Suspect Large Fiber Neuropathy As we mentioned above, the symptoms of large fiber neuropathy consist of tingling numbness and poor balance. Testing for large fiber neuropathy should include deep tendon reflex, vibration perception threshold (VPT) and proprioception testing. Deep tendon reflexes (DTR) can be helpful in identifying motor nerve involvement. One can test DTRs with a reflex hammer. The test provides information associated with the integrity of the central and peripheral nervous system. Generally, decreased reflexes indicate a peripheral problem and lively or exaggerated reflexes indicate a central nervous system defect. One may quantify DTRs with a grading system. The reflexes one may test in lower extremity examinations should include patellar reflex or knee jerk reflex (L3), Achilles reflex (S1), plantar reflex or Babinski reflex (S1). Elicit the plantar reflex (PR) by stroking the lateral or outer border of the sole of the foot with the thumbnail or a blunt point like the end of the handle of the reflex hammer or the tip of a key. Direct the stimulus from the heel forward toward the little toe. Upon reaching the foot pad, direct the stimulus transversely across the metatarsal pad from the little toe to the base of the great toe. The stimulus should stop short of the base of the toes because extending the stroke to the base of the toes produces unpredictable movements. The plantar response may signal: • a normal flexor plantar response (plantarflexion of the foot and adduction of toes); or • a pathologic or abnormal extensor plantar response (Babinski’s sign), which involves dorsiflexion or extension of the great toe with or without fanning or abduction of the other toes. One can obtain the vibration perception threshold with different modalities. The simplest of these modalities is a 128-Hz tuning fork. Using the timed method, one places the tuning fork on the dorsum of the distal phalanx of the hallux just proximal to the nail bed. Ask the patient to report the time at which vibration diminished beyond perception. Then apply the tuning fork to the distal phalanx of your thumb. A greater than 10 second perception or less than 2 second perception has a specificity and sensitivity of 98 percent and 80 percent respectively. One can also perform the on-off method by placing the tuning fork at the same dorsal location of the hallux and asking the patient to indicate when vibration starts and when dampening causes cessation of vibration. Specificity is 99 percent for five or more insensate responses and sensitivity is 56 percent for two or more insensate responses. One can test the VPT using a biothesiometer or vibration meter in the office. Literature has shown that VPT is an independent risk factor for foot ulceration. The VPT has a higher positive predictive value than the Semmes-Weinstein Monofilament (SWM). The VPT has a sensitivity of 80 to 100 percent and a specificity of 73 to 81 percent in predicting foot ulceration. If patients are unable to feel the device at greater than 25 volts, then they are at high risk for neuropathy. A measurement of 16 to 24 volts constitutes intermediate risk and less than 15 volts is considered low risk. The advantage of a biothesiometer/vibration meter is that it is quantitative and reproducible. Pertinent Pointers On Testing For Small Fiber Neuropathy The small nerve fibers in the lower extremity involve cold, warmth and pain sensation. The most common and simplest testing modalities include: sharp versus dull sensation, cold versus warmth sensation, and the use of the Semmes Weinstein 5.07 10-g monofilament to test for protective threshold. When it comes to testing sharp versus dull sensation, one would commonly use an instrument that has a reproducible sharp point when you apply it to the skin. In our facility, we also use a wooden cotton swab. We break the swab in half and use the sharp point created from the break to test sharp sensation, and use the cotton tip to assess the patient’s ability to feel dull sensation. Ask the patient to close his or her eyes. Perform the test by touching the patient’s foot in all dermatomes to assess whether there is symmetric loss of sensation. A patient who has diabetic peripheral sensory neuropathy will have a decrease or loss of sharp sensation to a pinprick in a stocking glove distribution. In other words, the patient will begin to feel the sharp sensation as one gets closer to the midfoot or ankle, and possibly even to the mid-leg. A patient who has asymmetric loss of sharp sensation will either have a mononeuropathy, entrapment of a single nerve or lumbosacral radiculopathy. It is paramount, before the practitioner begins testing the different areas of the feet, to show the patient what the sharp sensation should feel like by testing the patient’s hand, presuming that the dorsum of the hand has normal sensitivity. Repeat the test on