Evaluation of a Patient with a Referring Diagnosis of Bilateral Carpal Tunnel Syndrome and Lumbosacral Radiculopathy with Electrodiagnostic Findings of Generalized Peripheral Polyneuropathy
Greathouse DG, Painter EE. Evaluation of a Patient with a Referring Diagnosis of Bilateral Carpal Tunnel Syndrome and Lumbosacral Radiculopathy with Electrodiagnostic Findings of Generalized Peripheral Polyneuropathy. JCEWM. 3(1). doi:10.55566/JCEWM-D-24-00008
Electrodiagnostics
Evaluation of a Patient with a Referring Diagnosis of Bilateral Carpal Tunnel Syndrome and Lumbosacral Radiculopathy with Electrodiagnostic Findings of Generalized Peripheral Polyneuropathy
Greathouse,David G.PT, PhD, FAPTA1, Painter,Elizabeth E.PT, DSc, FAAOMPT2 1U.S. Army-Baylor University Doctoral Programs in Physical Therapy, 2Neurosurgery and Spine Consultants, San Antonio, TX
Keywords: polyneuropathy, nerve conduction studies, needle electromyography
https://doi.org/10.55566/JCEWM-D-24-00008
Journal of Clinical Electrophysiology and Wound Management
Vol.3, Issue 1, 2025
This case details the subjective and objective clinical exams, electrodiagnostic testing, and interventions for a 73-year-old man referred for electrodiagnostic testing with diagnoses of bilateral median mononeuropathy at or distal to the wrist or carpal tunnel syndrome (CTS) and lumbosacral radiculopathy. Findings in the subjective and objective clinical exams suggested that the patient may have a polyneuropathic process affecting his distal extremities in addition to likely median mononeuropathy at or about the wrists and lumbosacral radiculopathy affecting the lower extremities. The physical therapist performed additional clinical exam procedures and planned an electrodiagnostic exam that would evaluate the patient for these potential differential diagnoses. Electrodiagnostic testing, including nerve conduction studies (NCS) and needle electromyography (EMG), demonstrated a generalized, symmetrical, length dependent, sensorimotor, peripheral polyneuropathy in both upper extremities (BUE) and both lower extremities (BLE) with both significant axonal loss and demyelination. Chronic denervation was noted in BUE and BLE distal muscles tested.
A neurologist confirmed the generalized peripheral polyneuropathy (GPPN) in BUE and BLE and determined the etiology of this disease process as “idiopathic”. The patient was started on intravenous immunoglobulin therapy (IVIG) on a monthly basis and given steroid injections in both wrists by an orthopaedic hand surgeon. Six months following the start of IVIG, the patient characterized this intervention as “successful” with decreased pain and sensory disturbance in both hands and feet.
Nervous system dysfunction is complex and requires critical reasoning that combines both diagnostic and prognostic assessment.1–3 Planning the electrodiagnostic exam requires careful consideration of the referring clinical diagnosis, as well as evaluation of possible differential electrophysiological diagnoses that could account for the patient’s symptoms.1–3 A thorough subjective exam and tailored clinical exam are critical to planning an electrodiagnostic exam that adequately assesses the referring diagnoses and possible differential diagnoses.1–3 Throughout all exam components, the physical therapist must be alert for subjective and clinical exam findings that suggest alternative electrophysiologic pathology and necessitate additional exam procedures.
