Pathophysiological insight into transient global amnesia from quantitative electroencephalography

Transient global amnesia (TGA) is recognized as a benign memory disorder, with characteristic clinical and imaging features. However, the pathophysiology of TGA remains elusive. This study aims to elucidate the pathophysiological changes underlying TGA by exploring the brain activities. In total, 215 patients with TGA (age: 61.8 +/- 7.8 years; women: 146) with MRI (within 7 days) and EEG studies (within 90 days) were recruited. Quantitative EEG (QEEG) power spectra and network analysis were performed by the artificial intelligence EEG analysis platform (iSyncBrain (R)). Subgroup analyses were conducted for different clinical groups, based on symptom duration, EEG timing after onset, and cytotoxic lesions on the MRI. Compared with 252 age- and sexmatched subjects (age: 64.5 +/- 8.3 years, women: 182), TGA patients showed a global decrease in absolute power in all band waves, a relative decrease in alpha waves, a relative increase in theta waves, and atypical compensation activity. These QEEG changes were observed regardless of having cytotoxic lesions in MRI and they were significant up to 1 week after symptom onset. Network analysis showed that TGA was more activated than normal controls in alpha1 band-waves, exhibiting a compensatory process. TGA results in prolonged and widespread alterations of brain activity and connectivity. QEEG provide insight into pathophysiology of TGA.

Automated summary

This study aims to investigate the pathophysiological changes underlying transient global amnesia (TGA) by exploring brain activities. The results showed significant changes in EEG power spectra and network analysis in TGA patients. They exhibited a global decrease in absolute power, a decrease in alpha waves, an increase in theta waves, and atypical compensation activity. These changes were observed regardless of symptom duration, EEG timing after onset, and cytotoxic lesions on MRI. In addition, network analysis showed higher activation in TGA compared to normal controls.