GarciaLarrea.qxp 11/1/08 03:27 Page 40
Neuropathic Pain
Figure 1: Laser-evoked Potentials in a Case of Non-organic Pain Figure 2: Laser-evoked Potentials in Neuropathic Pain from
Brainstem Lesion
Stem L 1-left, pricking sensation (VAS 4/10)
Left-hand stimulation
FZ
Vertex
response
CZ
June 2006
0 100 200 300 400 500 600 700 800 900ms
Opercular
0 100 200 300 400 500 600 700 800 900ms
response
Right-hand stimulation
FZ
Activity maps
at 200ms
CZ
0 100 200 300 400 500 600 700 800 900ms
Stem L 1-right, no sensation reported
0 100 200 300 400 500 600 700 800 900ms December 2006
Laser-evoked potentials (LEPs) in a case of anaesthesia and pseudo-neuropathic pain that
developed immediately after a benign urological intervention at the pyelo–ureteral junction.
A 23-year-old woman complained of burning pain and hypaesthesia, which distributed A 65-year-old woman underwent a minor cranial trauma (temporal concussion, no loss of
roughly within the right L1 dermatome. The pain was considered neuropathic until its consciousness), and a computed tomography (CT) scan performed in the emergency room
distribution passed from L1 to S3, involving the perineal region and genitalia, and associated was considered normal. Four weeks later, she developed burning pain in the right upper
to hypaesthesia in the whole right side without clear nerve or root distribution. Laser stimuli limb, which was not considered neuropathic despite a new CT scan that showed an
yielded a satisfactory pricking sensation and high-amplitude cortical potentials to stimulation asymmetry at the mesencephalic level (June 2006). Clinical examinations for sensory
of the non-affected (left) limb (upper traces and maps). Stimulation of the affected territory symptoms were inconsistent from one neurologist to another. Laser-evoked potentials (LEPs)
at the same intensity did not yield any clinical report of sensation (complete clinical thermo- demonstrated significant abnormalities of conduction in pain–temperature pathways after
algaesic anaesthesia), but produced satisfactory cortical responses, including late-associative stimulation of the painful right hand (bottom left), and remained normal to stimulation of
components related to stimulus awareness (bottom traces and maps). Cortical responses to the non-painful side (top left). A gradient-echo magnetic resonance image (MRI) showed a
left and right stimuli were not significantly different. This demonstrated a satisfactory hypo-intense image in the posterior mesencephalon at the right side, suggesting
transmission through pain and temperature pathways, in contrast to the clinical presentation. haemorrhagic sequelae. The small mesencephalic lesion impinged with spinothalamic
The condition was consequently considered as non-neuropathic in origin. conduction and was responsible for the neuropathic pain.
transmission abnormalities in the pain pathways, and make the Normal Laser-evoked Potentials Argue Against the
condition enter the framework of neuropathic pain.
27
In central pain, Diagnosis of Central Neuropathic Pain
LEPs are attenuated to the stimulation of the painful territory, even if Although we ignore how much spinothalamic damage is still
the patients present enhanced pain reactions such as hyperalgaesia or compatible with a normal LEP response, available data suggest that
allodynia.
28–30
The reason for this is that LEPs index the activity of the the sensitivity of LEPs parallels that of a detailed neurological exam.
most synchronised and rapidly transmitted pain and temperature LEPs have been found to be abnormal in patients with even discrete
volleys. This system mediates elaborated and discriminative aspects of sensory loss due to peripheral or central damage.
28,34
Normal LEPs are
nociception and is subserved by the ‘lateral’ or ‘neo-spinothalamic’ obtained in patients with conversion disorder or malingering or non-
arrangement of spinal tracts and thalamocortical projections, whose organic pain,
30,35
but have never been described in the presence of
lesions are well reflected by LEPs. thermal hypesthaesia due to a proven lesion of pain pathways. Some
reports suggest that LEPs may be sensitive enough to detect deficits
The cortical networks that generate LEPs are able to detect abrupt that are suspected because of the history, symptoms or other aspects
changes in sensory input, but are much less qualified to reflect a of the neurological examination, but are not revealed by quantitative
slow-changing state. Thus, LEPs are inappropriate to reflect the sensory testing.
28,36
Inasmuch as central pain without pain and
slowly emerging, ill-defined and long-lasting phenomena that underlie temperature sensory deficits is exceptional, the recording of normal
over-reaction symptoms (hyperalgaesia and allodynia), which are LEPs to stimulation of a painful territory stands clearly, in most cases,
thought to depend on spino-reticulo-thalamic projection systems.
31–33
In against the diagnosis of CNP (see Figure 1).
other words, the slope of energy change associated to allodynic or
hyperalgaesic symptoms is commonly not abrupt enough to generate However, there are instances where central pain may present without
LEPs. Thus, LEPs accurately reflect the spinothalamic deafferentation clinically evident spinothalamic deficits. For instance, the patient may
leading to pain discrimination deficits, but do not index the neural be unable or unwilling to collaborate with a clinical examination. In
events underlying allodynia and hyperalgaesia. This is the such cases, LEPs are helpful to confirm diagnosis by demonstrating
electrophysiological counterpart of a clinical paradox commonly objective spinothalamic deficits (see Figure 2). Moreover, sensory
observed in CNP syndromes, namely the presence of exaggerated pain deficits may sometimes exclusively concern the dorsal column–medial
reactions within territories where pain discrimination is decreased or lemniscus system. These pure lemniscal lesions are rare sources of
abolished.
7
However, we shall see that some patterns of LEP CNP.
37,38
In these cases, standard SEPs will highlight deficiencies and
abnormality may indirectly reflect the existence of hyperalgaesic attest to the neuropathic origin of the pain. In rare cases, a proven
symptoms (see below). CNS lesion may transitorily induce pain with genuine central features,
40 EUROPEAN NEUROLOGICAL DISEASE 2007
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