each foot and record the responses. A patient with a neurologic deficit would not be able to differentiate between sharp and dull sensation, or will have hyperesthesia to the sharp stimulus. The Semmes-Weinstein 5.07 10-g Monofilament is likely the most widely utilized tool for screening a patient for peripheral neuropathy in podiatry clinics across the United States and the world. The monofilament test can assess whether a patient has lost the small fiber function of light touch and pain sensation. It is important to remember that the SWM tests small fiber neuropathy. A negative test does not rule out the presence of large fiber neuropathy. Therefore, one should only use it as an isolated test if the patient has a positive loss of protective threshold on examination. There is no universally accepted guideline on how to use the monofilament or interpret the results. Researchers have suggested a reasonable sensitivity (80 percent) and specificity (86 percent) in testing the plantar aspect of the first and fifth metatarsal head respectively. While the 5.07/10-g monofilament has an approximately 90 percent specificity to detect an insensate foot, there is considerably more variation and lower sensitivity ranging from 44 to 71 percent. The typical sites are the plantar tufts of the first, third and fifth toes, and plantar first, third and fifth metatarsal heads. Other research has tested the dorsal hallux just proximal to the nail bed with the SWM and noted a sensitivity and specificity of 77 percent and 96 percent respectively. Perhaps the take home point in regard to using 5.07 SWM is not to use it as a single testing modality. A normal response to the 5.07 SWM does not rule out peripheral neuropathy. In 1998, Armstrong, et al., found that combining VPT, SWM and a subjective symptom score increases the specificity of predicting foot ulceration in comparison to using one of the above modalities alone.1 What You Should Know About Other Diagnostic Modalities Nerve conduction studies are strongly correlated with underlying structural changes and are the least subjective and most reliable single criterion standard of testing for neuropathy. Electromyography (EMG) and nerve conduction velocities (NCV) are among the most standard and widely available techniques for neurophysiologic quantization of peripheral neuropathy in large fiber neuropathy. They do not correlate with the assessment of neurologic function of small fiber neuropathy. This test can be fairly uncomfortable for the patient and is not considered a screening modality. Pressure Specified Sensory Device (PSSD, Sensory Management) testing may also measure pressure thresholds sensed by the patient. These thresholds include touch, both static and in movement, on a continuous scale. Reports have shown that with this test, patients with diabetes have poorer sensibility in comparison to controls and those diabetics with ulcers showed poorer sensibility than those without ulcers.2 In regard to pressure perception, studies have shown that quantitative sensory testing with the PSSD has a high sensitivity but a low specificity in comparison to electrodiagnostic testing for the diagnosis of peripheral nerve entrapment.3 Although this test is helpful, it may not be necessary if one performs a good clinical examination. How To Diagnose Lumbosacral Radiculopathy Radiculopathy is defined as nerve root disease from a known origin. The most common cause of lumbosacral radiculopathy is disc herniation. L5 and S1 nerve roots are the most commonly involved nerve roots. The involvement of these two nerve roots is why it is so important for clinicians to be aware of the clinical presentation of patients who have L5 and/or S1 radiculopathy. Typically, patients will present with the onset of low back pain. However, in some patients, the back pain will disappear as the leg and foot pain begins. The pearl here is to not always expect low back pain to accompany the leg and foot pain. Radiculopathy/sciatic pain is usually rather diffuse and difficult for the patient to localize. In other words, patients will not always present complaining of pain radiating from the buttocks to the foot. The lower extremity examination should consist of a thorough neurological examination that includes sensation, strength and reflexes. Performing a straight leg raise test may provide evidence of increased dural tension, indicating an underlying nerve root pathology. Clinicians should also perform a thorough musculoskeletal examination because one may confuse focal joint involvement with a lumbosacral radiculopathy. Combining the history and physical examination findings increases the overall predictive value of the correct diagnosis. Most disc herniations are self limiting and do not require surgical therapy. Roughly one-fifth of pain-free people under age 60 have evidence of a herniated disc on the MRI and 50 