264
(median SBR 12/min), clinical stabilization (median 13.5/min)
and at 4-months follow-up (median 17/rain). There was no
significant difference between SBR across the three time points.
SBR was correlated with neither neuroleptic dosage, symptoms,
nor duration of untreated psychosis.
Conclusion: SBR was increased in first-episode schizophrenic
patients. In contrast with earlier reports, it was found not to
be significantly reduced after neuroleptics treatment. Although
clearly increased in patients, our data suggests that SBR is not
a simpe linear reflection of dopaminergic activity in
schizophrenia.
B,242. L O N G - L A S T I N G INTERMITTENT
TREATMENT OF RATS WITH
RISPERIDONE
A. Bille, R. Hemmingsen, B. G l e n t h o j
Department of Psychiatry E, Bispebjerg Hospital, DK-2400
Copenhagen NV, Denmark
Persisting increases in the number of vacuous chewing move-
ment (VCM) in rats following long-lasting antipsychotic treat-
ment, is believed to be an animal model of tardive dyskinesia
(TD).
In previous studies we have reported persisting increases in
the number of VCM following long-lasting intermittent treat-
ment of rats with haloperidol. No changes were found in rats
treated with either clozapine or a selected dopamine D1 antago-
nist. Furthermore, rats with persisting dyskinetic mouth move-
ments demonstrated cross-sensitivity between persisting
increases in VCM and electrical amygdala kindling. Risperidone
has high affinity to serotonin 5HT:A receptors and dopamine
D 2 receptors, and a lower risk for acute dyskinetic side-effects
is reported.
The aim of this study was to test if long-lasting intermittent
treatment with risperidone gives rise to persisting increases
in VCM.
The balance between serotonin 5HT2A and dopamine D2
receptor antagonism possibly provides a modifying effect on
the development of persisting increases in the number of
vacuous chewing movements after long-term intermittent treat-
ment with risperidone, but even with a relatively high serotonin
5HT2A-receptorbinding and a low dopamine
D2-receptorbinding the animals developed mouth movements.
No changes in seizure activity were found during electrical
kindling, and it was concluded that risperidone is situated
between clozapine and haloperidol regarding the risk of devel-
opment of tardive dyskinesia.
B.243. T H E R E L A T I O N S H I P BETWEEN
DYSKINETIC MOVEMENTS AND
PRIMITIVE REFLEXES
E. K e n n y ~, L. R a m s a y 2, J. Hillery
1 Department of Psychiatry, St Vincent's University Hospital,
Elm Park, Dublin 4, Ireland
2St Raphael& Celbrtdge, Co Kildare, lreland
Background: Dyskinetic movements have been extensively
researched in schizophrenia, and other psychiatric disorders.
There is some evidence that in certain individuals dyskinetic
movements may be an intrinsic part of the schizophrenic
disorder rather than simply a side effect of neuroleptic medica-
tion. If this were the case, vulnerability markers to tardive
dyskinesia would be helpful in monitoring those at risk. In this
study we evaluate the relationship between dyskinesia and
primitive reflexes in a population of individuals with moderate
learning disability.
Methods: A random sample of individuals who were attend-
ing two workshops were assessed, blind to medication status,
using the Abnormal Involuntary Movement Scale (AIMS).
Primitive reflexes were evaluated using a subsection from the
Condensed Neurological Evaluation Scale (CNE). The case
notes were then examined to establish diagnoses and medica-
tion status.
Results: Thirty-two individuals, (24 males and 8 females)
with a mean age of 38.5 years, sd= 11.4 were included in the
study. The average AIMS score was 4.3, sd=5.2. It was non-
significantly higher in those on neuroleptic medication (6.4 vs
3.7). In the total sample the rate of dyskinesia was 34%. The
rate of dyskinesia in the neuroleptic naive group was similar,
(32%). Primitive reflexes were significantly associated with
dyskinesia, (72% vs 33%, p =0.01 ).
Conclusion: The role of primitive reflexes as a possible
vulnerability marker to the development of tardive dyskinesia
merits further evaluation.
A. Is Movement Disorder Disease Related?
B.244. C H A N G E S I N N E G A T I V E S Y M P T O M S
AND THE RISK OF TARDIVE DYSKINESIA:
A LONGITUDINAL STUDY
J. van Os, E. Walsh, E. van H o r n , T. Tattan, R. Bale,
a n d S.G. T h o m p s o n on b e h a l f o f the U K 7 0 0 G r o u p
Dept. of Psychiatry and Neuropsychology, Maastricht
University, European Graduate Schools of Neuroscience, PO
Box 616, 6200 MD Maastricht, The Netherlands
Background It has been reported that the development of
tardive dyskinesia (TD) is accompanied by a parallel process
of worsening negative symptoms, suggesting an underlying,
illness-related cause. We examined this issue in a longitidunal
study.
Method A sample of 708 psychotic patients were followed
over a period of two years, using the Abnormal Involuntary
Movement Scale and the Scale for the Assessment of Negative
symptoms.
Results. Of 361 individuals with no prior evidence of dyskine-
sia, 46 (13%) developed TD by year 2. Independent of the