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The IASP classification of chronic pain for ICD-11: chronic neuropathic pain.

January 2019
Pain 160(1)

Authors:

Queen Mary, University of London

The upcoming 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD) of the World Health Organization (WHO) offers a unique opportunity to improve the representation of painful disorders. For this purpose, the International Association for the Study of Pain (IASP) has convened an interdisciplinary task force of pain specialists. Here, we present the case for a reclassification of nervous system lesions or diseases associated with persistent or recurrent pain for ≥3 months. The new classification lists the most common conditions of peripheral neuropathic pain: trigeminal neuralgia, peripheral nerve injury, painful polyneuropathy, postherpetic neuralgia, and painful radiculopathy. Conditions of central neuropathic pain include pain caused by spinal cord or brain injury, poststroke pain, and pain associated with multiple sclerosis. Diseases not explicitly mentioned in the classification are captured in residual categories of ICD-11. Conditions of chronic neuropathic pain are either insufficiently defined or missing in the current version of the ICD, despite their prevalence and clinical importance. We provide the short definitions of diagnostic entities for which we submitted more detailed content models to the WHO. Definitions and content models were established in collaboration with the Classification Committee of the IASP's Neuropathic Pain Special Interest Group (NeuPSIG). Up to 10% of the general population experience neuropathic pain. The majority of these patients do not receive satisfactory relief with existing treatments. A precise classification of chronic neuropathic pain in ICD-11 is necessary to document this public health need and the therapeutic challenges related to chronic neuropathic pain.

Classification of chronic neuropathic pain in ICD-11. Top and 2nd level diagnoses are part of ICD-11 Mortality and Morbidity Linearisation (MMS). 32 Specific entities of chronic neuropathic pain are included at the next level. According to the new concept of multiple parenting in ICD-11, these entities may be referred to from other divisions of the chronic pain classification, eg, chronic posttraumatic pain or chronic secondary headaches and orofacial pains.

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Narrative Review

The IASP classification of chronic pain for ICD-11:

chronic neuropathic pain

Joachim Scholz

a,b

, Nanna B. Finnerup

c,d

, Nadine Attal

e,f

, Qasim Aziz

, Ralf Baron

, Michael I. Bennett

Rafael Benoliel

, Milton Cohen

, Giorgio Cruccu

, Karen D. Davis

m,n

, Stefan Evers

o,p

, Michael First

Maria Adele Giamberardino

, Per Hansson

s,t

, Stein Kaasa

u,v,w

, Beatrice Korwisi

, Eva Kosek

Patricia Lavand’homme

, Michael Nicholas

, Turo Nurmikko

, Serge Perrot

, Srinivasa N. Raja

, Andrew S.

C. Rice

, Michael C. Rowbotham

, Stephan Schug

, David M. Simpson

, Blair H. Smith

, Peter Svensson

jj,kk

Johan W.S. Vlaeyen

ll,mm

, Shuu-Jiun Wang

nn,oo

, Antonia Barke

, Winfried Rief

, Rolf-Detlef Treede

pp,

*, Classification

Committee of the Neuropathic Pain Special Interest Group (NeuPSIG)

Abstract

The upcoming 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD) of the World

Health Organization (WHO) offers a unique opportunity to improve the representation of painful disorders. For this purpose, the

International Association for the Study of Pain (IASP) has convened an interdisciplinary task force of pain specialists. Here, we

present the case for a reclassification of nervous system lesions or diseases associated with persistent or recurrent pain for $3

months. The new classification lists the most common conditions of peripheral neuropathic pain: trigeminal neuralgia, peripheral

nerve injury, painful polyneuropathy, postherpetic neuralgia, and painful radiculopathy. Conditions of central neuropathic pain

include pain caused by spinal cord or brain injury, poststroke pain, and pain associated with multiple sclerosis. Diseases not explicitly

mentioned in the classification are captured in residual categories of ICD-11. Conditions of chronic neuropathic pain are either

insufficiently defined or missing in the current version of the ICD, despite their prevalence and clinical importance. We provide the

short definitions of diagnostic entities for which we submitted more detailed content models to the WHO. Definitions and content

models were established in collaboration with the Classification Committee of the IASP’s Neuropathic Pain Special Interest Group

(NeuPSIG). Up to 10% of the general population experience neuropathic pain. The majority of these patients do not receive

satisfactory relief with existing treatments. A precise classification of chronic neuropathic pain in ICD-11 is necessary to document

this public health need and the therapeutic challenges related to chronic neuropathic pain.

Keywords: Chronic pain, Neuropathic pain, Diagnosis, Classification, ICD-11, WHO

1. Neuropathic pain

Lesions or diseases involving the somatosensory nervous system

may paradoxically not only lead to a loss of function but also to

increased pain sensitivity and spontaneous pain. This neuro-

pathic pain is usually chronic, ie, it either persists continuously or

manifests with recurrent painful episodes. Pain may result from

etiologically diverse disorders affecting the peripheral or the

central nervous system. The cause can be a metabolic disease,

eg, diabetic neuropathy, a neurodegenerative, vascular or

autoimmune condition, a tumor, trauma, infection, exposure to

toxins, or a hereditary disease. Chronic pain also occurs in

neurological conditions of unknown etiology, eg, idiopathic

neuropathies.

The mechanistic underpinnings of pain hyper-

sensitivity and spontaneous pain in these conditions are complex,

and their relationship to the underlying pathological disease

process often remains unclear. On the other hand, differences in

pain phenotypes offer an opportunity to distinguish pain

syndromes clinically.

1,9,30

Neurophysiological investigations

may reveal some mechanistic clues, eg, activity increases in

somatosensory nerve fibers or changes in the endogenous

control of pain.

14,17

However, a lack of suitable noninvasive tests

usually precludes an in-depth evaluation of active pain mecha-

nisms in patients. Although imaging studies and quantitative

sensory tests help elucidate important pathophysiological

aspects of pain in patients, current knowledge of neuropathic

pain mechanisms is based largely on animal models.

Chronic neuropathic pain is a major factor contributing to the

global burden of disease.

Its prevalence ranges between 6.9%

and 10% of the general population.

How strongly pain is

associated with a particular neurological disease varies. Pain may

be the most prominent or sole disease manifestation as, eg, in

postherpetic neuralgia, or it may occur only in a subgroup of

patients with the same disease as, eg, in chemotherapy-induced

peripheral neuropathies. Even among patients with the same

underlying cause of neuropathic pain, painful symptoms and signs

usually differ.

