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M.P.H.

Editions, Royan, 1984

J. Psychiat. biol. ther., 1984, n 16, 26-28

Dexamethasone suppression test in tardive dyskinesia


A. Perenyi MD *, Z. Rihmer M.C.*, E. Frecska M.D.*, G. Faludi M.D. * *
* National Institute for Nervous and Mental Diseases 1281 Budapest, 27 Pf. I. Hungary
** St. John Hospital, Mental Health Service, 1125 Budapest, Dioscirok u.l.

ABSTRACT

RESUME

Dexamethasone Suppression Test (DST) were given


to 20 chronic schizophrenics w,lthlardive dyskiriesia
(TD) and 20 chronic schizophrenics without TD. The
mean cortisol levels and the frequency of the abnormal DST response in the two groups did not differ
significantly.

Les auteurs ont appliqu le test a la dexamethasone


chez 20 schizophrenes chroniques ayant ete atteints
de dyskinesies tardives. Le groupe controle a ete etabli
par 20 schizophrenes chroniques sans symptomes de
dyskinesies tardives. La moyenne du cortisol plasmatique et la frequence de la reponse anormale a la dexamethasone dans les deux groupes n'ont pas montre
une difference significative.

Tardive dyskinesia (TD) is charactized by stereotypic, repetitive, involuntary movements particularly


in the crofacial region and tongue, but it may be
accompained by choreiform movements of trunk and
extremities. Although it has been the target of a large
number of investigations, its pathomechanism is still
unclear (Jeste and Wyatt, 1981). The syndrome develops usually as a result of long-term neuroleptics.
Data have lately emerged in the literature which indicate a correlation between depression and TD. Thus,
Rosenbaum et al. (1980) reported on the succesful
treatment of 19 TD patients with the combination
of tricyclic antidepressants and lithium. Their patients
were suffering of major depressive illness according
to the Research Diagnostic Criteria (RDC ; Spitzer
et al., 1977). In all of them both the movement disorder and depression improved, which supports the
hypothesis that affective disorder is a predisposing
factor of TD. Rush et al. (1982) also claimed that
the depression was a risk factor contributing to the
development of TD. Recently Cutler and Post (1982)
described two cases of manic depressive psychosis
where TD appeard in the depressive phase only and
was absent in mania.

in a large number of patients, it would be hard to


decide whether abnormal DST is caused by depression, or as we supposed, by TD.
METHODS

The dexamethasone supression test (DST) has proved a useful tool in the diagnosis of endogenous
depression (Carrot et al., 1981). Relying on the above,
it appeared of interest to study the response of schizophrenic patients suffering of TD to the DST. It further justified the performance of our study that
Rosenbaum et al. (1979) reported to have found elevated or upper normal urinary free cortisol (UFC)
levels in 15 of their 18 TD patients.
Since we supposed and occasional common pathomechanism of the affective psychosis and TD based
on data mentioned above, we wanted to avoid the
participation of depressed patients with TD in the present study. Namely in case of finding DST positivity,

The DST was performed in 20 chronic schizophrenic patients diagnosed on the basis of RDC, suffering of TD, and in 20 chronic schizophrenics without
TD. We considered patients having TD if they achived at least one 3, or three 2 on the first seven items
of Abnormal Involuntary Movement Scale (Guy,
1976) at two ratings carried out at intervals of one
month. According to the ward psychiatrist the
patients'movement disorder had been present for at
least two years. The mean age of TD patients was
55,23 6,31 years (mean SD),. that of the patients
without TD was 51,42 8,9 years. The difference
between the mean age of the two groups. The difference between the mean age of the two groups was
statistically nonsignificant (t = 0,701, two tailed, df
= 38, p < 0,5). The mean duration of neuroleptic
treatment for the TD patients was 8,31 2,32 years,
for the patients without TD it was 7,12 4,85 years.
The difference is statistically nonsignificant (t = 0,412,
two tailed, df = 38, p < 0,7). None of the patients
was taking antidepressants during the study, but all were
on neuroleptics. Every patient was female inpatient.
The DST procedure was as follows : the patients
took an oral dose of 1 mg dexamethasone tablet at
10.00 p.m. and post-dexamethasone blood samples
were obtained on the following day at 8.00 a.m. and
3.00 p.m. The criterion of an abnormal DST response
was a higher than 5.00 microgram/dl postdexamethasone cortisol level. Plasma cortisol levels
were measured by a competitive protein binding
method described by Carrol et al. (1981). We had to
depart from the sampling times indicated byCarrol
et al. (1981) for technical reasons.
Every patients was able and willing to give informes consent.

