For the full versions of these articles see bmj.com
CLINICAL REVIEW
Diagnosis and management of
neuropathic pain
R Freynhagen,1 M I Bennett2
1
Department of Anaesthesiology,
Critical Care Medicine, Pain
Therapy & Palliative Care, Pain
Center Lake Starnberg, Benedictus
Krankenhaus Tutzing, 82327
Tutzing, Germany
2
International Observatory on End
of Life Care, School of Health and
Medicine, Lancaster University,
Lancaster LA1 4YT
Correspondence to: R Freynhagen
r.freynhagen@krankenhaustutzing.de
Cite this as: BMJ 2009;339:b3002
doi: 10.1136/bmj.b3002
Neuropathic pain arises from damage, or pathological
change, in the peripheral or central nervous system.
It is usually a chronic condition that can be difficult
to treat because standard treatment with conventional
analgesics does not typically provide effective relief of
pain. Patients with neuropathic pain commonly present
to primary care professionals, but making a diagnosis
may be difficult. Neuropathic pain is usually associated
with substantially greater impairment of quality of life
compared with other types of chronic pain, and the
disorder is a large cost burden on healthcare services.
In this review, we provide an overview of published
evidence to help clinicians recognise and manage
patients with neuropathic pain.
What is neuropathic pain and who gets it?
A group of specialists of the International Association
for the Study of Pain defines neuropathic pain as “pain
arising as a direct consequence of a lesion or disease
affecting the somatosensory system.”1 In contrast to
inflammatory or nociceptive pain, which is caused by
actual tissue damage or potentially tissue damaging
stimuli, neuropathic pain is produced either by damage
to, or pathological change in, the peripheral or central
nervous system, the system that normally signals pain.
As such, the term neuropathic pain represents a varying set of symptoms rather than a single diagnosis.
Damage to the somatosensory system can provoke
a range of responses; an absence of sensation and pain
is probably a more common response than new onset
of pain. Sensitisation of peripheral nerves with ectopic
SUMMARY POINTS
Neuropathic pain commonly presents in primary care and is
often unrecognised
Diagnosis is based on characteristic symptoms,
altered sensation, and a clinical history that matches a
neuroanatomical or dermatomal pattern
Less than half of patients achieve significant benefit with any
single drug
Management includes making pain tolerable and
maintaining emotional and physical functioning
Non-pharmacological approaches can be effective, but
referral for specialist help is indicated if pain persists or
remains uncontrolled
BMJ | 15 AUGUST 2009 | VOLUME 339
Box 1 | Examples of neuropathic pain syndromes
Peripheral nervous system focal and multifocal lesions
Post-herpetic neuralgia
Cranial neuralgias (such as trigeminal neuralgia,
glossopharyngeal neuralgia)
Diabetic mononeuropathy
Nerve entrapment syndromes
Plexopathy from malignancy or radiation
Phantom limb pain
Post-traumatic neuralgia (such as nerve root compression,
post-thoracotomy)
Ischaemic neuropathy
Peripheral nervous system generalised polyneuropathies
Metabolic/nutritional—Diabetes mellitus, amyloid,
pellagra, beriberi, multiple nutritional deficiency,
hypothyroidism
Toxic—Alcohol, platinum, or taxane based chemotherapy,
isoniazid, antiretroviral drugs
Infective/autoimmune—HIV, acute inflammatory
polyneuropathy (Guillain-Barré syndrome),
neuroborreliosis (Bannwarth’s syndrome)
Heriditary—Fabry’s disease
Malignancy—Carcinomatosis
Others—Idiopathic small fibre neuropathy
Central nervous system lesions
Spinal cord injury
Prolapsed disc
Stroke (brain infarction, spinal infarction)
Multiple sclerosis
Parkinson’s disease
Surgical lesions (such as rhizotomy, cordotomy)
Complex neuropathic disorders
Complex regional pain syndrome types I and II
or spontaneous activity and hyperexcitability in the
modulatory pathways of the central nervous system
are possible mechanisms that could cause neuropathic
pain.2 3
Neuropathic pain can be caused by several different
disease processes, which can often overlap, but currently there is no universally accepted classification for
the disorder. However, four broad classes of diseases
are recognised based on aetiology and anatomy2: focal
and multifocal lesions of the peripheral nervous system; generalised polyneuropathies of the peripheral
nervous system; lesions in the central nervous system;
and complex neuropathic disorders (box 1).
