ABSTRACT
Halperidol [HP] is a high potency antipsychotic drug used in treatment of schizophrenia. One of its major side effects is Tardive Dyskinesia [TDD] which is a syndrome of irreversible involuntary movements in tongue, face, arms and legs. Different mechanisms were proposed to explain the pathphysiology of TD and to suggest the proper treatment of this iatrogenic effect caused by HP. The most accepted theory could be histological alterations in the striatum caused by an oxidative stress mechanism and hence the trial of vitamin E [being an antioxidant] as a protective agent against HP-induced TD. The study was performed to investigate the effect of HP on the corpus striatum of rat and the possible neuroprotective role of vitamin E. The present study was carried out on forty adult male albino rats which were divided into four groups; the control group, vitamin E group received only vitamin E orally in a dose of 100 mg/kg/day for 4 consecutive weeks, the HP group received HP in a dose of 40 mg/kg/day for 4 consecutive weeks and the HP and vitamin E group received 100 mg/kg vitamin E in conjunction with HP for the same period. Clinical observation for VCMs [analogue of TD] was made during the period of experiment. At the end of four weeks, animals were sacrificed and brain specimens were prepare for histological study of the basal ganglia by light microscopy using H and E. and DOPA reaction. There were different histological alternations in neurons of the striatum in the HP-treated group, which were in the form of distortion, cellular infiltration,, shrinkage and hypereosinophilia of the cytoplasm. Other neurons showed cytoplasmic vacuolations, Co-administrations of vitamin E, reduced the HP-induced striatal neuronal changes, thus, vitamin E could be of value as a neuroprotective agent against HP-induced striatal changes in humans