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Dexamethasone suppression test in tardive dyskinesia

RESULTS
The mean of the plasma cortisol levels measured
at 8.00 a.m.. in the TD group was 2,39 3,13 microgram/di, that of the group without TD was 2,83
4,35 microgram/dl. The difference was statistically
nonsignificant (t = 0,367, two tailed, df = 38, p <
0,8). The mean plasma cortisol levels in the TD group
at 3.00 p.m. were 1,99 3,54 microgram/dl and 2,65

3,96 microgram/di, respectively. The difference


was neither statistically signific,ant(t = 0,558, two tailed, df = 38, p < 0,6). At 8.00 a.m. three patients
of both groups, at 3.00 p.m. one patient of TD group
and three ones of the control group had plasma cortisol levels above 5.00 microgram/di. The difference
was statistically nonsignificant between the two
groups at 3.00 p.m. either (X2 test with Yates' correction : 0,27, df = 1, p < 0,7).
DISCUSSION
Our examination have revealed no significant difference in the response to the DST between chronic
schizophrenic with and without TD. At the selection
of the patients of control group we relied on the hypothesis that even if the TD patient would have less frequently abnormal DST than those with depression
it would more frequently be positive than the DST
of schizophrenics without TD. This would have supported our presumption that TD patients, or at least
one of their subgroups had similar neuroendocrine
dysfunction to that in depression.
We can not explain the negative results with difference between the original method and the procedure used by us, since using a procedure similar to
the present study we had found abnormal DST in
twelve of sixteen patients with masked depression
(Rihmer et al., 1983). One may say, that nobody
would have expected anything other, than negative
results examining two groups of schizophrenics, but
we refer to the study of Dewan et al. (1982). They
found 30 07o nonsuppression in chronic schizophrenics, therefore we might suppose that a subgroup of
chronic schizophrenics (may be with a higher risk for
the development of TD) has abnormal DST. Our
expectations did not prove true in this study.
Data according to which a subgroup of TD patients
is characterized by noradrenergic hyperfunction (Jeste
and Wyatt, 1981), and the hypothesis put forward
by others (Sachar, et al., 1980) that abnormal DST
is correlated with central noradrenergic deficit would
possibly help to interpret our negative results. Nevertheless, we had to reject this interpretation, as noradrenergic hyperactivity would characterize only one
subgroup of TD patients, Cutler and Post (1982) e.g.
observed the symptoms of TD in the presence of low

