PRACTICE ISSUES


Test Utilization and Value
C O N T I N UU M A UD I O
I NT E R V I E W A V AI L A B L E
ONLINE
in the Evaluation of
Peripheral Neuropathies
By Brian C. Callaghan, MD, MS, FAAN

CITE AS:
CONTINUUM (MINNEAP MINN)
2020;26(5, PERIPHERAL NERVE AND
MOTOR NEURON DISORDERS):
1384–1391.
Address correspondence to
Dr Brian Callaghan, 109 Zina
Pitcher Pl, 4021 BSRB, Ann Arbor,
MI 48104, bcallagh@med.umich.
edu.
RELATIONSHIP DISCLOSURE:
Dr Callaghan serves on a
scientific advisory board for a
Patient-Centered Outcomes
Research Institute grant, on the
International Diabetes
Neuropathy Consortium board
for the Peripheral Nerve Society,
on the editorial board of
Neurology, and as a consultant
for DynaMed. Dr Callaghan has
received research/grant support
from the American Academy of
Neurology, JDRF, the National
Institutes of Health (R01
DK115687), and the US
Department of Veterans Affairs
(Clinical Science Research and
Development Merit I01CX001504)
and provided consulting services
for medicolegal cases and the US
Vaccine Injury Compensation
Program.
ABSTRACT
Peripheral neuropathies can be classified as typical or atypical. Patients
with atypical neuropathy have one or more of the following features:
acute/subacute onset, non–length dependence, motor predominance, or
asymmetry. This classification is important because it informs the appropriate
diagnostic evaluation of this highly prevalent condition. The evaluation of a
typical peripheral neuropathy, also known as distal symmetric
polyneuropathy, requires a thorough history, neurologic examination, and
focused laboratory testing. Electrodiagnostic testing and MRI account for
the majority of costs but rarely lead to changes in diagnosis or management.
These costs are increasingly being passed on to patients, especially those
with high-deductible health plans. In contrast, patients with atypical
neuropathy require more extensive testing, including electrodiagnostic
tests. These tests are much more likely to lead to the use of disease-
modifying therapies in these patients compared to in those with typical
peripheral neuropathy. This article describes two cases to illustrate the
appropriate diagnostic workup of those with typical or atypical neuropathy.
CASE 1
A 60-year-old man presented for an outpatient neurology consultation with
numbness, tingling, and pain in his feet. His symptoms started 3 years earlier
in his toes and slowly and steadily spread to his midshins with no involvement
of his hands. His symptoms were symmetric, and he denied weakness. He had
a past medical history of hyperlipidemia and hypertension but did not have
diabetes or significant alcohol consumption. No one in his family had a
diagnosis of neuropathy or similar symptoms.
Neurologic examination revealed normal strength, absent Achilles
reflexes, decreased pinprick sensation below the knees, and 3 seconds of
vibration sensation at the toes.

UNLABELED USE OF
PRODUCTS/INVESTIGATIONAL DISCUSSION

T
USE DISCLOSURE:
Dr Callaghan reports no
he patient in CASE 1 presented with symptoms and signs of a typical
disclosure. distal symmetric polyneuropathy. No atypical features such as
acute/subacute onset, non–length dependence, motor predominance,
© 2020 American Academy or asymmetry were present (PRACTICE FIGURE 1).1,2 The patient did
of Neurology. not have a condition known to cause neuropathy, such as diabetes or

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alcohol use disorder. In cases of
distal symmetric polyneuropathy,
the most important components
of the diagnostic evaluation are
the history and neurologic
examination.3 Laboratory tests
add slightly to the diagnostic yield,
whereas electrodiagnostic tests
and MRIs are rarely needed. Nerve
biopsies are not needed because of
the low diagnostic yield and high
morbidity associated with these
procedures. Testing for this
patient should include a glucose
tolerance test, vitamin B12 level,
serum protein electrophoresis
with immunofixation, complete
blood cell count, and
comprehensive metabolic panel.

