Tardive akathisia (TA) is a well-documented side-effect of neuroleptic treatment. The underlying mechanism is poorly understood, and treatment is unsatisfactory. In this case report, TA that occurred in the course of a tardive dyskinesia (TD) was successfully treated with the monoamine-oxidase-A inhibitor moclobemide. With respect to the mechanism of action, it may be hypothesized that dopaminergic supersensitivity in the mesocortical region is counteracted by enhanced inhibition of primarily noradrenergic neurotransmission.