Following thorough subjective and objective clinical exams, electrodiagnostic (EDX) evaluation of a patient with a referring diagnosis of bilateral median mononeuropathy at or distal to the wrist or CTS should include median motor and sensory nerve conduction studies (NCS), as well as testing of another motor and sensory nerve at a minimum to assess for other peripheral entrapments or polyneuropathic process.1–3 Needle electromyography of both proximal and distal muscles representing the C5-T1 myotome and cervical paraspinal muscles assesses for axonal injury to the median nerve and screens for conditions that can produce similar clinical symptoms, such as cervical radiculopathy, motor neuron disease and myopathy.1–3 Evaluation of lumbosacral radiculopathy should include at least one motor and sensory nerve conduction study and H-reflex in each limb with additional motor and sensory nerve conduction studies if abnormalities are identified.1–3 Needle EMG should be performed on at least five muscles in each limb representative of the L2-S2 myotomes and the lumbosacral paravertebral muscles.1–3 If abnormalities are noted on needle EMG, testing of additional muscles may be required to confirm or clarify the most involved nerve root level(s).1–3 These electrodiagnostic testing strategies should alert the physical therapist to other potential differential diagnoses and the need for additional subjective history, clinical exam or additional NCS and EMG to fully evaluate other suspected pathology.1–3 In patients with neurological symptoms in both upper and lower extremities, the physical therapist needs to consider the possibility of a systemic condition such as peripheral polyneuropathy, motor neuron disease or myopathy.1–3
Polyneuropathy is a disease process involving a number of peripheral nerves in multiple extremities and is often accompanied by sensory changes in a glove or stocking distribution, distal weakness, and hyporeflexia.1–3 Generalized peripheral polyneuropathy (GPPN) is typically diffuse, symmetrical, affects distal extremities greater than proximal, and is characterized by demyelination and/or axonal loss of multiple peripheral nerves and corresponding impairments in sensory, motor, and autonomic nervous system function.1–3 GPPN is often classified with regards to duration (acute versus chronic), structures involved (demyelination and/or axonopathy), type of neural fibers affected (small versus large fiber), distribution patterns (symmetric versus focal/multifocal), and pathology (e.g., idiopathic, systemic, immune response, infectious/inflammatory or hereditary).3
Electrodiagnostic testing, including NCS and needle EMG, provides a means to classify the chronicity, severity, distribution, and extent of large neural fiber sensory and motor involvement in patients with polyneuropathy.1–3 Patients with polyneuropathy are also susceptible to compression neuropathies, including CTS.1–3 CTS has been identified by EDX testing and ultrasound imaging in some patients with polyneuropathy secondary to hemodialysis4 and diabetic polyneuropathy.5–8
This case report will highlight subjective, clinical examination, and EDX including NCS and EMG testing in a patient with pain, paresthesia, and weakness secondary to generalized peripheral polyneuropathy in BUE and BLE.
A 73-year-old right hand dominant male was referred by his primary care provider (PCP) for EDX testing of bilateral lower extremities (BLE) and bilateral upper extremities (BUE) with a referring diagnosis of lumbosacral radiculopathy and bilateral CTS. Testing was performed over two testing sessions six days apart.
One month prior to EDX testing, the patient had an onset of acute low back pain (LBP) with pain in bilateral anterior thighs to the knees. He also complained of initially intermittent and then constant numbness/tingling (N/T) in both hands and feet, all aspects, which had been present one year prior to the onset of the LBP. He denied current or previous history of injury or trauma to the lower back, BLE, BUE or neck or incontinence of bowel or bladder. The patient had a past medical history of intermittent, central LBP that had previously been successfully treated with physical therapy. His current symptoms included pain in both buttocks and anterior thighs and constant N/T in the dorsum and plantar aspects of both feet. He denied other pain, N/T or weakness in BLE. The patient described a one-year history of constant pain and N/T in the dorsum and palm of both hands that affected all digits (D1-D5) and bilateral hand weakness including grip and fine movements. Otherwise, the patient denied any pain, N/T or weakness proximal to the wrists in BUE. The patient denied neck pain or radicular pain in BUE.
The patient’s report of constant N/T in the dorsum and plantar aspects of both feet in a stocking distribution and constant pain and N/T in the palm and dorsal surfaces of D1-D5 in both hands in a glove distribution was suggestive of a generalized peripheral polyneuropathic process. With these findings in both feet and hands, the physical examination and EDX studies focused on the possibility of a polyneuropathic process in BUE and BLE in addition to the referring diagnosis of bilateral CTS and lumbosacral radiculopathy.
The patient reported that his general medical health was good, and he was being treated for high cholesterol and anxiety by his PCP. Two years prior to the EDX testing, the patient had bilateral total hip arthroplasties. The patient denied diabetes, heavy metal exposure, thyroid disease, renal disease, or alcohol abuse. He also denied any recent infection or acute illness in the past year. A review of systems was non-contributory for cardiovascular, pulmonary, gastrointestinal, genitourinary or endocrine disease. The patient had no family history of neuromuscular disease. The patient denied problems with vision, chewing or swallowing.
The EDX testing, including NCS and needle EMG, was described for the patient, and the patient gave verbal and written consent for the EDX testing, and he also gave verbal permission for the use of his case including EDX testing results for educational purposes including presentation and publication.
The patient had a normal gait cycle without limp or apparent weakness in BLE and was not using any adaptive equipment for ambulation. In standing, the patient had decreased heel walk (ankle dorsiflexion) bilaterally, but he was able to perform normal toe walking (ankle plantar flexion) in both single and double stance and was able to squat to 60º of knee flexion bilaterally without pain or weakness in BLE. Decreased balance was noted during both the heel and toe walking maneuvers. Active mobility of BUE and BLE was normal.
