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Review

Management of neuropathic pain after knee surgery

Pascale Vergne-Salle
Service de rhumatologie, CHU Dupuytren, 2, avenue Martin-Luther-King, 87042 Limoges cedex, France

a r t i c l e

i n f o

Article history:
Accepted 25 January 2016
Available online xxx
Keywords:
Neuropathic pain
Knee surgery
Knee arthroplasty
Knee prosthesis
Chronic pain

a b s t r a c t
Chronic postsurgical pain (CPSP) affects 10 to 30% of surgical patients overall and 16 to 20% of patients
after knee surgery. Patients report persistent pain in the absence of infection, mechanical disorders, or
complex regional pain syndrome type I. In many cases, the mechanism is neuropathic pain related to
an intraoperative nerve injury or impaired pain modulation with central sensitization. The clinical risk
factors and pathophysiology of CPSP are being actively investigated. Risk factors include preoperative
pain; diffuse pain; severe pain during the immediate postoperative period; anxiety, depression, or cognitive distortions such as catastrophizing; and comorbidities. The diagnosis rests on clinical grounds and
should be established as early as possible to optimize the chances of improvement. The management of
CPSP combines a number of perioperative prophylactic strategies and the treatment of chronic neuropathic pain. Local treatments consist of transcutaneous electrical nerve stimulation and lidocaine patches
combined with tramadol. When this treatment is inadequately effective, an antidepressant or anticonvulsant can be added. A capsaicin patch is the third-line treatment, and step III opioids are the last option.
Rehabilitation therapy and physical exercises are benecial. Psychological counseling and/or cognitive
behavioral therapy should be offered, if indicated, by the results of the evaluation.
e francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.
2016 Societ

Chronic postsurgical pain (CPSP) is dened as pain that persists

longer than 2 months after a surgical procedure, has no identied
cause, does not continue from a preexisting pain problem, and is not
related to a postoperative complication [1]. In patients with pain
after knee surgery, the evaluation should rule out other causes of
pain such as infection, loosening, instability, and complex regional
pain syndrome type I. Although CPSP is multifactorial, there is often
a neuropathic component related to peripheral nerve injury during surgery or impaired pain modulation with central sensitization
[24]. Neuropathic pain is characterized by the combination of sensory loss with paradoxical oversensitivity. The incidence of CPSP is
difcult to assess, because available studies used a wide variety
of methodological approaches. In a recent population-based study
from Norway, the incidence of CPSP was 40% overall and 18% when
only moderate-to-severe pain was considered [5]. In France, longitudinal cohort studies of postsurgical patients found incidences
ranging from 5 to 30% depending on the intensity of the pain and,
most importantly, the type of surgery [6]. Neuropathic pain has
been reported in 16% of patients after simple, commonly performed
arthroscopic procedures on the knee [7]. After knee arthroplasty,
over 20% of patients are dissatised and their main complaint is

E-mail address: pascale.vergne-salle@chu-limoges.fr

persistent pain after more than 6 months [8]. One month after knee
arthroplasty, over half the patients report moderate pain and 16%
severe pain, with pain during motion being far more common (78%
of cases) than pain at rest. A 2012 systematic literature review
showed that 20% of patients had persistent pain after knee arthroplasty [9]. During a questionnaire survey conducted 3 to 4 years
after knee arthroplasty, 44% of 632 patients reported pain overall
and 16% reported severe pain [10].

1. Pathophysiology
In patients undergoing knee arthroplasty or arthroscopy, the
initial lesion may involve the infrapatellar branches of the saphenous nerve, the lateral femoral cutaneous nerve (medial edge of
the patella), the anterior cutaneous branches of the femoral nerve,
the common peroneal nerve, and/or the posterior tibial nerve [11].
The infrapatellar branches of the saphenous nerve may be injured
after knee arthroplasty or arthroscopy. The saphenous nerve penetrates the fascia between the gracilis muscle and the sartorious
muscle at the tip of the patella then courses in the subcutaneous
tissue before dividing, typically into three branches. Anatomic variants exist regarding the number of branches (one to four) and their
location between the tip of the patella and the tibial tuberosity
[12]. Injury to the infrapatellar branches of the saphenous nerve

http://dx.doi.org/10.1016/j.jbspin.2016.06.001
e francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.
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Fig. 1. A. Anterior view of the distribution of sensory nerves in the lower limb (http://coursenligne.u-picardie.fr). B. In this diagram, the shaded area approximately indicates
the location of sensory impairments caused by injuries to the femoral nerve (intermediate and medial femoral cutaneous nerve and saphenous nerve). The dotted line
circumscribes the area affected by injuries to the ends of the anterior cutaneous branches of the femoral nerve and to the infrapatellar branches of the saphenous nerve
during surgery on the knee (from [13]).

