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Opioid Intoxication
Opioid intoxication begins when opioids in the bloodstream reach the brain and attach to mu receptors.1 Opioid binding at the mu receptors stimulates release of dopamine into an area called the nucleus accumbens.1,2
This increased dopamine activity in the nucleus accumbens is associated with the euphoria and other pleasurable sensations (
) characteristic of opioid intoxication.1,2
Withdrawal
Repeated use of an opioid causes mu receptors to become tolerant—the first sign of physical dependence—and higher doses of the opioid are needed to produce the intended effect.1,3 Chronic use of escalating doses intensifies this physical dependence and alters the brain so that it functions more or less normally when opioids are present and abnormally when they are not.1
The hallmark of physical dependence is the emergence of opioid-specific withdrawal symptoms when opioid levels in the bloodstream (and, thus, the brain) decline.
Declining opioid concentrations in the brain mean that when opioid molecules leave the mu receptors, they are less likely to be replaced by other opioid molecules. The increasing number of unoccupied mu receptors corresponds to an overall decline in opioid-induced activity.
This decline in opioid-induced activity upsets the neurobiological balance that developed in order to accommodate chronic use of exogenous opioids.1,2 Most notably, the brain releases excessive noradrenaline (norepinephrine), which the patient experiences as clinical symptoms of opioid withdrawal (
).1,2 (Opioid cravings may also be present at this time, although it should be noted that cravings often occur independently of the opioid withdrawal syndrome.) Other neurochemical imbalances, such as low dopamine levels, are also thought to contribute to opioid withdrawal syndrome.2
SUBOXONE
Once the patient takes SUBOXONE sublingually, its buprenorphine component (
) travels through the bloodstream to the brain, where it binds to the mu receptors, reinitiating opioid activity in the brain (
). As a partial agonist, buprenorphine produces less euphoria than a full opioid agonist but is sufficient to suppress withdrawal and cravings.
Buprenorphine's high affinity for the mu receptor keeps it from being displaced by other opioids (and so blocks the effects of other opioids). With its prolonged therapeutic effect; once SUBOXONE maintenance dosing is established, most receptors remain filled and the patient's withdrawal and cravings are controlled.
| 1. | Kosten TR, George TP. The neurobiology of opioid dependence: implications for treatment. Science & Practice Perspectives. 2002;1:13-20. |
| 2. | Camí J, Farré M. Mechanisms of disease: drug addiction. N Engl J Med. 2003;349:975-986. |
| 3. | American Pain Society. Advocacy & Policy: Definitions Related to the Use of Opioids for the Treatment of Pain. American Pain Society Web site. Available at: http://www.ampainsoc.org/advocacy/opioids2.htm. Accessed September 21, 2004. |
