Laser-evoked potentials in post-herpetic neuralgia
Introduction
Herpes Zoster (HZ) is a localized infection caused by the varicella-zoster virus. After remaining dormant in the sensory ganglia since the primary infection (i.e. varicella), the virus reactivates and spreads along the nerve fibres to the skin causing a dermatomally distributed painful rash. In the ganglion, the virus causes neuronal death followed by degeneration of spinal and peripheral axons (Head and Campbell, 1900). The main complication of HZ is post-herpetic neuralgia (PHN), defined as a chronic painful condition lasting for at least 3 months after the HZ skin eruption (Dworkin and Portenoy, 1996). The sensory disturbances in PHN include hypoesthesia and allodynia to various modalities in one or more dermatomes. PHN-induced pains comprise constant (burning or aching) pain, paroxysmal (shooting) pain, and allodynia (most commonly dynamic mechanical allodynia) (Rowbotham and Fields, 1989).
The pathophysiological mechanisms leading to persistent pain in PHN remain unclear. Skin biopsy studies (Oaklander, 2001) have shown a severe loss of epidermal nerve endings in the affected dermatomes. Post-mortem histopathological studies have shown demyelination and axonal degeneration of dorsal root cells, together with dorsal horn atrophy, in patients with PHN but not in patients who had HZ without persistent pain (Watson et al., 1988, Watson et al., 1991). Psychophysiologic measures of mechanical, thermal, and pain thresholds in PHN, showed a multi-modality sensory impairment involving all groups of myelinated as well as unmyelinated fibres (Nurmikko and Bowsher, 1990, Bjerring et al., 1990).
Neurophysiological studies, using peripheral nerve conduction and dermatomal somatosensory evoked potentials, have confirmed damage to large-diameter myelinated fibres in patients with PHN and HZ (Leardi et al., 1994, Mondelli et al., 1996). The neurophysiological assessment of small-fibre function relies on the laser-evoked potentials (LEPs) after stimulation of the face, hand, and foot (Bromm and Treede, 1984, Bromm and Chen, 1995, Kakigi et al., 1992, Agostino et al., 2000b, Cruccu et al., 2001). Probably because HZ most frequently affects proximal dermatomes, LEPs have been studied in very few patients with PHN (Darsow et al., 1996, Innocenti et al., 1999).
To evaluate the reliability of LEPs as a diagnostic tool in radiculopathy, we recorded LEPs after stimulation of the supraorbital, upper cervical, lower cervical, upper thoracic, mid thoracic, and lower thoracic territories in control subjects and patients with PHN. To gain information on the pathophysiology of pain in PHN we also determined the correlation of LEP data with clinical variables (age, duration of disease, and the severity and quality of pain).
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Subjects
Twelve healthy volunteers, aged 45–82 years (mean 67 years), and 40 patients with PHN aged 54–87 years (mean 70 years) participated in the study. All subjects gave their informed consent to undergo the procedure, and the local Ethics Committee approved the research. All patients had unilateral PHN, involving the supraorbital territory (V1) in 9 patients, upper cervical dermatomes (C2–C5) in 4, upper thoracic dermatomes (T1–T4) in 12, mid thoracic dermatomes (T5–T8) in 11, and lower thoracic
Normative values for threshold, latency and amplitude
In all normal subjects laser stimulation readily evoked brain potentials consisting of a negative component (N) at about 200 ms latency, followed by a positive component (P) at about 300 ms latency, corresponding to the so-called N2-P2 components of the late LEPs commonly seen after hand stimulation and attributed to activation of A-delta nociceptors (Fig. 1).
The perceptive threshold and LEP latency differed at the various body sites (P<0.001, ANOVA). Post hoc analysis found a significant
Discussion
Our findings show that in healthy subjects, laser stimulation of proximal dermatomes readily evokes large brain potentials. The latency slightly increases with the distance from the brain, as does the perception threshold, probably because of the longer conduction distance and lower receptor density (Agostino et al., 2000a). In patients with PHN, stimulation of the affected dermatomes yielded markedly altered LEPs, thus demonstrating a severe impairment of A-delta nociceptive neurons. None of
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