Motor strength testing of BLE is presented in Table 1. There was weakness in the bilateral distal leg (ankle dorsiflexion/toe extensors) and intrinsic foot muscles, but there was no visible atrophy of the bilateral foot intrinsic muscles. Muscle stretch reflexes (MSRs) of the bilateral knee jerk (L2-L4) testing was present and equal (2/4). The bilateral ankle jerk (S1) MSRs were absent (0/4). The Babinski and Chaddock pathological reflexes were absent in BLE. There was decreased light touch and pain (pin prick) in the bilateral medial legs. Otherwise, light touch and pain sensory testing was normal in BLE including assessment of all dermatomes (L1-S3) and peripheral nerves in BLE. There was decreased vibration sensory testing in the bilateral great toes and medial malleoli with normal vibration testing at both tibial tuberosities. The bilateral pedal and posterior tibial artery pulses were palpable and equal. Bilateral straight leg raise tests were performed in both sitting and supine positions without reproduction of LBP or radicular symptoms in BLE.
The patient had mild to moderately decreased cervical motion in all planes, but he denied neck pain or radicular pain in BUE. The Spurling’s test was negative for neck pain or radicular symptoms in BUE. Motor strength testing of BUE is presented in Table 2. In addition to the weakness in the bilateral distal hand muscles, there was atrophy of the median and ulnar innervated hand intrinsic muscles bilaterally. Muscle stretch reflexes (MSRs) of the bilateral biceps brachii (C6), brachioradialis (C6), and triceps brachii (C7) testing was present and equal (2/4). The Hoffman pathological reflex was absent in BUE. There was decreased light touch and pain (pin prick) sensory testing in a glove distribution including both hands, affecting palmar and dorsal aspects of all digits and forearms distal to the elbows. Otherwise, light touch and pain sensory testing was normal in the bilateral arms. There was decreased vibration sensation testing at the left thumb (D1) and radial styloid but normal vibration testing of the right thumb and radial styloid. The bilateral radial and ulnar artery pulses were palpable and equal.
The procedures for performing NCS have been previously described in detail.1–3,11 The NCS results are presented in Table 3 (BUE) and Table 4 (BLE). The normal NCS values established for this EDX laboratory were adjusted using a correction factor for the patient’s age (73 years). There were no recordable sensory responses in the bilateral superficial fibular, sural, median, and ulnar nerves. There was no recordable motor response from the right tibial nerve, recorded at the abductor halluces, at distal or proximal stimulation sites. Extremely prolonged distal motor latencies (DMLs) were demonstrated in the left median motor (recurrent branch to the left APB, 26.6 ms; normal < 4.4 ms) and right median motor (recurrent branch to the right APB, 17.3 ms; normal < 4.4 ms) with concomitant decreased compound motor action potential amplitude (1.8 mV left; 2.0 mV right; > 5 mv normal), slowed velocities across the forearm (left 34 m/s, right 23 m/s) and likely partial conduction block across the forearm. (Figure 1A, 1B) These extremely prolonged DMLs were approximately 600% of the upper limit of normal on the left and 393% on the right. Additionally, abnormally prolonged DMLs, decreased compound motor action potential amplitudes, and slowed motor nerve conduction velocities were demonstrated in the bilateral ulnar and deep fibular nerves and left tibial nerve. Distal motor latencies were substantially prolonged and ranged from 160% (left tibial motor) to 210% (left ulnar motor) of the upper limit of normal. Despite the substantially prolonged distal motor latencies, temporal dispersion was not observed in any motor response (Figure 1A, 1B). Central conduction studies (F waves) in BUE and BLE were prolonged in the bilateral median, ulnar and deep fibular nerves and left tibial nerve.
