Vicodin, the
combination drug of
acetaminophen and the
opioid hydrocodone, is one of the most prescribed drugs on the market today.
Opioids have demonstrated the ability to paradoxically cause increased
pain sensitivity to users in a phenomena called
opioid-induced
hyperalgesia (OIH). While selected
opioids have been shown to produce OIH symptoms in an animal model,
hydrocodone and the
combination drug Vicodin have yet to be studied. The purpose of this study was to explore the effect of exposure to chronic high dose
Vicodin or its components on the sensitivity to both thermal and mechanical
pain. Animals were randomly divided into 4 groups,
Vicodin,
acetaminophen, hydrocodone, or vehicle control, and administered the
drug daily for 120 days. Rats were subsequently tested for thermal and mechanical sensitivity. The rats in the
Vicodin group displayed a significant decrease in withdrawal time to thermal
pain. The rats receiving
acetaminophen, hydrocodone, and vehicle showed no statistically significant
hypersensitivity in thermal testing. None of the groups demonstrated statistically significant
hypersensitivity to mechanical testing. The data suggests
Vicodin produces signs of OIH in a rodent model. However, increased
pain sensitivity was only noted in the thermal pathway and the
hypersensitivity was only seen with the
opioid combination drug, not the
opioid alone. The results of this study both support the results of previous rodent
opioid studies while generating further questions about the specific properties of
Vicodin that contribute to
pain hypersensitivity. The growing use of
Vicodin to treat
chronic pain necessitates further research looking into this paradoxical
pain response.