Under experimental conditions, CSD can be triggered in normal brain tissue by various methods including direct application of KCl/glutamate or mechanical/electrical stimulation ( Olesen and Jørgensen, 1986 Zandt et al., 2013). SD has been observed in the penumbra in patients with metabolically stressed brain tissue ( Mayevsky et al., 1996). Cortical Spreading DepressionĬSD or spreading depolarization (SD) perturbs the homeostasis of neurons and glial cells by increasing the levels of extracellular K +/glutamate and intracellular Ca 2+/Na +/water content, resulting in cell swelling and unresponsive cells ( Dreier, 2011). In this article, mechanisms underpinning a stress-induced locus coeruleus-noradrenaline (LC-NE)-related CSD–TGA model will be explored for the first time, demystifying this perplexing disorder and bridging the gap between clinical presentation and the possible electrophysiological alterations on a holistic perspective. Nevertheless, the relationship between the two has not been systematically delineated so far. These two distinct conditions seem to share many overlapping domains. Research findings on both TGA and CSD have accumulated over the past few decades. It was first proposed as a possible etiology of TGA in 1986 ( Olesen and Jørgensen, 1986).

As another postulated cause of TGA, cortical spreading depression (CSD) has been found to exert a detrimental impact on patients with critical conditions such as traumatic brain injury ( Dreier et al., 2017). But none of these disorders could sufficiently explain the disorder in its entirety. Several etiologies have been proposed, such as migraine, epilepsy, ischemia, venous congestion, and glutamate toxicity ( Romero et al., 2013 Ogawa et al., 2018 Han et al., 2019).

An anterograde memory gap is seldom recovered, but certain retrograde components may be regained ( Eustache et al., 1999). Other features include retrograde amnesia, mainly confined to recent events that happened prior to TGA, and/or vegetative symptoms such as headache or nausea ( Arena and Rabinstein, 2015). Anterograde amnesia manifests as an inability to acquire new information, and patients typically repeat the same question despite being repetitively provided with the answer ( Agosti et al., 2008). The chief complaint of TGA patients is anterograde amnesia, which lasts up to 24 h without focal neurological signs and symptoms ( Romero et al., 2013). Recurrence is relatively low but it may be increased in those with certain prior conditions such as head injury or psychological disorders ( Tynas and Panegyres, 2020). Gender differences in these precipitating incidents vary according to different studies, but men tend to have physical stress, while women are more likely to experience emotional turmoil prior to attacks ( Quinette et al., 2006). A large proportion of TGA cases are preceded by stressful events which may be emotional or physical ( Fisher, 1982). It typically occurs in middle-aged to elderly populations ( Arena and Rabinstein, 2015). Transient global amnesia (TGA) is an episodic memory disorder that affects the hippocampus ( Eustache et al., 1999). Thus, by deeply delving into the anatomic and electrophysiological properties of the CNS, the CSD-TGA model may render insights into the basic pathophysiology behind the façade of the enigmatic clinical presentation. Corresponding evidence regarding hemodynamic and morphological changes from TGA and CSD have been accumulated separately, but the resemblance between the two has not been systematically explored so far, which is surprising especially considering that CSD had been confirmed to cause secondary damage in the human brain. Being a regional phenomenon, CSD seems to affect every aspect of the micro-mechanism in maintaining the homeostasis of the central nervous system (CNS). Cortical spreading depression (CSD) was proposed as a possible cause decades ago. The prevalence of stressful events before a TGA attack makes it hard to overlook these precipitating factors, given that stress has the potential to organically effect the brain. Transient global amnesia (TGA) is a benign memory disorder with etiologies that have been debated for a long time. 2Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.1Department of Neurology, China-Japan Friendship Hospital, Beijing, China.

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