Restless legs syndrome (RLS) is an idiopathic movement disorder of uncertain etiology, where the patient feels an uncontrollable compulsion to move their lower limb, disturbing sleep. Tardive dyskinesia is an irreversible adverse effect of antipsychotic medication treatment and affects axial movements, muscles of the face and limbs. Both disorders are thought to reflect abnormalities of the basal ganglia. A growing literature has implicated abnormal iron metabolism in the basal ganglia in their pathogeneses. Blood ferritin and iron levels are decreased in RLS  and decreased brain iron levels can be visualized by MRI . RLS responds to treatment with iron supplements . However, there is no evidence that iron deficiency alone can cause RLS. Rather growing evidence suggests that iron uptake into the basal ganglia, which is mediated by the transferrin receptor, is diminished in the syndrome [30,31].
The association between iron or metal status and tardive dyskinesia is less clear. Antipsychotic drugs promote the uptake of iron into synapses, and so may increase the ROS burden on the neuron . However, clinical studies have found contradictory evidence of peripheral iron dysregulation in antipsychotic-related abnormal movement disorders [33,34].
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