cerebrospinal fluid nnorepinephrine concentration in


the depressive phasis of their patient with affective
illness, furthermore the results of others (Sternbach
et al., 1981) failed to support the opinion that positive DST is associated with central noradrenergic
deficit.
Rosenbaum et al. (1980), as well as Rush et al.
(1982) have only drawn the conclusion that depression is a risk factor in the development of TD. Neither do our results allow to draw further conclusion.
It is true that 15 of 18 TD patients of Rosenbaum
et al. (1979) had elevated or upper normal UFC level,
but 13 of the 15 patients were probably depressed and
one of them manic.
In view of the fact that, based on our present knowledge of the pathomechanism of TD, existence of
several subgroups has been suggested (Jeste and
Wyatt, 1981), and that a tendency to develop TD has
been observed in depressed patients (Rosenbaum et
al., 1980, Rush et al. 1982) we have come to the conclusion that the TD of depressed patients may constitute a biochemically separate subgroup and/or if
the pathomechanism of TD in depression does not
differ from that observed in schizophrenia, the biochemical alterations responsible for its development
are independent of the factors involved in abnormal
DST.
BIBLIOGRAPHIE
Carrot B.J., Feinberg M., Greden J.F., Tarika J., Albala A.A.,
Haskett R.F., James N. McI., Kronfol Z., Lohr N., Steiner M.,
tie Vigne J.P., Young E. A specific laboratory test for the diagnosis of melancholia. Arch. Gen. Psychiat. 1981, 38 : 15-22.
Cutler N.R., Post R.M. - State-related cyclical dyskinesias in
manic-depressive illness. J. Clin. Psychopharmacol. J982, 2 :
350-354.
Dewan M.J., Pandurangi A.K., Boucher M.L., Levy B.F.,
Major L.F. - Abnormal dexamethasone supression test results
in chronic schizophrenic patients. Am. J. Psychiat. 1982, 139 :
1501-1503.
Guy W. Ecdeu Assessment Manual for Psychopharmacology/NIMH, Bethesda, MD, 1976/.
Jeste D.V., Wyatt R.J. Dogma disputed : is tardive dyskinesia
due to postsynaptic dopamine receptor supersensitivity ? J. Clin.
Psychiat. 1981, 42 : 455-457.
Rihmer Z., Szadoczky E., Arato M. Dexamethasone suppression test in masked depression. J. Affect Dis. 1983, 5 : 293-294.
Rosenbaum A.H., Maruta T., Duane D.D., Auger R.G., Brenengen E.E. - Tardive dyskinesia in depressed patients : succesful therapy with antidepressants and lithium. Psychosomatics
1980, 21 : 715-719.
Rosenbaum A.H., Maruta T., Jiang N.S., Auger R.G., De La
Fuente J.R., Duane D.D. - Endocrine testing in tardive

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A. Perenyi M.D., Z. Rihmer M.D., E. Frecska M.D., G. Faludi M.D.


dyskinesia : preliminary report. Am. J. Psychiat. 1979, 136 :
102-103.
Rush M., Diamond F., Alpert M. - Depression as a risk factor in tardive dyskinesia. Biol. Psychiat. 1982, 17 : 386-392.
'-char E.J., Asnis G., Nathan S., Halbreich U., Tabrizi
Halpern F.S. - Dextroamphetamine and cortisol in
uepression. Arch. Gen. Psychiat. 1980, 33 : 755-757.

Spitzer R.L.. Endicott J., Robins E. - E. Research Diagnostic Criteria/RDC/for a selected group of functional disorders.
3rd edition, Biometric Research, NY State Psychiatric Institute,
New-York,/1977/.
Sternbach H., Gwirtsman H., Gerner R.H. - The dexamethasone suppression test and response to methylphenidate in depression. Am. J. Psychiat. 1981, 138 : 1629-1631.

L'INFORMATION PSYCHIATRIQUE
Sommaire n 8/1984

CORPS ET PSYCHOPATHOLOGIE
DE L'ENFANT
Nurnero special sous Ia direction de R. Mises
Fonctions du Moi-Peau

par D. Anzieu
Corps a corps ou tete a corps
par S. Lebovici
Corps et psychopathologie de ('adolescent

par Ph. Jeammet


Pathogenie des troubles somatiques de l'enfant et aspects transculturels : le kwaschiorkor

par R. Mises
L'expression corporelle dans Ia psychopathologie de l'enfant

par L. Kreisler
Le corps en question dans deux traitements analytiques d'enfants

par C. Druon
Des corps a constituer

Corps de l'enfant et corpus institutionnel


par J. Constant

Histoire de Ia psychiatrie
La Guerre par B. Bonfils

Documents administratifs
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Communiqus

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