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CLINICAL EVALUATION AND

INVESTIGATION OF NEUROPATHY
*
Hugh J Willison, John B Winer
ii3

J Neurol Neurosurg Psychiatry 2003;74(Suppl II):ii3ii8

T
he assessment and investigation of a possible neuropathy is one of the most common clinical
problems facing the general neurologist. Studies of the prevalence of neuropathy in the com-
munity are rare but suggest a figure of between 28%,1 making peripheral neuropathy at least
as common as stroke. Despite this high prevalence of neuropathy, it is only a small proportion of
patients with neuropathies who are referred for detailed evaluation, principally those individuals
with disabling disease, or with none of the obvious risk factors such as diabetes or alcoholism.
A logical approach to the assessment of such patients is essential and can be organised into a
number of basic questions. The neurologist faced with a patient with a neuropathy has to deal with
literally thousands of possible causes, many extremely uncommon, and these can only be simpli-
fied by defining the neuropathy by other features that lead to the select few of most likely
diagnoses. This is in part a process of pattern recognition but can be helped by a stepwise approach.
Several algorithms2 and review articles3 have been published to aid this process and a typical one
has been constructed here (fig 1).
The approach adopted in this article is to present the evaluation as a list of commonly asked
questions that, if correctly addressed and answered, are likely to yield diagnostically important
information, and hence direct appropriate management. This is not intended as an exhaustive
account of neuropathy but is a personal view, illustrative of a diagnostic process that is commonly
adopted.

DOES THE HISTORY AND EXAMINATION SUGGEST THAT THE PATHOLOGICAL

c PROCESS IS LOCALISED TO THE PERIPHERAL NERVE?

This question can usually be answered easily, but occasionally patients may present unusually, and
multiple pathologies may confound the diagnostic process. Spinal cord disease is one of the most
common differential diagnostic considerations in patients with neuropathic-type symptoms (box
1). Where sensory symptoms are present with few clinical signs, the classical features of a lower
motor neurone disorder may be absent and a transverse myelitis, myelopathy, or other central
nervous system disorder can masquerade as a neuropathy. Involvement of cranial nerves (for
example, facial numbness or weakness, oculomotor disturbance) in an acute inflammatory
neuropathy is helpful in excluding a cord lesion with a pseudo-lower motor neurone pattern of
presentation, as may occur in acute myelopathies.
A common co-occurrence, particularly in the elderly, is the combined presence of cervical
spondylotic myelopathy and late onset predominantly sensory axonal neuropathy. In the same
context, spondylotic radiculopathies may co-occur with upper limb entrapment neuropathies. In
these circumstances, experience and care is required to identify the dominant pathological process,
and this may not always be possible. Certain neuropathies co-exist with CNS disease, such as vita-
min B12 deficiency, adrenomyeloneuropathy, neuroacanthocytosis, spinocerebellar syndromes, to
name but a few of many. In these situations there is no substitute for pattern recognition and, if
this fails, a structured approach, both of which are more likely to succeed than random investiga-
tion.

HAS THE PRESENTING COMPLAINT BEEN FULLY DESCRIBED?

See end of article for authors It is surprising how often simple, clearly discernable features of the history can be overlooked. This
affiliations is particularly the case in inherited neuropathies and congenital syndromes. Funny feet, unevenly
worn shoes, and childhood and adolescent clumsiness, especially in sports and tasks requiring fine
Correspondence to: coordination, are all important clues to an illness that may extend back well beyond the duration
Professor Hugh J Willison,
Division of Clinical of the patients more obvious symptoms.
Neurosciences, Southern The duration of symptom development is important to define and the following categories are
General Hospital, Glasgow used as broad guidelines in neuropathy circles: acute (< 4 weeks), subacute (13 months), and
G51 4TF, UK;
h.j.willison@udcf.gla.ac.uk chronic (> 3 months). Vasculitic lesions are often hyperacute mononeuropathies, usually coming
on over 2472 hours. In some circumstances, such as early assessment following symptom onset,

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NEUROLOGY IN PRACTICE

Box 1: Diagnostic pitfalls in establishing a Box 2: Demyelinating neuropathies

neuropathy
c Acute
c Transverse myelitis Guillain Barre syndrome (GBS)
c Hypokalaemia c Chronic
c Spinal arteriovenous malformation chronic inflammatory demyelinating polyradiculo-

