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Restless legs syndrome (RLS) is a sensory-motor disorder with unknown etiology that is characterized as a strong sensation of moving legs and other extremities during resting. This unpleasant sensation has a strong circadian rhythm, which gets worse at nights and calms down after sleep, especially in the mornings. There are two types: One being idiopathic and the other being secondary. Anti-emetics, anti-psychotics, anti-histaminics, some anti-epileptics, tricyclic anti-depressants, and serotonin or serotonin-noradrenaline reuptake inhibitors may all cause RLS or lead to exacerbation of present symptoms. In this paper we report of a bipolar patient, who had RLS induced by quetiapine. Our patient was a 53 years old female. She applied to our clinic in 2007 reporting symptoms of depressive mood, anhedonia, asthenia, pessimism, distress, anxiety that had been going on since 1998. She was describing short hypomanic episodes after these depressive periods. Bipolar manic disorder type 2 was diagnosed according to DSM-IV and the patient has been in partial remission for the last 2 years with 150 mg/day venlafaxine and 900 mg/day Lithium bicarbonate treatment. Her lithium levels and thyroid function tests were checked monthly. She developed compensated hypothyroidism that had been got under control with low dose levothyroxine sodium. Despite having most of her symptoms revealed, insomnia and anhedonia were persistent. At this point quetiapine 300 mg/day was added on her treatment. 2 weeks after daily quetiapine administration, she started to complain about a weird feeling on her legs at nights and had a need to move them. Thus having her insomnia symptoms getting worse, she had stopped having her daily quetiapine after 5 days. All the organic reasons causing restless leg syndrome were ruled out by clinical and laboratory tests and patients symptoms were thought to be due to dosage of quetiapine. The dose had been reduced to 150 mg/day and was started again. She was called for supervision the week after. During her supervision she reported continuing her drug for only 2 days because of having her previous discomfort. The patient was started zopiclone 7.5 mg/day treatment. On her next control she had no symptoms of restless leg syndrome and her insomnia was partially relieved. Although the etiopathogenesis of restless leg syndrome is yet to be identified, the effectiveness of dopaminergic drugs in treatment gives a hint about its cause to be about abnormal functioning in central nervous system. Advanced radiological imaging shows decreased dopamine D2 receptor binding in striatum of restless leg syndrome patients. In our case, we think restless leg syndrome symptoms are induced by quetiapine’s weak blockage of dopaminergic pathway. Current literature reveals very few reports of RLS caused by quetiapine. With this aspect, we think our report will provide valuable information to literature.