An Approach to the Evaluation of Peripheral

Neuropathies
Mark B. Bromberg, M.D., Ph.D.1

ABSTRACT

The clinical evaluation of peripheral neuropathies can be challenging. This article

presents an approach based on a structured assessment that asks a series of yes or no
questions during the history and examination that leads to localization and characterization
of the neuropathy. The final assessment includes further characterization by electrodiag-

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nostic evaluation. At this point, a reasonable differential diagnosis can be generated and
appropriate laboratory tests ordered.

KEYWORDS: Peripheral neuropathy, diagnosis, neuropathy symptoms, neuropathy

signs

Objectives: On completion of this article, the reader will have a structured approach to localization and characterization of peripheral
neuropathies.
Accreditation: The Indiana University School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to
provide continuing medical education for physicians.
Credit: The Indiana University School of Medicine designates this educational activity for a maximum of 1 Category 1 credit toward
the AMA Physicians Recognition Award. Each physician should claim only those credits that he/she actually spent in the educational
activity.
Disclosure: Statement of disclosure has been obtained regarding the author’s relevant financial relationships. The author has nothing to
disclose.

Symptoms of distal numbness, tingling and pain,
and weakness are common complaints, and in the gen-
eral population, the prevalence of peripheral neuropathy
approaches 10%.1 It can be challenging to identify an
underlying cause of a neuropathy. A structured evalua-
tion is more efficient than an unstructured or shotgun
approach. Disadvantages of an unstructured approach
include false leads and expensive and unproductive
laboratory tests, and occasionally unnecessary surgery.2,3
The structured approach results in a full localiza-
tion and characterization of the neuropathy that focuses
the differential diagnosis and leads to a rational list of
laboratory tests.2,3 Localization and characterization are
discussed in terms of seven layers (Table 1). The history
should be conducted as an active process, with the goal of
an understanding of what the patient is experiencing.
With a full history, neurological findings during the
examination should be predictable. Assigning layers and
a sequence is somewhat artificial; the evaluation process
is dynamic, and layers will merge and the sequence will
vary depending upon the clinician’s experience and
clinical situations.

Peripheral Neuropathies; Editor in Chief, Karen L. Roos, M.D.; Guest Editor, Mark B. Bromberg, M.D., Ph.D. Seminars in Neurology, Volume 25,
Number 2, 2005. Address for correspondence and reprint requests: Mark B. Bromberg, M.D., Ph.D., Department of Neurology Room 3, University
of Utah School of Medicine, 50 North Medical Drive, Salt Lake City, UT 84132-0001. 1Department of Neurology, University of Utah School of
Medicine, Salt Lake City, Utah. Copyright # 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.
Tel: +1(212) 584-4662. 0271-8235,p;2005,25,02,153,159,ftx,en;sin00360x.
153
154 SEMINARS IN NEUROLOGY/VOLUME 25, NUMBER 2 2005

Table 1 Diagnostic Evaluation Layers Leading to Full Neuropathy Characterization

First layer
Within the peripheral nervous system? Exclude cortical, spinal, psychogenic loci
Second layer
What part of the peripheral nervous system? Root, plexus, single nerve, multiple nerves, peripheral neuropathy
Third layer
What is the time course? Acute, subacute, chronic, progressive, relapsing-remitting, event-linked
Fourth layer
What nerve fibers are involved? Sensory, motor, autonomic, combinations
Fifth layer
What is the primary pathology? Demyelination, axonal, mixed
Sixth layer
What are the other pertinent features? Family, medical, social histories
Seventh layer
What are the epidemiological features? Probability, age of onset, rarity, gender

