Inhibition of the cortex using transcranial magnetic stimulation in psychiatric populations: current and future directions.
Several lines of evidence suggest that deficits in γ-aminobutyric acid (GABA) inhibitory neurotransmission are implicated in the pathophysiology of schizophrenia, bipolar disorder, major depressive disorder and obsessive-compulsive disorder. Cortical inhibition refers to a neurophysiological process, whereby GABA inhibitory interneurons selectively attenuate pyramidal neurons. Transcranial magnetic stimulation (TMS) represents a noninvasive technique to measure cortical inhibition, excitability and plasticity in the cortex. These measures were traditionally specific to the motor cortex, which is an important limitation when nonmotor neurophysiological processes are of primary interest. Recently, TMS has been combined with electro encephalography (EEG) to derive such measurements directly from the cortex. This review focuses on neurophysiological studies related to inhibitory and excitatory TMS paradigms, linking dysfunctional GABAergic neurotransmission to disease states. We review evidence that suggests cortical inhibition deficits among psychiatric populations and demonstrate how each disorder has a specific neurophysiological response to treatment. We conclude by discussing the future directions of TMS combined with EEG, demonstrating the potential to identify biological markers of neuropsychiatric disorders.
The Centre for Addiction and Mental Health, University of Toronto, Toronto, Ont.
Natasha
N
Radhu
Lakshmi N
LN
Ravindran
Andrea J
AJ
Levinson
Zafiris J
ZJ
Daskalakis
D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology*; D005544:Forecasting / Q000379:methods; D006801:Humans; D001523:Mental Disorders / Q000378:metabolism / Q000503:physiopathology*; D009415:Nerve Net / Q000378:metabolism / Q000503:physiopathology*; D009433:Neural Inhibition / Q000502:physiology*; D050781:Transcranial Magnetic Stimulation / Q000379:methods* / Q000639:trends*