the inhibition of dopaminergic reuptake, and through the activation of noradrenergic and serotoninergic sites in the basal forebrain and cerebral cortex (Malanga and Kosofsky 1999). In preclinical studies, exposure to cocaine during gestation has been shown to affect brain function, particularly the dopaminergic systems, causing anatomical, physiological, and behavioural changes. However, human studies often reported only mild alterations in attention, language, and memory inuenced by environmental factors such as socioeconomic status and other drug use (Betancourt etal. 2011). Neurotoxic effects of in utero cocaine exposure can manifest in foetal and long-term growth outcomes, as well as structural abnormalities, determining an impaired neurodevelopment. Maternal complications following in utero cocaine exposure include cardiovascular complications (e.g., hypertension, myocardial infarction, ischaemia), renal failure, hepatic rupture, cerebral haemorrhage/isch­aemia/infarction and maternal death (Smid etal. 2019). Evidence supports that car­diovascular complications are not dose-dependent, by underlining that also small doses may lead to cardiac morbidity and mortality in healthy pregnant women. Moreover, clinicians should also consider that pregnancy may increase cardiovascu­lar toxicity due to an increased cardiac muscle’s sensitivity to cocaine through an increased progesterone concentration (Plessinger and Woods Jr. 1991). Cocaine toxicity may cause severe hypertension, hyperreexia, oedema, seizures and pro­teinuria in pregnant women (Smid etal. 2019). A systematic review and meta­analysis conducted by Gouin etal. (2011) on 31 studies reported an increased risk for preterm delivery, low birth weight, small for gestational age infants, earlier ges­tational age at delivery and reduced birth weight. Postpartum psychological distress experienced by mothers with prenatal cocaine exposure was greater compared to mothers not using cocaine (Smid etal. 2019). The long-term effects on child growth and development are uncertain, though some research indicates slower growth in children up to age 10. Cocaine exposure is linked to neurodevelopmental issues like cognitive impairments, behavioural problems (e.g., ADHD), and language delays. However, sociodemographic and environmental factors may contribute as much, or more, to these outcomes. Protective factors, such as family support and better socio­economic status, can help mitigate the negative effects of prenatal cocaine exposure (Cressman etal. 2014). Higher rates of psychopathological symptoms (e.g., depres­sion, anxiety, psychosis and paranoia) amongst cocaine-using women were reported by Singer etal. (2000) which were associated with higher levels of reduced head circumference and birthweight. A dose-response correlation between a prenatal cocaine exposure and a lower height and weight-for-height z scores at 6years was reported by Minnes etal. (2005). Several large longitudinal prospective cohort stud­ies reported stable negative effects on language skills in cocaine-exposed infants and children up to 7years of age, beyond the effect of the home environment or other confounding factors (Singer etal. 2001; Morrow etal. 2003; Bandstra etal.