248293248296
Site
NR
Peak (ms)
Norm Peak (ms)
P-T Amp (µV)
Norm P-T Amp
Site1
Site2
Delta-P (ms)
Dist (cm)
Vel (m/s)
Norm Vel (m/s)
Left Superficial Radial Anti Sensory (Base 1st Digit)
D1
2.8
<2.9
17.3
>
D1
Base 1st Digit
2.8
10.0
36
Right Superficial Radial Anti Sensory (Base 1st Digit)
Abbreviations: Abd Hall Brevis, abductor halluces; Amp, amplitude; Ant Lat Mall, anterior lateral malleolus; Anti, antidromic; BLE, both lower extremities; B Fib, fibular head; cm, centimeter; dist, distance; ms, EDB, extensor digitorum brevis; Lat Mall, lateral malleolus; millisecond; m/sec, meter/second; Mrkrs, markers; NR, no response; norm, normal; O-P, onset to peak; Poplt, popliteal space; P-T, peck to trough; SFN, superficial fibular nerve; vel, velocity; µV, microvolt;
The procedures for performing needle EMG have been previously described in detail.1–3,11 A monopolar needle electrode was used to perform the EMG testing in this study. The EMG results are presented in Table 5. Abnormal EMG findings, as demonstrated by increased insertional activity and the presence of abnormal spontaneous electrical activity (fibrillation potentials and positive waves) at rest were noted in the upper extremities including the bilateral 1st DI, ADM, and APB; and in the lower extremities including bilateral EHL, EDB, and abductor halluces. Fibrillation potentials observed were small amplitude (< 100 µV) which is compatible with chronic denervation.1–3 Abnormal motor unit morphology with prolonged duration (> 15 ms) was noted in the bilateral APBs. Otherwise, normal motor unit morphology (shape, duration and amplitude) was present in the other muscles tested during voluntary contraction in BUE and BLE. The recruitment and interference patterns were decreased during maximal voluntary contraction in these muscles in BUE (left APB, 25%; right APB, 75%; left 1st DI, 50%; right 1st DI, 75%; left ADM, 50%, and right ADM, 75%) and BLE (bilateral EHL, 75%: bilateral EDB, 50%; and bilateral abductor halluces (25%). The other muscles testing in BUE, BLE, and bilateral low lumbar PVM were normal on EMG examination (Table 3).
The electrophysiological evidence demonstrated a generalized, symmetrical, length dependent, sensorimotor, peripheral polyneuropathy in BUE and BLE with both significant axonal loss and demyelination. Chronic denervation with reduced recruitment and interference patterns was noted in all distal muscles tested in BUE (1st DI, ADM, and APB) and BLE (EHL, EDB, and abductor halluces). Electrophysiologic evidence also suggested superimposed, bilateral, median nerve mononeuropathies at or distal to the wrist, particularly given the extremely prolonged median motor DMLs, but the presence of polyneuropathy made it difficult to determine definitively or assign severity. Chronic denervation was noted in bilateral APB with increased duration MUPs which is compatible with motor unit remodeling.
There was no electrophysiological evidence on this exam of bilateral C5-T1 radiculopathy in BUE or bilateral L2-S2 radiculopathy in BLE and the bilateral low lumbar PVM. Given the significant EMG and NCS abnormalities, it was difficult to fully exclude bilateral ulnar mononeuropathies at or about the wrists and elbows or fibular mononeuropathy at or about the fibular heads. However, the abnormalities observed were considered most likely attributable to the GPPN.
The physical therapist recommended referral to a neurologist for further evaluation and intervention of the generalized peripheral polyneuropathy and to an orthopaedic hand surgeon for the evaluation and intervention for the suggested bilateral median nerve mononeuropathies at or distal to the wrist, most likely representing carpal tunnel syndrome.
After receiving the EMG/NCS report, the patient’s primary care provider referred the patient to a neurologist and an orthopaedic hand surgeon.
One month following the EDX testing, the patient was evaluated by a neurologist and had additional testing including a lumbar puncture with cerebrospinal fluid sampling that was reported as normal. The neurologist confirmed the generalized peripheral polyneuropathy in BUE and BLE and stated that the GPPN was “idiopathic” (classification/etiology). The neurologist started the patient on intravenous immunoglobulin fusion therapy (IVIG) on a monthly basis. The patient continues to be followed by the neurologist.
The patient was evaluated by an orthopaedic hand surgeon two months following the EDX testing, and had steroid injections in each wrist on two clinic visits. The patient is being followed by this hand surgeon, but he has not had any hand or wrist surgery.
The neurologist also referred the patient to physical therapy for mobility and strengthening exercises for BUE and BLE. The patient completed an in-clinic physical therapy program and continues a home exercise program.
Six months following the EDX testing, the patient stated that the monthly IVIG intervention had been “successful,” and this intervention decreased the pain and N/T in both hands and feet. He reported that the N/T in his plantar feet continued to be his most “bothersome” symptom. The symptoms in both hands also decreased following the two steroid injections in both wrists. He felt that the physical therapy intervention had “helped” and noted that the weakness in both hands was improved, characterizing his grip strength as “almost normal”. From these combined interventions, the patient feels like he is “90%” improved since the EDX testing. The patient continues to be followed by his neurologist and orthopaedic hand surgeon.