percent have evidence of a bulging disc. When working up a patient, be sure to check for the presence of fever, weight loss, and chills indicating an infectious process. Bear in mind that patients who are younger than 20 and older than 50 may be at increased risk for malignancies and infections. The importance of understanding lumbosacral radiculopathy is simply to avoid misdiagnosing foot conditions such as Morton’s neuroma, tarsal tunnel syndrome, plantar fasciitis and many other musculoskeletal conditions affecting the foot. The goal of the clinical examination should first confirm that the patient’s pain is lumbosacral in nature. With the physical exam, one must aim to identify symptoms that are present in a dermatomal or myotomal distribution. Whenever you suspect lumbosacral radiculopathy, one test that is essential is the straight leg raise test. The patient lies in the supine position and lifts a single leg with the knee extended. The physician can elucidate symptoms when the leg is between 30 to 70 degrees off the table. If no symptoms are present, the examiner may dorsiflex the foot in an effort to place additional tension on the sciatic nerve. At this point, note the location, quality and quantity of paresthesias created. This test serves to identify a potential problem between L5 and S1. If one suspects lumbosacral radiculopathy in a patient based on the previous in-office tests, the physician can often confirm the diagnosis via electrodiagnostic tests that one may obtain from a neurologist or a physiatrist. Once one makes the diagnosis of lumbosacral radiculopathy, refer the patient to an orthopedic spine specialist for future management. A Guide To Assessing Entrapment Neuropathy Entrapment neuropathy can be defined as “a group of syndromes resulting from entrapment or compression of a short segment of a nerve at a specific site. Frequently, the nerve is vulnerable where it passes through a fibro-osseous tunnel or an opening in fibrous or muscular tissue.” Any neighboring anatomic structure with the capability of irritating a nerve trunk, including muscle bellies, osseous surfaces and fibrous bands, can create compression. The best diagnostic tools for entrapment neuropathies are a thorough history and physical exam. The clinical picture of this process involves burning, tingling, pain and numbness, including shooting pain or an electric shock-like sensation. One may usually locate pain over the sensory distribution of the involved nerve. Podiatric physicians may also note dysesthesia, hypoesthesia and hyperesthesia with entrapment neuropathies, and can use those conditions to help localize a specific nerve at the entrapment site. The physical exam should be focused on sensorimotor findings. One may use physical exam findings such as Tinel’s sign, Valleix’s sign, active and passive manipulation of the extremity, and muscle strength testing (in advanced cases) to localize an entrapment point. Nerve conduction velocity studies, the PSSD and diagnostic local steroid/anesthesia injection are also helpful in diagnosing this condition. What About Tarsal Tunnel Syndrome? Tarsal tunnel syndrome, as described in 1962 by Keck and Lam, is the condition created by compression of the tibial nerve within the fibro-osseous tunnel posterior to the medial malleolus.4,5 This term is now more broadly accepted as including both the tibial nerve and any of its branches that may become entrapped in this area. The symptoms of tarsal tunnel syndrome are commonly localized to the medial aspect of the ankle or the bottom of the foot. However, the symptoms may extend to the heel, arch, toes or even the calf along the involved nerves. A positive Tinel’s sign and sensory impairment are the two most common clinical findings in tarsal tunnel syndrome. The best way to diagnose this condition is through a thorough history and physical although objective tests such as quantitative sensory testing, electrodiagnostic studies and MRI may be helpful. It is important to keep in mind that S1 radiculopathy or sciatica can mimic tarsal tunnel syndrome. A missed proximal nerve pathology stemming from the lower back may frequently be the cause of a failed tarsal tunnel decompression. Pertinent Perspectives On Entrapment Of The Peroneal Nerves And The Sural Nerve Common peroneal nerve entrapment is frequent due to its anatomical location over the periosteum while crossing over the fibula, also coursing through the fibrous hiatus in the origin of the peroneus longus. Patients with common peroneal nerve entrapment often present with pain and altered sensation over the dorsum of the foot and lateral aspect of the leg along with weakness or a lack of foot eversion and ankle dorsiflexion. A positive Tinel’s sign over the common peroneal nerve is the best clinical test. However, quantitative sensory testing (PSSD) and electrodiagnostic studies are important