Substance abuse and the heterogeneity of schizophrenia a population-based study.
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Adult↗
Biomedical subjects
Brian Kirkpatrick
Publications and source records attributed to Brian Kirkpatrick.
Interstitial cells of the white matter in the dorsolateral prefrontal cortex in deficit and nondeficit schizophrenia.
An increased density of neurons in the white matter of the neocortex has been found in schizophrenia, and the original reports suggested this abnormality was restricted to a subgroup of patients. In a study of the inferior parietal cortex, we found that deficit schizophrenia subjects, but not nondeficit subjects, had an increased density of ICWMs. We extended that finding by comparing the density of microtubule-associated protein 2-immunoreactive ICWMs in deficit schizophrenia (N = 3), nondeficit schizophrenia (N = 4), and control (N = 5) subjects, using postmortem tissue from the dorsolateral prefrontal cortex (Brodmann area 46). The deficit group differed significantly from the other two groups; the respective mean (SD) density values for the deficit, nondeficit, and control groups were 1.27 (.10),.53 (.39), and.76 (.20) cells per 10-6 cubic microns. These group differences provide further evidence that deficit and nondeficit schizophrenia differ in their pathophysiology.
Adult↗
Novel factor-based symptom scores in treatment resistant schizophrenia: implications for clinical trials.
To study the factor structure of symptoms in patients with treatment resistant schizophrenia and whether it is altered by treatment, we analyzed ratings on the Brief Psychiatric Rating Scale (BPRS) from two independent groups of patients with treatment resistant schizophrenia. With confirmatory factor analysis of pre-clozapine BPRS scores in 1074 patients in an administrative data base, the Clozapine Authorization and Monitoring Program (CAMP), we assessed the fit of published factor models and developed a better-fitting model. Model fit was validated in an independent group of 197 research unit participants. Stability of model fit six months post-clozapine was assessed in 834 CAMP patients. A new 4-factor model (negative symptoms, reality distortion, disorganization, and anxiety/depression) had better fit in both data sets than two commonly used factor models, and also fit better post-clozapine. We recommend these four factor scores as clinical trial outcomes in patients with treatment resistant schizophrenia.
Adolescent↗
Glucocorticoid hormones and early brain development in schizophrenia.
While genetic factors play a role in the etiology of schizophrenia, environmental factors contribute to the etiology of the disorder as well. If a woman is exposed during the second trimester of gestation to stressors such as the death of a loved one, influenza infection, or natural and man-made disasters, her baby has an increased risk of developing schizophrenia later in life. A common mechanism may mediate the effects of these diverse risk factors: a stress response during a restricted period of gestation may affect fetal brain development and, given the appropriate genetic predisposition, result in schizophrenia in adult life. Findings in animals exposed to prenatal stress strengthen the hypothesis that exposure to high glucocorticoid levels and/or other components of the stress response increases the risk of schizophrenia. These clinical and preclinical studies could be used to develop hypotheses that could then be tested in patients with schizophrenia.
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Summer birth and deficit schizophrenia: Cantabria, Spain.
An association between deficit schizophrenia and summer birth has previously been reported. The authors attempted to replicate this association in a population-based study of incident cases of psychosis in the autonomous region of Cantabria, in northern Spain. Schizophrenia patients were categorized into deficit (N = 22) and nondeficit (N = 55) groups, and the pattern in the two groups was compared. After accounting for the variance due to disorganization, hallucinations and delusions, and demographic variables, deficit schizophrenia had a significant association with summer birth; this association did not depend on a single definition of summer. For instance, among the deficit patients, 59% were born from May to August, in contrast to 18% of nondeficit patients and 34% of the general population. These results confirm the association between summer birth in the Northern Hemisphere and deficit as opposed to nondeficit schizophrenia. The existence of a different risk factor for the two groups suggests a difference in etiology and pathophysiology.
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Summer birth and deficit schizophrenia in Dumfries and Galloway, southwestern Scotland.
OBJECTIVE: An association between deficit schizophrenia and summer birth has previously been reported. Confirmation of a separate risk factor for this group of patients is potentially important, but the number of subjects with deficit schizophrenia in previous reports has been small. This analysis used data from an epidemiological study of incident cases of psychosis to test the hypothesis that deficit schizophrenia is associated with summer birth. METHOD: Data were drawn from records for the first year of clinical contact for all new patients coming into treatment for psychosis in the region of Dumfries and Galloway, Scotland, from 1979 to 1998. Patients with schizophrenia were classified as having deficit (N=65) or nondeficit (N=277) schizophrenia. Time of birth in the deficit and nondeficit groups was compared, and time of birth in the deficit group was compared with that for all births in Dumfries and Galloway during the study period. RESULTS: The deficit schizophrenia group had an excess of summer births, compared to both the nondeficit schizophrenia group and all births in Dumfries and Galloway. The difference between the deficit and nondeficit schizophrenia groups remained significant after accounting for demographic characteristics and symptoms of disorganization and hallucinations plus delusions. A measure of negative symptoms (as opposed to deficit schizophrenia) was a weaker predictor of summer birth. CONCLUSIONS: This study confirmed an association between deficit schizophrenia and summer birth in the nontropical regions of the Northern Hemisphere. The existence of a risk factor for deficit but not nondeficit schizophrenia is also consistent with other evidence that the pathophysiology of deficit schizophrenia differs from that for other types of the disorder.
Adult↗