LAYER 1: LOCALIZATION TO THE may have incorporated the patient’s symptoms,

PERIPHERAL NERVOUS SYSTEM and giving the patient a therapeutic way out of

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Although usually assumed, this layer deserves mention
because not all symptoms of distal numbness, tingling
and pain, and weakness are referable to the peripheral
nervous system. Failure to consider this step can lead
to diagnostic errors. Examples referable to the central
nervous system include asymmetry, unusual symptom
patterns, and pathological tendon reflexes.
It is also important to consider that some patterns
of symptoms may not be attributable to definable lesions
within either the central or peripheral nervous systems,
and a somatoform disorder should be considered.4
Somatoform disorders represent distressful physical
symptoms causing impaired social or occupational dys-
function with no diagnosable condition to account for
them.5 Symptoms of numbness, paresthesias, pain,
weakness, and fatigue are considered to be ‘‘pseudoneuro-
logical’’ when no neurological basis can be found.
Whether a patient fulfills full DSM-IV criteria for
somatization or undifferentiated somatoform disorders
is less important than recognizing that further evaluation
is unlikely to lead to a physical diagnosis.5 Every patient
deserves a considered evaluation because somatization
can accompany true diseases,4 but when reasonable
localization cannot be achieved, neurological and labora-
tory examinations are normal, and the temporal
pattern does not fit known pathological processes, it is
highly unlikely that the symptoms represent a definable
pathology.
When this occurs, an understanding discussion
seeking other factors is appropriate. Opening the con-
versation to consideration of internal factors that may be
causative or contributory should be taken slowly. Con-
ditions such as depression, anxiety, and panic disorders
may coexist.6 Replacing long-standing symptoms with
the ‘‘good news’’ of ‘‘good health’’ is rarely successful.
With long-standing symptoms, the family milieu
their dilemma, such as physical therapy, should be
considered.
LAYER 2: LOCALIZATION WITHIN THE
PERIPHERAL NERVOUS SYSTEM
This layer is based on peripheral nervous system anat-
omy. Symptoms expected from lesions from root to
plexus to peripheral nerve can be queried during the
history. This article focuses on peripheral neuropathy
and assumes that localization to roots, plexus, and single
nerves has been excluded.
Peripheral Neuropathy Pattern
There are several patterns of peripheral neuropathy
(Table 2). The prototypic and most common pattern is
symmetric and length-dependent, involving sensory loss
and pain and, less frequently, distal weakness. As pro-
gressively shorter nerves are affected, symptoms and
signs unroll up the leg as a stocking. Nerve length at
knee level is approximately equal to the length innervat-
ing the hand, and with further progression, symptoms
and signs unroll up the arm as a long glove. In the
extreme, a shield loss over the chest and abdomen can
be observed when nerve length involvement reaches the
circumference of the thorax. Most length-dependent
peripheral neuropathies are chronic and involve axonal
pathology.7 Causes of peripheral neuropathy are
many and are felt to reflect metabolic abnormalities.
Diabetes mellitus is the most common underlying
cause of this type of neuropathy, followed by hereditary
(genetic) neuropathies. The cause for many neuropathies
of this type is unknown, and idiopathic or crypto-
genic neuropathies represent up to 25% of peripheral
neuropathies.8,9
 AN APPROACH TO THE EVALUATION OF PERIPHERAL NEUROPATHIES/BROMBERG 155

Table 2 Patterns of Peripheral Neuropathy and Examples of Disorders and Causes

Sensory-motor symmetric (length-dependent pattern)
Sensory-motor symmetric (proximal and distal pattern)
Sensory-motor asymmetric (nerve or plexus pattern)
Sensory-motor asymmetric
Sensory symmetric or asymmetric
Motor symmetric or asymmetric
Autonomic symmetric or asymmetric
Diabetes, medications, toxins, metabolic disorders, hereditary
Acute inflammatory demyelinating polyradiculopathy, chronic inflammatory
demyelinating polyradiculopathy
Diabetic amyotrophic, idiopathic plexopathy, vasculitic mononeuritis
multiplex
Porphyria, leprosy
Paraneoplastic neuronopathy, Sjögren’s syndrome, idiopathic ganglionitis,
vitamin B6 toxicity, leprosy
Amyotrophic lateral sclerosis, multifocal motor conduction block
neuropathy, lower motor neuron syndrome, poliomyelitis, West
Nile syndrome
With other neuropathies (diabetes, acute inflammatory demyelinating
polyradiculopathy), isolated involvement (amyloidosis)

When the pattern of symptoms and signs includes history of clear remissions and exacerbations suggests
both proximal and distal limb segments, the pathological CIDP or other form of immune-mediated neuropathy.
process is usually demyelination at multifocal sites along When the time course clearly starts in adult life, an