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CLINICAL REVIEW
Box 2 | Common side effects of first line drugs for
neuropathic pain
Tricyclic antidepressants (amitriptyline, nortriptyline,
desipramine)
Drowsiness
Confusion
Dry mouth
Orthostatic hypotension
Weight gain
Urinary retention
Screening electrocardiography is recommended before
beginning treatment in patients over 40 years
α2-δ anticonvulsants (gabapentin and pregabalin)
Drowsiness
Dizziness, cognitive or gait impairment
Peripheral oedema
Serotonin and norepinephrine reuptake inhibitors
(duloxetine, venlafaxine)
Nausea
Dizziness
Dry mouth
Sexual dysfunction
Topical 5% lidocaine patch
Mild skin reactions (such as redness or swelling under
patch, erythema)
How common is neuropathic pain?
Estimates of neuropathic pain associated with specific
aetiologies are well described. A 2008 study reported
age standardised incidence rates of 27.3 per 100 000
person years for post-herpetic neuralgia, 26.7 for trigeminal neuralgia, 26.7 for painful diabetic neuropathy,
and 0.8 for phantom limb pain.4 The prevalence of
neuropathic pain typically rises with age and severity
of the underlying condition.5 6
By contrast, the overall prevalence of neuropathic
pain in the general population is difficult to quantify,
and exact data are lacking because of the large number
of underlying causes and the lack of standardised measurement methods. Nevertheless, epidemiological surveys suggest that 6-8% of the general population report
chronic pain with neuropathic characteristics.7 8 Neuropathic back pain with radiating pain to the arm or leg,
and post-traumatic neuropathic pain (from accidental or
surgical injury) are probably the most common causes.
Among every 1000 patients registered with a general
practitioner, about 60-80 patients will have symptoms
of chronic neuropathic pain; in half of these patients,
pain will require medication and regular support.9
How does neuropathic pain present in clinical practice?
Abnormal responses to nerve damage can account for
many of the clinical characteristics of neuropathic pain.
Symptoms can be unusual and are unlike more common pain symptoms that patients will have previously
experienced (see the box “A patient’s perspective”).
Painful symptoms arising in an area of altered sensation (numbness or hyperexcitability) are the hallmark of
neuropathic pain.
Cardinal symptoms can be spontaneous pain (pain
arising without stimulus) and abnormal responses to non392
painful or painful stimuli. In the clinic patients can complain of dysaesthesias (unpleasant and strange sensations
in the skin, such as tingling and pins and needles), deep
seated gnawing pain, and abnormal thermal sensations
(burning, on fire, or ice cold). Less commonly, patients
complain of paroxysmal pains classically described as
shooting, stabbing, or electric shocks. Patients may complain that the painful area is abnormally sensitive to any
innocuous mechanical or thermal stimulus; sometimes
clothes brushing against the area or a cold draught of air
can be intensely painful.
Features of neuropathic pain may be evident within
days of nerve damage or can take months to develop.
Sometimes, a minor insult to an area of previous injury
that had healed without problem can trigger neuropathic
pain.
How is neuropathic pain diagnosed?
