Postmortem structural studies of the thalamus in schizophrenia

Abstract

In this review, we seek to answer the following question: Do findings in the current literature support the idea that thalamo-cortical dysfunction in schizophrenia is due to structural abnormalities in the thalamus? We base our review on the existing literature of design-unbiased stereological studies of the postmortem thalamus from subjects with schizophrenia. Thus, all reported results are based upon the use of unbiased principles of sampling to determine volume and/or total cell numbers of thalamus or its constituent nuclei. We found 28 such papers covering 26 studies. In a series of tables we list all positive and negative findings from the total thalamus, the mediodorsal, pulvinar and anterior nuclei, as well as less frequently studied thalamic regions. Only four studies examined the entire thalamus and the results were inconsistent. We found largely consistent evidence for structural changes (reduced volume and cell numbers) in the pulvinar located in the posterior thalamus. In contrast, findings in the mediodorsal thalamic nucleus are inconsistent, with the largest and most recent studies generally failing to support earlier reports of a lower number of neurons in schizophrenia. Thus, the current findings of stereological studies of the thalamus in schizophrenia support the idea that thalamo-cortical dysfunction in schizophrenia might be attributable, at least in part, to structural alterations in the pulvinar that could impair thalamic inputs to higher order cortical association areas in the frontal and parietal lobes. However, more studies are needed before robust conclusions can be drawn.

The medial pulvinar: function, origin and association with neurodevelopmental disorders

“…; Kemether et al. ; for review Dorph‐Petersen & Lewis, ). Postmortem quantification of neurones in PM reveals decreased density in SCZ patients, which in the absence of signs of neurodegeneration and scarring has been attributed to disrupted neurogenesis (Byne et al.…”

A Meta-analysis of Retinal Cytoarchitectural Abnormalities in Schizophrenia and Bipolar Disorder

“…to note that the thalamus, through its higher order nuclei, is a major relay center with connections to the cerebral cortex, striatum, and cerebellum, which modulate a number of cognitive domains. 37 The thalamus is also one of the brain regions that is most affected in SZ and BD as evidenced by alterations in neuronal number, volume, neurochemistry, functional activation, and structural connectivity. [37][38][39] Thus, axonal damage caused by aberrations in the microvasculature or in inflammatory and oxidative stress pathways may result in RTSD that can be examined through the eye, but no studies to date have tested this hypothesis in SZ or BD.…”

“…33 It is possible that thinning of the GCL-IPL may be related to neuronal loss and/or synaptic pruning, which are prominent pathophysiologic hypotheses in SZ, though further systematic studies are needed. 37,45…”

Partial‐volume modeling reveals reduced gray matter in specific thalamic nuclei early in the time course of psychosis and chronic schizophrenia

“…Postmortem studies of these nuclei have reported smaller volume and lower number of neurons and/or oligodendrocytes in SCHZ patients as compared with healthy individuals (Byne et al, 2009; Dorph‐Petersen & Lewis, 2017). However, there is a large discrepancy in findings across postmortem studies (Dorph‐Petersen & Lewis, 2017).…”