History and Examination

As in most clinical conditions, the
history and examination are
essential in determining the PRACTICE FIGURE 1
underlying cause of a distal Diagnostic algorithm for distal symmetric
polyneuropathy. Testing for distal symmetric
symmetric polyneuropathy. Distal
polyneuropathy is based on whether atypical
symmetric polyneuropathy can be features are present and whether a known cause
caused by a lengthy list of is already established based on the history and
conditions, including, but not neurologic examination. Most cases of distal
symmetric polyneuropathy require limited
limited to, diabetes, prediabetes,
diagnostic testing.
alcohol use disorder, nutritional EMG = electromyography.
deficiencies, paraproteinemias, Modified with permission from Callaghan BC, et al, JAMA.1
medications, chronic kidney © 2015 American Medical Association.
4
disease, and genetic causes. Most
of these conditions are diagnosed or suspected by taking a thorough medical,
family, and social history. Idiopathic neuropathy accounts for at least one-fourth
of distal symmetric polyneuropathies and increases greatly after the age
of 40.3,5–8 The lack of recognition of the high prevalence of idiopathic distal
symmetric polyneuropathy likely drives unnecessary testing. Community-
based neurologists are able to diagnose the underlying cause of distal
symmetric polyneuropathy in 64% of cases before further diagnostic testing.3

Laboratory Testing
Laboratory testing is important to attempt to diagnose the underlying cause of
distal symmetric polyneuropathy in those in whom the history does not lead to
a clear etiology. The American Academy of Neurology (AAN) guideline
supports testing for hyperglycemia and vitamin B12 deficiency, testing for
a monoclonal gammopathy with a serum protein electrophoresis with
immunofixation, complete blood cell count, and comprehensive metabolic
panel (PRACTICE FIGURE 1).9

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TEST UTILIZATION AND VALUE IN PERIPHERAL NEUROPATHIES

Testing for hyperglycemia is the most important diagnostic step, as

diabetes and prediabetes are the most common causes of distal symmetric
polyneuropathy.3,6,7,10,11 Hemoglobin A1c and fasting glucose can be used to test
for hyperglycemia, but a glucose tolerance test has a higher sensitivity.11 Since
the diagnosis of diabetes or prediabetes is important to the management of
patients with distal symmetric polyneuropathy, using the most sensitive test is
essential. Vitamin B12 level is one of the few tests with a yield higher in distal
symmetric polyneuropathy than expected in the general population, and
vitamin B12 deficiency has been associated with worsening neuropathy.12,13
Vitamin B12 replacement is inexpensive and has the potential to improve
neuropathy and prevent further worsening, highlighting the need for this test.
The prevalence of a monoclonal gammopathy (abnormal serum protein
electrophoresis with immunofixation) is 10% in patients with otherwise
idiopathic neuropathy, which is much greater than in population-based
studies.14 These tests have the potential to uncover monoclonal gammopathies
that may indicate underlying malignancy or may be the precursor to future
malignancy. Complete blood cell counts and comprehensive metabolic panels
do not have great evidence to support their use, but the majority of
neurologists would order them, based on a national survey.15 In contrast,
rheumatologic tests (such as an antinuclear antibody test) and
thyroid-stimulating hormone (TSH) do not have a higher yield in those with
distal symmetric polyneuropathy compared to those without neuropathy.16
Previous studies have also demonstrated that more extensive laboratory testing
does not increase the yield and that repeat testing is not helpful.13,17,18 The AAN
guideline–recommended tests are also the tests most likely to change clinical
management.3 Guideline-supported diagnostic tests are not just a starting point
but are usually the only tests needed for patients presenting with typical distal
symmetric polyneuropathy.

Electrodiagnostic Testing
Nerve conduction studies and EMG enable clinicians to determine the pattern of
nerve injury and whether underlying axon loss or primary demyelination is
present. However, these tests rarely change the pretest diagnosis or management
of patients with distal symmetric polyneuropathy.3 In a study of 458 patients,
only two patients had a change in diagnosis (from distal symmetric
polyneuropathy to “no neuropathy”) and no patients had a change in
management based on these tests. Interestingly, the chance of patients
undergoing an electrodiagnostic test is highly dependent on which neurologist
they see and not on other demographic or clinical factors.3 These results have led
to a position statement from the American Diabetes Association stating that
routine electrodiagnostic tests are not needed in patients with diabetes and distal
symmetric polyneuropathy unless atypical features are present, the diagnosis is
unclear, or another etiology is suspected.19 Which neuropathy patients would
benefit from these tests is unclear, but it would likely be those with atypical
features. An editorial has criticized this work based on four studies that reported
a different yield of electrodiagnostic studies.20 However, the largest study
with the most rigorous study design came to the same conclusion that
electrodiagnostic tests are not routinely needed in those with distal symmetric
polyneuropathy of clear cause.3,21 Two of the other studies focused on all tertiary
electrodiagnostic referrals and only included a small number of patients with

