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Neuropathic Pain
Diagnostic Role of Laser-evoked Potentials in Central Neuropathic Pain
a report by
Luis Garcia-Larrea and Fabio Godinho
INSERM U879, Central Integration of Pain, University Claude Bernard, and Hospices Civils de Lyon
Until the 1980s, central neuropathic pain (CNP) was mainly viewed as superficial layers of the hairy skin and excite type II mechano-thermal
a ‘release’ phenomenon caused by a lesion that removed inhibitory nociceptors related to small myelinated (AMH) or unmyelinated (CMH)
influences of the lemniscal pathways on pain systems.
1–3
However, fibres, as well as thermal C receptors (C warmth units). Gas-state (CO
2
,
detailed sensory analysis of CNP patients later demonstrated that argon) or solid-state laser stimulators – yttrium aluminium garnet (YAG)
almost all cases had lesions affecting the major pathways for or yttrium aluminum perovskite (YAP) – are the most commonly used.
temperature and pain sensation (the spino-thalamo-cortical pathways),
while concomitant injury to the medial lemniscal system was not Although laser stimuli most often simultaneously excite Aδ and C
essential for the development of CNP.
4
Accordingly, impairment of receptors, both the sensation and the concomitant laser-evoked cerebral
spinothalamic pathways is now regarded as a crucial or even sine qua potentials (LEPs) reflect, almost exclusively, the transmission by Aδ
non condition for the occurrence of CNP.
4–8
channels. The reason for this is beyond the purpose of this paper, but
the interested reader can consult detailed papers on this matter.
16–17
However, damage to the nociceptive pathways is not a sufficient Selective excitation of the amyelinic C fibres can be achieved by diverse
condition for CNP to occur, as lesions entailing identical deficits may procedures, mainly based on the elimination of the Aδ component by a
induce chronic pain in some subjects and not in others.
6–9
These pressure-block,
18
stimulation of tiny skin areas
19
or stimulation of large
differences may arise in part from genetic susceptibility
10
and in part from areas at low intensity.
20–21
All of these manipulations yield the so-called
pathophysiological dissimilarities that are not detected by standard ‘ultra-late’ LEPs, rising to about 1,000ms after stimulation and
clinical exams, but may be disclosed by more sophisticated analyses. The depending exclusively on C-fibre activation.
proteiform nature of mechanisms triggered by a given lesion is supported
by the variety of physiological responses that can be obtained in patients Laser-evoked Potentials in Central Neuropathic Pain
with similar anatomical damage. This has prompted the search for The value of LEPs in the diagnosis of neuropathic pain relies on their
neurophysiological techniques selective for spinothalamic pathways and aptitude to detect dysfunction of pain and temperature pathways, which
powerful enough to detect subtle abnormalities in their function. is the basis of CNP syndrome development. During the 1990s, extensive
validation efforts were carried out to record LEPs in proven lesions of the
The Problem of Selective Stimulation of nervous system, which showed that LEPs can detect even minute injury
Nociceptive Afferents of the spinothalamic pathways provided that the stimulus is correctly
Standard neurophysiological responses, i.e. nerve conduction studies applied to the affected regions. This has been shown for spinal,
and somatosensory-evoked potentials (SEPs), do not selectively assess brainstem, thalamic and thalamo-cortical lesions;
22,23
it is now reasonable
the function of the thin fibres that convey pain sensations, because to assert that if one central nervous system (CNS) lesion is able to induce
electrical stimuli preferentially excite the large, non-nociceptive a deficit in pain and temperature perception, it will also be able to alter
afferents with the lowest electrical threshold (Aα and Aβ fibres). the LEPs. In cases of dissociated sensory loss, LEPs are abnormal while
Special techniques have been proposed to improve the selectivity of conventional SEPs exploring the dorsal column–medial lemniscal system
electrical stimuli for pain pathways, such as selective blocks of large commonly remain within normal limits.
24–26
In general terms, there is a
fibres
11–12
and intra-neural or intra-epidermal stimulation.
13–14
strict overlap between conditions that are able to decrease LEPs and
those able to induce neuropathic pain.
However, all of these techniques have significant technical limitations, are
confined to restricted territories and whether they provide a reliable On the basis of studies published so far, the European Federation of
specific correlate of the nociceptive input is controversial. Radiant-heat Neurological Societies (EFNS) has recommended the use of LEPs as an
stimulation can circumvent these difficulties by providing selective ancillary tool in the evaluation of neuropathic pain, and regrets that
activation of Aδ and C thermosensitive nociceptors, without concomitant few university hospitals currently use this technique.
27
The main points
activation of mechano-receptors. However, most common sources of relevant to the use of LEPs in the diagnosis and management of
thermal stimulation, such as light bulbs or Xenon lamps, cannot activate neuropathic pain are summarised below.
nociceptors synchronously enough to allow the recording of
neurophysiological responses.
15
Abnormal Laser-evoked Potentials to Stimulation of a
Painful Territory Substantiate the Neuropathic
Monochromatic high-intensity light sources provided by laser stimulators Nature of the Pain
eliminate most of these problems. Laser stimulators are able to deliver Attenuated, delayed or absent LEPs to stimulation of a painful territory
brief (1–100ms) pulses that rapidly raise the temperature in the (while remaining normal to stimulation of non-painful sites) reveal
© TOUCH BRIEFINGS 2007 39
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