Crack cocaine is a highly addictive and dangerous substance that can trigger or worsen epileptic seizures. However, the molecular mechanisms underlying crack cocaine's effects on epilepsy are not fully elucidated. Recent evidence involves the inhibition of acetylcholinesterase (AChE) by crack cocaine, increasing the levels of acetylcholine in the brain, leading to overstimulation of cholinergic receptors and neuronal excitability. Another alarming factor is the exposure of fetuses to crack cocaine during the gestational period. Studies indicate that crack cocaine and its metabolites cross through the placenta, causing premature delivery, fever, irritability, sweating, and seizures in the first months of life. In children, the effects of crack cocaine have been associated with cognitive impairments, verbal difficulties, aggression, and depression, as well as an increased risk of epileptic seizures, including Status Epilepticus (SE) in adulthood. In animal models crack cocaine exposure during the gestational period leads to an increased propensity to anxiety and depression, long-term memory deficit and reduction of the threshold of epileptic seizures associated with neuronal death, which predispose crack cocaine babies to develop epilepsy and other neuropsychological disorders. Here, we will address the latest research on the impact of crack cocaine on animal models and their offspring. Additionally, will be discussed the mechanisms and consequences of direct and prenatal exposure to crack, and how they relate to the development of epilepsy and other neurological disorders. The aim of the discussion is to provide a comprehensive overview of the current state of knowledge and future directions in this research field.