However, when present, neuropathic pain frequently

causes major suffering and disability. Therapeutic management is

challenging. Medications recommended as first-line treatments

provide less than satisfactory relief in many patients.

A suspected diagnosis of neuropathic pain requires specific

investigations to ascertain that the pain originates in the nervous

system. The distribution of pain must correspond to the

underlying lesion or disease of the somatosensory nervous

system. The neuroanatomical relation to the underlying cause

must still be recognizable even if pain is not felt in the entire

innervation territory of an affected peripheral nerve or root, or the

somatotopic representation corresponding to a lesion or disease

of the central nervous system, or if pain extends somewhat

outside these boundaries. Objective signs of a sensory disorder in

January 2019·Volume 160 ·Number 1 www.painjournalonline.com 53

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

the distribution of pain increase diagnostic certainty. These signs

may indicate a sensory deficit or exaggerated responses to

normally painful (hyperalgesia) or painless stimuli (allodynia). The

definite diagnosis of neuropathic pain requires demonstration of

the cause, eg, neurophysiological tests confirming a peripheral

neuropathy or imaging results showing the involvement of

somatosensory fiber tracts after spinal cord injury.

6,10,25

Neuro-

pathic pain also requires specific treatment, involving both

pharmacological and nonpharmacological approaches.

8,11

Evi-

dence of high or moderate quality supports the use of

gabapentin, pregabalin, and inhibitors of serotonin and nor-

adrenalin reuptake, and tricyclic antidepressants as medications

of first choice. Dermal patches releasing lidocaine or capsaicin

and subcutaneous injection of botulinum toxin offer topical

treatment options. Opioids should be reserved for patients not

responding to therapeutic alternatives with a lower risk of adverse

effects.

Analgesics such as nonsteroidal anti-inflammatory

drugs have no proven efficacy against pain of neuropathic

origin.

18,29

These particular requirements for evaluation and

treatment call for an accurate representation of neuropathic pain

in diagnostic classifications of the relevant clinical conditions.

2. Shortcomings of ICD-10

A structured classification of conditions associated with neuropathic

pain is critically needed.

To date, the International Classification of

Headache Disorders (ICHD) is the only disease classification

providing systematic coverage of neuropathic pain conditions, but

these are limited to cranial nerve injuries and neuralgias.

12,15

Despite its clinical and economic significance, neuropathic

pain is not adequately represented in the current version of the

International Statistical Classification of Diseases and Related

Health Problems (ICD) of the World Health Organization (WHO).

The ICD is the most widely used source for diagnostic codes and

the standard instrument for disease classification in clinical

practice, epidemiology, and health management.

The ICD

organizes diseases and clinical syndromes by etiology, affected

organ, or body region. In the current version of the ICD (ICD-10),

painful conditions that do not fit this scheme can be classified as

acute (R52.0) or chronic pain (R52.2), with a separate code for

chronic intractable pain (R52.1). These codes can be combined

with neurological diagnoses, eg, diabetic polyneuropathy

(G63.2*). The asterisk behind the code indicates a clinical

syndrome in need of another etiological code, marked by

a dagger. In this example, type 2 diabetes mellitus with

neurological complications (E11.4†) would be a suitable speci-

fication. Thus, 3 codes are required to fully describe painful

diabetic polyneuropathy, one of the most common manifesta-

tions of neuropathic pain that affects up to 30% of patients with

type 2 diabetes.

There are very few explicit references to conditions of

neuropathic pain in ICD-10. They include trigeminal neuralgia

(G50.0), postzoster neuralgia (G53.0* B02.2†), and phantom limb

syndrome with pain (G54.6). The code for postzoster neuralgia,

better known as postherpetic neuralgia, applies only if the

disorder involves a cranial nerve, although thoracic nerve roots

are far more commonly affected by the disease.

Hereditary

neuropathies that are predominantly characterized by painful

symptoms or signs are not listed at all or incorrectly classified. For

example, erythromelalgia is designated as peripheral vascular

disease (I73.8) because painful episodes associated with the

disease are accompanied by an erythema. A hereditary variant of

the disease, in which intense pain, not reddening, is the leading

symptom, remains unspecified.

The complexity of ICD-10 codes and the incomplete or

inaccurate coverage of relevant clinical conditions risk

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

J. Scholz and N.B. Finnerup contributed equally to this manuscript. A. Barke, W. Rief, and R.-D. Treede contributed equally to this manuscript.

Departments of

Anesthesiology and,

Pharmacology, Columbia University Medical Center, New York, NY, United States,

Department of Clinical Medicine, Danish Pain

Research Center, Aarhus University, Aarhus, Denmark,

Department of Neurology, Aarhus University Hospital, Aarhus, Denmark,

INSERM U 987, Assistance

Publique—H ˆopitaux de Paris, H ˆopital Ambroise Par ´e, Boulogne Billancourt, France,

Universit ´e Versailles Saint Quentin en Yvelines, Versailles, France,

Centre for

Neuroscience and Trauma, Wingate Institute of Neurogastroenterology, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of

London, London, United Kingdom,

Department of Neurology, Universit¨atsklinikum Schleswig-Holstein, Kiel, Germany,

Academic Unit of Palliative Care, University of

Leeds, Leeds, United Kingdom,

Department of Diagnostic Sciences, Rutgers School of Dental Medicine, Newark, NJ, United States,

St. Vincent’s Clinical School,

University of New South Wales, Sydney, Australia,

Department of Human Neuroscience, Sapienza University, Rome, Italy,

Department of Surgery and Institute of Medical

Science, University of Toronto, Toronto, ON, Canada,

Division of Brain, Imaging and Behavior-Systems Neuroscience, Krembil Research Institute, Univer sity Health

Network, Toronto, ON, Canada,

Department of Neurology, Krankenhaus Lindenbrunn, Coppenbr ¨ugge, Germany,

Faculty of Medicine, University of M ¨unster, M ¨unster,

Germany,

Department of Psychiatry, Columbia University, New York State Psychiatric Institute, New York, NY, United States,

Department of Medicine and Science of

Aging, CeSI-MeT, G D’Annunzio University of Chieti, Chieti, Italy,

Department of Pain Management and Research, Division of Emergencies and Critical Care, Oslo University

Hospital, Oslo, Norway,

Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockh olm, Sweden,

European Palliative Care Research Centre (PRC), Oslo,

Norway,

Department of Oncology, Oslo University Hospital, Oslo, Norway,

Institute of Clinical Medicine, University of Oslo, O slo, Norway,

Division of Clinical Psychology

and Psychotherapy, Department of Psychology, Philipps-University Marburg, Marburg, Germany,