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distal symmetric polyneuropathy, which limits making any conclusions about
the value of electrodiagnostic testing in patients with distal symmetric
polyneuropathy.22,23 One other small study did not have a clear definition of
distal symmetric polyneuropathy and provided minimal details of what
constituted a change in management.24 Therefore, the current evidence does not
support routine electrodiagnostic tests in the evaluation of distal symmetric
polyneuropathy. Defining the exact scenarios that warrant testing requires
further studies, but the answer to whether all patients with distal symmetric
polyneuropathy should have electrodiagnostic tests is probably not.25

MRI
MRI of the neuraxis can help determine the cause of peripheral nervous system
lesions, especially with localizations such as polyradiculopathies, plexopathies,
and radiculoplexus neuropathies (PRACTICE FIGURE 2).26 However, the yield of

PRACTICE FIGURE 2
Diagnostic algorithm for atypical distal symmetric polyneuropathy. Testing for atypical distal
symmetric polyneuropathy is based on the localization of nerve injury from the nerve
conduction study and EMG. Most cases of atypical distal symmetric polyneuropathy require
extensive diagnostic testing.
Abs = antibodies; AMA = antimitochondrial antibody; ANA = antinuclear antibody; ANCA = antineutrophil
cytoplasmic antibody; ASMA = antismooth muscle antibodies; BJS = Bence Jones screen; CBC = complete
blood cell count; COMP = comprehensive metabolic panel; CRP = C-reactive protein; CXR = chest x-ray;
dsDNA = double-stranded deoxyribonucleic acid; EMG = electromyography; ESR = erythrocyte sedimentation
rate; FLC = free light chain; GM1 = ganglioside M1; HIV = human immunodeficiency virus; HTLV = human T-cell
lymphotropic virus; MRI = magnetic resonance imaging; RF = rheumatoid factor; SPEP/IF = serum protein
electrophoresis/immunofixation; SSA = Sjögren syndrome A; SSB = Sjögren syndrome B; UA = urinalysis;
UPEP/IF = urine protein electrophoresis/immunofixation; VEGF = vascular endothelial growth factor;
WNV = West Nile virus.
Reprinted with permission from Callaghan BC, et al, JAMA Neurol.26 © 2015 American
Medical Association.

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TEST UTILIZATION AND VALUE IN PERIPHERAL NEUROPATHIES

MRI is extremely low in those with distal symmetric polyneuropathy.3 One large
study demonstrated that none of the 458 patients with distal symmetric
polyneuropathy had a change in etiologic diagnosis or management after MRI
despite almost 30% of the patients receiving these tests.3,27 Despite the low yield,
MRIs of the neuraxis are ordered frequently, even in a survey that presented a
vignette with classic distal symmetric polyneuropathy symptoms, signs, and the
label of distal symmetric polyneuropathy to neurologists and primary care
physicians.15,27,28 These findings have led to a Choosing Wisely recommendation
from the American Association of Neuromuscular and Electrodiagnostic
Medicine that states that physicians should not order an MRI of the spine or
brain for those with only peripheral neuropathy.29 MRI should be reserved for
presentations consistent with polyradiculopathies, plexopathies, and
radiculoplexus neuropathies.

Cost
The cost of the diagnostic evaluation of distal symmetric polyneuropathy is
largely driven by electrodiagnostic tests and MRIs.30 These tests account
for 88% of the total diagnostic expenditures. The costs of the evaluation and
management (E/M) by neurologists and other physicians and the few
laboratory tests are quite small by comparison. In 2016, the mean estimated
reimbursements were $1076 for electrodiagnostic tests, $1265 for MRI,
and $253 for the physician visit (E/M) (unpublished data using the Clinformatics
Datamart, OptumInsight, Eden Prairie, Minnesota). Whereas out-of-pocket
costs for these diagnostic tests were previously quite small, they have risen
dramatically over the past 15 years. With deductibles rising, these costs are
now substantial for the approximately 40% of patients in commercial insurance
plans who pay out-of-pocket costs. The median out-of-pocket cost for these
patients is $230 for electrodiagnostic tests, $204 for MRI, and $40 for the
physician evaluation.

