896 BIOL PSYCHIATRY Correspondence 1995;37:895-897 changes in cortical indices of 5-HT function. This is in contrast to previous reports, which found a relationship between depres- sion, agitation, and psychosis and decreases in 5-HT in various brain areas (Zubenko et al 1990, 1991; Palmer et al 1988). However, it is possible that important relationships between behavior and 5-HT were missed by limiting our analyses to the temporal cortex. Furthermore, the fact that our patients were on the mild end of the behavioral disturbance spectrum may also have militated against demonstrating a significant finding for the behavioral disturbances in this study. Future studies that examine different brain areas, in patients with a broader range of cognitive impairment and with more severe behavioral complications, will be necessary to address the methodological deficiencies apparent in the present study. Brian A. Lawlor 1 Theresa M. Ryan 2 Linda M. Bierer 2 James Schmeidler 2 Vahram Haroutunian 2 Richard Mohs 2 Kenneth L. Davis 2 1 Department of Psychiatry St. James's Hospital Dublin, Ireland 2 Mount Sinai/Bronx VAMC New York, NY SSDI 0006-3223(95)00035-F References Altman HJ, Normile HJ (1985): What is the nature of the role of the serotonergic nervous system in learning and memory: Prospects for the development of an effective treatment strategy for senile dementia. Neurobiol Aging 9:627-638. Bowen DM, Allen SJ, Benton JS, et al (1983): Biochemical assessment of serotonergic and cholinergic dysfunction and cerebral atrophy and Alzheimer's disease. J Neurochem 41:266 -272. Cross AJ, Crow TJ, Ferrier IN, et al (1984): Serotonin receptor changes in dementia of the Alzheimer type. J Neurochem 53:1574-1581. Khachaturian ZS (1985): Diagnosis of Alzheimer's disease. Arch Neurol 42:1097-1105. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM (1984): Clinical diagnosis of Alzheimer's dis- ease. Report of the NINCDS-ADRDA Work Group. Neurol- ogy 34:939-944. Mirra SS, Heyman A, McKeel D, Sumi SM, Crain BJ, Brownlee LM, Vogel FS, Hughes JH, vanBelle G, Berl I (1991): The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part II. Standardization of the neuropathological assessment of Alzheimer's disease. Neurology 41:479-486. Palmer AM, Francis PT, Benton JS, et al (1987): Presynaptic serotonergic dysfunction in patients With Alzheimer's dis- ease. J Neurochem 48:8-15. Palmer AM, Statman GC, Procter AW, et al (1988): Possible neurotransmitter basis of behavioral changes in Alzheimer's disease. Ann Neurol 34:616-620. Rosen WG, Mohs RC, Davis KL (1984): A new scale for Alzheimer's disease. Am J Psychiatry 141:1356-1364. Zubenko GS, Moosy J (1988): Major depression in primary dementia: clinical and neuropathological correlates. Arch Neurol 45:1182-1186. Zubenko GS, Moossy J, Kopp U (1990): Neurochemical corre- lates of major depression in primary dementia. Arch Neurol 47:209-214. Zubenko GS, Moosy J, Martinez AJ, et al (1991): Neuropatho- logical and neurochemical correlates of psychosis in primary dementia. Arch Neurol 48:619-623. Zweig RM, Ross CA, Hedreen JC, et al (1988): The neuropa- thology of aminergic nuclei in Alzheimer's disease. Ann Neurol 24:233-242. Does Vitamin E Prevent Tardive Dyskinesia? To the Editor: In a recent paper in Biological Psychiatry Nagesh Pai et al. (1994) reported on a depletion of glutathione and enhanced lipid peroxidation products in the cerebrospinal fluid (CSF) of psy- chotic patients following 2 weeks of haloperidol treatment. Similar findings were observed in rat brains, suggesting in- creased oxidative stress after neuroleptic treatment (Shivakumar and Ravindranath 1993). It has been hypothesized that the oxidative stress caused by neuroleptics may underlie the devel- opment and persistence of tardive dyskinesia (TD) (Cadet et al 1986). It is therefore conceivable that the coadministration of antioxidants such as vitamin E with neuroleptics may prevent TD. In rodents chronic treatment with haloperidol increases the behavioral sensitivity to dopamine (DA) agonists. We used this animal model for TD to investigate the effects of the coadministration of vitamin E with haloperidol on apomor- phine-induced locomotion and stereotypies (Gattaz et al. 1993). Two groups of adult male Wistar rats (n = 14 in each group) were treated with haloperidol (0.05 mg/kg/day) over 4 weeks. One group received concomitantly vitamin E-enriched food (mean daily intake 400 mg/kg vitamin E), starting 2 weeks before the haloperidol therapy until the end of the trial. A control group received haloperidol plus normal food during the same period. Apomorphine-induced locomotion and stereotypies (with 0.25 mg/kg apomorphine subcutaneously [s.c.]) were assessed before and after the haloperidol treat- ment. Vitamin E attenuated significantly the increase of behavioral sensitivity to apomorphine after chronic haloperidol-treatment compared to animals receiving haloperidol alone (p < 0.01 for locomotion and p < 0.01 for stereotypies). This finding supports the idea that the concomitant administration of high-doses of vitamin E with neuroleptics may prevent the development of TD in humans. A number of clinical trials with vitamin E on patients with TD showed contradictory results or, at best, a modest thera-