A possible association between venous thromboembolic disease and the use of antipsychotics has been suggested since the 1950s following the introduction of phenothiazines. Several case studies have supported the idea of increased risk of deep vein thrombosis for those on antipsychotics, but the relative impactof this risk factor remains unclear. Deep vein thrombosis is often the result of a combination of several risk factors. The direct implication of a molecular action of antipsychotics began to be considered after several publications illustrating cases of deep vein thrombosis of the lower limbs and serious pulmonary embolism, paradoxically occurring in young psychiatric patients free from any other risk factors. Many hypotheses have been mentioned to explain the mechanisms of occurrence of thromboembolic events: neuroleptics can induce sedation and weight gain indirectly promoting the thromboembolic risk by reducing mobilization; they may also be responsible for an increase in anti-phospholipid antibody levels, increased platelet aggregation, hyperhomocysteinemia, an increase in serotonin and prolactin levels as well as peripheral vasodilation (responsible venous stasis) thus promoting the occurrence of thromboembolic events. We discuss the role of antipsychotics in the ethiopathogenesis of deep vein thrombosis through a literature review as well as a clinical case of a young patient with a schizoaffective disorder who presented deep vein thrombosis on antipsychotics during hospitalization.