can cause pain in the anterior knee and proximal tibia (Fig. 1A and
B). In some individuals, the end of the lateral femoral cutaneous
nerve communicates with the infrapatellar branch of the saphenous nerve and the anterior cutaneous branches of the femoral
nerve, forming a peripatellar plexus. The pain then tends to be
located at the medial knee, in the most distal part of the cutaneous
distribution of the femoral nerve (Fig. 1A and B).
The common peroneal nerve may be injured during knee arthroplasty. The frequency of this event varies widely across orthopedic
studies, from 0 to 9.5%. In a retrospective study of 1476 arthroplasties, 1.3% of patients experienced common peroneal nerve injury;
however, only cases with combined sensory and motor involvement were included [14]. Among patients with common peroneal
nerve injury, 20% also had an injury to the posterior tibial nerve. Risk
factors for common peroneal nerve injury are preoperative knee
valgus greater than 15 , xed knee exion, and a longer tourniquet
time during surgery [15]. The pain tends to localize to the lateral
and anterolateral aspects of the leg (Fig. 2A and B).
The risk of nerve injury depends on the approach [16]. With
the anteromedial approaches used for total and medial unicompartmental knee arthroplasty, there is a theoretical but small risk
of injury to the saphenous nerve or its branches. Nerve injuries
are rare with the anterolateral approach used for lateral unicompartmental arthroplasty or total knee arthroplasty in a patient
with valgus malalignment. The medial posterolateral approach carries a risk of injury to the branches of the saphenous nerve. This

approach is indicated for excision of the posterior horn of the

medial meniscus, synovectomy, and ligament reconstruction procedures. The common peroneal nerve may be injured when using
the lateral posterolateral approach, which is indicated for excision of the posterior horn of the lateral meniscus, synovectomy,
ligament reconstruction, and internal xation of fractures [17]. A
neuroma is a growth of Schwann cells and axons packed within
brous tissue at a nerve ending. During the physical examination,
a neuroma may be detected as a nodule whose palpation triggers
the pain (trigger zone).
Intraoperative tissue damage due to inammation and/or nerve
injury (stretching, laceration, or section) induces sensitization of
not only the peripheral, but also the central, nervous system.
Peripheral sensitization is related to nerve damage or local inammation induced by the surgical procedure. Damaged cells release
mediators of inammation (histamine, bradykinin, prostaglandins,
and others) and attract immune cells, which produce proinammatory cytokines. The various mediators of inammation sensitize
the peripheral nerve, whose action potentials are triggered by
lower levels of stimulation [11]. In the spinal cord, the expression of the enzymes cyclooxygenase 1 and 2 increases 3 to 6 h
after surgery. Spinal cord inammation results in the production
of excitatory neurotransmitters such as glutamate and substance P
in the dorsal horn and in decreased production of inhibitory neurotransmitters such as glycine. Glutamate activates the N-methyl
D-aspartate (NMDA) receptors, thereby inducing long-lasting

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Fig. 2. A. Posterior view of the distribution of sensory nerves in the lower limb (http://coursenligne.u-picardie.fr). B. In this diagram, the shaded area approximately indicates
the location of sensory impairments caused by injuries to the common peroneal nerve [13].