Department of Clinical Neuroscience, Karolinska Institute, Stockholm,

Sweden,

Department of Anesthesiology and Acute Postoperative Pain Service, Saint Luc Hospital, Catholic University of Louvain, Bruss els, Belgium,

Pain Management

Research Institute, Royal North Shore Hospital, University of Sydney, Sydney, Australia,

Institute of Aging and Chronic Disease, University of Liverpool, Liverpool, United

Kingdom,

INSERM U 987, Pain Clinic, Cochin Hospital, Paris Descartes University, Paris, France,

Division of Pain Medicine, Department of Anesthesiology and Critical

Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States,

Pain Research, Department of Surgery and Cancer, Imperial College, London,

United Kingdom,

California Pacific Medical Center Research Institute, San Francisco, CA, Uni ted States,

Anaesthesiology and Pain Medicine, Medical School, University

of Western Australia and Royal Perth Hospital, Perth, Australia,

Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States,

Division

of Population Health and Genomics, University of Dundee, Dundee, Scotland,

Section of Clinical Oral Physiology, School of Dentistry, Aarhus University, Aarhus, Denmark,

Department of Dental Medicine, Karolinska Institute, Huddinge, Sweden,

Research Group Health Psychology, University of Leuven, Leuven, Belgium,

Experimental

Health Psychology, Maastricht University, Maastricht, the Netherlands,

Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan,

Brain Research Center,

National Yang-Ming University, Taipei, Taiwan,

Department of Neurophysiology, CBTM, Medical Faculty Mannheim of Heidelberg University, Mannheim, Germany

*Corresponding author. Department of Neurophysiology, Centre for Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Heidelberg University,

Ludolf-Krehl-Str.13-17, 68167 Mannheim, Germany. Tel.: 149 (0)621 383 71 400; fax: 149-(0)621 383 71 401.E-mail address: Rolf-Detlef.Treede@medma.uni-heidelberg.

de (R.-D. Treede).

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the

journal’s Web site (www.painjournalonline.com).

PAIN 160 (2019) 53–59

http://dx.doi.org/10.1097/j.pain.0000000000001365

54 J. Scholz et al.·160 (2019) 53–59 PAIN

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

underreporting of chronic pain. This has practical consequences

for clinicians, hospitals, and other health care providers. Under-

reporting also hinders efficient resource management by insurers

and the development of sound public health strategies by

policymakers. The current epidemic of opioid abuse in North

America illustrates the importance of a reliable classification of

chronic pain to enable the monitoring of safe and effective

analgesics use in cancer and noncancer pain, including pain of

neuropathic origin.

3. The IASP Task Force Initiative for the classification

of chronic pain in the International Classification

of Diseases

To generate a systematic and improved classification of conditions

associated with clinically relevantpain and to ensure representation

of these diagnoses in the upcoming revision of the ICD, the

International Association for the Study of Pain (IASP) established

a Task Force that works in close cooperation with WHO

representatives.

The classification is dedicated exclusively to

chronic pain syndromes, defined as persistent or recurrent pain

lasting $3 months. As we have previously outlined, conditions of

neuropathic pain are divided into 2 broad categories for peripheral

or central nervous disorders. Diseases not explicitly listed in the

classification will be captured in residual categories.

During the

process of drafting and editing the definitions of individual diseases

and detailed content models of neuropathic pain, the Task Force

conferred with the Classification Committee of the IASP’s

Neuropathic Pain Special Interest Group (NeuPSIG). Content

models underwent initial field testing in Australia, Germany, Japan,

and Norway. Revised models were subjected to further field testing

by the WHO in WHO-led field tests. We will report the results of

these field tests separately. Overall, utility and specificity of the

diagnostic criteria were ranked highly. A version for preparing

implementation of ICD-11 was released by the WHO in June

2018.

The complete revision will be submitted to the WHO’s

Executive Board in January and the World Health Assembly in May

2019. After endorsement, member states are expected to report

health statistics according to ICD-11 from 2022 onward.

4. The classification of chronic neuropathic pain

Some conditions of persistent neuropathic pain produce distinct

symptoms that would allow for diagnosing chronic pain before the

3-month threshold. One example is trigeminal neuralgia, which is

characterized by a pain distribution in one or more branches of the

fifth cranial nerve, abrupt pain paroxysms, and provocation of

these pain attacks by normally innocuous mechanical stimuli or

orofacial movements. Periods of remission vary, but the neuralgia

never disappears completely.

6,15

Similarly, pain associated with

polyneuropathy caused by type 2 diabetes or central pain after

spinal cord injury usually persists sothat it may seem unnecessary

to wait 3 months before diagnosing chronic neuropathic pain.

3,23

Nonetheless, in the absence of objective markers delineating

acute and chronic phases of pain, the arbitrary definition of 3

months was chosen because it provides for clear operationaliza-

tion in line with widely used research criteria and subject enrolment

in analgesic treatment trials.

The proposed classification differentiates neuropathic pain of

peripheral and central origin.

It comprises 9 common con-

ditions associated with persistent or recurrent pain (Fig. 1 and

supplementary Table 1, available at http://links.lww.com/PAIN/

A658). Short definitions of these conditions are listed below.

These definitions are part of more detailed content models

included in the so-called foundation layer of ICD-11. The models

provide minimum criteria of possible neuropathic pain and

describe investigations that support a definitive diagnosis.

6,10

They also contain extension codes for pain severity (combining

intensity, distress, and disability), temporal characteristics, and

psychological or social factors,

as well as a link to the

International Classification of Functioning (ICF).

19,33

4.1. Chronic neuropathic pain

Chronic neuropathic pain is chronic pain caused by a lesion or

disease of the somatosensory nervous system.

The pain may

be spontaneous or evoked, as an increased response to a painful

stimulus (hyperalgesia) or a painful response to a normally

nonpainful stimulus (allodynia). The diagnosis of chronic neuro-

pathic pain requires a history of nervous system injury or disease

and a neuroanatomically plausible distribution of the pain.

Negative (eg, decreased or loss of sensation) and positive

sensory symptoms or signs (eg, allodynia or hyperalgesia)

indicating the involvement of the somatosensory nervous system

must be compatible with the innervation territory of the affected

nervous structure. These criteria apply to all diagnostic entities of

chronic neuropathic pain.

4.1.1. Chronic peripheral neuropathic pain

Chronic peripheral neuropathic pain is chronic pain caused by

a lesion or disease of the peripheral somatosensory nervous

system.