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roots and nerves (inflammatory polyradiculoneuro-
pathy). Acute inflammatory demyelinating polyradicu-
loneuropathy (AIDP) and chronic inflammatory
demyelinating polyradiculoneuropathy (CIDP) occur.
Asymmetric patterns are less common and in-
clude different lesion sites and pathological processes.
Unilateral and focal symptoms and signs in a limb must
be distinguished from radiculopathy, plexopathy, or
mononeuropathy (mononeuritis multiplex). In some
situations, the most frequent being diabetes mellitus,
length-dependent neuropathies coexist with radiculopa-
thies, plexopathies, and mononeuropathies. Atrophic
weakness without sensory loss that does not follow
a radicular, plexopathy, or mononeuropathy pattern
suggests motor neuron disease (amyotrophic lateral
sclerosis).
LAYER 3: WHAT IS THE TIME COURSE?
Definitions of time course applied to peripheral neuro-
pathies are different than those used in general neurol-
ogy (Table 3). True acute or apoplectic events are rare in
neuropathies. More commonly, acute onset is defined as
days to several weeks, and suggests AIDP (Guillain-
Barré syndrome), a metabolic event, or a toxic exposure.
Chronic neuropathies progress over months to years. A
acquired neuropathy is more likely, and when the time
course cannot be dated, a hereditary neuropathy should
be considered. Our understanding of hereditary neuro-
pathies is expanding, and several ‘‘idiopathic’’ neuro-
pathies beginning in adulthood may represent mild
forms of hereditary neuropathies.
LAYER 4: WHAT NERVE FIBERS
ARE INVOLVED?
The peripheral nervous system includes somatic and
autonomic components, and somatic nerves are further
divided into sensory and motor functions. Within the
somatic nervous system, involvement of sensory and
motor fibers can be assessed, and there are neuropathies
affecting either sensory or motor or both types of fibers.
Detailed assessment of components of the autonomic
nervous system is difficult, and it is usually sufficient to
determine whether there is some autonomic involve-
ment. Neuropathies with isolated autonomic nervous
system involvement are rare (Table 4).
Symptoms
The chief complaint may not indicate which types of
nerves are involved. Nerve dysfunction can be expressed

Table 3 Peripheral Neuropathy Time Courses and Examples of Associated Neuropathies