*
ii4
c
c
Conus tumour
Carcinoma prostate
neuropathy (CIDP)
paraproteinemia related
amiodarone toxicity
Refsums disease
this cannot be clarified at presentation but becomes evident Charcot-Marie-Tooth (CMT) types 1, X and AR CMT 1
later. Guillain-Barr syndrome (GBS), for example, by defini- metachromatic leucodystrophy
tion reaches its nadir within four weeks of onset, and any pro- statins
gression beyond this may suggest relapsing disease or
evolution into chronic inflammatory demyelinating polyra-
diculoneuropathy (CIDP), both of which would require even to peripheral nerve, but they do give an indication of fibre
further treatment. A frequent difficulty in the history is type involvement, and hence narrow down the likely causes.
encountered in separating residual deficit following an acute
event, from a chronic process. The time course helps to limit
the differential diagnosis, especially for acute and chronic HAVE I OBTAINED ADEQUATE PAST, FAMILY,
demyelinating syndromes (box 2). OCCUPATIONAL, AND DRUG HISTORIES?
One often undervalued aspect of clinical history taking A very important consideration is to establish whether the
relates to the precise details of the site and character of neuropathy is an isolated illness of peripheral nerve, or
sensory symptoms. Detailed accounts of this are available whether it is occurring in the context of disease elsewhere, or
from many sources.4 Focal symptoms can provide vital clues to other historical factors. Important background clues and
individual nerve or root disorders, that in themselves may be information are often missed in the first round of assessment
sufficient to make a firm diagnosis of, for example, meralgia and only come to light retrospectively.
parasthetica. Distal dying back axonopathies have a very Concurrent systemic diseases are clearly important, particu-
characteristic length dependent pattern of symptom evolu- larly organ failure, endocrine disorders, and connective tissue
tion, that is usually symmetrical, affecting feet, then hands, disease. Diabetes, and latent diabetes, should always be
then anterior trunk. Demyelinating neuropathy may also have sought. The detailed family history is often crucial, even if
a length dependent pattern of sensory evolution because in a negative, provided that the family is of a sufficient size to be
diffuse process longer fibres have a higher probability of informative. This may include an opportunistic examination
becoming blocked. In contrast, multi-segmental patterns of of accompanying relatives, even if restricted to tapping the
sensory involvement, including the trunk, suggest dorsal root ankle jerks, or recording a lower limb motor conduction veloc-
ganglionopathies as may occur in the neuropathy of Sjogrens ity.
syndrome, for example. Toxic exposure in the workplace is becoming less prominent
Apart from the site of onset, the character of sensory symp- a risk factor as industrial environments improve. Thus lead,
toms needs to be pinned down from the history, as it is often arsenic, acrylamide, and volatile solvents are all rare as causes
poorly described by patients and can be diagnostically useful. of neuropathy. However, a drug history is crucial, both
Pain, loss of temperature appreciation, and autonomic symp- prescribed and recreational. The list of prescribed medications
toms are all features of selective small fibre involvement. The resulting in neuropathy is too long to list, major culprits being
negative sensory symptom of unsteadiness that is more amiodarone, phenytoin, statins, many antibiotics, and chemo-
prominent in the dark, or on eye closure, is characteristic of therapies: if in doubt, look it up in your BNF! Abused drugs
sensory ataxia caused by large fibre involvement. These provide a twofold risk: the drug itselffor example, tobacco
patterns of sensory involvement do not localise the lesion, (paraneoplastic), alcohol (toxic), cocaine (vasculitic)and

Figure 1 Algorithm showing a

stepwise approach to the assessment
and investigation of a possible
neuropathy. CIDP, chronic
inflammatory demyelinating
polyradiculoneuropathy; CMT,
Charcot-Marie-Tooth; EMG,
electromyography; GBS,
Guillain-Barr syndrome; HNPP,
hereditary neuropathy with liability to
pressure palsies; NCS, nerve
conduction studies.

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NEUROLOGY IN PRACTICE

the behaviour related consequences, including HIV or hepati-

Box 3: Focal and multifocal neuropathies
tis C infection, and nutritional deficiency.
Within the ethnic diversity and globalisation of travel seen c Entrapment neuropathyfor example, carpel tunnel syn-
in multiracial Britain, certain types of neuropathy may be drome (CTS), ulnar nerve at elbow, common peroneal nerve
more prominent in particular groups. There is no point over fibular head
c Myxoedema, acromegaly

*
suspecting a Scottish highlander of having leprosy, but he may
c Amyloid
have acquired neuroborreliosis locally, or have returned with it ii5
c Diabetes
from a walking tour of the Black Forest. The contrary applies c Hereditary neuropathy with liability to pressure palsies
to an immigrant from India, leprosy being one of the most (HNPP A)
common causes of neuropathy worldwide. Vegans are vulner- c Vasculitis
able to nutritional deficiency; intrafamilial marriages throw c Multifocal motor neuropathy
up recessive neuropathies.

