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Neurogenic hyperalgesia versus painful hypoalgesia: two distinct mechanisms of neuropathic pain

Baumgärtner, Ulfa,b; Magerl, Waltera; Klein, Thomasa,b; Hopf, Hanns Christianb; Treede, Rolf-Detlefa,∗

doi: 10.1016/S0304-3959(01)00438-9
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Patients with sensory disturbances of painful and non-painful character show distinct changes in touch and/or pain sensitivity. The patterns of sensory changes were compared to those of human surrogate models of neuropathic pain to assess the underlying mechanisms. We investigated 30 consecutive in-patients with dysaesthesia of various origins (peripheral, spinal, and brainstem lesions) and 15 healthy subjects. Tactile thresholds were determined with calibrated von Frey hairs (1.1 mm ∅). Thresholds and stimulus–response functions for pricking pain were determined with a series of calibrated punctate mechanical stimulators (0.2 mm ∅). Allodynia was tested by light stroking with a brush, Q-tip, and cotton wisp. Perceptual wind-up was tested by trains of punctate stimuli at 0.2 or 1 Hz. Intradermal injection of capsaicin (n=7) and A-fiber conduction blockade (n=8) served as human surrogate models for neurogenic hyperalgesia and partial nociceptive deafferentation, respectively. Patients without pain (18/30) showed a continuous distribution of threshold shifts in the dysaesthetic skin area with a low to moderate increase in pain threshold (by 1.52±0.45 log2 units). Patients with painful dysaesthesia presented as two separate groups (six patients each): one showing lowered pain thresholds (by −1.94±0.46 log2 units, hyperalgesia) and the other elevated pain thresholds (by 3.02±0.48 log2 units, hypoalgesia). The human surrogate model of neurogenic hyperalgesia revealed nearly identical leftward shifts in stimulus–response function for pricking pain as patients with spontaneous pain and hyperalgesia (by a factor of about 5 each). The sensory changes in the human surrogate model of deafferentation were similar to patients with hypoalgesia and spontaneous pain (rightward shift of the stimulus–response function with a decrease in slope). Perceptual wind-up did not differ between symptomatic and control areas. There was no exclusive association of any parameter obtained by quantitative sensory testing with a particular disease (of either peripheral or central origin). Our findings suggest that neuropathic pain is based on two distinct mechanisms: (I) central sensitization (neurogenic hyperalgesia; in patients with minor sensory impairment) and (II) partial nociceptive deafferentation (painful hypoalgesia; in patients with major sensory deficit). This distinction as previously postulated for postherpetic neuralgia, is obviously valid also for other conditions. Our findings emphasize the significance of a mechanism-based classification of neuropathic pain.

aInstitute of Physiology and Pathophysiology, Johannes Gutenberg-University, Saarstrasse 21, D-55099 Mainz, Germany

bDepartment of Neurology, Johannes Gutenberg-University, Langenbeckstrasse 1, D-55101 Mainz, Germany

Corresponding author. Tel.: +49-6131-3925715; fax: +49-6131-3925902

E-mail: treede@mail.uni-mainz.de

Submitted April 27, 2001; revised September 18, 2001; accepted October 2, 2001.

© 2002 Lippincott Williams & Wilkins, Inc.
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