Cortical excitability in neuroleptic-naive first-episode schizophrenic patients
| Autor: | Göran Hajak, Harald Binder, Peter Eichhammer, Berthold Langguth, Alexander Kharraz, Rainer Wiegand |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Adult
Male Psychosis Time Factors medicine.medical_treatment Central nervous system Neural Conduction Differential Threshold Magnetics medicine Humans Biological Psychiatry First episode Muscles Motor Cortex Dose-Response Relationship Radiation Neural Inhibition medicine.disease Evoked Potentials Motor Electric Stimulation Functional imaging Transcranial magnetic stimulation Psychiatry and Mental health Electrophysiology medicine.anatomical_structure Schizophrenia Case-Control Studies Female Psychology Neuroscience Motor cortex |
| Zdroj: | Schizophrenia research. 67(2-3) |
| ISSN: | 0920-9964 |
| Popis: | Transcranial magnetic stimulation (TMS) provides an intriguing in vivo method to investigate motor cortex excitability in men. This offers new insights into the neurophysiological basis of neuropsychiatric diseases. Earlier TMS studies in patients with schizophrenia revealed inconsistent results, probably due to major confounding variables like state of medication and stage of illness. To control for these effects, we studied two TMS paradigms in 21 drug-naive first-episode schizophrenic patients and 21 age- and sex-matched healthy controls. The patient group demonstrated a significant lower resting motor threshold as compared with healthy controls, whereas TMS paradigms of intracortical inhibition and intracortical facilitation failed to show significant differences between patients and controls. This pattern of TMS parameters is similar to that obtained in healthy volunteers investigated under increasing doses of ketamine, a central acting drug known to produce psychosis-like effects. In agreement with recent results of functional imaging, our neurophysiological findings suggest that drug-induced and naturally occurring psychosis may share a common pathway, which may base on dysfunctional glutamatergic mechanisms. |
| Databáze: | OpenAIRE |
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