diagnostic modalities to utilize for objective evidence of the common peroneal nerve pathology. This nerve and its branches are at increased risk of entrapment simply due to their superficial location. The common entrapment points for the superficial peroneal nerve are the deep crural fascia approximately 10 cm above the ankle joint, and over the first metatarsocuneiform joint. An inversion ankle sprain can result in a traction injury of the superficial peroneal nerve where it exits the deep crural fascia above the ankle. We recommend using a pinprick test to map out the nerve deficit. Injury to the superficial peroneal nerve where it exits the fascia is purely a sensory injury and results in chronic pain. Aside from the pinprick test to map out nerve deficit, PSSD testing can give objective evidence of an injury. Electrodiagnostic testing will rarely show abnormalities with such a distal superficial peroneal nerve injury. The second entrapment site for the superficial peroneal nerve occurs at the level of the first metatarsocuneiform joint. One of the major risk factors for such an entrapment is the dorsal exostosis at the first metatarsocuneiform joint. This nerve is so superficial that it is frequently seen by the naked eye. The first metatarsocuneiform exostosis and the shoe gear worn by the patient causes compression of the nerve, which takes a very superficial course in this area. Percussing the area and getting a positive Tinel’s sign is pathogneumonic for the entrapment of this nerve. In addition, a pinprick test will aid in identifying the abnormal sensation in this anatomical area. Electrodiagnostic testing is not helpful when one is faced with this pathology. Deep peroneal nerve entrapment typically occurs at the level of the midfoot where the extensor digitorum brevis muscle crosses and entraps the deep peroneal nerve at the level of the base and shaft of the first metatarsal. The physical exam will likely reveal a Tinel’s sign at this site. Using the PSSD can aid in providing objective evidence of neurological deficit within the first interspace dorsally. The sural nerve and its branches travel in close proximity to the tendo Achilles, the lateral malleolus, lateral collateral ligaments and along the lateral fifth metatarsal. Entrapment of the sural nerve usually results from direct trauma and/or scarring secondary to surgical procedures in this vicinity. Fifth metatarsal base fractures can also cause entrapment by tenting the nerve. Physical examination consists of a pinprick test and looking for abnormal sensation along the sural nerve distribution. The PSSD and electrodiagnostic studies can provide objective evidence of sural nerve pathology. Keys To Diagnosing Morton’s Neuroma Podiatric physicians usually make the diagnosis of Morton’s neuroma from the patient history alone because the symptoms are usually characteristic and specific to this condition. The patient commonly describes pain and/or numbness in the distribution of the affected nerve and the inability to wear tight shoes. Patients will often describe the sensation of walking with an object in their shoe or a wrinkled sock. The adjacent toes may spread apart if the neuroma is large enough. A palpable click of the neuroma sliding between the metatarsal heads (Mulder’s click) may be present when one applies transverse pressure and simultaneously applies dorsal and plantar pressure to the intermetatarsal space. Diagnostic tests for Morton’s neuroma include radiographs, MRI and ultrasonography. The neuroma itself is not visible in plain radiographs but one can evaluate other pathological conditions such as juxtaposition, enlargement and rotation of the adjacent metatarsals. Radiographs can also rule out other pathologies. The neuroma will appear as hypointense relative to fat tissue on T-1 weighted MRI, and is difficult to differentiate from other surrounding tissues on T-2 weighted MRI. High resolution ultrasound can be a very accurate tool to visualize this type of neuroma but the accuracy is dependent upon the person administering the test. It is important to point out that not all forefoot pain is a neuroma and not all perceived neuromas should be surgically removed. One should approach forefoot pain with caution and the differential diagnosis should include lumbosacral radiculopathy. Dr. Reyzelman is the Chairman of the Department of Medicine at the California College of Podiatric Medicine at Samuel Merritt College. He practices privately in San Francisco. Mr. Fiorito, Mr. Hoover and Mr. Brewer are fourth-year students at the California College of Podiatric Medicine at Samuel Merritt College.
References:
1. Armstrong DG, Hussain SK, Middleton J, Peters EJ, Wunderlich RP, Lavery LA. Vibration perception threshold: are multiple sites of testing superior to single site testing on diabetic foot examination? Ostomy Wound Manage 44(5):70-74,76, May 1998.
