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I often ask my patients who have relapsed why they restarted their drug use.  Sometimes, the reasons for the relapse seem easy to understand.  There was some particular stressor or or some turn of events that the person could identify..  These cravings were easy to understand (see the article on cravings)  But often, the person has no clue.  They found themself using before they knew it.  It was akin to a kneejerk reflex and the person had relapsed before they knew what was going on.  I had also asked the patient if there were a lot of cravings- sometimes there were.  However, sometimes they were using with their first craving, it was that intense. 

How does it come about that such a "reflex" to relapse develops?
    To understand why this happens, one needs to understand normal functioning of the brain.  Imagine a lab rat placed in an unfamiliar maze with the smell of food emanating from wherever the goal is.  Outwardly, they sniff around and move quite slowly.  This belies lots of internal brain activity; the brain is ferociously active and involves the analytic parts of the brain including the prefrontal cortex and nucleus accumbens.  The neurotransmitters,glutamate and dopamine, are released in the accumbens  which provides the motivation to seek out the food.  This pathway involves multiple neurological connections with various parts of the brain and is a relatively slow process. 

As  the rat, learns the maze, he moves more, and his brain becomes less active.  The behavior still needs to be motivated but it is no longer motivated by the accumbens.  Rather a nearby area, called the posterior striate cortex  (PSC), which  also releases glutamate and dopamine, motivates the behavior.  In comparison to the accumbens, the connections between the stimulus (smell) and the effect (movement) are fewer.  The behavior is accomplished faster and with less brain activity.  It is also accomplished more automatically and with less conscious thought.

Human learning is chock full of comparable examples. When we first learn a sport, each skill is thought out, and than practiced over and again until hopefully it becomes automatic.  A major league shortstop does not have time to think about catching a line drive- he has to react quickly.  The better athletes among us are those who can get these skills learned efficiently and reproduce them consistently- it is why we practice.  As we repeat the behavior over and over and see good outcomes, we imprint the behavior into our PSC.  The motivation for the behavior has moved from our accumbens to the PSC.  These behaviors now are a reaction to a stimulus (the ball coming at us) and we act without thinking.  

Of course, we did not evolve to play ball, rather the ability to make these adaptations helped make our hunting, gathering and survival skills more efficient.

So how does this relate to drug cravings.  A person looking forward to a good movie, or a pay check at the end of the week, or a good grade for work well done, is certainly  motivated by the  benefits they are anticipating.  However,  it is a conscious, analytic motivation involving the relatively cumbersome acumbens.  A non-addict thinking about the pleasurable aspects of a drug (or another addictive behavior) will also be motivated by the acumbens.  However, it has been shown that by the time an addiction has been set in, that motivation has moved to the PSC.

An alcoholic, who is shown pictures of an alcoholic beverage, will release dopamine in the PSC.  This motivates alcohol seeking behavior.  Even if alcohol is not obtained, the desire to use alcohol, or craving, is similarly caused by the dopamine release.  In fact, it has also been shown that the greater the amount of dopamine released, the more intense the cravings will be.  A similar finding is seen when a heroin addict is shown a needle or a compulsive food addict is shown a plate of cookies.  We therefore see this dopamine release in response to a trigger that causes a behavior (the cravings is the behavior).  Even when we don't use the drug, the cravings  can persist as long as 20 minutes and can keep recurring throughout the day.  Even if the trigger is subliminal (below the awareness of the person) it has been shown to lead to dopamine release and cravings.  I have termed this the "I want" reflex.

The drugs have taken advantage of an evolutionary adaptation.  Behaviors that have been shown to be beneficial though multiple episodes of expression and reward eventually get imprinted into the PSC so they can be performed quickly and automatically for the benefit of the person.  However, drugs cause such a release of dopamine that they fool the brain into treating them as beneficial behaviors.  Drug using behavior may be imprinted after only a few expressions of the behavior.  Unfortunately, once, imprinted, they are extremely persistent and difficult to get rid of.

Even though we have this drive to use drugs or act inappropriately, there are still other parts of our brain that are supposed to help us inhibit inappropriate behavior.  Unfortunately, a separate abnormality found in the addicted brain is a deterioration of these self control parts of the brain.

Any medication that minimizes the release of dopamine or gluatamate in the PSC will reduce the intensity of cravings.  Topiramate stabilizes glutamate levels as does N-acetyl cystine.  Ondansetron (zofran), in ultra low doses only, has been shown to reduce the release of dopamine.  All these medications have shown the ability to reduce cravings.

Stuart Wasser MD  2/12, 6/13

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