Elsevier

Journal of the Neurological Sciences

Volume 368, 15 September 2016, Pages 187-190
Journal of the Neurological Sciences

Transient global amnesia: Only in already disrupted neuronal integrity of memory network?

https://doi.org/10.1016/j.jns.2016.05.035Get rights and content

Highlights

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    Not every signal in the memory network of TGA patient is associated with symptoms.

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    Recurrent transient hippocampal lesions do not affect the neuronal integrity.

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    Transient memory impairment of TGA is related to the disrupted neuronal integrity.

Abstract

Transient global amnesia is a well-described clinical syndrome; however, the pathophysiology is perplexing. Structural imaging indicates that punctuate hippocampal lesions are the representative pathophysiology, although functional neuroimaging studies have reported that the various regions comprising the episodic memory network are involved. We hypothesized that the neuronal integrity of the memory network might correlate with amnesia symptoms when there is any insult that can affect the hippocampus. Diffusion tensor images of 5 patients with variable diffusion-weighted imaging findings with or without transient global amnesia symptoms were analyzed. Diffusion tensor image analyses were performed using DTI studio software. A patient with a typical restricted diffusion involving the right hippocampus, but without memory symptoms, had more abundant cingulum fibers. However, the serial cingulum fibers of patients having experienced multiple attacks did not show a decremental tendency. The volume of fibers in the affected side was lower than that of the opposite side. This report suggests that memory-related symptoms of transient global amnesia are related to the disrupted neuronal integrity of cingulum fibers.

Introduction

Transient global amnesia (TGA) is a well-described clinical syndrome, which is defined by an anterograde and retrograde amnesia of sudden onset that lasts up to 24 h. Despite clear clinical criteria, the pathophysiology is perplexing [1]. Numerous neuroimaging studies based on diffusion weighted imaging (DWI) have indicated that that punctuate hippocampal lesions which mainly include the CA1 field are the representative imaging findings [2], and the detection rate is increasing to up to 88% by using the modified DWI protocol. However, previous functional neuroimaging studies using positron emission tomography (PET), single photon emission computed tomography (SPECT) and resting-state functional magnetic resonance imaging (RSfMRI) have reported that various regions, especially the bilateral hippocampi and connected parts comprising the episodic memory network, are involved in TGA patients [1], [3]. These findings might suggest that transient weakness of the memory network is manifested as TGA.

Based on this evidence, it is suggested that the neuronal integrity of the memory network might correlate with TGA symptoms when there is any lesion affecting the hippocampus and related structures. Our hypothesis was the magnitude of neuronal integrity is related with TGA “symptom”, which is the degree of neuronal integrity would be different in patients with “TGA symptom” and patients without “TGA symptom”, in situation with both of them have focal hippocampal DWI lesions. We further evaluated the inverse theory via a case who had 4 episodes of TGA attack.

Section snippets

Patient 1 (PA1): typical DWI lesions involving the right hippocampus without memory symptoms

A 58-year-old woman visited the hospital due to abrupt dizziness associated with nausea and vomiting. The dizziness lasted 2–3 min and was made worse by a change in position, especially when right side down. Neurological examination did not show spontaneous nystagmus in the primary position; however, Dix-Hallpike test showed torsional and upbeat nystagmus at right side down position. There was no other cranial nerve sign, motor or sensory deficit, or dysmetria on finger to-nose and heel-to-shin

Results

The volumes of bilateral cingulum fibers of each patient are described in Fig. 2. The cingulum fibers of PA1 and PA2 were more abundant and connected to the dorsolateral prefrontal, and medial frontal cortices compared to PA3 and PA4 (Fig. 2-A, B, C, D). However, the serial cingulum fiber tracking of PA5 did not show a decremental tendency or much less amount of cingulum fiber than the other patients (Fig. 2-E1, E2, E3).

PA1, PA2 and PA3 had a more disrupted fiber track in one side where

Discussion

PA1 had vomiting, which is one of the precipitating factors of TGA, and a typical DWI lesion involving the right hippocampus which is usually present with TGA patients. However, she did not have any memory-related symptoms. It is assumed that the hippocampus might play a certain role in generating symptoms of dizziness or giddiness [5]. Another assumption is that the memory network is not affected by the focal lesion. PA2 did not even have any symptom. We considered the main reason is the

Conflict of interest

All authors declare no conflict of interest.

Acknowledgments

This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (HI14C2339).

The authors thank Boram Kim, MD, PhD and Chung-Hwan Kang, RT for their support in the imaging data analysis and acquisition.

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