PRIMEVIEW

NEUROPATHIC PAIN
For the Primer, visit doi:10.1038/nrdp.2017.2

Neuropathic pain is caused by lesions Determining whether the pain in question MECHANISMS
DIAGNOSIS is neuropathic (as opposed to, for example,
or diseases of the somatosensory nociceptive caused by damage to body tissue or PATIENT
system, including peripheral fibres (Aβ, Aδ other chronic pain syndromes) is important to HISTORY In neuropathic pain, peripheral sensory and central
and C fibres) and central neurons, and is provide appropriate treatments neurons show a gain of excitation and facilitation
associated with allodynia, burning and
and a loss of inhibition. Several mechanisms can
tingling sensations. Conditions associated
contribute to the neuropathy, including changes
with neuropathic pain include trigeminal
in the function and expression of voltage-gated
neuralgia, postherpetic neuralgia,
sodium, calcium and potassium channels; in the
radiculopathy, diabetic neuropathy, Possible neuropathic pain
• Fits with the patient’s history function of second-order nociceptive neurons
HIV infection, stroke and amputation.
• Neuroanatomically plausible (which convey sensory information to the thalamus
for further processing); and in the function of
inhibitory interneurons. These changes contribute
EPIDEMIOLOGY to a shift in the sensory pathways to a state of
EXAMINATION
hyperexcitability in which the brain receives
Estimating the incidence and prevalence of Quantitative
abnormal sensory messages. Over
neuropathic pain has been difficult owing to the sensory tests use
time, this hyperexcitability might
lack of simple diagnostic criteria that can be used standardized mechanical
contribute to the neuropathic
and thermal stimuli to test
for large epidemiological surveys of the general pain state becoming chronic.
the afferent nociceptive and
population. However, new screening tools have
non‑nociceptive systems, assessing
been developed; the population prevalence of Probable neuropathic pain
loss and gain of function of
chronic neuropathic pain has been estimated • Requires clinical evidence
the nerves
to be 7–10%.

The available data indicate that chronic CONFIRMATION

neuropathic pain is more frequent in women
Neurophysiological
than in men and in individuals >50 years of age
tests can be used to identify
damage along the somatosensory MANAGEMENT
pathways and skin biopsies can be used
to diagnose small-fibre neuropathies Typically, patients with neuropathic pain
QUALITY OF LIFE undergo conservative pharmacological and
Definite neuropathic pain integrative treatments (such as cognitive–
Neuropathic pain can substantially impair • Requires objective evidence that behavioural therapy and physical therapy)
quality of life, as it is often associated with confirms the lesion or disease of the  before interventional treatments are attempted.
other problems such as anxiety, depression, somatosensory system Medical treatments include γ-aminobutyric
disturbed sleep and high prescription drug use. acid (GABA; an inhibitory neurotransmitter)
Patient-reported scores in, for example, physical analogues, serotonin–noradrenaline reuptake
functioning and emotional role functioning inhibitors and tricyclic antidepressants. The
can be significantly OUTLOOK effects of these agents are mediated by their
lower in those with actions on descending inhibitory control
neuropathic The development of novel polypharmacy in patients with the pain and improved clinical systems. Interventional treatments are largely
pain than in interventions with improved neuropathic pain. Drug discovery trial designs that incorporate and surgical and include spinal cord stimulation and
the general efficacy and tolerability relies on improved understanding stratify patients according to their implanted intrathecal pumps, which provide
population. is paramount to reduce of the mechanisms underlying genotypic and phenotypic profiles. targeted drug delivery, as well as repetitive
transcranial magnetic stimulation.

Written by Mina Razzak; designed by Laura Marshall Article number: 17003; doi:10.1038/nrdp.2017.3; published online 16 Feb 2017
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