WHAT SPECIAL FEATURES OF DIAGNOSTIC HELP

proves true in modern practice. In length dependent
MIGHT I PICK UP FROM THE EXAMINATION?
axonopathies, such as Charcot-Marie-Tooth 2 (CMT 2) or
We all know of the apocryphal stories of the eager specialist
metabolic neuropathies, this may be the case. Demyelinating
registrar who leaves the urine pot on the windowsill to diag-
neuropathy, such as GBS and CIDP, is often characterised by
nose porphyria. However, picking up special diagnostic
proximal dominant weakness, since multiple roots are often
features from the general examination is not easy to approach
affected by conduction block, and may even produce a
systematically, and often it requires a return visit to the patient
pseudo-pyramidal pattern of weakness.
to seek something other tests might lead you to suspect. Thus
The examination hallmark of neuropathy is to elicit the
the umbilical keratomas of Fabrys disease, the Mees lines of
tendon reflexes. Focal reflex loss with preservation at other
arsenic toxicity, and the orange tonsils of Tangiers disease are
sites has clear implications. Distal reflex loss, manifested by
but a sprinkling of the rarified diagnostic opportunities avail-
absent ankle jerks but preserved reflexes elsewhere, is very
able to the well tutored.
characteristic of the length dependent axonopathies. In the
Certain aspects of the peripheral nerve examination are
acquired demyelinating neuropathies, reflex loss is usually
more practically useful. Convention dictates that we start with
generalised, as is also usually the case in CMT 1.
the cranial nerves. Thus anosmia occurs in Refsums disease
The sensory examination is best approached by testing
and B12 deficiency; optic atrophy when not associated with
modalities that subserve large fibre (vibration sense and pro-
mixed central and peripheral demyelinating disease may sug-
prioception) and small fibre (pinprick, pain, and temperature)
gest an inherited syndrome. Anisocoria and impaired pupil-
function, in conjunction with a consideration of both focal and
lary light reflexes indicate parasympathetic damage and may
length dependent features, since this can provide key clues to
be isolated, as in Adies syndrome, or direct a more careful
the likely cause. Sensory examination must be approached
search for autonomic involvement elsewhere, as may occur in
with a clear diagnostic purpose and guided by knowledge of
diabetic neuropathy or the acute dysautonomia occasionally
the major cutaneous nerve and root patterns, otherwise it is
seen in the GBS spectrum. Impaired ocular mobility suggests
likely to be unrewardingly circumspect.
botulism or Miller Fisher syndrome, facial weakness is a
frequent feature of GBS, and trigeminal sensory loss of
Sjogren neuropathy. Lower cranial nerve palsies are typical of IS THE NEUROPATHY FOCAL, MULTIFOCAL OR
Kennedys disease, which along with gynaecomastia will allow GENERALISED?
you to make a confident bedside diagnosis when confronted The pattern of distribution of peripheral nerve involvement is
with a case of diffuse motor neuronopathy. very helpful in reaching a diagnosis. Thus mononeuropathies,
Assessing muscle strength is conventionally conducted especially if an entrapment site, are often an isolated
using the Medical Research Council scale and nothing has phenomenon, possibly related to pregnancy, thyroid disease or
superseded this despite the uncomfortably broad range of occupation, but importantly may also occur as features of a
power in band 4. This is not a shortcoming of the design of the more generalised disorder, such as hereditary neuropathy with
scale which originated in 1941 for assessing the severe nerve liability to pressure palsies (HNPP) or amyloidosis. Mono-
injuries sustained in military combat, but a pleasant reminder neuropathies occurring outside entrapment sites are more
that today we tend to complain about smaller things than our important to investigate fully, especially if vasculitis is
predecessors. Dynamometry can be used for the more precise suspected as this need careful evaluation for treatment. If the
measurements needed for clinical trials or for assessing pattern suggests a single nerve or plexus lesion at an unusual
responses of individual muscle groups to treatment, such as site of compression or invasion, such as a radial nerve lesion
intravenous immunoglobulin (IVIg) in multifocal motor neu- compressed on a chair in a patient following an overnight
ropathy (MMN). binge, or invasion of the brachial plexus with breast
However recorded, power measurement is important to malignancy, this is clearly important to detect. The list of pos-
conduct and record properly and distribution of weakness is sible causes for focal or multifocal neuropathies is consider-
crucial to diagnosis. A broad knowledge of peripheral nerve ably reduced compared with generalised neuropathies (box 3).
territories and root values is our neurological bread and butter. Another issue is to consider whether the neuropathy involves
Difficulties can arise when multiple mononeuropathies upper or lower limbs in a preferential pattern. Most length
become confluent since they can be hard to separate from dependent axonopathies will commence in the legs, but occa-
polyneuropathies, and when examining complex brachial and sionally inherited neuropathies and neuronopathies begin in
lumbar plexus lesions. Electrophysiological help is often the hands in some families. In hereditary amyloid neuro-
required in these situations. The medical student view that pathies, the hands are often affected early. In acquired de-
weakness in polyneuropathy is invariably distal also rarely myelinating neuropathies, the arms may be prominently

