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Conclusion. These data suggest increased FAS in schizophrenia and provide quantitative evidence of developmental instability. Acknowledgements: Supported by the Health Research Board.

I X . F . 4

M I N O R P H Y S I C A L A N O M A L I E S I N

S C H I Z O P H R E N I C P A T I E N T S A N D T H E I R

R E L A T I V E S

*T. Sigmundsson, T. Griffiths, P. Birkitt, T. Sharma, S. Frangou, A. Revely and R. M u r r a y

*The Department of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE58AF, U.K.

Several studies have shown an excess of minor physical anomalies (MPA), in schizophrenic patients and an association with a positive family history has been reported. Data from the Maudsley Family Study was used to examine the relation- ship between MPA and family history. Six groups were com- pared; 33 schizophrenic patients and 67 of their first degree relatives from multiply affected families, 28 schizophrenic patients without a family history of psychosis and 42 of their relatives, 42 normal controls and 20 relatives of patients with affective disorder. The patients met DSM-IIIR criteria for schizophrenia. A modified Waldrop scale (Green et al. 1989) for minor physical anomalies was used by a single rater who was blind to diagnosis and group.

No significant differences in MPA scores were found between the groups using mean MPA score or a cutoff score of 3 or higher. Schizophrenic patients with a negative family history had the highest MPA score and when compared with all subjects without schizophrenia this difference was significant (p<0.05). In this group, 5 of 7 patients with a high MPA score (>3) were male.

These preliminary results suggest that MPA may be associ- ated with nongenetic forms of schizophrenia, particularly in males.

I X . G . O t h e r

I X . G . 1

L O C A T I O N O F T H E H A N D E D N E S S G E N E

O N T H E X A N D Y C H R O M O S O M E S

M.C. Corballis, K. Lee, I.C. M c M a n u s and T.J. Crow

Departments of Psychology, University of Auckland, NZ and University College London; and POWIC, University Department of Psychiatry, Warneford Hospital, Oxford, U.K.

Psychological studies of sex chromosome aneuploidies are consistent with the suggestion (Crow, 1994) that a gene for

cerebral asymmetry is present on X and Y chromosomes. A prediction is that pairs of siblings concordant for handedness would be more likely than chance to be of the same sex although if, as suggested by Annett (1985) and McManus (1985), a substantial random clement is also present the effect would be expected to be small.

We have accumulated an effective sample of 15 106 sibling pairs from 5 handedness surveys with the following findings.

Handedness pairings

R x R R x L L x L

Totals M x M 3258 865 106 M x F 5511 1531 176 F x F 2642 603 63

Same sex/opposite sex 1.070 0.959 0.964

~=0.0215 2(1)=6.81 p<0.01

The overall qb is close to that predicted by sex linkage and the genetic models, and therefore supports complete rather than partial X-Y linkage--that is an homologous gene in the sex- specific rather than in the pseudo-autosomal region of the sex chromosomes. Such a conclusion is consistent with a sex difference such as is seen for handedness and cerebral asymmetry.

References

Annett, M. (1985) Left, Right, Hand and Brain. Lawrence Erlbaum, London.

Crow, T.J. (1994) Cytogenet Cell Genet 67: 393-394. McManus, I.C. (1985) Psychol Med, Monogr Suppl 8: 1-40.

I X . G . 2

A N E W A N D F A M I L I A L V A R I A N T O F

S C H I Z O P H R E N I A ?

G.A. Doody, W.J. Muir , E.C. Johnstone , D.G.C. Owens

University Dept. of Psychiatry, Royal Edinburgh Hospital Morningside Park, Edinburgh, Scotland, EHIO 5HF, U.K.

It is widely believed that the point prevalence of schizophre- nia in individuals with mild learning disability is three times that of the general population. This large Edinburgh study seeks to explore reasons for this observation. Three sex and age matched populations are under study; subjects with a dual diagnosis of mild learning disability and schizophrenia (obtained from a National register), subjects with DSMIII-R schizophrenia and normal premorbid I.Q. (randomly matched from the Lothian Psychiatric Case Register) and subjects with mild learning disability alone. A detailed family history has been obtained in over 85% of cases.