4.1.1.1. Trigeminal neuralgia

Trigeminal neuralgia is a manifestation of orofacial neuropathic

pain restricted to one or more divisions of the trigeminal nerve.

The pain is recurrent, abrupt in onset and termination, triggered

by innocuous stimuli, and typically compared with an electric

shock or described as shooting or stabbing. Some patients

experience continuous pain between these painful paroxysms.

The diagnosis comprises idiopathic trigeminal neuralgia,

classical neuralgia produced by vascular compression of the

trigeminal nerve, and secondary neuralgia caused by a tumor or

cyst at the cerebellopontine angle or multiple sclerosis.

As for other conditions of chronic neuropathic pain, the

detailed content model includes a discussion of the etiology.

4.1.1.2. Chronic neuropathic pain after peripheral nerve

injury

Chronic neuropathic pain after peripheral nerve injury is persistent

or recurrent pain caused by a peripheral nerve lesion. History of

a plausible nerve trauma, pain onset in temporal relation to the

trauma, and pain distribution within the innervation territory of

a peripheral nerve (or nerves) are required for the diagnosis.

Negative and positive sensory symptoms or signs must be

compatible with the innervation territory of the affected nerve (or

nerves). Formation of a neuroma may lead to pain at the lesion site.

Consistent with the new concept of “multiple parenting” in ICD-

11 (Fig. 1), the diagnosis of chronic neuropathic pain after

peripheral nerve injury is also listed in the section on postsurgical

and posttraumatic pain.

However, the content model for the

diagnosis is stored in the foundation layer of ICD-11.This

hierarchical structure of the classification allows for multiple

referencing of a content model without duplicating the diagnosis.

January 2019·Volume 160 ·Number 1 www.painjournalonline.com 55

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

4.1.1.3. Painful polyneuropathy

Chronic pain occurs in polyneuropathies caused by metabolic,

autoimmune, familial or infectious diseases, exposure to environ-

mental or occupational toxins, or treatment with a neurotoxic drug.

Chronic pain also occurs in polyneuropathies of unknown etiology.

Pain may be the initial symptom of a neuropathy or develop over the

course of the disease (Case vignette 1). Negative and positive sensory

symptoms or signs must be compatible with the anatomical

distribution pattern of the polyneuropathy. Chemotherapy-induced

peripheral neuropathy is one form of painful polyneuropathy included

in the classification of chronic cancer-related pain.

4.1.1.4. Postherpetic neuralgia

Postherpetic neuralgia is defined as pain persisting for $3

months after the onset or healing of herpes zoster. The

innervation territory of the first (ophthalmic) branch of the

Figure 1. Classification of chronic neuropathic pain in ICD-11. Top and 2nd level diagnoses are part of ICD-11 Mortality and Morbidity Linearisation (MMS).

Specific entities of chronic neuropathic pain are included at the next level. According to the new concept of multiple parenting in ICD-11, these entities may be

referred to from other divisions of the chronic pain classification, eg, chronic posttraumatic pain or chronic secondary headaches and orofacial pains.

56 J. Scholz et al.·160 (2019) 53–59 PAIN

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

trigeminal nerve and thoracic dermatomes are the locations most

frequently affected by chronic pain after herpes zoster. Post-

herpetic neuralgia may emerge in continuation of the acute pain

associated with the skin rash or develop after a painless interval.

Negative and positive sensory symptoms or signs must be

compatible with the innervation territory of the affected cranial

nerve or peripheral dermatome (or dermatomes).

4.1.1.5. Painful radiculopathy

Chronic painful radiculopathy is persistent or recurrent pain caused

by a lesion or disease involving the cervical, thoracic, lumbar, or

sacral nerve roots. Degenerative changes of the spinal column

including ligaments and intervertebral disks are the most frequent

cause, but painful radiculopathy may also result from trauma, tumor,

or neoplastic meningitis, from infections, hemorrhage or ischemia,

diabetes mellitus, rheumatoid arthritis, or from an iatrogenic lesion,

eg, during injection therapy or surgery. Pain within the affected

dermatomes (radicular pain) is required for the diagnosis. The pain

may be spontaneous but is typically exacerbated or provoked by

taking or maintaining a certain body position or during movement.

Negative and positive sensory symptoms or signs must be

compatible with the innervation territory of the affected nerve root

(or roots). Musculoskeletal pain associated with painful radiculop-

athy should be classified separately.

4.1.1.6. Other specified and unspecified chronic peripheral

neuropathic pain

ICD-11 contains a residual category for other specified conditions

of chronic peripheral neuropathic pain that are not covered by the

diseases listed above, eg, chronic neuropathic pain caused by

a carpal tunnel syndrome. An additional category for unspecified

conditions provides for the classification of disorders for which

insufficient information is available to assign a precise diagnosis.

4.1.2. Chronic central neuropathic pain

Chronic central neuropathic pain is chronic pain caused by

a lesion or disease of the central somatosensory nervous system.

4.1.2.1. Chronic central neuropathic pain associated with

spinal cord injury

Chronic central neuropathic pain associated with spinal cord

injury is caused by a lesion or disease of the somatosensory

pathways in the spinal cord. The definition of spinal cord injury

comprises impairments of spinal cord function resulting from

external force or a disease process. The pain may be

spontaneous or evoked, as an increased response to a painful

stimulus (hyperalgesia) or a painful response to a normally

nonpainful stimulus (allodynia). The diagnosis requires a history of

spinal cord lesion or disease and a neuroanatomically plausible

distribution of the pain, ie, pain felt in dermatomes at or below the

level of injury in areas with sensory disturbance (Case vignette 2).

This cause of central neuropathic pain is also included in the

classification of chronic postsurgical and posttraumatic pain.

4.1.2.2. Chronic central neuropathic pain associated with

brain injury

Chronic central neuropathic pain associated with brain injury is

caused by a lesion or disease of the somatosensory cortex,

connected brain regions, or associated pathways in the brain.

History of a plausible brain trauma, pain onset in temporal relation

to the trauma, and a pain distribution that is neuroanatomically

plausible are required for the diagnosis. Negative or positive

sensory symptoms or signs indicating the involvement of the brain

must be present in the body region corresponding to the brain

injury.

See also the classification of chronic postsurgical and post-

traumatic pain.

