Ondansetron, a 5HT3-antagonist, does not alter dynamic mechanical allodynia or
spontaneous ongoing pain in peripheral neuropathy.
Author(s): Tuveson B, Leffler AS, Hansson P.
Affiliation(s): Department of Molecular Medicine and Surgery, Clinical Pain Research, Karolinska
Institute, Danderyd Hospital, Stockholm, Sweden. Birgitta.Tuveson@ds.se
Publication date & source: 2011, Clin J Pain. , 27(4):323-9
OBJECTIVES: The aim of this study was to examine whether the intensity of dynamic
mechanical allodynia and spontaneous ongoing pain in patients with neuropathic
pain associated with peripheral neuropathy was influenced by an intravenous
infusion of the 5HT3-antagonist, ondansetron.
METHODS: A randomized, double-blind, and placebo-controlled single intravenous
infusion of 8 mg ondansetron or saline was administered to 15 patients during 10
minutes on 2 different occasions with an interval of at least 3 days. To monitor
the brush-evoked allodynic percept over time, a computerized visual analog scale
(VAS) was used allowing the patient to continuously rate the intensity and
duration of pain. The area under the VAS curve was used to calculate the total
brush-evoked pain intensity. Ongoing pain was rated using a VAS before each
assessment of dynamic mechanical allodynia, that is, before and immediately after
the infusion and at every 15 minutes over a period of 3 hours.
RESULTS: There was no influence of the factors with or without pain medication
and treatment sequence (ie, ondansetron/saline or saline/ondansetron) on
brush-evoked or ongoing pain intensity. No significant change over time was found
after the infusion of either ondansetron or saline in the total brush-evoked pain
intensity, in duration and frequency of aftersensation or in ongoing pain
CONCLUSIONS: No influence from 8 mg of ondansetron could be shown on the
intensity of brush-evoked or spontaneous ongoing pain in patients with peripheral
neuropathy, indicating the lack of involvement of 5HT3-receptors in an earlier
proposed spinobulbospinal loop with descending facilitation acting on spinal
mechanisms related to dynamic mechanical allodynia.