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None of the learning disabled group have schizophrenic relatives. A third of the schizophrenic group have a family history of schizophrenia in first or second degree relatives.

Karyotypic analyses of 20 dual diagnosis probands show chromosomal variants to be common.

Over 60% of the dual diagnosis group have a family history of schizophrenia. 50% of these have a family history of schizo- phrenia alone, and 50% have a family history of dual diagnosis. It is possible that the latter 50% constitute a previously undescribed variant of schizophrenia, the psychosis developing in adulthood, but associated with cognitive impairment present since childhood. This disorder is highly familial with probands originating from multiply affected families.

I X . G . 3

L E A R N I N G D I F F I C U L T I E S I N F A M I L I A L

S C H I Z O P H R E N I A

A.I .M. Glen, E.M.T. Glen, L.E.F. MacDonel l , F.K. Skinner, J. Suther land, P.E. Ward

Highland Psychiatric Research Group, Craig Dunain Hospital, Inverness, U.K.

The co-existence of manic depressive illness in the families of schizophrenic probands is well recognised but the presence of learning difficulties in members of these families has received little attention, possibly because of the absence of a unifying hypothesis. The evidence now accumulating for a lipid abnor- mality in schizophrenia provides an opportunity for such a hypothesis. The subjects of this study so far are 22 families from a wider study in the north of Scotland of familial schizophrenia. At this stage the data are descriptive and cannot be subjected to statistical analysis purposes. 22 families were identified as having schizophrenic probands and at least one first-degree relative with a psychotic illness. At present, 5 of the probands and 4 of the affected relatives show borderline handicap (IQ below 80) or clinical evidence of learning diffi- culties. The evidence from the hypothesis (reviewed by Horrobin et al, 1994) is that levels of fatty acids essential for normal brain development, particularly arachidonic and doco- sahexaenoic, will be abnormal in these subjects.

References

Horrobin et al (1994) Schizophr. Res. 13, 195-207.

I X . G . 4

S Y N D R O M E S T R U C T U R E I N

S C H I Z O P H R E N I A IS I N D E P E N D E N T O F

G E N E T I C P R E D I S P O S I T I O N

J.B. Loftus, N.J. Bass, L.E. DeLisi and T.J. Crow

University Department of Psychiatry, Warneford Hospital, Oxford, OX3 7JX, U.K.

Family, twin and adoption studies have established the genetic contribution to schizophrenia but the influence of genetic factors in determining symptom patterns has been unclear. Studies looking at this problem in terms of the traditional subtypes generally have shown non-significant rela- tionships. A limitation of this approach is that it may impose boundaries where non exist. An alternative is to look at the concordance of subsyndromes in sib-pairs collected in the course of a linkage study. This study compares the frequency of subsyndromes using a modified Krawiecki rating scale based on all available case notes and interview information. Expected numbers were calculated using the binomial theorem.

No significant deviations from a random assortment were observed (see table) although the deviation for disorganisation approached significance. The main finding is contrary to what one would expect if genetic factors determined syndrome structure in schizophrenia. These results suggest that symptom patterns within schizophrenia are independent of the genetic contribution. The findings are compatible with the operation of a single genetic influence that interacts with independent personality dimensions to generate the manifestations of this disorder.

Subsyndromes Total sib-pairs = 53

concordant +ve concordant - v e discordant x p

Expected Observed Expected Observed Expected Observed

Positive 47.98 49 0.12 0 4.90 3 0.88 Negative 23.11 22 6.11 7 23.11 22 0.18 Affective 29.44 30 3.44 4 20.12 19 0.16 Disorganised 34.89 37 1.9 4 16.24 12 3.56

0.7 0.95 0.95 0.2