Acute
Apoplectic Vasculitic mononeuritis multiplex, idiopathic plexopathy
Days to weeks Acute inflammatory demyelinating polyradiculopathy, porphyria, acute toxic exposure, proximal diabetic
neuropathy, paraneoplastic sensory neuronopathy
Chronic
Years Diabetic polyneuropathy, chronic inflammatory demyelinating polyradiculopathy, idiopathic
Insidious Hereditary
156 SEMINARS IN NEUROLOGY/VOLUME 25, NUMBER 2 2005
Table 4 Positive and Negative Symptoms Associated
with Nerve Damage
Negative
Positive Symptoms Symptoms
Somatic Nerves
Sensory Pain Numbness
Tingling Lack of feeling
Motor Cramps Weakness
Fasciculations Atrophy
Autonomic Nerves
Hyperhydrosis Orthostatic
hypotension
Diarrhea Impotence
Anhydrosis
Constipation
as negative and positive symptoms (Table 4). Positive
symptoms reflect inappropriate spontaneous nerve activ-
ity detected by the patient as uncomfortable and painful
sensations, or other spontaneous phenomena. Negative
symptoms reflect loss of nerve signaling. An important
clinical difference between sensory and motor somatic
nerves is the compensatory mechanism that follows
motor nerve loss, when surviving motor nerves undergo
collateral reinnervation to reinnervate orphaned muscle
fibers. The compensatory process blunts weakness due to
mild motor nerve loss, and clinical weakness may not be
apparent to the patient or on physical examination until
50% of motor nerve fibers are lost (80% in slowly
progressive denervating disorders).10 However, positive
symptoms of cramps and fasciculations may be present as
the only clinical indication of motor nerve involvement.
The needle electromyography is sensitive in detecting
early motor fiber loss and will confirm motor nerve
involvement.
Signs
The neurological examination is sensitive for detecting
peripheral nerve loss and dysfunction and is informative
for localization. The accuracy and interpretation of
the examination is facilitated by an appreciation of nerve
physiology and pathology and the limitations of clinical
testing. The sensory examination can be challenging and
confusing because responses are indirect and represent
a patient’s interpretation of the test and test questions. It
is important that the patient clearly understands the
object of the test, and attention and cooperation are
imperative. It is worthwhile asking specific questions
during the neurological examination. For example,
does the sensory loss follow a stocking-glove (distal-
predominate), dermatomal, or radicular pattern?
The question of ‘‘large fiber’’ or ‘‘small fiber’’
involvement is usually based on bedside clinical tests
performed using cool instruments (tuning fork, reflex
hammer) and sharp objects of varying shape (safety pin,
broken wooden stick, commercial pin probe). However,
formal psychophysical testing of nociception is per-
formed using hot and cold stimuli and special equip-
ment. Such testing suggests that distinctions between
the two are more apparent than real because of overlap
between nociception, touch, and pressure stimulus prop-
erties. Nociceptive information is mainly conveyed by
small-diameter nerve fibers, but some nociceptive recep-
tors are innervated by myelinated fibers, and subjects can
distinguish sharp from dull stimuli without feeling pain.
Cutaneous mechanoreceptors are mainly innervated by
large-diameter nerve fibers and are activated by a variety
of moving stimuli. Touch stimulus threshold changes
modestly with age. A comparison of quantitative sensory
testing in neuropathy patients indicates that vibratory
thresholds are well correlated with touch pressure
thresholds, and vibratory thresholds are suitable
indicators of large-diameter sensory nerve dysfunction.11
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With these principles in mind, specific questions can be
answered by using an informative battery of sensory
tests.
SENSORY LEVEL
Patients are generally able to determine the level of
involvement on a limb by asking them to make a line
of demarcation, below which sensations are abnormal
and above which they are normal.
TOUCH STIMULI
The lightest touch to the dorsum of the hand and foot
represents a measure of low threshold mechanorecep-
tion. Monofilaments probes can be applied to grade the
severity of touch loss. Ten-gram filaments are useful
because lack of perception at this level of pressure is
associated with risk for unappreciated trauma.12
VIBRATION STIMULI
Tuning forks of 128 Hz assess larger-diameter nerve
fiber function, and it is important that patients fully
attend and understand the need to indicate complete
disappearance of the vibration. Comparisons between
patient and examiner for the disappearance of the vibra-
tion can be measured in seconds. The time for the
vibration to disappear for the patient after the tuning
fork is forcefully struck can be measured in seconds.
Empiric data from the great toe indicate that young
adults lose vibration perception after 15 seconds, with a
loss of 1 second per decade of age, and a loss of vibratory
perception in less than 10 seconds is abnormal at any
age.13
SHARP STIMULI
The goal is to apply a sharp stimulus without also
applying undue touch pressure on the skin. A distinction
 AN APPROACH TO THE EVALUATION OF PERIPHERAL NEUROPATHIES/BROMBERG
between noxious and light pressure stimuli can be made
by gently applying the two ends of a safety pin (sharp end
and dull end) in association with a three-part question:
‘‘Which is sharper, the first application, the second
application, or are both the same?’’ Inability to distin-