With a referring diagnosis of bilateral CTS and lumbosacral radiculopathy, a thorough subjective (history and review of systems) and physical clinical examination of BUE and BLE was performed prior to initiating the EDX studies.1–3 The findings on the patient’s physical examination fit the triad of polyneuropathy with decreased sensation to light touch, pain and vibratory sensation in a glove distribution in both hands and forearms, decreased sensation to vibration in both feet and lower legs, weakness in distal muscles in both hands and feet, and absent bilateral ankle jerk (S1) MSRs.1–3 EDX testing confirmed the physical exam findings and demonstrated a generalized, length dependent, sensorimotor, peripheral polyneuropathic process affecting BUE and BLE with both prominent axonal loss and demyelinating features.1–3 The patient did not have any of the more common etiologies of generalized peripheral polyneuropathy to include diabetes, renal disease, chronic alcohol abuse, critical illness or known family history of neuromuscular disease.1–3 After additional testing, including a lumbar puncture and cerebrospinal fluid assessment, a neurologist confirmed the GPPN in BUE and BLE and stated the polyneuropathy was “idiopathic”.
While EDX testing can only characterize peripheral nerve pathology by its electrophysiologic features, the severely prolonged distal motor latencies in multiple BUE and BLE nerves and the patient’s reported improvement with IVIG suggested that these findings may represent an inflammatory or immune mediated polyneuropathy.12–14 While the patient had features that may suggest chronic inflammatory demyelinating polyneuropathy (CIDP), particularly the severely prolonged distal motor latencies, the lack of proximal weakness and slow, insidious onset of symptoms suggested that these findings may represent a rare variant such as distal acquired demyelinating symmetric neuropathy (DADS).12–14 DADS is characterized by distal sensory and motor impairments that are typically worse in the legs and requires CIDP confirming motor nerve conduction abnormalities in at least two upper limb nerves.12–14 One motor nerve conduction criterion includes DML prolongation of greater than or equal to 50% above the upper limit of normal and with distal CMAPs of at least one millivolt. This patient had distal motor prolongations of 160-600% of the upper limits of normal with amplitudes of >1 mV in bilateral median and ulnar and left tibial motor nerves.12–14
Patients with polyneuropathy are also susceptible to compression mononeuropathies including CTS.1–3 Carpal tunnel syndrome has been identified by EDX testing and ultrasound imaging in patients with polyneuropathy secondary to maintenance hemodialysis4 and diabetic polyneuropathy.5–8 This patient had EDX findings that suggested superimposed bilateral median mononeuropathies at or distal to the wrist or CTS based on the significantly greater prolongation of the median DMLs as compared to the bilateral ulnar DMLs.1,2 It is difficult to fully characterize how much the GPPN contributed to the findings noted in bilateral median nerves, particularly considering the absence of both ulnar and median sensory responses. While there is no published CTS classification system for patients with GPPN and CTS, comparison with findings in the ulnar nerves is frequently used to distinguish between superimposed median mononeuropathy from the polyneuropathy, but this technique has limitations when there are severe abnormalities in both median and ulnar nerves.1,2 Additional EDX testing including inter-latency difference between 2nd lumbricale and median DML,4,5 median nerve inching, 2nd lumbricale-interossei test8 and ultrasound imaging6,7 may assist in determining the presence of bilateral CTS in patients with polyneuropathy. Treatment directed at the median mononeuropathy may help clinically distinguish between the two conditions, but the patient had both systemic treatment (IVIG) and local treatment (steroid injection in the wrists), making it difficult to determine the relative contribution of either treatment.
A thorough subjective exam and tailored clinical exam are critical to planning an electrodiagnostic exam that adequately assesses the referring diagnoses and possible differential diagnoses.
Throughout all exam components, the physical therapist must be alert for subjective and clinical exam findings that suggest alternative pathology and necessitate additional exam procedures.
Electrodiagnostic testing (including nerve conduction studies and diagnostic EMG) is performed to confirm the findings of a thorough history and physical examination and may identify neurological injury associated with generalized peripheral polyneuropathy.
Polyneuropathy is a disease process involving multiple peripheral nerves in multiple extremities and consists of a triad of sensory changes in a glove or stocking distribution, distal weakness, and hyporeflexia.
Generalized peripheral polyneuropathy (GPPN) is typically diffuse, symmetrical, affects distal extremities greater than proximal, and is characterized by demyelination and/or axonal loss of multiple peripheral nerves and corresponding impairments in sensory, motor, and autonomic nervous system function.
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