4.1.2.3. Chronic central poststroke pain

Chronic central poststroke pain is caused by a cerebrovascular

lesion, infarct or hemorrhage, of the brain or brainstem. The pain

may be spontaneous or evoked, as an increased response to

a painful stimulus (hyperalgesia) or a painful response to

a normally nonpainful stimulus (allodynia). The diagnosis of

central poststroke pain requires a history of stroke and a neuro-

anatomically plausible distribution of the pain, ie, pain felt in the

body region represented in the central nervous structures

affected by the stroke. Negative or positive sensory symptoms

or signs indicating the involvement of the brain must be present in

the body region affected by the stroke.

4.1.2.4. Chronic central neuropathic pain caused by multiple

sclerosis

Chronic central neuropathic pain in multiple sclerosis is caused

by a lesion of somatosensory brain regions or their connecting

Case vignette 1: Chronic painful polyneuropathy

A 56-year-old woman with type 2 diabetes mellitus for 2 years complains about pain in the feet that started approximately 4 months ago. The pain intensity is 5 to 7 on a scale from

0 to 10. The pain may get worse at night or when she is walking. In addition, she noticed numbness and tingling in the feet. The examination reveals a stocking-like distribution of

deficits in the sense of touch. The Achilles tendon reflex is weak. An electrophysiological examination shows slow conduction in the sural and peroneal nerves. The patient has

a body mass index of 30. Her fasting blood glucose concentration is 132 mg/dL, and the HbA1 measures 7%. Painful polyneuropathy caused by type 2 diabetes mellitus was

diagnosed. The treatment plan consisted of improved blood glucose management, medication for neuropathic pain, and foot care education.

Case vignette 2: Chronic central neuropathic pain associated with spinal cord injury

A 40-year-old man, who 5 years ago suffered an incomplete spinal cord injury at the thoracic level, reports diffuse pain in both legs. He desc ribes an ongoing pain of burning

and squeezing character as well as sensations of pins and needles. The average pain intensity is 6/10. In addition, he sometimes experiences pain provoked by light touch.

These painful sensations developed gradually over the first 6 months after the injury. On physical examination, he exhibits decreased detection of both mechanical and

thermal stimuli from dermatome T4 down, hypersensitivity to cold and touch-evoked allodynia on the lower legs. The diagnosis was chronic central neuropathic pain

associated with spinal cord injury. Following referral to a multidisciplinary center for pain therapy, he received comprehensive care including medication for neuropathic

pain, physical and cognitive behavioral therapy.

January 2019·Volume 160 ·Number 1 www.painjournalonline.com 57

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

pathways. The pain may be spontaneous or evoked, as an

increased response to a painful stimulus (hyperalgesia) or a painful

response to a normally nonpainful stimulus (allodynia). The

diagnosis requires a history of multiple sclerosis and a neuro-

anatomically plausible distribution of the pain. Negative or positive

sensory symptoms or signs indicating the involvement of the brain

or spinal cord must be present in the area of the body affected by

pain. Pain primarily related to spasticity should be classified as

musculoskeletal pain.

4.1.2.5. Other specified and unspecified chronic central

neuropathic pain

Residual categories are available for other specified or un-

specified conditions of chronic central neuropathic pain.

5. Discussion

Neuropathic pain commonly persists beyond the natural healing

process of the underlying disease, eg, in postherpetic neuralgia,

or despite treatment directed at the disease cause. Combining

a code for the underlying disease with the explicit diagnosis of

neuropathic pain has the advantage that for the first time, patients

with specific treatment needs for their pain will be distinguished

from those with a painless manifestation of the same neurological

disorder. Although the neurological diagnosis will guide treatment

of the disease that is responsible for the pain, the neuropathic

pain diagnosis will provide for appropriate pain management.

Different from previous editions of the ICD, the new codes for

chronic neuropathic pain will be concise and embedded in

a systematic classification of chronic pain. They will cover the

epidemiologically most relevant conditions and provide clear

diagnostic criteria that are backed by literature references and

suggestions for additional investigations to increase the level of

diagnostic certainty.

ICD-11 includes cross-references to other conditions of

chronic pain in separate “parent” chapters. Examples are painful

chemotherapy-induced polyneuropathy, which are mentioned

under chronic cancer-related pain,

or pain after amputation,

which are listed under chronic postsurgical and posttraumatic

pain.

Cross-referencing in ICD-11 facilitates the coding of

painful disorders within the most fitting treatment-relevant

category of the classification.

The proposed classification is a compromise balancing the

length of this important division with those of 6 other groups of

chronic pain conditions, eg, musculoskeletal and visceral pain.

Diseases not explicitly listed in the classification are captured in

residual categories for “Other specified chronic peripheral neuro-

pathic pain” or “Other specified chronic central neuropathic pain.”

6. Summary and conclusions

The classification of chronic neuropathic pain represents the first

systematic and most comprehensive classification to date of

common painful neurological disorders. Precise diagnostic

criteria and literature references are included in the full-content

description of the disorders to minimize ambiguity. The criteria

match the grading system for evidence supporting the diagnosis

of neuropathic pain in clinical practice and research.

These

provisions generate a valuable tool for diagnostic code assign-

ment, appropriate allocation of health care services, and the

collection of epidemiological data. Clear definitions combined

with a seamless evaluation of the evidence leading to the

diagnosis of chronic neuropathic pain will facilitate patient

identification for enrolment in clinical trials and promote the

translation of research findings into practice.

Conflict of interest statement

J. Scholz has received research support from the Thompson Family

Foundation and Acetylon, and is now an employee of Biogen. This

work was completed before he joined the company. Biogen did not

have a role in the design, conduct, analysis, interpretation, or funding

of the research related to this work. N.B. Finnerup has received

honoraria for serving on advisory boards or speaker panels from

Astellas, Gr ¨unenthal, Mitshubishi Tanabe, Novartis, and Teva. N.

Attal has received speaker fees from Pfizer and consultant fees from

Aptinyx, Gr ¨unenthal, Mundipharma, Novartis, Sanofi Pasteur, and

Teva. R. Baron reports receiving research grants from Genzyme,

Gr ¨unenthal, Mundipharma, and Pfizer, and honoraria for serving on

advisory boards or speakers panels from Abbvie, Allergan, Astellas,

AstraZeneca, Bayer, Biogen, Biotest, Boehringer Ingelheim, Bristol-

Myers Squibb, Daiichi Sankyo, Desitin, Eisai, Galapagos NV,

Genentech, Genzyme, Glenmark, Gr ¨unenthal, Kyowa Kirin, Lilly,

Medtronic, Merck MSD, Mundipharma, Novartis, Pfizer, Sanofi

Pasteur, Seqirus, TAD, Teva, and Vertex. He is also member of the

Innovative Medicines Initiative (IMI), a public–private partnership

between the European Union and the European Federation of

Pharmaceutical Industries and Associations (EFPIA). G. Cruccu

reports grants or personal fees from Alfa sigma, Angelini, Biogen,

Mundipharma, and Pfizer. M. First reports personal fees from

Lundbeck International Neuroscience Foundation, outside the

submitted work. M.A. Giamberardino reports personal fees from

IBSA Institute Biochimique, personal fees from EPITECH Group,

personal fees from Helsinn Healthcare, grants from EPITECH Group,

and grants from Helsinn Healthcare, outside the submitted work. S.