There is no standard diagnostic procedure for neuropathic pain, so making a diagnosis is based on clinical
judgment. The essential elements of this process are
to identify painful symptoms, altered sensation, and
a clinical history that all match a neuroanatomical or
dermatomal pattern.10 Screening methods for neuropathic pain consist mostly of characteristic verbal
descriptors, though some have simple bedside tests in
addition. Examples of the latter are the Leeds assessment of neuropathic symptoms and signs (LANSS)
pain scale11 or the painDETECT questionnaire,5 which
have an approximate accuracy of 80% compared with
expert clinical judgment in identifying patients with
neuropathic pain. Screening methods, however, are not
a substitute for good clinical assessment and are not
intended to be diagnostic methods.12
Bedside examination is straightforward; the aim is
to identify altered sensation in the painful area, and so
responses should be compared with a non-painful adjacent or contralateral area. A painful response to lightly
stroking the skin with a finger or cotton wool is a sign of
allodynia (pain caused by a stimulus that does not usually provoke pain), a common characteristic of neuropathic pain. Numbness (hypoalgesia) or an exaggerated
painful response (hyperalgesia) to pin prick testing with
A patient’s perspective—neuropathic facial pain resulting
from oropharyngeal cancer
As far as I can remember my pain started during the second
week of the radiotherapy and chemotherapy. In total I had
six chemotherapy and 30 radiotherapy sessions over a
six week period. I found the radiotherapy was the most
painful. Not during treatment—it was the after effects. The
headache seemed to get worse on a daily basis.
Trying to explain the pain is difficult. It is like hundreds of
needles inside my head. I ended up trying to relate it to
other pain I have suffered over my lifetime. For instance,
ear infection at its worst, very bad migraine, tonsillitis. If
you could imagine all this pain in one blast it is about right,
maybe even worse. At this time of my life I was lucky if I
managed to have an hour or two of undisturbed sleep. Now
10 months down the line, I am finding it much easier to cope
as my nerve ends are healing. The medication as a pain patch
has definitely been a great help with the nerve pain.
BMJ | 15 AUGUST 2009 | VOLUME 339
CLINICAL REVIEW
a monofilament or sharp object confirms an altered pin
prick threshold. Finally, inability to distinguish warm
from cold objects suggests an altered thermal threshold.
A combination of characteristic painful symptoms in an
area of altered sensation on bedside testing is usually
enough to make a diagnosis of neuropathic pain. When
there is doubt, more detailed examination using quantitative sensory testing is helpful though not commonly
available, and it is costly and time consuming.13
Patients usually present with a spectrum of features
(mixed pain) and it is more helpful to ask yourself the
question “does this pain have any neuropathic component?”14 It is important to identify neuropathic components because different classes of analgesic drugs are
usually required to manage this type of pain effectively.
Recently, criteria for categorising neuropathic pain as
definite, probable, or possible have been proposed; this
would better indicate the reality of clinical practice than
a simple “nociceptive versus neuropathic” dichotomy.1
What are the personal and societal costs of
neuropathic pain?
Patients with chronic neuropathic pain usually report
poorer physical and mental health compared with
patients with other types of chronic pain, even when
adjusting for pain intensity.5 15 16 This association with
poor physical and mental health suggests that the
nature, and not simply the intensity, of neuropathic
pain adversely affects quality of life and that successful
management requires more than drug treatment alone.
The cost of neuropathic pain to society is not known,
but recent economic modelling of neuropathic low
TIPS FOR NON-SPECIALISTS
• Make sure that the chronic pain type has been diagnosed
correctly: a neuropathic pain screening tool may help
(such as painDETECT, the LANSS pain scale)
• In general, start with monotherapy, but consider
combination therapy from early on (for example, start with
amitriptyline or duloxetine but then add gabapentin or
pregabalin, or vice versa)
• Provide adequate time for any drug trial (two to eight
weeks; at least one to two weeks at maximum tolerated
dosage)
• Address physical and emotional aspects, as well as pain,
by encouraging physical activity, improving poor sleep,
and treating depression and anxiety
• A multidisciplinary approach to treatment is often the
most successful; this includes seeking specialist help if
your patient is not improving despite initial treatment
back pain in Germany estimated the annual cost to be
about €7.6bn (£6.4bn; $10.9bn).17
What is a sensible therapeutic approach for patients
with neuropathic pain?
