Assessment of Cortical Plasticity in Schizophrenia by Transcranial Magnetic Stimulation

Abstract

Neural plasticity refers to the capability of the brain to modify its structure and/or function and organization in response to a changing environment. Evidence shows that disruption of neuronal plasticity and altered functional connectivity between distinct brain networks contribute significantly to the pathophysiological mechanisms of schizophrenia. Transcranial magnetic stimulation has emerged as a noninvasive brain stimulation tool that can be utilized to investigate cortical excitability with the aim of probing neural plasticity mechanisms. In particular, in pathological disorders, such as schizophrenia, cortical dysfunction, such as an aberrant excitatory-inhibitory balance in cortical networks, altered cortical connectivity, and impairment of critical period timing are very important to be studied using different TMS paradigms. Studying such neurophysiological characteristics and plastic changes would help in elucidating different aspects of the pathophysiological mechanisms underlying schizophrenia. This review attempts to summarize the findings of available TMS studies with diagnostic and characterization aims, but not with therapeutic purposes, in schizophrenia. Findings provide further evidence of aberrant excitatory-inhibitory balance in cortical networks, mediated by neurotransmitter pathways such as the glutamate and GABA systems. Future studies with combining techniques, for instance, TMS with brain imaging or molecular genetic typing, would shed light on the characteristics and predictors of schizophrenia.

Genetic polymorphism and neuroanatomical changes in schizophrenia

“…There is significant evidence regarding the functional connectivity of neural networks connecting brain regions in patients with schizophrenia. Research conducted with transcranial magnetic stimulation technology has demonstrated that there is a malfunction of cortical networks [ 131 , 132 ] thus leading to severe cognitive dysfunction. The occurrence of these abnormalities is determined, most of the time, by the expression of genetic polymorphisms or mutations [ 133 ].…”