<scp>THC</scp> may reproducibly induce electrical hyperalgesia in healthy volunteers

Walter, Carmen; Oertel, B.; Lötsch, Jörn

doi:10.1002/ejp.575

Cited by 17 publications

(15 citation statements)

References 17 publications

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“…This finding was independently reproduced in a cohort of 30 healthy young men or women who had received oral doses of either 20 mg THC or placebo. In this study, pain tolerance to nociceptive electrical stimuli decreased from 3.7 ± 2.1 mA to 2.5 ± 1.3 mA following THC administration, while it remained fairly stable after placebo (Walter et al., ). As in both studies, electrical noxious stimuli were involved, the particular pain model may play a role in the unexpected outcomes that were not reported with other pain models.…”

Section: Human Experimental Evidence Of Analgesic Effects Of Cannabinmentioning

confidence: 67%

Current evidence of cannabinoid‐based analgesia obtained in preclinical and human experimental settings

Lötsch

Weyer-Menkhoff

Tegeder

2017

European Journal of Pain

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109

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Section: Human Experimental Evidence Of Analgesic Effects Of Cannabinmentioning

confidence: 67%

Current evidence of cannabinoid‐based analgesia obtained in preclinical and human experimental settings

Lötsch

Weyer-Menkhoff

Tegeder

2017

European Journal of Pain

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109

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“…As proposed by Walter et al. (), this narrow therapeutic window may be the result of co‐activation of TRPA1 and TRPV1 channels along with CB1 receptors by Δ9‐THC at higher concentrations. The dose of 10 mg of the oral formulation of Δ9‐THC was the highest single dose that is administered to healthy volunteers of this formulation to date (Klumpers et al., ).…”

Section: Discussionmentioning

confidence: 90%

Effect profile of paracetamol, Δ9‐THC and promethazine using an evoked pain test battery in healthy subjects

Amerongen

Siebenga

Kam

et al. 2018

European Journal of Pain

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“…This is owed to the risk of illicit use (Hall and Solowij, 1998) and also to the incomplete mechanistic understanding of its analgesic effects. It should be noted that studies in humans produced remarkably heterogeneous outcomes with respect to the effects of cannabis on pain, ranging from analgesia to hyperalgesia (Kraft, 2012;Walter et al, 2015b).…”

Section: Introductionmentioning

confidence: 99%

Brain Mapping-Based Model of Δ9-Tetrahydrocannabinol Effects on Connectivity in the Pain Matrix

Walter

Oertel

Felden

et al. 2015

Neuropsychopharmacol

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Cannabinoids receive increasing interest as analgesic treatments. However, the clinical use of Δ 9 -tetrahydrocannabinol (Δ 9 -THC) has progressed with justified caution, which also owes to the incomplete mechanistic understanding of its analgesic effects, in particular its interference with the processing of sensory or affective components of pain. The present placebo-controlled crossover study therefore focused on the effects of 20 mg oral THC on the connectivity between brain areas of the pain matrix following experimental stimulation of trigeminal nocisensors in 15 non-addicted healthy volunteers. A general linear model (GLM) analysis identified reduced activations in the hippocampus and the anterior insula following THC administration. However, assessment of psychophysiological interaction (PPI) revealed that the effects of THC first consisted in a weakening of the interaction between the thalamus and the secondary somatosensory cortex (S2). From there, dynamic causal modeling (DCM) was employed to infer that THC attenuated the connections to the hippocampus and to the anterior insula, suggesting that the reduced activations in these regions are secondary to a reduction of the connectivity from somatosensory regions by THC. These findings may have consequences for the way THC effects are currently interpreted: as cannabinoids are increasingly considered in pain treatment, present results provide relevant information about how THC interferes with the affective component of pain. Specifically, the present experiment suggests that THC does not selectively affect limbic regions, but rather interferes with sensory processing which in turn reduces sensory-limbic connectivity, leading to deactivation of affective regions.

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THC may reproducibly induce electrical hyperalgesia in healthy volunteers

Cited by 17 publications

References 17 publications

Current evidence of cannabinoid‐based analgesia obtained in preclinical and human experimental settings

Current evidence of cannabinoid‐based analgesia obtained in preclinical and human experimental settings

Effect profile of paracetamol, Δ9‐THC and promethazine using an evoked pain test battery in healthy subjects

Brain Mapping-Based Model of Δ9-Tetrahydrocannabinol Effects on Connectivity in the Pain Matrix

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