transient global amnesia
Recently Published Documents


TOTAL DOCUMENTS

950
(FIVE YEARS 155)

H-INDEX

48
(FIVE YEARS 4)

BMC Neurology ◽  
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Eckhard Schlemm ◽  
Tim Magnus ◽  
Leander D. Rimmele ◽  
Justine Münsterberg ◽  
Maxim Bester ◽  
...  

Abstract Background We report the case of a patient with recurrent episodes of disturbed memory suggestive of transient epileptic amnesia, and a focal hippocampal lesion typically associated with transient global amnesia. We argue how careful consideration of clinical, electrophysiological and imaging findings can resolve this apparent contradiction and lead to a diagnosis of early symptomatic post-stroke seizures that links brain structure to function in a new, clinically relevant way. Case presentation A 70-year-old patient was identified in clinical practice in our tertiary care centre and was evaluated clinically as well as by repeated electroencephalography and magnetic resonance imaging. The presenting complaint were recurrent episodes of short-term memory disturbance which manifested as isolated anterograde amnesia on neurocognitive evaluation. EEG and MRI revealed predominantly right frontotemporal spikes and a punctate diffusion-restricted lesion in the left hippocampus, respectively. Both symptoms and EEG changes subsided under anticonvulsant treatment with levetiracetam. Conclusions Our report contributes to the current discussion of clinical challenges in the differential diagnosis of transient memory disturbance. It suggests that focal diffusion-restricted hippocampal lesions, as seen in TGA, might be ischemic and thus highlights the importance of considering post-stroke seizures as a possible cause of transient memory disturbance.


2021 ◽  
Vol 34 (4) ◽  
pp. 319-322
Author(s):  
Jonathan Morena ◽  
Hera A. Kamdar ◽  
Amir Adeli

2021 ◽  
pp. svn-2021-001384
Author(s):  
Michele Romoli ◽  
Lorenzo Muccioli

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi148-vi148
Author(s):  
Shannon Higgins ◽  
Andrew Lassman ◽  
Laura Lennihan ◽  
Joshua Willey ◽  
Tony Wang ◽  
...  

Abstract INTRODUCTION Radiation induced cerebral vasculopathy encompasses a complex and broad range of effects such as ischemia, hemorrhage, vascular malformation, capillary telangiectasias, and large vessel stenosis caused by pathological reorganization of tissue after radiation exposure. Necrosis and inflammation induce damage and demyelinating changes to other vessels over the corresponding areas that may occur months to years after brain irradiation. Here we report an unusual case of hemorrhagic basal ganglia/internal capsule glioblastoma followed by contralateral basal ganglia/internal capsule acute infarct with resulting acute transient global amnesia followed by chronic memory impairment. CASE REPORT A 58-year old man was diagnosed with a hemorrhagic left basal ganglia/internal capsule mass after presenting with severe headaches, agitation, and vomiting. Glioblastoma (IDH wild type by sequencing, MGMT unmethylated) was identified on resection. He underwent radiotherapy and concurrent and adjuvant (12 cycles) temozolomide. Serial surveillance brain MRI scans demonstrated multiple incidental vascular abnormalities including subacute right basal ganglia/internal capsule ischemic infarct, right temporal cavernoma, and right temporal intra-parenchymal hemorrhage approximately 1, 2, and 3 years after diagnosis, respectively. Approximately 4 years after diagnosis, he presented with transient global amnesia and imaging demonstrated right basal ganglia/internal capsule ischemic stroke. DISCUSSION Bilateral basal ganglia/internal capsule damage from stroke has been reported as causing memory impairment (Tatemichi TK et al, Neurology 1992;42:1966-79; PMID 1407580). Here we report memory impairment from unilateral basal ganglia/internal capsule tumor and contralateral infarct following brain radiotherapy as another mechanism of neurocognitive injury. Our case highlights the significance of continuing to surveil for these findings as new neurologic symptoms may mimic tumor progression.


2021 ◽  
Vol 12 ◽  
Author(s):  
Andreas Rogalewski ◽  
Anne Beyer ◽  
Anja Friedrich ◽  
Jorge Plümer ◽  
Frédéric Zuhorn ◽  
...  

