Human Brain Mapping - Recreational Drugs, Alcohol and Addictions

Recreational Drugs, Alcohol and Addictions

• Disease theory of alcoholism - problem drinking is sometimes caused by a disease of the brain, characterized by altered brain structure and function. For wider scope see: Disease model of addiction
• Long-term impact of alcohol on the brain
• Wernicke–Korsakoff syndrome - vitamin B1 (thiamine) deficiency usually secondary to alcohol abuse causing vision changes, ataxia and impaired memory.
• Alcoholic polyneuropathy - primarily caused by chronic alcoholism, this is a neurological disorder in which multiple peripheral nerves throughout the body malfunction simultaneously. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally.
• Other areas: Alcohol dependence, Delirium tremens, Alcoholic hallucinosis, Short-term effects of alcohol
• Search "fMRI alcoholic" or "fMRI alcohol" for extensive coverage not yet available on Wikipedia
• Cannabis and memory – With legalization in some states and increasing use, the effects of cannabis on memory is a salient research topic. Efforts are focused on which areas of the brain are most significantly affected, for what duration, and what the effects are. See also sections in Long-term effects of cannabis.
• Gambler's fallacy a cognitive bias and fallacy that arises out the erroneous belief that small samples must be representative of the larger population. Its further divided into "classic" gambler's fallacy (Type I), when individuals believe that a certain outcome is "due" after a long streak of another outcome or Type II when a gambler underestimates how many observations are needed to detect a favorable outcome (such as watching a roulette wheel for a length of time and then betting on the numbers that appear most often). . Functional magnetic resonance imaging has revealed that, after losing a bet or gamble ("riskloss"), the frontoparietal network of the brain is activated, resulting in more risk-taking behavior. In contrast, there is decreased activity in the amygdala, caudate and ventral striatum after a riskloss. Activation in the amygdala is negatively correlated with gambler's fallacy - the more activity exhibited in the amygdala, the less likely an individual is to fall prey to the gambler's fallacy. These results suggest that gambler's fallacy relies more on the prefrontal cortex (responsible for executive, goal-directed processes) and less on the brain areas that control affective decision-making. The desire to continue gambling or betting is controlled by the striatum, which supports a choice-outcome contingency learning method. The striatum processes the errors in prediction and the behavior changes accordingly. After a win, the positive behavior is reinforced and after a loss, the behavior is conditioned to be avoided. In individuals exhibiting the gambler's fallacy, this choice-outcome contingency method is impaired, and they continue to take risks after a series of losses.