Combination therapy with drugs that result in additive
or synergistic effects to target different pain mechanisms is a logical approach because less than half of
all patients will achieve a significant benefit with any
single medical treatment for neuropathic pain.18 The
evidence, however, to support the idea that combination therapy is likely to be more efficacious and safer
than each drug alone is less developed than that for
single drugs (see the box “Tips for non-specialists”).18
Table 1 | Treatment recommendations for peripheral neuropathic pain adapted from recent guidelines and algorithms19-22
Medication class/drug
Antidepressants
Tricyclics (nortriptyline, desipramine,
amitriptyline, imipramine)
Duloxetine
Venlafaxine
Paroxetine, citalopram, bupropion
Anticonvulsants
Pregabalin
Gabapentin
Carbamazepine
Lamotrigine
Oxcarbazepine
Topiramate
Valproate
Opioids*
Oxycodone
Morphine
Tramadol
Methadone
Miscellaneous
Topical lidocaine (patch 5%; gel)
Cannabinoids
Topical capsaicin
Dose range (mg/day) for
maintenance
Combined NNH for study withdrawal Combined NNT for 50% pain relief
(range)
(range)
25-150; secondary amine tricyclic
antidepressants are in favour
(nortriptyline, desipramine)
60-120
150-225
14.7 (10.2-25.2)
2.1/2.5/3.1 (1/8-3.7)
Relative risk not significant
Relative risk not significant
Relative risk not significant
4.1/5.2 (2.9-8.5)
4.6 (2.9-10.6)
6.8 (3.4-441)
First
First
First (only for trigeminal neuralgia)
Second or third
Second (only for trigeminal
neuralgia)
Third
Third
150-600
1200-3600
200-1200
200-400 (slow titration)
600-1800 (fewer safety concerns)
11.7 (8.3-19.9)
17.8 (12-30)
21.7 (12.6-78.5)
Relative risk not significant
Relative risk not significant
4.2/4.9 (3.7-7.6)
4/4,4 (3.3-6.1)
2.0 (1.3-2.2)
4.9 (3.5-8.1)
NA
200-400
1000
6.3 (5-8)
Relative risk not significant
7.4 (4.3-28)
2.8 (2.1-4.2)
Second or third
Second or third
Second or third
Second or third
10-120
15-300
200-400
15
Relative risk not significant
Relative risk not significant
9 (6.0-17.5)
NA
2.6 (1.9-4.1)
2.5 (1.9-3.4)
3.9/4.8 (2.6-26.9)
NA
First or second (only for localised
areas of pain, focal neuropathy,
allodynia)
Third
Third
1-3 patches/day applied for 12 h
Relative risk not significant
4.4 (2.5-17.5)
5-15
Relative risk not significant
11.5 (8.1-19.8)
9.5 (4.1-∞)
6.7 (4.6-12)
Recommended stage of treatment
First
First or second
First or second
Third
NNH=number needed to harm on the basis of withdrawal from neuropathic pain studies owing to adverse effects.
NNT=number needed to treat on the basis of 50% pain relief from baseline.
*The combined NNH for study withdrawal (range) for opioids overall = 17.1 (10-66).
BMJ | 15 AUGUST 2009 | VOLUME 339
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CLINICAL REVIEW
Table 2 | Treatment recommendations for central neuropathic pain adapted from current evidence
based literature19-22 26
Medication class/drug
Antidepressants
Tricyclics (amitriptyline)
Serotonin and norepinephrine reuptake inhibitors (duloxetine,
venlafaxine)
Anticonvulsants
Pregabalin
Gabapentin
Lamotrigine
Valproate
Recommended stage of treatment
First or second
First or second
First or second
First or second
Second or third (in pain after stroke)
Third
Opioids*
Levorphanol
Miscellaneous
Cannabinoids
Mexiletine
Second (in multiple sclerosis)
Third
*Second or third (no specification).
What are the recommendations from clinical guidelines
and algorithms?
