Cocaine is a highly stimulating drug derived from the leaves of the coca plant, which grows both naturally and under human cultivation in various highland areas of South America. An illicit and extremely addictive drug, the two chemical forms of cocaine that people abuse are a water-soluble hydrochloride salt and water-insoluble cocaine base (or freebase). The street name crack refers to freebase cocaine, and the characteristic crackling sound it makes when the mixture is smoked.1 Although the drug presents a serious risk for the onset of physical dependence and addiction, not all people who use cocaine develop these problems.
Regardless of the method of consumption (injection, smoking or nasal inhalation), the drug rapidly increases the brain’s dopamine supply. Dopamine plays a critical role in an area of the brain called the limbic system, which triggers pleasurable sensations in response to certain actions and behaviors. When levels of this chemical rise, feelings of pleasure generated in the limbic system increase. In turn, this increase creates a rewarding feedback loop that reinforces the likelihood of future participation in the action or behavior in question.4,5
Physical dependence on cocaine (or any other common drug of abuse) occurs when the brain starts to treat its altered dopamine levels as the normal or default situation. When dopamine levels fall below this new normal, withdrawal symptoms kick in, and the severity of these symptoms typically gives the user a strong incentive for continued drug use. Addiction occurs when this incentive becomes compulsive, with cocaine or other drugs being the focal point of daily existence.4,5
The connection between cocaine use and aneurysm-like bleeding and stroke has been known since the first cocaine-induced stroke was reported in 1977. The exact details of how cocaine impacts the brain’s blood vessels remains elusive. Using a laser-based method to measure how cocaine disrupts blood flow in the brains of mice, researchers now have clues as to how cocaine induces microischemia, a precursor to stroke. This is a condition in which there is insufficient blood flow to the brain to meet metabolic demand, albeit to a smaller degree than brain ischemia. The images reveal that after 30 days of chronic cocaine injection or repeated acute injection of cocaine, there is a dramatic drop in blood flow speed.6
The basal ganglia is the collective term for a group of brain structures that sit above and around the limbic system. Initially, scientists thought the singular purpose of these structures was to control various types of body movement. It is now known the basal ganglia is also closely related to an advanced part of the brain called the neocortex, which helps humans perform higher mental functions such as learning and memory formation. Furthermore, the basal ganglia plays a significant role in creating the pleasurable, dopamine-related rewards previously only associated with the main structures of the limbic system.7
A study published in the journal Brain in 2011 examined the basal ganglia in a large group of known cocaine users. Compared to study participants who were not cocaine users, all those who used the drug had an abnormally enlarged basal ganglia. However, the same amount of enlargement appeared in new cocaine users and long-term, habitual users. The uniform degree of change implies basal ganglia enlargement was a pre-existing abnormality before cocaine use occurred. Researchers theorized the uniform abnormality might be responsible for a built-in sensitivity to cocaine’s effects, thereby helping to explain why some cocaine users become addicted while others do not.8
As cocaine addiction develops, users can experience a wide range of health problems related to escalating drug consumption. Some of the most common behavioral side effects include:
Prolonged use of cocaine can result in “crashing,” which is characterized by anxiety, depression, fatigue, irritability and thoughts of suicide. Other common cocaine withdrawal symptoms include restlessness, nightmares, a general feeling of discomfort and extremely strong cravings for the drug. Cocaine dependent users have a statistically higher risk for other substance use disorders, as well as personality disorders, post-traumatic stress disorder and depressive disorders. The mental health aspects of cocaine withdrawal are particularly challenging and need to be incorporated into treatment strategies.9
Cocaine addicts often use alcohol, sedatives, hypnotics, or antianxiety medicines to treat withdrawal symptoms. This is not a solution because it simply shifts addiction from one substance to another. Currently, there is little evidence-based research on medication-managed withdrawal, although some studies have shown amantadine and bromocriptine may help reduce cravings, increase energy and normalize sleep.9
While basal ganglia enlargement and other inborn or genetic factors may help lay the foundation for addiction to cocaine or other drugs, the overall picture of dependence and addiction is far more complex. Other factors that operate in combination with or instead of genetic tendencies include family and social environments, personality traits, drug-related peer pressure or emotional and/or physical trauma, exposure to stress and susceptibility to impulsive behavior. The virtually limitless potential for interaction among these variables makes the science behind addiction highly complex.
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