Abstract
Baclofen, commonly used to reduce severe muscle spasms in patients with spinal cord injuries, is also active in the brain. A patient with pre-existing bipolar affective disorder developed increased depression while on baclofen, which progressed to a delusional depression when baclofen and haloperidol were rapidly decreased. When the dose of haloperidol was increased to a previously well tolerated dose to deal with the depressive delusion, a pseudoparkinson's state developed. This case demonstrates the interactive effects of baclofen and haloperidol on central noradrenergic and dopaminergic systems and suggests a possible neurochemical basis for the difference between delusional and nondelusional depression that is consistent with the different therapeutic response to psychotropic drugs of patients with these illnesses The paradoxical appearance of the pseudoparkinson state in this patient when much higher doses of haloperidol had been free of such side effects, may reflect baclofen-induced alterations in receptor sensitivity. It appears that baclofen should be used with caution in patients with neuropsychiatric problems and that, when used, the withdrawal of baclofen should be continued over several weeks to allow receptor sensitivity to return to normal levels.