Study factors influencing ventricular enlargement in schizophrenia: A 20year follow-up meta-analysis

Abstract

A meta-analysis was performed on studies employing the ventricular-brain ratio to compare schizophrenic subjects to that of normal controls. This was a follow-up to a similar meta-analysis published in 1992 in which study-, in addition to clinical-, factors were found to contribute significantly to the reported difference between patients with schizophrenia and controls. Seventy-two (N=72) total studies were identified from the peer reviewed literature, 39 from the original meta-analysis, and 33 additional studies published since which met strict criteria for inclusion and analysis– thus representing ~30 years of schizophrenia ventricular enlargement research. Sample characteristics from schizophrenics and controls were coded for use as predictor variables against within sample VBR values as well as for between sample VBR differences. Additionally, a number of factors concerning how the studies were conducted and reported were also coded. Obtained data was subjected to unweighted univariate as well as multiple regression analyses. In particular, results indicated significant differences between schizophrenics and controls in ventricular size but also the influence of the diagnostic criteria used to define schizophrenia on the magnitude of the reported VBR. This suggests that differing factors of the diagnostic criteria may be sensitive to ventricular enlargement and might be worthy of further examination. Interestingly, we observed an inverse relationship between VBR difference and the number of co-authors on the study. This latter finding suggests that larger research groups report smaller VBR differences and may be more conservative or exacting in their research methodology. The diagnostic criteria used for defining schizophrenia were also predictive of between group differences. Analyses weighted by sample size provided identical conclusions. The effects of study factors such as these are helpful for understanding the variation in the size of the reported differences in VBR between patients and controls as well as for understanding the evolution of research on complex clinical syndromes employing neuroimaging morphometrics.

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

“…In both studies, ventricular size returned to baseline with 7 days of recovery. Enlargement of the lateral ventricles, observed in normal aging (Pfefferbaum et al, 1994;Walhovd et al, 2011), and many pathologies including traumatic brain injury (Bigler and Maxwell, 2011), Alzheimer's disease (Fox and Schott, 2004), and schizophrenia (Sayo et al, 2012), is often interpreted as a marker of atrophy (ie, cell loss) of the surrounding brain regions. In the current study, however, measurement of selective brain regions (ie, dorsal and ventral hippocampi, caudate-putamen, thalamus) did not detect volume changes that could explain ventricular expansion.…”

“…Cerebral ventricular enlargement occurs in numerous conditions including normal aging (Pfefferbaum et al, 2006), traumatic brain injury (Bigler and Maxwell, 2011), Alzheimer's disease (Fox and Schott, 2004), and schizophrenia (Sayo et al, 2012). The frequency and consistency of this finding may reflect the ease and reliability of lateral ventricle measurement with ultrasound, computed tomography, and magnetic resonance imaging (MRI).…”

Approaches to neuromodulation for schizophrenia

“…20 Reduction of cortical grey matter may be progressive and lead to ventricular enlargement, and may occur at an accelerated rate in prodromal subjects who subsequently convert to psychosis 50. Hippocampal volume reduction has a larger effect size noted in male patients 22.…”

Rethinking schizophrenia through the lens of evolution: shedding light on the enigma

“…It is well documented that the cerebral cortex has a key role in cognition (Zola-Morgan and Squire 1993, Goel et al 1998, Miller 2000, Muller and Knight 2006, Hickok 2009, Apps et al 2016, Filley and Fields 2016, Lockwood 2016, Millan et al 2016, Ramirez-Cardenas and Viswanathan 2016, Rosenthal and Soto 2016, Eichenbaum 2017) so we would expect a significant structural impairment in the cortex of schizophrenic patients. However, the results obtained are contradictory, inconsistent and controversial (Weinberger and Berman 1998, Harrison 1999, Manoach 2003, Sayo et al 2012, thus allowing us to conclude that schizophrenia is characterized by a lack of a unifying neuropathology , Catts et al 2013, Dorph-Petersen and Lewis 2011, at least as far as the cerebral cortex is concerned.…”