guish between sharp and dull supports loss of nociceptive
fibers relative to low-threshold mechanoreceptor fibers.
POSITION SENSE
The ability to distinguish changes in digital joint posi-
tion is normally exquisite (2 degrees). Patients must
understand the degree of sensitivity requested and
be blinded to the testing. Reduced perception of
joint movements (including falsely perceived position
changes) indicate loss of large-diameter fibers.
DEEP TENDON REFLEXES
Tendon reflexes are objective measures of sensory nerve
function. The myotatic reflex is a monosynaptic arc with
large-diameter afferent nerve fiber input from muscle
spindle fibers and large-diameter efferent nerve fiber
output from a motor neuron fibers. The reflex is much
more vulnerable to sensory nerve fiber than to motor
nerve fiber damage. An absent Achilles reflex indicates
significant dysfunction of large-diameter sensory fibers,
but it is important that the reflex is truly absent, and
reinforcing maneuvers, such as clinching the jaw or fists
and the Jendrassic maneuver, should be used before the
reflex is considered absent. Several grading systems for
tendon reflexes have been proposed, and the National
Institute of Neurological Disorders and Stroke
(NINDS) scale has good intraobserver reliability
(Table 5).14 Tendon reflexes diminish with age, and
although precise data are not available, an absent
Achilles reflex after the age of 80 years may be normal.
MOTOR SIGNS
Motor nerve fiber loss initiates collateral innervation that
obscures early effects of denervation. Inspection of the
extensor digitorum brevis muscle can reveal early loss in
the feet, and inspection of the first dorsal interosseous
Table 5 NINDS Scale for Deep Tendon Reflexes
Grade Reflex Response
0 Reflex absent
1 Reflex small, less than normal; includes trace
response, or response brought out only with
reinforcement
2 Reflex in lower half of normal range
3 Reflex in upper half of normal range
4 Reflex enhanced, more than normal; includes clonus,
which optionally can be noted in an added verbal
description of the reflex
Modified from Litvan et al.14
157
muscles can show early changes in the hands. A degree of
age-related motor fiber loss occurs after 65 years of age.
Inspection for contraction fasciculations, which are visi-
ble twitches of a muscle during early activation and
represent the discharge of individual motor units, is
useful to detect motor fiber loss.15 They are not visible
in muscles with normal numbers of motor units, but
enlarged motor units from denervation and collateral
reinnervation are readily observed.
Strength testing can be optimized to detect mild
degrees of weakness by assessing muscles that can be just
overcome on manual muscle testing in normal indivi-
duals. Informative muscles in the legs include flexors and
extensors of the lesser toes and extensors of the great toe,
and in the arms include abductors of the second and fifth
digits and extensors of the fingers. Ankle dorsiflexion
weakness occurs in more severe neuropathies, but ankle
plantar flexion weakness is evident only in the most
severe neuropathies.16 Subtle weakness of ankle dorsi-
flexion and plantar flexion can be tested best during gait
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assessment by having patients walk on their heels and
toes or hop on one leg at a time.
ORTHOPEDIC SIGNS
Limb inspection can reveal structural changes in the
feet, lower legs, and hands. The following changes may
be encountered in normal individuals but in the setting
of a peripheral neuropathy evaluation suggest a long-
standing condition. The angle between the shin and the
unsupported foot is normally
130 degrees, and a larger
angle suggests weakness of ankle dorsiflexor muscles.
High arches and hammertoe deformities suggest long-
standing differences in muscular forces exerted on the
bones of the foot leading to foreshortened feet.
Fallen arches can also be observed in severe neuropa-
thies. Toe and foot injuries unnoticed by the patient
suggest a marked degree of sensory loss. In the hands,
atrophy of the first dorsal interosseous muscle indicates
denervation.
OTHER SIGNS
Dependent pedal edema, rubor, and coolness and shini-
ness of the lower leg and foot despite good distal arterial
pulses suggest decreased movements of distal leg muscles
due to mild muscle weakness, reducing vascular return of
blood and lymph.
AUTONOMIC SYSTEM SIGNS
The autonomic nervous system is involved in many
peripheral neuropathies, but symptoms and signs of
dysautonomia are uncommonly voiced by the patient
and must be asked for. Orthostatic dizziness and changes
in blood pressure (a drop of > 30 mm Hg systolic
pressure and > 15 mm Hg diastolic pressure recorded
60 to 90 seconds after standing following 5 minutes of
supine rest) support autonomic involvement. Impotence
158 SEMINARS IN NEUROLOGY/VOLUME 25, NUMBER 2 2005
has many causes but is frequently associated with auto-
nomic neuropathy. Sicca symptoms (dry eyes and
mouth) are associated with the Sjögren’s syndrome
and represent end-organ failure of salivary and tear
glands. Sjögren’s syndrome is associated with sensory
neuropathies.
LAYER 5: WHAT IS THE PRIMARY
PATHOLOGY?
Determining between the primary pathological process
of demyelination and axonal loss is important for diag-
nosis, treatment, and prognosis. They may also occur
together, especially when the primary process is demye-
lination, because demyelination frequently involves
immune attack and axons can also be damaged. Electro-