Kaasa reports that he is Eir solution—stockholder. T. Nurmikko has

received personal fees from Abide, Astellas, Mundipharma, and

Nexstim. S.N. Raja has received research grants from Medtronic,

and serves in the advisory boards of Allergan, Daiichi Sankyo, and

Aptinyx. A.S.C. Rice has received research funding from Orion, has

consulted or participated in advisory boards for Imperial College

Consultants, including remunerated work for Abide, Astellas,

Galapagos, Lateral, Peter McNaughton from King’s College London

and Cambridge University, Merck, Mitsubishi, Novartis, Orion,

Pharmaleads, Quartet, and Toray. He owned share options in

Spinifex from which personal benefit accrued upon the acquisition

of Spinifex by Novartis, and from which future milestone payments

may occur. A.S.C. Rice is also named inventor on patents WO

2005/079771, EP13702262.0, and WO2013/110945. S.A. Schug:

The Discipline of Anaesthesiology and Pain Medicine at the

University of Western Australia, but not S.A. Schug personally,

has received research and travel funding and speaking and

consulting honoraria from Andros Pharmaceuticals, Aspen, bioCSL,

Eli Lilly, Grunenthal, Invidior, Janssen, Luye Pharma, Mundipharma,

Pfizer, Pierre Fabre, Seqirus and iX Biopharma, outside the

submitted work. S.-J. Wang reports personal fees from Eli-Lilly,

personal fees from Daiichi Sankyo, grants and personal fees from

Pfizer, Taiwan, personal fees from Eisai, personal fees from Bayer,

and personal fees from Boehringer Ingelheim, outside the submitted

work. A. Barke reports personal fees from IASP, during the conduct

of the study. W. Rief reports grants from IASP, during the conduct of

the study; personal fees from Heel, personal fees from Berlin

Chemie, outside the submitted work. R.-D. Treede reports grants

from Boehringer Ingelheim, Astellas, AbbVie, and Bayer, personal

fees from Astellas, Gr ¨unenthal, Bauerfeind, Hydra, and Bayer,

grants from EU, DFG, and BMBF, outside the submitted work. The

remaining authors have no conflicts of interest to declare.

58 J. Scholz et al.·160 (2019) 53–59 PAIN

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

Acknowledgements

The authors gratefully acknowledge financial support by the IASP

and the excellent discussions with Dr. Robert Jakob of the WHO.

Members of the Taskforce: Rolf-Detlef Treede (Chair), Winfried

Rief (Co-chair), Antonia Barke, Qasim Aziz, Michael I. Bennett,

Rafael Benoliel, Milton Cohen, Stefan Evers, Nanna B. Finnerup,

Michael First, Maria Adele Giamberardino, Stein Kaasa, Beatrice

Korwisi, Eva Kosek, Patricia Lavand’homme, Michael Nicholas,

Serge Perrot, Joachim Scholz, Stephan Schug, Blair H. Smith,

Peter Svensson, Johannes Vlaeyen, Shuu-Jiun Wang.

Appendix A. Supplemental digital content

Supplemental digital content associated with this article can be

found online at http://links.lww.com/PAIN/A658. SDC includes

a complete reference list of the diagnoses entered into the

foundation with the foundation IDs as well as the extension codes

(specifier). Since the complete list is contained, the material is

identical for all papers of the series.

Article history:

Received 14 June 2018

Received in revised form 25 July 2018

Accepted 30 July 2018

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January 2019·Volume 160 ·Number 1 www.painjournalonline.com 59

Copyright Ó2018 by the International Association for the Study of Pain. Unauthorized reproduction of this article is prohibited.

Impact of Erector Spinae Plane Blocks on Pain Management and Postoperative Outcomes in Patients with Chronic Pain Undergoing Spine Fusion Surgery: A Retrospective Cohort Study

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Nov 2024

Objetivos: Identificar a prevalência e a incidência de dor crônica com e sem características neuropáticas em pacientes com câncer em hospitais públicos de São Luís, Maranhão. Metodologia: Trata-se de um estudo de corte transversal. A amostra foi composta de pacientes com diagnóstico de câncer que estiveram internados nas clínicas dos dois hospitais oncológicos da rede pública de saúde do município de São Luís – MA. Foi identificada a prevalência e incidência de dor crônica nos pacientes oncológicos e em seguida foi descrito o perfil sociodemográfico e clínico e utilizados questionários validados na língua portuguesa para identificar a presença do componente neuropático na dor. Resultados: A amostra final deste estudo foi de 1020 pacientes. A prevalência de dor crônica nos pacientes oncológicos foi de 35,3%. Desses, 62,5% apresentavam dor de características neuropáticas. Além disso, a incidência foi de 21,4%. Os indivíduos portadores de DNRC foram, em sua maioria, mulheres de baixa renda, com menor nível educacional, afrodescendentes, provenientes da zona rural e com diagnóstico de câncer de mama e câncer de colo de útero, principalmente.Conclusão: Grande parte dos pacientes com o diagnóstico de câncer convivem com dor crônica, seja ela com ou sem componente neuropático, atingindo principalmente mulheres de baixa renda com menor nível educacional.

Zgoda na udzielanie świadczeń medycznych wyrażona przez pacjenta w silnym bólu a wyłączenie swobody podjęcia decyzji w rozumieniu art. 82 Kodeksu cywilnegoConsent to Medical Services Expressed by the Patient in Severe Pain with Regard to Removal of the Freedom to Choose within the Meaning of Article 82 of the Civil Code

Article

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Nov 2024

Dominika Fajka

Praca ma na celu omówienie prawa pacjenta do leczenia bólu i prawa do wyrażenia zgody na udzielenie świadczenia zdrowotnego, a także ocenę relewantności prawnej zgody na udzielenie takiego świadczenia, wyrażonej przez pacjenta odczuwającego ból, w odniesieniu do ewentualnego ograniczenia lub wyłączenia swobody podjęcia decyzji w rozumieniu art. 82 Kodeksu cywilnego (k.c.), przy uwzględnieniu aspektów praktycznych realizacji tych praw oraz z uwzględnieniem obowiązków lekarza. Należy bowiem uznać, że stan psychofizyczny, w którym znajduje się pacjent odczuwający silny ból, może być postrzegany jako stan wyłączający swobodę powzięcia decyzji w rozumieniu art. 82 k.c., a co za tym idzie – może mieć znaczący wpływ na ważność udzielonej zgody.

Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11).

Article

Full-text available

Jan 2019

Chronic pain is a major source of suffering. It interferes with daily functioning and often is accompanied by distress. Yet, in the International Classification of Diseases, chronic pain diagnoses are not represented systematically. The lack of appropriate codes renders accurate epidemiological investigations difficult and impedes health policy decisions regarding chronic pain such as adequate financing of access to multimodal pain management. In cooperation with the WHO, an IASP Working Group has developed a classification system that is applicable in a wide range of contexts, including pain medicine, primary care, and low-resource environments. Chronic pain is defined as pain that persists or recurs for more than 3 months. In chronic pain syndromes, pain can be the sole or a leading complaint and requires special treatment and care. In conditions such as fibromyalgia or nonspecific low-back pain, chronic pain may be conceived as a disease in its own right; in our proposal, we call this subgroup "chronic primary pain." In 6 other subgroups, pain is secondary to an underlying disease: chronic cancer-related pain, chronic neuropathic pain, chronic secondary visceral pain, chronic posttraumatic and postsurgical pain, chronic secondary headache and orofacial pain, and chronic secondary musculoskeletal pain. These conditions are summarized as "chronic secondary pain" where pain may at least initially be conceived as a symptom. Implementation of these codes in the upcoming 11th edition of International Classification of Diseases will lead to improved classification and diagnostic coding, thereby advancing the recognition of chronic pain as a health condition in its own right.

The IASP classification of chronic pain for ICD-11: chronic cancer-related pain

Article

Full-text available

Jan 2019

Worldwide, the prevalence of cancer is rising and so too is the number of patients who survive their cancer for many years thanks to the therapeutic successes of modern oncology. One of the most frequent and disabling symptoms of cancer is pain. In addition to the pain caused by the cancer, cancer treatment may also lead to chronic pain. Despite its importance, chronic cancer-related pain is not represented in the current International Classification of Diseases (ICD-10). This article describes the new classification of chronic cancer-related pain for ICD-11. Chronic cancer-related pain is defined as chronic pain caused by the primary cancer itself or metastases (chronic cancer pain) or its treatment (chronic postcancer treatment pain). It should be distinguished from pain caused by comorbid disease. Pain management regimens for terminally ill cancer patients have been elaborated by the World Health Organization and other international bodies. An important clinical challenge is the longer term pain management in cancer patients and cancer survivors, where chronic pain from cancer, its treatment, and unrelated causes may be concurrent. This article describes how a new classification of chronic cancer-related pain in ICD-11 is intended to help develop more individualized management plans for these patients and to stimulate research into these pain syndromes.

The IASP classification of chronic pain for ICD-11: functioning properties of chronic pain

Article

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Dec 2018
PAIN

Physical, mental, and social well-being are part of the concept of health according to the World Health Organization, in addition to the absence of disease and infirmity. Therefore, for a full description of a person's health status, the International Classification of Functioning, Disability and Health (ICF) was launched in 2001 to complement the existing International Classification of Diseases (ICD). The 11th version of the ICD (ICD-11) is based on so-called content models, which have 13 main parameters. One of them is functioning properties (FPs) that, according to the WHO, consist of the activities and participation components of the ICF. Recently, chronic pain codes were added to the 11th edition of the ICD, and hence, a specific set of FPs for chronic pain is required as a link to the ICF. In addition, pain is one of the 7 dimensions of the generic set of the ICF, which applies to any person. Thus, assessment and management of pain are also important for the implementation of the ICF in general. This article describes the current consensus proposal by the International Association for the Study of Pain (IASP) and the International Society of Physical and Rehabilitation Medicine (ISPRM) for a specific set of FPs of chronic pain, which will have to be empirically validated in a next step. The combined use of ICD-11 and ICF is expected to improve research reports on chronic pain by a more precise and adequate coding, as well as patient management through better diagnostic classification.

The IASP classification of chronic pain for ICD-11: chronic secondary musculoskeletal pain

Article

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Dec 2018

Chronic musculoskeletal pain is defined as chronic pain arising from musculoskeletal structures such as bones or joints. Although comprising the most prevalent set of chronic pain conditions, it was not represented appropriately in the 10th edition of the International Classification of Diseases (ICD-10), which was organized mainly according to anatomical sites, was strongly focused on musculoskeletal disease or local damage, and did not consider the underlying mechanisms of pain. The new ICD-11 classification introduces the concept of chronic primary and secondary musculoskeletal pain, and integrates the biomedical axis with the psychological and social axes that comprise the complex experience of chronic musculoskeletal pain. Chronic primary musculoskeletal pain is a condition in its own right, not better accounted for by a specific classified disease. Chronic secondary musculoskeletal pain is a symptom that arises from an underlying disease classified elsewhere. Such secondary musculoskeletal pain originates in persistent nociception in musculoskeletal structures from local or systemic etiologies, or it may be related to deep somatic lesions. It can be caused by inflammation, by structural changes, or by biomechanical consequences of diseases of the nervous system. It is intended that this new classification will facilitate access to patient-centered multimodal pain management and promote research through more accurate epidemiological analyses.

The IASP classification of chronic pain for ICD-11: chronic postsurgical or posttraumatic pain

Article

Full-text available

Dec 2018
PAIN

Chronic pain after tissue trauma is frequent and may have a lasting impact on the functioning and quality of life of the affected person. Despite this, chronic postsurgical and posttraumatic pain is underrecognised and, consequently, undertreated. It is not represented in the current International Classification of Diseases (ICD-10). This article describes the new classification of chronic postsurgical and posttraumatic pain for ICD-11. Chronic postsurgical or posttraumatic pain is defined as chronic pain that develops or increases in intensity after a surgical procedure or a tissue injury and persists beyond the healing process, ie, at least 3 months after the surgery or tissue trauma. In the classification, it is distinguished between tissue trauma arising from a controlled procedure in the delivery of health care (surgery) and forms of uncontrolled accidental damage (other traumas). In both sections, the most frequent conditions are included. This provides diagnostic codes for chronic pain conditions that persist after the initial tissue trauma has healed and that require specific treatment and management. It is expected that the representation of chronic postsurgical and posttraumatic pain in ICD-11 furthers identification, diagnosis, and treatment of these pain states. Even more importantly, it will make the diagnosis of chronic posttraumatic or postsurgical pain statistically visible and, it is hoped, stimulate research into these pain syndromes.

