In any case, there is substantial evidence that addiction is related to loss of frontal lobe function and increased impulsivity. The limbic system isn't the only part of the brain affected by long-term drug or alcohol abuse. The frontal lobe of the brain also suffers. It shrinks and loses its ability to function properly.
This part of the brain regulates decisions, choices, and the ability to know the difference between good and evil. When the frontal lobe doesn't work as it should, you can't control the urge to drink or use drugs. Ironically, the essential part of the brain that you would use to change your harmful habits is affected by those harmful habits and you can't make the right decisions. Addiction is a complex disease that affects brain function.
The part of the brain that causes addiction is called the mesolimbic dopamine pathway. It's sometimes called a brain reward circuit. Let's take a deeper look at the causes of addiction and how this area of the brain is affected. Another way to describe the prefrontal cortex is to think of it as a brake system.
The prefrontal cortex acts as a brake on the brain. Send signals to inhibit particular behaviors or actions. When addiction damages this area of the brain, it also limits the brain's ability to control other behavioral systems. Imagine how difficult it would be to operate a car without brakes.
At this point, we could say that the brain is drugged by addiction. The prefrontal cortex also projects into other regions of the brain associated with addictive problems. These include the reward system, memory and emotions, and the brain's stress regulation centers. Therefore, damage to the prefrontal cortex can also further interfere with the functioning of these other brain regions.
There are two regions of the brain that are commonly discussed when it comes to addictions: the prefrontal cortex and the midbrain. These areas of the brain are two very different regions with functional differences that corroborate the maintenance of homeostasis. Here we review the results of neuroimaging studies that have evaluated the effects of drug administration on functional measures, such as glucose metabolism and cerebral blood flow (CBF). Few studies have measured regional brain activity during drug poisoning, and most of these studies have used a single drug exposure.
These studies have demonstrated lower glucose metabolism throughout the brain, including the frontal cortex, during cocaine, morphine, or alcohol poisoning (27—30). In contrast, marijuana poisoning is associated with higher levels of glucose metabolism in the prefrontal cortex, orbitofrontal cortex, and striatum in marijuana users, but not in non-abusers (3). Similarly, faster metabolism in the prefrontal cortex, the anterior cingula, the orbitofrontal cortex, and the striatum has been reported in cocaine users after sequential intravenous administration of methylphenidate, which cocaine users report is similar to intravenous cocaine (1). It should be noted that activation in the orbitofrontal cortex was only observed in subjects in whom methylphenidate induced intense desire and in the prefrontal cortex in subjects in whom mood improved.
Excessive desire or excessive desire for drugs, or other more automatic processes, such as attention bias and conditioned responses, can pave the way to additional drug use, even when the addicted person is trying to abstain (see TABLE 1 for the clinical characteristics of addiction in context of iRISA and the role of PFC in addiction). Although the question of how these networks and other interconnected brain regions affect drug addiction has recently begun to be explored, studies of functional connectivity in resting states have already shown promise by revealing patterns that predict disease severity and treatment outcomes. Therefore, we conceptualize drug addiction as a syndrome of altered response inhibition and attribution of salience and called it the “I-RISA syndrome” of drug addiction. .