Unfortunately, there is no absolute consistency from the
four most recently published guidelines and algorithms
regarding the assessment of first, second, and third line
drug treatments for neuropathic pain, although consistency exists for the classes of medication.19-22 There are
several limitations of this evidence. The evidence is
focused on a limited range of peripheral neuropathic
pain disorders (in particular, post-herpetic neuralgia
and painful diabetic peripheral neuropathy) rather than
central neuropathic pain (box 1); past studies have usually examined monotherapy rather than sequential or
parallel combinations; priorities in guidelines are not
derived from head to head studies but from comparisons
of separate and heterogenous controlled trials; and the
duration of studies is usually limited to six to eight weeks,
which tells us little about managing chronic neuropathic
pain that lasts for many years. Table 1 shows data for
different classes of treatments.
First line approaches
A sensible first line approach is to use an anticonvulsant
that binds on the α2-δ subunit of presynaptic, voltagegated calcium channels (gabapentin or pregabalin)
or a tricyclic antidepressant. Comparisons of tricyclic
antidepressants did not show any significant difference
between them, but tertiary amine tricyclic antidepressants (amitriptyline, imipramine, clomipramine) are usually associated with more severe side effects than with
other tricyclic antidepressants, and secondary amine tricyclic antidepressants (nortriptyline and desipramine)
are better tolerated (box 2). The newer mixed serotonin
and norepinephrine reuptake inhibitors (such as duloxeSOURCES AND SELECTION CRITERIA
We searched PubMed and Medline for articles whose titles included the keywords “neuropathic
pain” with the limits “meta-analysis, review and randomised controlled trial”, and we restricted
the search to articles published in English in the previous five years. We individually reviewed
the titles of the resulting articles to identify major themes. We identified all systematic reviews
in the Cochrane Controlled Trials Register with the same terms. Finally we checked recent
recommendations and published clinical guidelines from different international pain associations
and societies and reviewed contemporary textbooks and personal files.
394
tine and venlafaxine)20-22 are recommended as either
first or second line treatment, as is the use of topical 5%
lidocaine patches (for localised small areas of pain).19-22
Meta-analyses show that tricyclic antidepressants are
more efficacious and more cost effective than serotonin
and norepinephrine reuptake inhibitors, although the
latter have a better side effect profile and may therefore
be more suitable for elderly patients or those with cardiac disease (box 2).19 As new studies on serotonin and
norepinephrine reuptake inhibitors emerge, these drugs
may soon replace the use of tricyclic antidepressants.
Topical lidocaine patches can be used preferentially for
localised small areas of peripheral neuropathic pain with
mechanical allodynia (such as in post-herpetic neuralgia)
or for focal neuropathy, but not for patients with central
neuropathic pain. As systemic side effects are extremely
rare with topical treatments, they are safe particularly for
elderly patients. Data about impact on quality of life and
comorbidities are only available for newer drugs such as
gabapentin, pregabalin, and duloxetine, which have all
shown positive effects.9 16 19
Second line approaches
Randomised controlled trials have shown that controlled
release opioid analgesics, such as morphine, oxycodone,
and tramadol, are effective in neuropathic pain.18-22 There
is no evidence that one opioid is any more effective than
another, or less effective than other drug classes for neuropathic pain, however, due to potential safety concerns
such as tolerance, addiction, cognitive impairment, these
drugs are usually recommended as second or third-line
treatments.
Opioids can be considered as a first-line approach in
selected clinical circumstances, such as intractable pain,
episodic exacerbations of severe pain, acute neuropathic
pain, and neuropathic cancer pain.20 The treatment of
trigeminal neuralgia has distinct recommendations: carbamazepine (stronger evidence) or oxcarbazepine (better
tolerability) should be offered as first-line treatment for
patients with this disorder, but are otherwise not recommended for the management of neuropathic pain.23
There are encouraging results from studies regarding
cannabinoids, but their future role in the treatment of
neuropathic pain has still to be determined.24
Third line approaches
Even with well established drugs, effectiveness is
unpredictable, dosing can be complicated, analgesic
onset is delayed, and dose limiting adverse effects are
common. So patients who are refractory to any first or
second line treatment may benefit from other drugs, but
recommendations are based on much weaker evidence
or only expert clinical opinion. There is insufficient support for the use of non-steroidal anti-inflammatory drugs
such as aspirin, diclofenac, naproxen, or ibuprofen.
