The brain reward system is known to be the neuroanatomical basis of addictive behaviors. Systemic, cognitive and functional consequences of crack-cocaine addiction are clinically evident, but the neuroanatomical underpinnigs are not yet well understood. We aim to assess the neuroanatomical differences between crack-cocaine patients and paired healthy controls. Fifteen crack-cocaine patients recently discharged from the Addiction Unit of the Hospital de Clínicas de Porto Alegre and fifteen controls matched for gender, age, education and handedness were scanned using a Philips Achieva 1.5T MRI equipment. All subjects had negative positive tests at admission and patients had at least 15days of detoxification. Active neurologic, inflammatory, cardiovascular or systemic comorbidities were excluded. Subcortical structure volumes were determined using Freesurfer v5.1. Controls had greater volumes in the left accumbens (t=3.604, df=28, p=0.001) compared to patients. Right accumbens volumes were also greater in controls (t=2.098, df=28, p=0.045). Groups did not differ regarding intracranial volumes (p=0.514). This preliminary and innovative data on crack-cocaine dependence suggests that there is a volumetric reduction of the accumbens, a region that has a significant role in motivation, pleasure, reward and reinforcement learning, and it could play a central role in the pathophysiology of this drug addiction. Therefore, these findings may contribute to understand some behavioral and cognitive deficits in this population.

Data suggest that cocaine use could be associated with HCV infection due to the specificities of cocaine consumption pattern, even in those subjects who do not inject drugs, in addition to other risky behaviors, such as tattooing and unprotected sex. Injectable cocaine users seem to be more susceptible to contamination than users who do not inject drugs. However, evidence is pointing to the possibility of infection by sharing drug paraphernalia other than syringes. Moreover, specific immune system impairments caused by cocaine use are also being linked with HCV infection susceptibility, persistence and increased pathological effects.

There is a growing body of evidence suggesting that neuroprogression occurs in addiction in the same way as in other psychiatric disorders. Biological markers of neuroprogression will be reviewed in the light of the staging model of addiction proposed by Volkow and Koob (intoxication, withdrawal and negative affect, and preoccupation and anticipation) and of allostatic load theory. Chronic exposure to drugs leads to allostatic load or overload through these stages. Neuroadaptation in this process disrupts brain morphology and function. Evidence regarding neuroprogression in drug addiction will focus on neuroimaging findings as well as neurotrophins, inflammatory markers, oxidative stress, and accelerated ageing.