diagnostic testing can distinguish between the two and is
discussed in another article. Nerve biopsy is less infor-
mative in this regard because it evaluates only a small
segment of sensory nerve and the relevant pathological
process may be missed; axonal loss is common to both
primary pathological processes, and evidence for demye-
lination is elusive. Biopsies are rarely repeated, and the
time course of changes cannot be followed. A nerve
biopsy leaves permanent dysfunction, and biopsies of
sensory nerves are better tolerated because a localized
area of numbness is tolerable whereas permanent weak-
ness is not. A biopsy is important when vasculitis is a
consideration and can detect rare causes of neuropathy
due to amyloid, sarcoid, or malignant cells but is not
more successful than electrodiagnostic studies in diag-
nosing demyelinating pathology.17,18
LOCALIZATION SUMMARY
At this point in the evaluation, a full characterization
of the neuropathy should have emerged, and Table 6
summarizes the clinical, electrodiagnostic, and patholo-
gical features. The next two layers focus on factors
unique to the patient under evaluation and help refine
Table 6 Clinical, Electrodiagnostic, and Pathological
Characteristics of Peripheral Neuropathies
Clinical characteristics
Acute or chronic
Symmetric or asymmetric
Distal length-dependent or distal and proximal
Electrodiagnostic and pathological characteristics
Uniform demyelinating; sensory þ motor
Segmental demyelinating; motor > sensory
Axonal; motor > sensory
Axonal; sensory neuropathy or neuronopathy
Axonal; motor neuropathy or neuronopathy
Axonal and demyelinating; sensory þ motor
diagnostic considerations and the order of laboratory
testing.
LAYER 6: WHAT ARE THE OTHER
PERTINENT FEATURES?
Determining the underlying causes of peripheral neuro-
pathies must include a thorough review of the patient’s
medical and family history.
Medical History
Past and current medical histories are obviously impor-
tant, but there are relatively few medical conditions
clearly associated with peripheral nerve disorders.13
The spectrum of appropriate laboratory tests is debated,
but the yield of informative tests falls markedly after
2-hour glucose tolerance, creatinine, and B12 tests are
considered.9 Other tests are appropriate when there is
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clinical suspicion for collagen vascular disorders and
HIV infection. When there is electrodiagnostic evidence
for primary demyelinating disorders, immunofixation
and cerebrospinal fluid analysis are appropriate.
However, many laboratory tests are frequently ordered
in the evaluation of a neuropathy, but many of these tests
represent general medical tests that are not truly infor-
mative or pertinent to the evaluation of peripheral nerve
disorders. Ganglioside antibody panels are not informa-
tive, and if positive titers are detected they rarely provide
a specific diagnosis not considered from the clinical and
electrodiagnostic data.19 Serum testing for monoclonal
proteins is appropriate with inflammatory neuropathies
to look for coexistent plasma cell dyscrasias. Of note, the
presence of monoclonal antibodies of uncertain signifi-
cance increases with age, especially over age 70.
Medications and Other Compounds
A review of medication use is important, and inquiry
should include vitamins and over-the-counter com-
pounds. Although the list of drugs, compounds, and
vitamins associated with peripheral neuropathies is
limited, drug-induced neuropathies represent readily
treatable causes and are discussed in another article.
Family History
Hereditary neuropathies are more common than appre-
ciated. With very chronic neuropathies a detailed
family inquiry is appropriate. Table 7 lists useful ques-
tions that can be addressed to parents, siblings, and
children. Interestingly, in large families with known
Charcot-Marie-Tooth neuropathy, less than 30% of
affected individuals seek medical attention for their
symptoms.20
 AN APPROACH TO THE EVALUATION OF PERIPHERAL NEUROPATHIES/BROMBERG
Table 7 Questions Pertinent to Chronic Neuropathies
Difficulty with running, sports, or military activities
High-arched feet
Hammer or curled-up toes
Claw hands
Wasting of distal muscles
Foot troubles, foot ulcers
Use of braces
Foot troubles attributed to ‘‘arthritis’’ or ‘‘poliomyelitis’’
(incorrect diagnoses)
Difficulty walking on heels
Difficulty rising from a kneeling position
LAYER 7: WHAT ARE PERTINENT
EPIDEMIOLOGICAL FACTORS?
Investigating epidemiological factors, the final step, can
help establish disease probability. The maxim of hoof-
beats being more likely from horses than from zebras
applies to peripheral neuropathies. Premature concern
about zebras in the form of rare and unlikely diseases
causing a neuropathy and the fear of ‘‘not missing
something’’ frequently overrides good epidemiological
sense. Knowledge about epidemiology patterns and dis-
ease probability, and comfort with these issues, comes
from the literature on specific types of neuropathies.
SUMMARY
The diagnostic process may take many forms, but there
is a core of information that is necessary to make an
efficient and accurate differential diagnosis. This article
focuses on the major points as a series of layers that can
be followed during the history and examination. This
approach is efficient and economical. It also recognizes
that a significant number of peripheral neuropathies will
be idiopathic, and an expansive series of tests will not
yield a true diagnosis.
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