functional changes in the dorsal horn neurons, which manifest

as central sensitization. The glial cells, microglia (nervous system
immune cells), and astrocytes make a major contribution to sensitization by producing proinammatory cytokines, potentiating
the excitatory system, and depressing the inhibitory system [18].
Peripheral and central sensitization is amplied by opioids (with
step III opioids inducing hyperalgesia during the postoperative
period) and probably also by genetic susceptibility factors.
2. Risk factors for chronic pain after surgery
Many studies have sought to identify risk factors for CPSP [19].
Pain and functional impairment before surgery are associated with
CPSP [2,11]. Knee arthroplasty is often performed because of severe
pain and functional disability due to knee osteoarthritis. Severe and
long-standing pain before surgery may alter the somatosensory
system, impair pain modulation, and increase the risk of chronic
pain even after surgery. Pain with central sensitization has been
extensively documented in patients with knee osteoarthritis [20].
Increased sensitivity to pressure and heat, as well as temporal
summation, are indicators of central sensitization that can be documented by a detailed neurological evaluation. A more accurate
evaluation can be obtained by quantitative sensory testing (QST), in
which pain and other sensory perceptions in response to mechanical and thermal stimuli of various intensities are recorded. QST
measures the degree of hyperalgesia and allodynia by allowing a
comparison of pain thresholds to those on the normal contralateral
side or in healthy individuals. Nevertheless, QST is not available in
everyday practice (Table 1).
Thus, preoperative pain at the surgical site is a major risk factor
for CPSP. Another risk factor is preoperative pain at other sites (e.g.,
chronic pain or bromyalgia). In a prospective observational cohort
study, patients completed the 2011 bromyalgia survey questionnaire before undergoing knee or hip arthroplasty [21]. Patients
who met criteria for bromyalgia (6%) were excluded. Among the
remaining patients, a high questionnaire score independently predicted a smaller improvement in pain. Thus, the 2011 bromyalgia

survey questionnaire may be a useful predictor of postsurgical

pain.
Other risk factors are greater severity of preoperative pain, one
or more comorbidities (e.g., diabetes or rheumatoid arthritis), and
female gender [19].
Several psychosocial characteristics are also associated with the
risk of CPSP, including psychological vulnerability (stress and anxiety disorders) and cognitive distortions such as catastrophizing
[19]. In a prospective study of 55 patients, a high preoperative score
on the Pain Catastrophizing Scale predicted chronic pain 24 months
after knee arthroplasty [22]. A prospective longitudinal investigation in surgical patients looked for associations linking cognitive
factors (executive function, visual memory, and attention) to the
presence of chronic pain 6 and 12 months after total knee arthroplasty or breast cancer surgery [23]. Altered cognitive performance
predicted postsurgical pain independently from affective variables.
Furthermore, impaired cognitive test scores predicted pain intensity and neuropathic symptoms. Thus, cognitive exibility and
memory performance may be linked to the mechanisms responsible for pain chronicity.

Table 1
Methods for assessing the features of neurological sensitization.
Sensory symptom

Physical examination

Quantitative
sensory testing

Static mechanical
hyperalgesia

Blunt tip
Finger pressure

Calibrated von Frey

laments
Pressure algometer

Dynamic mechanical
hyperalgesia
Heat hyperalgesia

Brush

Cold hyperalgesia

Temporal summation

Tube lled with hot water

Thermo roll (at 40 C)

Thermotest

Tube lled with cold water

Thermo roll (at 25 C)
Drop of acetone
Repetitive stimuli (10 in all,
1/second) with a blunt tip

Thermotest

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a brush) or hyperalgesia (exaggerated pain in response to a stimulus

normally associated with mild pain, such as pin prick or repeated
simulation) (Table 2). Several validated tools for assisting in the
diagnosis of neuropathic pain are available. The DN4 questionnaire
is a four-item screening tool for neuropathic pain that is simple and
requires little time (Appendix A). Scores of 4/10 or more indicate
neuropathic pain with 89.9% specicity and 82.9% sensitivity [26].
The use of the DN4 is recommended in everyday practice to assist
in the diagnosis of neuropathic pain [25].
4. Management of neuropathic pain after knee surgery
4.1. Prophylactic preoperative management
Fig. 3. Risk factors for the development of chronic postsurgical pain [24].

