DEPENDENCE ON CRACK/COCAINE: A NEUROBIOLOGICAL AND SOCIAL ANALYSIS

ANA LETÍCIA AMARAL, BRENDA ARNOLD, MARIZE VITÓRIO, THIAGO JUSTINO

Resumo


Introduction: Chemical addiction is a chronic, relapsing disease in which the use of psychoactive
substances causes structural and functional changes in the brain leading to behavioral and social
repercussions. In the 1990s, crack was introduced in Brazil, making the country its largest market
currently1. This is the smoked form of cocaine, seeking for faster and more intense effects, with higher
addictive potential2,3. They differ in the pharmacokinetics, as physical/chemical form, route of
administration, genetics and effects on body4. Cocaine/crack are seen as a public health problem due to
the growth of consumption3, but for its higher compulsivity, crack has brought major social consequences
such as violence and sexual risk behaviors5,1. Objective: To execute a neurobiological and social analysis
of drugs, focusing on crack/cocaine. Methods: A literature review was conducted during the month of
August 2015 in the databases of PubMed and BVS, with the following keywords: crack/cocaine, addiction
and treatment. Articles published prior to 2010 were excluded. Discussion: Drugs operate on
mesocorticolimbic pathway of the dopaminergic neurotransmission, mainly in the nucleus accumbens
(feeling of pleasure and reinforcement in search behavior) and prefrontal cortex (inhibitory control,
hypofunctioning in dependents), composing the brain reward system3. There are three interacting stages
that are gradually intensified leading to addiction, they are also involved in the neuroplasticity of neural
circuits: excess/intoxication, abstinence/negative affect, preoccupation/anticipation; impulse control
disorders appear in the early stages and compulsive disorders in the later ones6. Cocaine inhibits the
presynaptic dopamine transporter, increasing its quantity in the synaptic cell and unchaining the
repetitive behavior behind the drug, reducing this neurotransmitters postsynaptic receptors;
simultaneously, glutamatergic neurons are activated in the prefrontal cortex and glutamate is liberated,
responsible for regulating the locomotor sensitization, drug seeking and conditioned responses to drugassociated stimuli3,7. Crack conduces to addiction faster, to withdrawal stronger and to prognosis worse
than cocaine8: a five-years follow-up study developed with 131 Brazilian crack users revealed that 18,5%
died during this time, 56,6% of these related to homicides3,2. The tendency toward compulsiveness
generated by the use of crack is one of the responsible for those higher rates of violence, beyond others
social conflicts, such as sexual promiscuity that increases the STDs, and also the transmission of
respiratory diseases, like tuberculosis5,2. Chronical use of crack disturbs the general cognitive functioning,
verbal memory and attention8, such cognitive sequelae may prove a hindrance to the effectiveness and
adherence to treatment. Conclusion: The crack/cocaine consumption rebounded in all social classes,
although the predominance of users still remains on marginalized groups3, overlapping the profile of
young man, low socioeconomic and educational levels and with larger family problems3,1. In Brazil, the
stigma over the dependents has been hampered the providence of effective and humane treatment9. This
must be multidisciplinary and interdisciplinary, in need of support in social, physical, mental and legal
areas, such as in the quality of life and relapse prevention strategies3. Treatments also must contain social
reintegration strategies supported by health professionals, family and community10, seeking approaches
that improve neurocognitive functioning of these patients.


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