Background The developmental taxonomic theory proposes that there are two subtypes of antisocial behaviour. The first is a neurodevelopmental disorder which emerges in early childhood and follows a life‐course persistent course, whereas the second emerges in adolescence, remits in early adulthood and reflects peer processes such as mimicry of antisocial peers. The aim of this review was to evaluate the developmental taxonomic theory in the light of recent empirical research. Methods We conducted a comprehensive literature review comparing these subtypes of antisocial behaviour based on searches on PubMed and other scientific databases covering the period from 1993 to 2013. We focused on research encompassing psychiatric epidemiology, personality assessment, neuropsychology, neuroendocrinology, genetics, and structural and functional neuroimaging. Sixty one empirical studies were identified that investigated one of these forms of antisocial behaviour separately or explicitly compared childhood‐onset and adolescence‐onset forms of antisocial behaviour. Results Empirical research provides support for the hypothesis that life‐course persistent antisocial behaviour is a neurodevelopmental disorder which emerges in the transactions between individual vulnerabilities and environmental adversity. In contrast to the developmental taxonomic theory, however, empirical findings suggest that severe antisocial behaviour that emerges in adolescence frequently has a negative prognosis and is rarely limited to the adolescent period. In addition, both forms of antisocial behaviour are associated with emotion processing deficits, changes in brain structure and function, alterations in cortisol secretion, and atypical personality traits (such as increased callous‐unemotional traits). Conclusions We conclude that the developmental taxonomic theory is in need of revision, as differences between life‐course persistent and adolescence‐onset forms of antisocial behaviour appear to be quantitative, rather than qualitative, in nature. In addition, evidence is accumulating that adolescence‐onset antisocial behaviour may also be a neurodevelopmental disorder. To account for the similarities between these groups, despite the differences in their age‐of‐onset, we propose that the quality of the child's early environment moderates the relationship between individual vulnerabilities and the age‐of‐onset of antisocial behaviour.