BIOL PSYCHIATRY 1990;27:457-467

457

CORRESPONDENCE Letters of 600 words or less, with minimal allowance for tables, figures, and references, will be considered for publication. Rules regarding prior publication, conflict of interest, etc., are the same as for full manuscrtpts. All letters are subject to editing and condensation. Proofs will not be distributed.

Olfacto~ Functioning in Schizophrenia and Depression To the Editor: Various theories on the olfactory deficits encountered in the psychiatric patient population have been proposed on the basis of neurochemical imbalances, medication use, cognitive deficits, decreased attention span, and increased fatigue effect. Since Doty, et al. (1984) published his standardized smell identification test, investigators have systematically evaluated olfactory deficits in patients with Alzheimer's disease (Serby et al. 1985; Warner et al. 1986), Down's syndrome (Warner et al. 1988), depression (Amsterdam et al. 1987), and schizophrenia (Hurwitz et al. 1988). An olfactory deficit has been suggested in each of these disorders with the exception of depression (Amsterdam et al. 1988). We recently did a little s~udy using the standardized University of Pennsylvania smell identification test (UPSIT) to assess olfactory functioning in depressed and schizophrenic patient groups. Some depressed patients complain of a decreased ability to taste food, which might be ascribed to olfactory deficits. Both schizophrenic and depressive disorders are believed to involve limbic system pathology and, as olfactory function is subserved in part by limbic structures, olfactory deficits were postulated in both groups. Of the 26 male subjects who participated in our study, 18 were inpatients at the Palo Alto Veterans Administration Medical Center: 12 of these met Research Diagnostic Criteria (RDC) (Spitzer et al. 1977) for schizophrenia and 6 met criteria for major depressive disorder (MDD). An additional eight subjects served as normal controls. The sample was restricted to subjects 50 years and younger to ensure age comparability across groups. Exclusion criteria for all subjects included (1) severe medical problems, (2) viral infections in the past 2 weeks, (3) history of head injury with resultant loss of consciousness or ongoing neurological deficits, (4) use of psychotropic medication in the past 2 weeks, and (5) ,any disease associated with olfactory deficits (Schiffman 1983). ~MI subjects understood the ~sting procedure and gave written informed consent. © 1990 Society of Biological Psychiatry

The UPSIT consists of 40 chemically impregnated tapes which when scEatched, release an odor. Testretest reliability in a large normative sample of 0.92. Each subject was read aloud four possible answers. Regardless of whether or not subjects could smell the odor, they had to choose among the four alternatives. Neither the parametric nor the nonparametric analysis of variance showed differences among the three groups regarding subjects' UPSIT scores or ages (Table 1). However, with only 26 subjects, these results do not eliminate the possibility that difl~rences exist. Our results are consistent with those of Amsterdam et al. (1987) who found no difference between 51 depressed patients and 51 age- and gender-matched control subjects on the UPSIT. However, no information was given concerning the medication status of subjects. Hurwitz et al. (1988) administered the UPSIT to 18 schizophrenic patients on neurleptics, 11 nonschizophrenic patients on neuroleptics, and 10 normal controls. Schizophrenic patients did significantly worse than the other groups. However, it is difficult to interpret these results because the groups were not ageor gender-matched nor were the patients drug free. It is not known if neuroleptics interfere with olfa ~tion, but UPSIT scores are known to be lower w~th increased age and male gender (Dory et al. 1984). There have been very few standardized studies assessing olfactory function in depressed or schizophrenic patients. Further well-controlled studies are needed before any conclusions can be drawn.

Table I. UPSIT Scores and Ages

Group

Schizophrenic n=12 MDD n=6 Normal control n=8

Mean UPSIT scores (SD)

Mean age in years (age range)

36 (3.0)

34 (20-42)

38 (1.3)

37 (28-50)

38 (I.I)

32 (20--44)

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458

Correspondence

BIOL PSYCHIATRY 1990;27:457-467

M. Dhyanne Warner Cecilia A. Peabody John G. Csernansky Dept. of Psychiatry University of Texas Medical School 2800 S. McGregor Way P.O. Box 20708 Houston, TX 77225

References Amsterdam JD, Settle G, Dory RL, Abelman E, Winokar A (1987): Taste and smell per~:eption in depression. Biol Psychiatry 22:1477-1481. Doty RL, Shaman P, Dann W (1984): Development of the University of Pennsylvania Smell Test: Standardized microencapsulated test of olfactory function. Physiol Behav 32:489-502. Hurwitz T, Kopala L, Clark C, Jones B (1988): Olfactory deficits in schizophrenia. Biol Psychiatry 23:123-128. Schiffman S (1983): Taste and smell in disease. N E~gl J Med 308:1275-1279. Serby M, Corwin S, Conrad P, Rotrosen J (!985): Olfactory dysfunction in Alzheimer's disease and Parkinson's disease. Am J Psychiatry 142:781782. Spitzer RL, EnoS' " J, Robins E (1977): Research diagnostic crll "m for a selected group of functional disorders. New York State Psychiatric Institute, New York. Warner MD, Peabody CA, Berger PA (1988): Olfa,.'tory deficits and Down's syndrome. Biol Psy. chiatry 23:836-839. Warner MD, Peabody CA, Flattery JJ, Tinklenberg JR (1986): Olfactory deficits in Alzheimer's disease. Biol Psychiatry 21:116-118.

Response I o the Editor: On first glavce the results of this study appear to conflict with our own findings. As the sample sizes

are quite small, we took the liberty of reanalyzing the data provided by the authors. If one does a standard one-way analysis of variance, tl-.e resulting Fvalue is not significant (F2.23 = 2.56, i~ < 0.0988) but a trend is present. However, if one does a contrast between the depressed and normal subjecgs versus the patients with schizophrenia, the contrast is significant (t - 2.25, p < 0.034, df = 23.0 for the pooled variance estimate and t - 2.16, p < 0.049 df = 14.1 for the separate variance estimate0. This contrast essentially increase.:, the sample size of the normal group to 14. As the normal and depressed group means are identical, such a combination is statistically acceptable. Tilerefore, we suggest that this study replicates our initial findings for patients with schizophrenia and that neuroleptic medications were not a confound. We suggest that the authors have made a type II error and did not analyze their data thoroughly enough to justify their conclusions. Such an analysis is warranted when one wishes to refute a previous finding based on small sample sizes. There are two other points that should be addressed. First, the authors did not use the standard method for administering the SIT and this change may have biased the results. Second, in our original study, the normal controls were on average 10 years older than the patients with schizophrenia and hence, one would expect the normals to sco~e lower titan me patients with schizophrenia, as olfactory identifications decreases with age. Therefore, age could not account for the effect in the original study. In contrast, in the Warner et al. letter, the controls are slightly younger than the patients with schizophrenia. This difference in age may also introduce a slight bias. S~atistical details will be supplied upon request. T. A. Hurwitz Campbell Clark

University of British Columbia Department of Psychiatry. 2255 Westbrook Mall Vancouver, B.C., Canada V6T 2AI

Olfactory functioning in schizophrenia and depression.

BIOL PSYCHIATRY 1990;27:457-467 457 CORRESPONDENCE Letters of 600 words or less, with minimal allowance for tables, figures, and references, will be...
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