Central neuropathic pain
The treatment of central pain is even more controversial.
The evidence base is limited, and responders typically
experience only partial pain relief at tolerable doses.
Based on recent evidence,25 26 the first line approach that
BMJ | 15 AUGUST 2009 | VOLUME 339
CLINICAL REVIEW
ADDITIONAL EDUCATIONAL RESOURCES
• Special Interest Group on Neuropathic Pain of the IASP (NeuPSIG) (www.neupsig.org)—Leading
professional forum for science, practice, and education in the field of neuropathic pain; news,
guidelines on diagnosis and treatment; international educational meetings and symposiums
• German Research Network on Neuropathic Pain (DFNS) (www.neuro.med.tu-muenchen.de/
dfns/e_index.html)—Provides excellent information about neuropathic pain and ongoing
research (the central Integrative Network Project of the DFNS is a large neuropathic pain data
bank funded by the German Federal Ministry of Education and Research)
• Neuropathic Pain Network (NPN) (www.neuropathicpainnetwork.org/english/coalition/index.
asp)—Coalition of organisations and patient support groups actively supporting people with
neuropathic pain
• International Association for the Study of Pain (IASP) (www.iasp-pain.org)—Large
multidisciplinary organisation focused specifically on pain research and treatment
• Oxford Pain Internet Site (Bandolier) (www.medicine.ox.ac.uk/bandolier/booth/
painpag/#Chronic)—Based on the principles of evidence based medicine, this site has pulled
together systematic reviews with pain as an outcome
is recommended for peripheral neuropathic pain conditions can be used for central pain; α2-δ anticonvulsants,
tricyclic antidepressants, and serotonin and norepinephrine reuptake inhibitors are considered to be first or
second choice. Table 2 gives data for therapeutic options
in detail.
Is there a role for non-pharmacological treatments?
Surgical and chemical sympathectomy have been used
to treat neuropathic pain, but the evidence base is weak
and complications may be substantial.27 Microvascular
decompression is a recognised treatment for some types
of trigeminal neuralgia. The use of neurodestructive procedures to treat painful disorders that are due to nerve
damage is misguided and can lead to even more pain.
Recent systematic reviews have shown that neurostimulation, including the use of transcutaneous electrical nerve stimulation, electroacupuncture, and
repetitive transcranial magnetic stimulation, were all
found to be better than placebo, though these recommendations were not based on high grade evidence.28 29
The evidence for spinal cord stimulation supports its
use in patients with refractory neuropathic back and
leg pain (particularly in failed back surgery syndrome)
and complex regional pain syndrome.30 Although the
role of traditional acupuncture in neuropathic pain is
not supported by current evidence, it is popular among
patients, and as it is relatively harmless it is often used
in addition to drug treatment.
Questions for future research
Important areas for future research include developing a specific diagnostic method for neuropathic pain;
identifying associations between symptoms, signs, and
pathology to guide mechanism based treatment strategies; comparing combination treatments with monotherapy; and conducting pharmacogenomic studies to
guide prescribing.
Contributors: RF and MIB contributed equally to the article. Both authors
read and approved the final manuscript and are guarantors.
Competing interests: In the past three years RF has received research
support and consulting or speaking fees from Grünenthal, Janssen-Cilag,
Lilly/Boehringer, Mundipharma, Organon, Pfizer, and Schwarz Pharma. MB
has received honorariums, consultancy fees, and research grants from Pfizer,
NAPP, and Cephalon.
Provenance and peer review: Commissioned; externally peer reviewed.
BMJ | 15 AUGUST 2009 | VOLUME 339
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