In any case, there is substantial evidence that addiction is related to loss of frontal lobe function and increased impulsivity. Just as the liver is meant to regulate toxins, but falters when there is too much alcohol to regulate it, the prefrontal cortex is damaged by addiction. The prefrontal cortex keeps under control the reward observed by the nucleus accumulbens by inhibiting the decision to use drugs when there are obvious negative consequences. Continued drug and alcohol use, despite the negative consequences, is a definite feature of addiction and a strong indication that damage to the prefrontal cortex has occurred.
When the prefrontal cortex is damaged and begins to lose its function, it can no longer regulate the reward system. As a result, drugs freely dominate the brain, prioritizing the experience of pleasure, while the ability to “just say no” fades. 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.
These images show how scientists can use imaging technology to measure brain and heart function. Higher activity is shown in reds and yellows, and reduced activity in blues and purples. Both healthy brains and hearts show greater activity than sick brains and hearts, because both addiction and heart disease cause changes in function. In drug addiction, the frontal cortex, in particular, shows less activity.
It is the part of the brain associated with judgment and decision-making (NIDA). However, a key area of the brain affected by substance use disorders (SUD) is the prefrontal cortex (PFC). PFC is responsible for self-regulation, goal setting, and predicting behavioral consequences (Miller, J. During chronic substance use, the prefrontal cortex is connected in memory of the dopamine reward).
Every time this reward circuit is activated, the brain takes notes of it and teaches people to do it over and over again. Once memory is formed, it becomes reflexive, creating an SUD. Fortunately, during addiction recovery, exercise can promote the same mechanism of action in PFC. New frontiers in addiction research and treatment are using exercise as a targeted therapy to help regulate impulsivity and drug cravings, resulting in a healthier, substance-free lifestyle.
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, a faster metabolism in the prefrontal cortex, the anterior ongulus, the orbitofrontal cortex, and the striatum has been reported in cocaine users following 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). .