Older patients may be at increased risk for chronic pain after

orthopedic surgery [5]. In addition, genetic factors probably inuence not only the perception of pain, but also the metabolism of
analgesics.
Finally, highly invasive surgery involving extensive dissection
clearly increases the likelihood of CPSP. Minimally invasive techniques associated with milder local inammation are benecial.
Recommendations about the management of CPSP issued by the
French Society for Anesthesia and Intensive Care (SFAR) include an
evaluation to identify risk factors for CPSP [6], which are shown in
Fig. 3 [24].
3. Diagnosis of neuropathic pain after surgery
Establishing the diagnosis is of paramount importance, because
early treatment offers the best chances of obtaining pain relief.
Recommendations about the diagnosis, evaluation, and treatment of neuropathic pain issued by the French Society for the Study
and Treatment of Pain (SFETD) state that the diagnosis rests on
careful history taking and a thorough physical examination [25].
Patients should be asked about the features of neuropathic pain,
which usually include continuous or paroxysmal spontaneous pain
and pain triggered by various stimuli (e.g., touch or temperature
changes). These two components may exist in isolation or in combination. Patients frequently report burning sensations, electrical
shocks, and/or a painful cold sensation. Also common are abnormal
and unpleasant sensations such as paresthesia, dysesthesia, itching, and numbness. The neurological examination should include
tests to rule out loss of sensation (to touch, prick, heat, and cold).
Patients should be examined for allodynia (pain triggered by a normally non-painful stimulus such as gentle touching or stroking with

Table 2
Features of neuropathic and inammatory pain.

Positive symptoms
Spontaneous pain in the damaged
areas
Oversensitivity to heat
Cold allodynia
Hyperalgesia
Delayed pain sensation
Paroxysmal pain
Burning sensations
Stabbing pain
Negative symptoms
Sensory impairments in the
distribution of the damaged nerve
Motor impairments in the
distribution of the damaged nerve

Neuropathic
pain

Inammatory
pain

Yes

Yes

Rarely
Often
Often
Often
Often
Often
Rarely

Often
Rarely
Never
Rarely
Never
Rarely
Often

Yes

No

Often

No

The main preoperative prophylactic measures are patient education to diminish risk factors, particularly those related to
psychological and cognitive disturbances; optimal management of
preoperative pain; and selection of the best time for the surgical
procedure. An important measure that probably deserves to be
taken routinely is testing for preoperative central sensitization and
increased intensity of perioperative analgesia (see the section on
risk factors for CPSP and Table 1).
4.2. Perioperative management
The objective is to minimize immediate postoperative pain
and subacute pain, which set the scene for chronic pain. Patients
should receive multimodal analgesia combining several drugs
and techniques that act on different sites in order to induce
additive or even synergistic interactions [11,27]. Combining a
nonsteroidal antiinammatory drug (NSAID) and acetaminophen
during the perioperative period decreases step III opioid requirements, diminishes opioid-induced hyperalgesia, and lessens the
intensity of the pain, particularly after orthopedic surgery [11,27].
Caution is in order, as these drugs can induce adverse events,
particularly in older patients. Other options include nefopam, tramadol, and gabapentinoids. Ketamine combats hyperalgesia by
blocking the NMDA receptors and decreases both postoperative
pain intensity and morphine requirements [27]. In a randomized
placebo-controlled trial in 50 knee arthroplasty patients, duloxetine decreased the use of morphine after the procedure [28]. There
is also a recommendation to provide not only systemic analgesics,
but also regional anesthesia (epidural anesthesia or femoral nerve
block for knee surgery) or the more recently introduced practice
of injecting a variety of local anesthetics (e.g., ropivacaine) into the
posterior capsule and into the surgical wound in the knee. Multimodal analgesia decreases the intensity of immediate and midterm
postoperative pain, thereby probably combating one of the risk factors for chronic pain, despite the absence to date of direct proof of
a decrease in long-term pain.
4.3. Management of neuropathic pain
4.3.1. Patient information
The mechanisms of neuropathic pain and treatment goals
should be explained to the patient in simple, clear terms. The
patient must understand that the pain is caused by damage to
nerve bers and not to a relapse of the underlying disease or a
complication of the surgical procedure.
4.3.2. Local treatments
Local measures should be given preference for the rst-line
treatment. Transcutaneous electrical nerve stimulation (TENS) is
a noninvasive method with useful analgesic effects, particularly
in neuropathic pain [29]. Neurostimulation modalities fall into
two main categories: conventional high-frequency low-intensity

