Cocaine-induced seizures (CIS) and cocaine-induced psychosis (CIP) may be complications of acute cocaine intoxication. CIS could result from a kindling process, involving the glutamate NMDA receptor (NMDAR) phosphorylation state, which is enhanced by activation of the dopamine D1 receptor (D1R). CIP is considered to be more specifically associated with the activity of the dopamine D2 receptor (D2R). The authors describe the case of a 21-year-old woman who presented with recurrent CIP during a period of increased cocaine abuse that ended in two consecutive CIS. This case report may illustrate a possible overlap in the mechanisms underlying CIS and CIP, disclosing some subtle interactions occurring between dopaminergic and glutamatergic receptors during cocaine chronic intoxication. Chronic cocaine exposure usually induces the formation of a NMDAR-D2R complex, which seems to be linked to the usual clinical effects of the drug, but also causes complex formation not to occur in both D2R-based CIP and D1R-based CIS. To explain the case of this patient, we propose a pharmacological hypothesis based on a literature review and implying the lack of formation of this complex, which triggers CIP and CIS. On a more practical level, this case report also encourages practitioners to be aware of the possible co-occurrence of CIP and CIS in cocaine abusers, especially with respect to antipsychotic medications that could be administered in such situations.