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NEUROLOGY IN PRACTICE

Box 4 Box 5: Small fibre and autonomic neuropathies

c Predominantly sensory neuropathies c Diabetes
diabetes c Amyloidosis
thiamine deficiency c Fabrys disease
malignancy c Tangier disease

*
ii6


leprosy
hereditary sensory neuropathies
c
c
c
Hereditary sensory and autonomic neuropathies
Chronic idiopathic small fibre sensory neuropathy
Sjogrens syndrome
amyloid
uraemia
sarcoid
c Predominantly motor neuropathies duction velocities in several nerves, assessment of conduction
Guillain-Barre syndrome and CIDP block, measurement of sensory action potentials, and
porphyria measurement of distal latencies and F wave latencies, as
diphtheria described below.
botulism However, there are some clinical clues that can be helpful.
lead Widespread reflex loss, including in muscle groups that are
Charcot-Marie-Tooth not particularly weak or wasted, is more a feature of demyeli-
nation. In contrast, selective loss of the ankle jerks in the pres-
ence of distal wasting and weakness is more typical of an
affected to a greater extent than would be expected from the axonopathy, especially if accompanied by a stocking distribu-
degree of involvement in the legs. tion of sensory loss.
Thus the complete assessment of a patient with a
WHAT IS THE RELATIVE EXTENT OF MOTOR AND
neuropathy might characterise the clinical syndrome as a
SENSORY NERVE INVOLVEMENT?
chronic multifocal, predominantly motor, demyelinating neu-
It is clear that some neuropathy syndromes are purely motor,
such as multifocal motor neuropathy with conduction block ropathy. This type of neuropathy would have a restricted
(MMNCB), whereas other are purely sensory, such as a differential diagnosis and would target investigations towards
subacute sensory neuronopathy (SSN) caused by paraneo- distinguishing CIDP from a paraproteinemia and amiodarone
plastic or other autoimmune dorsal root ganglionopathies toxicity.
(box 4). However, clinical life is rarely so simple and the The largest and most difficult group is the mixed motor
majority of neuropathies are mixed, if not symptomatically, sensory neuropathy with a pattern to suggest a dying back
then at least on clinical or electrophysiological examination. axonopathy and confirmation of an axonal neuropathy on
Even in MMNCB, some very minor sensory symptoms or signs electrophysiology (box 6). Here a careful history is paramount
(including electrophysiological) in motor affected territories with detailed enquiry into other systemic disease and a
are sometimes evident and should not exclude the diagnosis, detailed family tree. Constructing a family tree may bring out
although may encourage one to consider the closely related details of forgotten relatives with stigmata of an inherited
syndrome, multifocal acquired demyelinating sensory and neuropathy such as high arched feet.
motor neuropathy (MADSAM, Lewis-Sumner syndrome). In
WHAT ADDITIONAL INFORMATION CAN I EXPECT
contrast sensory involvement should never be the case in
FROM A NEUROPHYSIOLOGICAL ASSESSMENT?
motor nurone disease (MND), and would cast serious doubt Detailed consideration of this is outwith the scope of our
on this diagnosis. Similarly motor involvement should never introduction, but it is worth making a few points. The neuro-
occur in a pure dorsal root ganglionopathy; however, the neu- physiological examination cannot be conducted in isolation
ropathy associated with anti-Hu antibody is not as uniform an from the clinical assessment, but has to be led by the histori-
SSN as text books state in that motor involvement can often be cal and clinical findings. Many clinical electrophysiologists
found in this patient group.5 Thus this question is intended as take a history and perform an examination before their elec-
a helpful guideline to diagnosis rather than an immutable trophysiological studies in order to guide their choice of sites
rule. and testing methods, but this by necessity is often rather lim-
ited. It is therefore extremely helpful for the clinician to high-
IS THERE PROMINENT SMALL FIBRE AND
AUTONOMIC INVOLVEMENT? light the most pertinent questions sought from the laboratory,
Autonomic features, including pupillary, sweat gland, cardio- ideally by discussion or alternatively on the request form. In
vascular, and gastrointestinal involvement are features of dia- the latter case, the neurologist should succinctly specify the
betic and amyloid neuropathy, and can occasionally be promi- information required from the neurophysiological assessment
nent in GBS (box 5). This requires a careful history for of the patient, but should refrain from specifying the
symptoms of light intolerance, postural hypotension, noctur- individual tests required to achieve that!
nal diarrhoea, impaired sweating, and bladder dysfunction. Sensory studies are often the first approach to determining
Examination can include careful analysis of pupillary light the presence of a neuropathy. If objective sensory loss affecting
responses, lying and standing blood pressure measurement, large fibres is clinically evident, the presence of normally pre-
and assessment of sinus arrhythmia with ECG measurement served sensory nerve action potentials (SNAPs) points away
during deep breathing. from the cause being distal to the dorsal root ganglion, and
suggests a central or root disorder. Focal entrapments can
IS THE NEUROPATHY AXONAL OR DEMYELINATING often be readily picked up by side to side comparisons on sen-
ON CLINICAL GROUNDS? sory nerve examination. Length dependent large fibre
This cannot be determined clinically with any degree of accu- neuropathies are characterised by disappearance of distal leg
racy and requires neurophysiology with measurement of con- SNAPs (that is, superficial peroneal and sural nerve) before