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stimulation and acupuncture-like low-frequency high-intensity

stimulation. The patient should be taught to use the device by specially trained personnel. In France, the cost of renting the TENS
device is reimbursed by the statutory health insurance system provided the prescription is from a pain management clinic. The device
can be rented for up to 6 months then, in some cases, purchased.
Depending on the severity of the pain, the patient can then use the
device several times a day. Regular follow-up is indispensable to
check that the patient is using the device properly and to reevaluate
the therapeutic effect. An implanted medical device and pregnancy
are contraindications to TENS.
Lidocaine patches, despite their modest effect, are recommended for focal neuropathic pain in French, European, and
international guidelines [25,30,31]. This topical treatment is fairly
well suited to pain after knee surgery, given the often limited size of
the painful area. Nevertheless, the only available data come from a
single randomized controlled trial, which showed benets in various types of neuropathic pain including CPSP; and from a Cochrane
review that found no evidence of an effect after thoracotomy or
mastectomy [32]. In Europe, lidocaine patches are licensed only for
the treatment of postherpetic neuralgia, although they are often
prescribed to treat focal neuropathic pain.
High-concentration capsaicin patches (applied every 3 months)
can only be used in hospitals by specially trained personnel. Benets have been reported in patients with peripheral neuropathic
pain [33]. Capsaicin patches may constitute a useful alternative
when more conventional treatments fail to provide adequate relief.
They are licensed for use in Europe in nondiabetic adults with
peripheral neuropathic pain.
A randomized placebo-controlled trial of intraarticular
botulinum toxin A in knee arthroplasty patients showed signicant improvements in pain and function after 2 months [34].
Botulinum toxin has been proven effective against neuropathic
pain, particularly in inammatory conditions. Further studies of
this treatment option would be of interest.

4.3.3. Systemic treatments

The drugs recommended for the rst-line treatment of neuropathic pain are antidepressants and gabapentinoid anticonvulsants
[25,30,31] (Table 3). A high level of evidence supports the efcacy of tricyclic antidepressants, gabapentin, and pregabalin in
neuropathic pain due to a broad range of causes [35]. The drug
class should be selected based on the setting, comorbidities,
safety prole, and cost. Regarding comorbidities, both anticonvulsants (gabapentin and pregabalin) improve sleep disturbances, and

pregabalin also alleviates anxiety disorders. Furthermore, antidepressants have proven benecial effects on depression and anxiety.
However, they also have many adverse effects and should be used
with caution in elderly individuals. Tricyclic antidepressants are
considered to have a less favorable safety prole than anticonvulsants.
Duloxetine and venlafaxine (antidepressants that inhibit the
reuptake of both serotonin and noradrenaline) have proven benets in neuropathic pain due to a smaller number of conditions
(e.g., diabetes). Duloxetine is licensed only for pain due to diabetic
neuropathy. Both drugs are also effective against depression and
generalized anxiety.
Tramadol has a dual mechanism of action that combines opioid
and monoaminergic effects. It has been proven effective in sensory
polyneuropathy. Tramadol has no effect on comorbidities. It has
the advantage of also alleviating nociceptive pain, which makes it
useful for the treatment of mixed pain [35].
Step III opioids (oxycodone, morphine, methadone) have been
convincingly shown to alleviate peripheral neuropathic pain. High
doses are often needed to obtain an effect, and a dose titration
procedure should be conducted in each individual patient. Step III
opioids should be used only when the other available treatments
have failed, in combination with other drugs if appropriate, and
with the usual precautions [35,36].

4.3.4. Rehabilitation therapy and physical activity

The links between pain and movement have been the focus
of many recent studies [37]. Physical activity is the best measure for preventing pain. In addition to the rehabilitation therapy
required after knee arthroplasty or other surgical procedures on
the knee, information and education should be provided to the
patient to encourage physical activity, functional restoration, and
self-sufciency.

4.3.5. Management of psychological and cognitive disturbances

Anxiety and depression set the scene for chronic pain and should
be identied and treated. Cognitive disturbances such as catastrophizing, kinesiophobia, and defective coping are well established
risk factors for progression to chronicity. They can be improved by
cognitive behavioral therapy [38], which seeks to modify behaviors,
emotions, cognitions, self-afrmation, and problem solving. Examples of useful goals are improvements in physical tness, sleep, and
stress management, as well as decreased dependency on analgesic
drugs.

