Biomedical subjects
Publications and source records attributed to M A Reveley.
The rationale and limitations of discriminating between cases of schizophrenia with and without a family history are reviewed. It is concluded from the evidence available that, by identifying subgroups of greater aetiological homogeneity, the strategy can be a useful starting point for research into likely causes.
Computer-assisted methods of CT brain scan analysis offer considerable advantages over visual inspection, particularly in research; and several semi-automated methods are currently available. A new computer-assisted program is presented which provides fully automated processing of CT brain scans, depending on "anatomical knowledge" of where cerebrospinal fluid (CSF)-containing spaces are likely to lie. After identifying these regions of interest quantitative estimates are then provided of CSF content in each slice in cisterns, ventricles, Sylvian fissure and interhemispheric fissure. Separate measures are also provided of mean brain density in each slice. These estimates can be summated to provide total ventricular and total brain volumes. The program shows a high correlation with measures derived from mechanical planimetry and visual grading procedures, also when tested against a phantom brain of known ventricular volume. The advantages and limitations of the present program are discussed.
Ninety-one schizophrenics (mean age 34 years) were examined for tardive dyskinesia (TD) during chronic neuroleptic treatment. Dyskinesia was found in 23 (25.3%). The only variable that showed an association with TD was the current doses of neuroleptics: in none of the TD patients did the dose of fluphenazine decanoate (or equivalent) exceed 45 mg/week, whereas it was higher in 23 of the 68 without TD (p less than 0.01). When these 23 "high-dose" patients were disregarded, the TD group differed significantly from the 45 dose-matched non-TD subjects in that it had more common anticholinergic drugs, more common parkinsonian symptoms, and less instances of good remission (p less than 0.05 in each case). There was no association between TD and other considered variables (drug history, age, sex, clinical characteristics, size of the lateral brain ventricles, neurological "soft" signs, cognitive impairment). The results illustrate a relationship between TD prevalence and current doses of neuroleptics and indicate that differences in doses between the groups with and without TD may obscure associations between dyskinesia and other factors.
Seventy-seven patients with diagnosis of schizophrenia (62) or schizoaffective disorder (15) were studied 2-20 years since onset of illness, when in a stable condition. The investigation included clinical assessment, measurement of plasma concentrations of neuroleptics and prolactin, computed tomography brain scan, neuropsychological and neurological examination. Outcome of illness was classified according to the presence of chronic psychiatric symptoms and social impairment, and response to neuroleptics according to the effect of treatment in the most recent psychotic episode. Neither outcome nor response to neuroleptics was related to duration of illness. The groups with good and poor outcome differed in premorbid adjustment, age at onset and symptoms of the initial episode, but not in drug bio-availability or prolactin response. Large cerebral ventricles and cognitive impairment, but not neurological 'soft' signs, were associated with unfavourable outcome. The three measures of organicity were not inter-related. No clinical differences were found between chronic patients with and without signs of organic dysfunction. The findings suggest that schizophrenia with good and unfavourable outcome may be separate sub-types. However, the role of organic factors in the latter group remains unclear.
Computer tomography brain scans were carried out on 40 patients with schizophrenia or schizo-affective disorder of 2-20 years duration. Ventricular-brain ratio (VBR) was significantly greater than that of the control group. In six patients the VBR exceeded the control mean + 2 s.d. Among the 13 whose VBR was more than 1 s.d. above the control mean, none had schizo-affective disorder, all but one had chronic illness, and patients with negative symptoms and those with premorbid schizoid traits were over-represented. VBR was unrelated to medical history, age, duration of illness, or neuroleptic treatment. It was not associated with neurological 'soft' signs or cognitive deficit. Among chronic patients, clinical features showed no association with ventricular size. The findings suggest that large ventricles may be related to a sub-type of chronic schizophrenia rather than to its particular clinical features.
Cerebrospinal fluid (CSF) from 20 chronically hospitalised male schizophrenics and from 12 patients admitted with acute schizophrenia were examined for antibodies against cytomegalovirus. A sensitive and specific enzyme-immunoassay was used to detect IgG or IgM classes of antibodies in the CSF of the schizophrenic patients and of ten orthopaedic patients, who served as controls. No significant amounts of IgM antibody were found in the CSF of either group. A significant titre of IgG was found in only one of the 32 schizophrenics, an acute patient, but in four of the orthopaedic patients. The results do not support an association of cytomegalovirus infection with schizophrenia; if such an association occurs, it must be unusual.
There has been a considerable range in both the prevalence of ventricular enlargement and values for ventricular size of both schizophrenics and controls, in studies using computerised tomography (CT). The CT scans of 19 unrelated chronic schizophrenics, all of monozygotic (MZ) twin birth, and 36 age-and-sex-matched normal twins from 18 MZ pairs were examined by linear, planimetric, and semi-automated computerised methods. All methods distinguished schizophrenics from controls at approximately the same level of significance, but partial volume artefact led to a greater than two-fold variation in apparent ventricular size, and significantly reduced the validity and reliability of mechanical planimetric and linear measures. Measurement error may be an important source of artefact in uncontrolled studies using those techniques, and when comparing absolute values across studies, but the use of computerised methods should significantly reduce this source of artefact and allow more meaningful comparison.
21 pairs of monozygotic twins discordant for alcoholism and heavy drinking were examined by computerised tomography. Brain and ventricular volumes were calculated by the use of a semiautomated method with the rater blind to twinship and drinking history. 11 severely dependent alcoholics had larger ventricular volumes and ventricle/brain ratios than did their normal cotwins. These changes correlated best with the length of time the alcoholic twin had been drinking eight centilitres pure alcohol, equivalent to a bottle of wine, a day.
Cerebral ventricular volume, assessed by computed tomography, is a genetically determined trait. In a series of 18 monozygotic and 18 dizygotic twins, heritability values ranged from 82% to 85% depending on the method of calculation.
In a group of schizophrenics of twin birth, no evidence of ventricular enlargement was found where there was a family history of major psychiatric disorder. Among those schizophrenics without such a family history, cerebral ventricular size was significantly increased (P less than 0.01), and there was also evidence of birth complications. Among normal control twins, those who reported complicated births had significantly larger ventricles.
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Three patients with hydrocephalus and aqueduct stenosis are described, who also have schizophrenia defined according to strict diagnostic criteria. There are no previous reports of such an association.
Platelet monoamine oxidase (MAO) activity was compared in four age and sex-matched groups: monozygotic (MZ) twins discordant for schizophrenia, normal MZ twins, normal dizygotic (DZ) twins and unrelated individuals. Among the twin groups, schizophrenic and normal there was a remarkably consistent degree of genetic control amounting to 70-80 per cent of the variation in activity. The mean platelet MAO activity of the schizophrenic twins was significantly lower than that of controls, but not than that of their psychiatrically well, neuroleptic-free cotwins; indeed the correlation for the MZ twins discordant for schizophrenia was almost exactly the same as that for the normal MZs. Thus, lower platelet MAO activity in schizophrenia, where it is found, is genetically modulated and not the result of the illness or its treatment.
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Comparison of the computerised tomographic scans of 11 pairs of healthy monozygotic (MZ) with those of 8 pairs of dizygotic (DZ) twins showed that ventricular size for seven pairs of MZ twins discordant for schizophrenia was not as high as in normal MZ twins. Furthermore, the schizophrenics had significantly larger ventricles than both control twins and their own co-twins, although there was a non-significant trend for their co-twins also to have larger ventricles than the controls. Some common environmental factor, possibly perinatal damage, may have led to the increase in ventricular size in the schizophrenia-discordant pairs, with schizophrenia developing in the more severely affected twin.