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NEUROLOGY IN PRACTICE

Box 6: Chronic axonal neuropathies Box 7: First round screening tests

c Drugs or toxins c Blood sugar
alcohol c Liver function tests
chemotherapeutic agentsfor example, vincristine, c Vitamin B12
cisplatinum c Paraprotein screen
organophosphate
phenytoin
c
c
c
Thyroid function
Full blood count
Erythrocyte sedimentation rate, vasculitic screen
*
ii7
antibioticsfor example, metronidazole, dapsone
statins
c Infections
leprosy neuropathy affecting the upper limbs, is there is evidence of
Borrelia conduction block to suggest a diagnosis of multifocal motor
HIV, HTLV1
c
neuropathy, as opposed to MND?11 Such studies need to
Connective tissue diseases
include assessment of proximal block by stimulating at Erbs
Sjogrens syndrome
point, which may not be done routinely. The multifocal
systemic lupus erythematosus
rheumatoid arthritis pattern of involvement seen in vasculitic neuropathy can often
c Metabolic be very helpfully separated from multiple entrapments or root
diabetes lesions. In Miller Fisher syndrome or bulbo-spinal neuronopa-
c Paraneoplastic thy, the salient question might be whether the sensory action
lung, ovarian carcinoma potentials reduced in size.
c Inherited
CMT 2 and X
familial amyloid neuropathies
WHAT SCREENING TESTS SHOULD I PERFORM?
c
Box 7 shows a reasonable first screen for a new presentation of
Vitamins
vitamin B12 an axonal neuropathy without an obvious cause.
vitamin E If no cause is found from the above and there are no clinical
pyridoxine toxicity clues in the past medical history, it would be reasonable to
c Endocrine delve further into the family history and try if possible to
hypothyroidism examine the relatives. Further tests are usually performed at
c Paraprotein this stage according to clinical clues that suggest more
myeloma unusual or esoteric causes for neuropathy. An example might
Waldenstroms disease be the measurement of anti-Hu antibodies to detect occult
benign monoclonal gammopathies chest or gynaecological malignancy.5 It is impossible to list all
investigations that might be of use and it should be
emphasised that these should be targeted to the clinical situ-
upper limb SNAPs. It is rare for sensory nerve studies to be ation. After these second line tests most recent studies suggest
completely normal in neuropathies with sensory symptoms, that there will be at least 15% of patients for which no cause
except in the difficult category of late onset, painful small fibre can be found.12 Studies of this group suggest that some may be
neuropathies, such as occur with restless legs. immune in origin and others unrecognised genetic neuro-
The simplest and most frequently asked question of motor pathies. The main clinical concern in patients that are deterio-
conduction studies (although not necessarily the easiest to rating is the presence of a vasculitis restricted to the peripheral
answer) is whether or not there is evidence of demyelination. nerves. Such a diagnosis can only be made on nerve biopsy, but
Protocols specifying agreed criteria for demyelination have the yield from biopsy in the chronic idiopathic symmetrical
been prepared for patients suspected as having GBS6 or CIDP7 neuropathies is very small. If the neuropathy is of recent onset
and these are useful. Establishing that the patient has a clearly and progressive, or if there is a suggestion of systemic disorder
demyelinating neuropathy is crucial to the subsequent or raised erythrocyte sedimentation rate (ESR), biopsy should
sequence of investigations. Interpretation of the pattern of be considered. Otherwise continued follow up is wise. Anti-Hu
demyelination is a rather specialised area best left to your antibodies are important, since their presence is closely asso-
neurophysiologist, but one that is very useful. Thus uniform ciated with a paraneoplastic neuropathy13 and undisclosed