Table 3
Dosage of the drugs recommended for the rst-line treatment of neuropathic pain (from the French drug compendium Vidal ).
Drugs

Starting dosage

Gabapentin

300 mg/d
in 3 divided doses

Pregabalin

Amitriptyline

SNRI

100150 mg/d
in 2 divided doses
1020 mg/d
in a single evening dose

Effective dosage: ED
Maximum dosage: MD

Renal dysfunction

ED = 9001800 mg/d
MD = 3600 mg/d

GFR 3060: 40014,00 mg

bid
GFR 1530:
200700 mg once daily

ED = 150 mg/d
MD = 600 mg/d

GFR 3060: 75300 mg/d

GFR 1530:
25150 mg once daily

ED = 25150 mg/d
MD = 150 mg/d

No dosage modication

ED = 6090 mg/d
MD = 120 mg/d

Contraindicated if GFR <30

by 30 mg after 2 weeks
by 75 mg every 2 weeks

ED = 150225 mg/d
MD = 375 mg/d

GFR 3015:
37.5112.5 mg/d

Titration

by 300 mg/d
at 27 day intervals

by 150 mg at 7-day
intervals if needed
by 515 mg at 7-day
intervals if needed

Duloxetine: 3060 mg/d

Venlafaxine: 75 mg/d

GFR: glomerular ltration rate in mL/min; SNRI: serotonin and norepinephrine reuptake inhibitor.

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4.3.6. Treatment strategy

An appropriate rst-line regimen is a combination of local therapy by TENS and lidocaine patches with systemic tramadol. The
next step is single-drug therapy with either a tricyclic antidepressant or an anticonvulsant. Both efcacy and safety must be
monitored regularly. The treatment should be continued for several months. If this rst-line treatment fails, switching from an
antidepressant to an anticonvulsant or vice versa is appropriate.
A combination of drugs can be used to improve a partial response.
High-concentration capsaicin can be viewed as a third-line treatment. Step III opioids are suitable only as a treatment of last resort,
given the risk of adverse effects and dependency. This strategy complies with French and European recommendations and with the
more recent recommendations issued by the International Association for the Study of Pain (IASP) [25,30,31].
In addition, the management strategy should include rehabilitation therapy and physical exercise. The need for psychological
counselling or cognitive behavioral therapy should be assessed
on a case-by-case basis. If needed, the patient should be
referred fairly rapidly to a pain clinic to receive multidisciplinary
management.

Question 2: Is the pain associated with one or more of the following symptoms in the same area?

5. Conclusion

TO COLLATE: Score 1 to each YES answer; Score 0 to

each NO answer. If the score is 4 or higher then the pain is likely to
be neuropathic pain; If the score is less than 4 then the pain is
unlikely to be neuropathic pain.

In patients with CPSP after knee surgery, the most common

diagnosis is neuropathic pain or pain with central sensitization,
once infection, mechanical complications, and complex regional
pain syndrome Type I have been ruled out. As with all chronic
pain syndromes, a thorough clinical workup including evaluations of biological, psychological, and social factors should be
conducted, as many of the factors that contribute to chronicity
are associated with impaired function of the somatosensory system. Careful history taking may identify risk factors such as severe
or diffuse preoperative pain, severe pain during the immediate
postoperative period, cognitive distortions, anxiety and/or depression, and comorbidities. The physical examination should look for
evidence of neuropathic pain. The optimal management requires
a multidisciplinary team to provide physical therapy, analgesic
interventions, and the treatment of psychological factors. Analgesic interventions may consist of TENS, topical treatments and,
should these measures fail, an antidepressant or anticonvulsant
drug.
Disclosure of interest
The author declares that he has no competing interest.
Appendix A. Diagnosing Neuropathic Pain - DN4
Questionnaire
DN4 questionnaire to screen for neuropathic pain [26].
This four-item questionnaire is intended as a screening tool for
neuropathic pain. Scores of 4/10 or more indicate neuropathic pain
with 82.9% sensitivity and 89.9% specicity.
Please complete this questionnaire by ticking one answer for
each item in the 4 questions below.
Question 1: Does the pain have one or more of the following
characteristics?
1: Burning

Yes

No

2: Painful Cold

Yes

No

3: Electric Shocks

Yes

No

4: Tingling

Yes

No

5: Pins and Needles

Yes

No

6: Numbness

Yes

No

7: Itching

Yes

No

Question 3: Is the pain located in an area where the physical

examination may reveal one or more of the following characteristics?
8: Hypoesthesia to touch

Yes

No

9: Hypoesthesia to prick

Yes

No

Question 4: In the painful area, can the pain be caused or

increased by.
10: Brushing?

Yes

No

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