Abstract
Acute perturbation of the hippocampus, one of the connector hubs in the brain, is a key step in the pathophysiological cascade of transient global amnesia (TGA). We tested the hypothesis that network efficiency, meaning the efficiency of information exchange over a network, is impaired during the acute stage of TGA. Graph theoretical analysis was applied to resting-state EEG data collected from 21 patients with TGA. The EEG data were obtained twice, once during the acute stage (< 24 hours after symptom onset) and once during the resolved stage (> 2 months after symptom onset) of TGA. Characteristic path lengths and clustering coefficients of functional networks constructed using phase-locking values were computed and normalized as a function of the degree in the delta, theta, alpha, beta 1, beta 2 and gamma frequency bands of the EEG. We investigated whether the normalized characteristic path length (nCPL) and normalized clustering coefficients (nCC) differed significantly between the acute and resolved stages of TGA at each frequency band using the Wilcoxon signed-rank test. For networks where the nCPL or nCC differed significantly between the two stages, we also evaluated changes in the connections of the brain networks. During the acute stage of TGA, the nCPL of the theta band networks with mean degrees of 8, 8.5, 9 and 9.5 significantly increased (P < 0.05). During the acute stage, the lost edges for these networks were mostly found between the anterior (frontal and anterior temporal) and posterior (parieto-occipital and posterior temporal) brain regions, whereas newly developed edges were primarily found between the left and right frontotemporal regions. The nCC of the theta band with a mean degree of 5.5 significantly decreased during the acute stage (P < 0.05). Our results indicate that TGA deteriorates the network efficiency of the theta frequency band. This effect might be related to the desynchronization between the anterior and posterior brain areas.
Highlights
Transient global amnesia (TGA) is an interesting syndrome of unknown etiology that is characterized by the abrupt onset of repetitive questioning
Because focal hyperintense diffusion-weighted imaging (DWI) lesions in area CA1 of the hippocampus have been reported during the acute stage of TGA [3], hippocampal CA1 injury and the subsequent perturbation of corticohippocampal circuits have been regarded as key steps in the pathophysiological cascade of TGA [4]
The effect sizes for the normalized characteristic path length (nCPL) and normalized clustering coefficients (nCC) were medium, with Cohen’s d ranging from 0.416 to 0.587 [24]
Summary
Transient global amnesia (TGA) is an interesting syndrome of unknown etiology that is characterized by the abrupt onset of repetitive questioning. Despite the presence of profound amnesia, patients with TGA appear to have intact general cognition during the attack. They remain alert and communicative without focal neurological signs [1], and their memory usually starts to recover after a few hours, returning to normal within a day [2]. Before the documentation of these hippocampal DWI lesions, mesiotemporal hypoperfusion with concomitant involvement of various cortical and subcortical structures had been noted in patients with TGA, suggesting alterations of the hippocampus and corticohippocampal circuits [5]. Corticohippocampal disruption was identified within the episodic memory network during a TGA attack in a resting-state functional MRI study [6]
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