demyelination rather favours an inherited neuropathy, malignancy usually of the lung or ovary.
whereas patchy findings with differences between nerves, and
segments within a nerve, are more in favour of an acquired CSF analysis
syndrome.8 9 F wave latencies are useful in the early stages of Cerebrospinal fluid (CSF) analysis is useful to distinguish
GBS for assessing proximal conduction slowing, and may immune mediated neuropathies such as CIDP or chronic
indeed be the only abnormality early in the course of the immune mediated axonal neuropathies where the CSF protein
disease.10 Some syndromes have peculiarly individual features; is frequently notably raised. The presence of a significant
thus the demyelinating neuropathy associated with immu- pleocytosis in a subacute neuropathy should raise suspicion of
noglobulin IgM anti-myelin associated glycoprotein (MAG) other acute inflammatory neuropathies such as Borrelia or
antibodies is characteristically associated with prolonged dis- sarcoidosis.
tal motor latencies.
Another common clinical question in which the electro- Special tests
physiologist is crucial is in determining whether the Genetic testing for neuropathy has thankfully mushroomed in
neuropathy is symmetrical and confluent or whether focal or recent years and has solved many diagnostic conundrums. The
multifocal features are present. In the case of an asymmetric area is covered in detail by Reilly and Hanna.14 Another area

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NEUROLOGY IN PRACTICE

where tests have increased dramatically is in dysimmune syn- with CIDP do not have inflammatory cells in their sensory
dromes, especially antibody testing. It is obligatory to diagnose nerves and biopsy is probably unnecessary in patients with
paraneoplastic syndromes by antibody testing in patients with typical electrophysiology and clinical features of CIDP.18 The
subacute sensory neuronopathies, and in practice the net is yield from biopsying chronic axonal neuropathies is very small
often cast wider than this clinical indication. A wide range of and is probably not justified when a vasculitis seems unlikely.
Patients with axonal neuropathy simulating an axonal form of

*
other antineuronal antibody tests are also available for specific
indications. CMT can occasionally turn out to have amyloid, especially if
ii8 there are small fibre features. The diagnosis in these patients
Anti-ganglioside antibodies are sought in patients with
suspected MMN. Anti-GM1 IgM antibodies are present in can frequently be made by looking for transthyretin mutations
around 50% of patients with this syndrome, so their absence in most patients without recourse to biopsy, but if the genetics
does not exclude the diagnosis, but their presence is diagnos- are unhelpful then a biopsy seems reasonable.
tically helpful.
.....................
Anti-GQ1b IgG antibodies are a highly reliable marker for
Authors affiliations
Miller Fisher syndrome where they are invariably present in H J Willison, Division of Clinical Neurosciences, Southern General
acute phase sera. In the motor axonal variant of GBS, Hospital, Glasgow, UK
J Winer, Department of Neurology, University Hospital Birmingham,
anti-GM1 and anti-GD1a antibodies are also frequently found, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK
being present in over 50% of cases.
In chronic neuropathy syndromes, particularly those REFERENCES
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CLINICAL EVALUATION AND INVESTIGATION

OF NEUROPATHY
Hugh J Willison and John B Winer

J Neurol Neurosurg Psychiatry 2003 74: ii3-ii8

doi: 10.1136/jnnp.74.suppl_2.ii3

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Topic Articles on similar topics can be found in the following collections

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