Table 3.
A summary of the main findings of the studies investigating the effects of TMS on the glutamatergic system.
| Glutamatergic system | ||||
|---|---|---|---|---|
| Study | Design | Population (n) | Intervention | Result |
| Fregni et al., 2011 | Crossover randomized double-blind placebo-controlled study | Chronic pancreatitis/visceral pain N=17 Sham group: 8 Real group: 9 |
Ten sessions of real or sham rTMS of SII spectroscopy evaluation. |
No significant changes in glutamate and N-acetyl aspartate (NAA) levels for either left or right SII-rTMS in the sham group Significant increases in glutamate and NAA levels in the active group |
|
| ||||
| De Andrade et al., 2013 | Crossover randomized double-blind placebo-controlled study | Healthy volunteers. N=36 |
Active rTMS of the right M1; active rTMS of the right DLPFC/PMC; or sham, after either intravenous saline or ketamine pretreatment | Ketamine significantly decreased the analgesic effects of both M1- and DLPFC/PMC-TMS |
|
| ||||
| Wischnewski et al., 2018 | Clinical study | Healthy volunteers. N=11 |
20 Hz beta tACS to M1, after intake of dextromethorphan (DMO) or placebo. | Motor evoked potential significantly increased after tACS in placebo group compared with baseline. However, this effect was not found in the DMO group. Resting-state beta oscillatory activity increases when compared to baseline in the placebo group, but not in the DMO group |