Neuropathic pain

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Feb 2017

Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibres (Aβ, Aδ and C fibres) and central neurons, and affects 7–10% of the general population. Multiple causes of neuropathic pain have been described and its incidence is likely to increase owing to the ageing global population, increased incidence of diabetes mellitus and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signalling, alterations in ion channels and variability in the way that pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. The burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain owing to increased drug prescriptions and visits to health care providers, as well as the morbidity from the pain itself and the inciting disease. Despite challenges, progress in the understanding of the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain.

Peripheral Neuropathic Pain: A mechanism-related organizing principle based on sensory profiles

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Nov 2016

Patients with neuropathic pain are heterogeneous in etiology, pathophysiology, and clinical appearance. They exhibit a variety of pain-related sensory symptoms and signs (sensory profile). Different sensory profiles might indicate different classes of neurobiological mechanisms, and hence subgroups with different sensory profiles might respond differently to treatment. The aim of the investigation was to identify subgroups in a large sample of patients with neuropathic pain using hypothesis-free statistical methods on the database of 3 large multinational research networks (German Research Network on Neuropathic Pain (DFNS), IMI-Europain, and Neuropain). Standardized quantitative sensory testing was used in 902 (test cohort) and 233 (validation cohort) patients with peripheral neuropathic pain of different etiologies. For subgrouping, we performed a cluster analysis using 13 quantitative sensory testing parameters. Three distinct subgroups with characteristic sensory profiles were identified and replicated. Cluster 1 (sensory loss, 42%) showed a loss of small and large fiber function in combination with paradoxical heat sensations. Cluster 2 (thermal hyperalgesia, 33%) was characterized by preserved sensory functions in combination with heat and cold hyperalgesia and mild dynamic mechanical allodynia. Cluster 3 (mechanical hyperalgesia, 24%) was characterized by a loss of small fiber function in combination with pinprick hyperalgesia and dynamic mechanical allodynia. All clusters occurred across etiologies but frequencies differed. We present a new approach of subgrouping patients with peripheral neuropathic pain of different etiologies according to intrinsic sensory profiles. These 3 profiles may be related to pathophysiological mechanisms and may be useful in clinical trial design to enrich the study population for treatment responders.

Trigeminal neuralgia: New classification and diagnostic grading for practice and research

Article

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Jun 2016

Trigeminal neuralgia (TN) is an exemplary condition of neuropathic facial pain. However, formally classifying TN as neuropathic pain based on the grading system of the International Association for the Study of Pain is complicated by the requirement of objective signs confirming an underlying lesion or disease of the somatosensory system. The latest version of the International Classification of Headache Disorders created similar difficulties by abandoning the term symptomatic TN for manifestations caused by major neurologic disease, such as tumors or multiple sclerosis. These diagnostic challenges hinder the triage of TN patients for therapy and clinical trials, and hamper the design of treatment guidelines. In response to these shortcomings, we have developed a classification of TN that aligns with the nosology of other neurologic disorders and neuropathic pain. We propose 3 diagnostic categories. Classical TN requires demonstration of morphologic changes in the trigeminal nerve root from vascular compression. Secondary TN is due to an identifiable underlying neurologic disease. TN of unknown etiology is labeled idiopathic. Diagnostic certainty is graded possible when pain paroxysms occur in the distribution of the trigeminal nerve branches. Triggered paroxysms permit the designation of clinically established TN and probable neuropathic pain. Imaging and neurophysiologic tests that establish the etiology of classical or secondary TN determine definite neuropathic pain.

New technologies for the assessment of neuropathies

Article

Mar 2017

Technical advances are rapidly changing the clinical and instrumental approach to peripheral nerve diseases. Magnetic resonance neurography, diffusion tensor imaging and nerve ultrasonography are increasingly entering the diagnostic workup of peripheral neuropathies as tools that complement neurophysiology and enable investigation of proximal structures, such as plexuses and roots. Progress in the design of magnetic resonance scanners and sequences, and the development of high-frequency ultrasound probes mean that high-resolution peripheral nerve imaging is possible, enabling detailed examination of nerve size, morphology and internal fascicular structure that can integrate nerve conduction studies into clinical practice. In the growing field of small-fibre neuropathy, in which traditional nerve conduction studies are of little or no use, skin biopsy has become a reliable tool for diagnosis. Corneal confocal microscopy, nociceptive evoked potentials and microneurography are emerging techniques that are mainly used in clinical research settings, but have increasing relevance to clinical practice. We review these new and emerging techniques and their effects on diagnosis, treatment strategies and prognosis in a variety of peripheral neuropathies, including entrapments, brachial plexopathies, immune and inherited neuropathies, and small-fibre neuropathies. We discuss the most promising research findings and their potential for future application in clinical practice.

Reliability of Conditioned Pain Modulation: a Systematic Review

Article

Aug 2016

A systematic literature review was undertaken to determine if conditioned pain modulation (CPM) is reliable. Longitudinal, English language observational studies of the repeatability of a CPM test paradigm in adult humans were included. Two independent reviewers assessed the risk of bias in 6 domains; study participation; study attrition; prognostic factor measurement; outcome measurement; confounding and analysis using the Quality in Prognosis Studies (QUIPS) critical assessment tool. Intraclass correlation coefficients (ICCs) less than 0.4 were considered to be poor; 0.4 and 0.59 to be fair; 0.6 and 0.75 good and greater than 0.75 excellent. Ten studies were included in the final review. Meta-analysis was not appropriate because of differences between studies. The intersession reliability of the CPM effect was investigated in 8 studies and reported as good (ICC50.6-0.75) in 3 studies and excellent (ICC.0.75) in subgroups in 2 of those 3. The assessment of risk of bias demonstrated that reporting is not comprehensive for the description of sample demographics, recruitment strategy, and study attrition. The absence of blinding, a lack of control for confounding factors, and lack of standardisation in statistical analysis are common. Conditioned painmodulation is a reliable measure; however, the degree of reliability is heavily dependent on stimulation parameters and study methodology and this warrants consideration for investigators. The validation of CPM as a robust prognostic factor in experimental and clinical pain studies may be facilitated by improvements in the reporting of CPM reliability studies.