ArticlesNeuroanatomy of comorbid schizophrenia and learning disability: a controlled study
Introduction
Epidemiological studies consistently show that people with mild learning disability have a higher frequency of mental disorder than the general population.1 The prevalence of mild learning disability in northern Europe is about 0·5%.2 The point prevalence of schizophrenia in these individuals is about 3%3–ie, three times that in the general population. The reasons for this higher frequency are uncertain, but possibilities include that the presence of schizophrenia (whether diagnosed or destined to develop) increases the likelihood of an individual being diagnosed as having learning disability, and that the presence of learning disability increases the likelihood of an individual being diagnosed as having schizophrenia. The former possibility is consistent with the view that cognitive dysfunction, and sometimes motor and social impairment, in childhood may be the initial features of severe schizophrenia.4 The latter possibility implies that the cognitive deficits of some individuals with learning disability convey an increased susceptibility to develop the impairments associated with schizophrenia.5 By way of analogy, people with deafness are more susceptible to the development of paranoid psychoses.6 and the suggested mechanism behind this association is the overload on comprehension imparted by partly understood stimuli.
Knowledge of the biological basis of schizophrenia remains limited, although the view that there are underlying structural brain abnormalities in a large proportion of cases of schizophrenia7 is widely accepted. Evidence of structural brain abnormalities provided by imaging8 and post-mortem studies9, 10 has been assessed alongside data on perinatal events,11 minor physical anomalies,12 and childhood development in individuals destined to develop schizophrenia in adult life.13 These elements have been drawn together to form the basis of the neurodevelopmental hypothesis of schizophrenia.7, 14 If the view that comorbid learning disability and schizophrenia represents schizophrenia in a very severe form is correct, individuals with this disorder would be expected to have particularly profound neurodevelopmental deficits and to show an exaggeration of the findings in individuals with schizophrenia alone.
We investigated this issue in terms of structural imaging, by examining matched groups of patients with comorbid learning disability and schizophrenia, schizophrenia alone, and learning disability alone.5 Initial reports of structural imaging in patients with schizophrenia showed enlarged ventricles and reduced brain substance, and these findings have been widely replicated.15, 16 Such general findings are, of course, not diagnosis-specific,17 but several structures, particularly the amygdala and hippocampus, are affected to a greater extent than would be expected from the overall reductions in brain volume.8 The structural brain changes in schizophrenia may thus be classified as general (ie, reduction of brain volume, ventricular enlargement, cortical sulcal dilatation) and focal (eg, reductions in amygdala or hippocampal size). We postulated that if comorbid learning disability and schizophrenia represents a particularly severe form of schizophrenia of neurodevelopmental origin, the focal changes in schizophrenia (ie, the reduction in amygdalo-hippocampal size), will appear in an exaggerated form, and, in general, the brains of the group with both disorders will resemble those of the schizophrenic group. If, on the other hand, the schizophrenic psychosis in the comorbid group is a result of a tendency of people with learning disability to develop psychotic symptoms, probably as a consequence of overload imposed by partial comprehension, the focal changes in the comorbid group will be less than those of the schizophrenic group, and, in general, the brains of the comorbid group will resemble those of the learning-disabled group. Brain structure in all three groups will differ from that of an appropriately matched control group of normal individuals, but the nature of the difference will vary.
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Patients
We studied patients who took part in a clinical comparison of matched patients with learning disability and schizophrenia, schizophrenia alone, and learning disability alone.5 The patients with both schizophrenia and learning disability had been identified from the database held by the Information and Statistics Division of the Scottish Health Service. We identified from this database 248 individuals with at least one episode of inpatient care in one of two Scottish health districts between
Results
Scans were carried out on 23 patients with learning disability and schizophrenia, 20 learning-disabled patients, 25 schizophrenic patients, and 29 normal controls. The mean ages of the individuals were 48·6 years (SE 1·9), 46·3 years (2·4), 51·1 years (1·7), and 42·8 years (1·8), respectively (normal controls p<0·01). The proportions of male individuals were 57%, 45%, 60%, and 45%, respectively.
Whole brain volume could be measured in all 97 scans. The scan of one patient in the
Discussion
Many studies have examined the brain structure of schizophrenic patients by neuroimaging,8 but studies of patients with learning disability (with or without comorbid psychosis) have been few,24 and the numbers of patients examined have been small.
The main aim of this study was to assess the extent to which the scans of the comorbid group resembled those of the schizophrenic group and of the learning-disabled group in terms of general brain structure (eg, total brain volume and ventricular
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