2. Castro-Ferreriaz M, Rodriguez L, Fels K. New method for evaluation of cutaneous sensibility in diabetic feet. Rev Hosp Clin 59(5):286-290, 2004.
3. Tassler PL, Dellon AL. Correlation of measurements of pressure perception using the Pressure Specified Sensory Device with electrodiagnostic testing. J Occup Environ Med 37(7):862-66, July 1995.
4. Keck C. Tarsal tunnel syndrome. Orthop Clin N Am 44A:180, 1962.
5. Lam SJ. A tarsal-tunnel syndrome. Lancet 2:1354-1355, 1962.
Additional references
6. Rutkove SB. Focal cooling improves neuronal conduction in peroneal neuropathy at the fibular neck. Muscle Nerve 24:1622-1626, 2001.
7. Helionovara M, Knekt P, Aromaa A. Incidence and risk factors of intervertebral disk or sciatica leading to hospitalization. J Chronic Dis 40(3):251-258, 1987.
8. Hughes RAC. Peripheral neuropathy. BMJ 324:466-469, 2002.
9. Clinical Practice Recommendations 2007. Diabetes Care 30 Sup 1, January 2007.
10. Cavanah PR, Ulbrecht JS, Caputo GM. The biomechanics of the foot in diabetes mellitus. In The Diabetic Foot, 6th ed, p 138, 2001.
11. Mackinnon SE, Dellon AL. Surgery of the Peripheral Nerve. Thieme Publishers, 1988.
12. Vinik AL, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care 26:3333-3341, 2003.
13. Boulton AJ, Vinik AL, Arezzo JC, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care 28:956-962, 2005.
14. Olney RK. Clinical trials for polyneuropathy: the role of nerve conduction studies, quantitative sensory testing and autonomic function testing. J Clin Neurophysiol 15(2):129-137, March 1998.
15. Dyck PJ, Lehman KA, et al. The Rochester diabetic neuropathy study: design, criteria for types of neuropathy, selection bias and reproducibility of neuropathic tests. Neurology 41:799-807, 1991.
16. Resnick HL, Vinik AL, Schwartz AV, et al. Independent effects of peripheral nerve dysfunction on lower-extremity physical function in old age: the women’s health and aging study. Diabetes Care 23: 1642-1647.
17. Vinik AL Mehrabyan A. Diabetic neuropathies (Review). Med Clin North Am 88:947-999, xi, 2004
18. Dyck PJ, O’Brien PC. Meaningful degrees of prevention or improvement of nerve conduction in controlled clinical trials of diabetic neuropathy. Diabetes Care 12:649-52, 1989.
19. Liang MH, Katz JN. Clinical evaluation of patients with a suspected spine problem. In: The adult spine: principles and practice. Frymoyer JW, ed. New York: Raven, p. 223-39, 1991.
20. Charnley J. Orthopedic signs in the diagnosis of disc protrusion with special reference to the straight leg raising test. Lancet (4):186-92, 1951.
21. Moore KL. Clinically Oriented Anatomy. Baltimore: Williams & Wilkins; 1992.
22. Dyck P. The femoral nerve traction test in lumbar disc protrusion. Surg Neurol 6(3): 163-6, 1976.
23. Oh SJ, Meyer RD. Entrapment neuropathies of the tibial (posterior tibial) nerve. Neurol Clin 17:593-615, 1999.
24. Khwaja G. Plantar reflex. JIACM 6(3): 193-197, July-September 2005.
25. Pham H, Armstrong DG, Harvey C, et al. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care. 23(5):606-11, May 2000.
26. McGill M, Molyneaux L, Spencer R, Heng LF, Yue DK. Possible sources of discrepancies in the use of the Semmes-Weinstein monofilament. Impact on prevalence of insensate foot and workload requirements. Diabetes Care. 22(4):598-602, April 1999.
27. Perkins BA, Olaleye D, Zinman B, Bril V. Simple screening tests for peripheral neuropathy in the diabetes clinic. Diabetes Care. 24(2):250-6, Feb. 2001.
28. Britland ST, Young RJ, Sharma AK, Clarke BF: Association of painful and painless diabetic polyneuropathy with different patterns of nerve fiber degeneration and regeneration. Diabetes 39:898-908, 1990.