Policy Implications
The most valuable aspect of the diagnostic evaluation of peripheral neuropathy is
the physician visit (E/M service). However, the US Centers for Medicare &
Medicaid Services (CMS) recently proposed grouping E/M levels 2 through 5 and
later proposed grouping levels 2 through 4. This policy would have adversely
impacted neurologists more than any other specialty since neurology is
largely an E/M-based specialty and neurologists more frequently use
level 4 and 5 codes than any other specialist.31,32 One likely reason that
this policy proposal did not go into effect was the AAN’s advocacy on this
topic in conjunction with other medical societies. In contrast to E/M, CMS
substantially reduced reimbursement for nerve conduction studies in 2013,
which led to decreased use of nerve conduction studies much more so than
use of EMG, which did not experience the same change in reimbursement.33
Furthermore, non-neurologists drastically reduced nerve conduction
study use. These results demonstrate that the magnitude of reimbursement
affects diagnostic test utilization. Incentivizing value in the care of patients
with distal symmetric polyneuropathy would likely require higher payments
for services that are more likely to lead to changes in management, such as
physician visits, compared to payments for other diagnostic tests that are
often not needed.

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CASE 2
A 60-year-old man presented for an outpatient neurologic consultation
with numbness, tingling, and pain in his right foot more than his left foot. He
had a past medical history of hyperlipidemia and hypertension but did not
have diabetes or significant alcohol consumption. The symptoms had
started 4 weeks earlier in his right foot and 1 week earlier in his left foot. He
stated that his right foot was also weak.
Neurologic examination revealed right dorsiflexion strength of 4/5 and
left plantar flexion strength of 4+/5; he was otherwise strong. He had an
absent left Achilles reflex with 2+ reflexes elsewhere; decreased pinprick
sensation in the dorsum of the right foot, the right lateral leg, and the sole
of the left foot; and 3 seconds of vibration sensation at the right toe and
7 seconds at the left toe.

DISCUSSION
The patient in CASE 2 presented with symptoms and signs of an atypical
peripheral neuropathy. The atypical features included a subacute onset, motor
predominance, and asymmetry. In contrast to CASE 1, the diagnostic evaluation
should consist of electrodiagnostic studies to further localize the nerve injury and
to evaluate for demyelinating features. Possible localizations include multiple
mononeuropathies, non–length-dependent neuropathy, polyradiculopathy,
and radiculoplexopathy, each of which requires specific diagnostic tests
(PRACTICE FIGURE 2).4 The most likely localization from this presentation is
multiple mononeuropathies given the pattern of sensory deficits in the
distribution of specific nerves (right fibular [peroneal] and left tibial), and the
most likely diagnosis is a vasculitic neuropathy, also known as mononeuritis
multiplex. For more information on mononeuritis multiplex, refer to the article
“Peripheral Neuropathies Associated With Vasculitis and Autoimmune
Connective Tissue Disease” by Chafic Karam, MD,34 in this issue of Continuum.
After electrodiagnostic testing, tests that are often needed for the investigation of
vasculitic neuropathy include antinuclear antibody, antineutrophil cytoplasmic
antibody (ANCA), rheumatoid factor, Sjögren syndrome A (SSA)/Sjögren
syndrome B (SSB), double-stranded DNA, cryoglobulins, human
immunodeficiency virus (HIV), hepatitis B and C serologies, urinalysis, chest
x-ray, complete blood cell count, comprehensive metabolic panel, and a nerve
biopsy. In contrast to the evaluation of patients with distal symmetric
polyneuropathy, these evaluations are likely to lead to treatment with a
disease-modifying therapy. In the case of ANCA-positive vasculitic neuropathy,
rituximab induction and maintenance has been shown to be effective at
preventing relapse.35,36

CONCLUSION
Typical peripheral neuropathies are much more common than atypical
peripheral neuropathies. The diagnostic evaluation can be quite extensive for
atypical peripheral neuropathies and should be limited for those with typical
peripheral neuropathies; all patients require a complete history, neurologic
examination, and simple laboratory tests, with more extensive testing, such as
electrodiagnostic tests and MRIs, reserved for atypical presentations or special

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TEST UTILIZATION AND VALUE IN PERIPHERAL NEUROPATHIES

situations. Costs, including patient out-of-pocket costs, should be considered to

ensure maximum value in the diagnostic evaluation of peripheral neuropathy.

ACKNOWLEDGMENT
The author would like to thank Raymond Price, MD, for his editorial assistance.

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