What do ERPs and ERFs reveal about the effect of antipsychotic treatment on cognition in schizophrenia?
Cognitive dysfunction is considered to be a core feature in schizophrenia. It is believed that antipsychotic drugs, especially atypical ones, could improve cognitive functions in schizophrenia patients. Auditory event-related potentials (ERPs) such as mismatch negativity (MMN) and P300 response are potential candidates for objective investigation of pre-attentional and attention-dependent processing in schizophrenia patients, respectively. Both these responses were found to be altered in schizophrenia. Moreover, neurotransmitters play important role in generation of MMN and P300 components. Therefore, these ERPs are potential candidates for monitoring the cognitive changes caused by neurochemical modulation during antipsychotic treatment in schizophrenia patients. In addition, neurochemical ERP generation mechanisms discovered during drug-challenge studies in healthy subjects could explain these ERP findings in patients. To date, no effect of antipsychotic treatment on MMN was observed, whereas certain antipsychotics (e.g. clozapine) could modulate P300 response. At the same time, adjunctive glutamate-system affecting therapy seems to influence MMN response. The explanation of these phenomena could be a weak relationship between dopaminergic activities and MMN response and a strong connection between glutamate NMDA receptors and MMN generation. As to the P300 component, because of the multiple generators, it is more sensitive to the influences of different neurochemical activities. In the future, the combination of transcranial magnetic stimulation (TMS) and functional magnetic resonance imaging (fMRI) with electroencephalography (EEG) will open new possibilities for understanding the drug-induced changes on the neural substrates of information processing in schizophrenia patients.
Korostenskaja
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Division of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA. milena.korostenskaja@gmail.com
Kähkönen
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S
D014150:Antipsychotic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D003071:Cognition / Q000187:drug effects* / Q000502:physiology; D004298:Dopamine / Q000502:physiology; D004569:Electroencephalography / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects* / Q000502:physiology; D005072:Evoked Potentials, Auditory; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D015225:Magnetoencephalography / Q000379:methods*; D011619:Psychotropic Drugs / Q000494:pharmacology / Q000627:therapeutic use; D012559:Schizophrenia / Q000188:drug therapy* / Q000503:physiopathology; D012565:Schizophrenic Psychology
D014150:Antipsychotic Agents; D011619:Psychotropic Drugs; D018698:Glutamic Acid; D004298:Dopamine