Background: Transient global amnesia (TGA) is defined by an acute memory disturbance of unclear etiology for a period of less than 24 h. TGA occurs as a single event in most cases. Prevalence rates of recurrent TGA vary widely from 5.4 to 27.1%. This retrospective study aimed to determine predictors for TGA recurrence.Methods: Cardiovascular risk profile and magnetic resonance imaging (MRI) of 340 hospitalized TGA patients between 2011 and 2020 were retrospectively analyzed. The median follow-up period amounted to 4.5 ± 2.7 years. Comparisons were made between TGA patients with and without subsequent recurrence.Results: TGA patients with subsequent recurrence were significantly younger (recurrent vs. single episode, 63.6 ± 8.6 years vs. 67.3 ± 10.5 years, p = 0.032) and showed a lower degree of cerebral microangiopathy compared to TGA patients without recurrence. The mean latency to recurrence was 3.0 years ± 2.1 years after the first episode. In a subgroup analysis, patients with at least five years of follow-up (N = 160, median follow-up period 7.0 ± 1.4 years) had a recurrence rate of 11.3%. A 24.5% risk of subsequent TGA recurrence in the following five years was determined for TGA patients up to 70 years of age without microangiopathic changes on MRI (Fazekas' score 0).Conclusion: Younger TGA patients without significant microangiopathy do have an increased recurrence risk. In turn, pre-existing cerebrovascular pathology, in the form of chronic hypertension and cerebral microangiopathy, seems to counteract TGA recurrence.


2021 ◽  
pp. svn-2021-001006
Author(s):  
Sang Hum Lee ◽  
Keon-Yeup Kim ◽  
Jeong-Woo Lee ◽  
So-Jeong Park ◽  
Jin-Man Jung

BackgroundThe exact pathophysiological mechanism of transient global amnesia (TGA) is unknown. It is debatable whether TGA is a risk factor for stroke. Therefore, here we investigated the possibility of TGA as a risk factor for stroke in a real-world setting using large-scale nationwide health claims data.MethodsWe used health claims data from the Korean National Health Insurance Service (NHIS). Patients diagnosed with TGA between 2007 and 2013 were selected. We initially extracted patients without TGA who were preferentially matched for age and sex with the patients with TGA at a ratio of 10:1 from the whole dataset. Further, we performed 1:2 propensity score matching analysis to balance the baseline characteristics between the two groups. In the propensity score-matched dataset, we performed multivariable Cox regression analysis to investigate the association between TGA and stroke type, including ischaemic, haemorrhagic and all stroke types.ResultsPatients with TGA (n=14 673) were selected from the NHIS database. After extracting from the whole database (n=140 486) and propensity score matching their data at a 1:2 ratio, a total of 10 448 and 20 442 patients were finally assigned to the TGA and control groups, respectively. The multivariable Cox regression analysis demonstrated that the TGA group had a higher risk of ischaemic stroke and all types of stroke (adjusted HR=1.194; 95% CI: 1.043 to 1.368; and HR=1.197; 95% CI: 1.056 to 1.357, respectively).ConclusionsAnalysis of the nationwide claims database showed that TGA could be an important risk factor for stroke, especially for ischaemic stroke.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Geon Ha Kim ◽  
Bori R. Kim ◽  
Min Young Chun ◽  
Kee Duk Park ◽  
Soo Mee Lim ◽  
...  

AbstractTriple intrinsic brain networks including the salience network (SN), default mode network (DMN), and central executive network (CEN), are known to be important in human cognition. Therefore, investigating those intrinsic brain networks in transient global amnesia (TGA) may offer novel insight useful for the pathophysiology of TGA. Fifty TGA patients underwent the resting state functional magnetic resonance imaging (rsfMRI) within 24 h, at 72 h, and 3 months after TGA onset. Twenty-five age, gender matched controls also underwent rsfMRI. Within 24 h of TGA onset, TGA patients showed greater functional connectivity in the SN and lower functional connectivity in the DMN, while relatively preserved functional connectivity was observed in the CEN. Interestingly, TGA patients continued to show decreased connectivity in the DMN, while no alterations were shown in the SN 72 h after illness onset. Three months after TGA onset, alterations of functional connectivity in the SN or the DMN were normalized. Our findings suggest that TGA is associated with transient greater functional connectivity in the SN and lower connectivity in the DMN.


2021 ◽  
Vol 12 ◽  
Author(s):  
Céline Becquet ◽  
Julien Cogez ◽  
Jacques Dayan ◽  
Pierrick Lebain ◽  
Fausto Viader ◽  
...  

The subjective experience associated to memory processing is the core of the definition of episodic autobiographical memory (EAM). However, while it is widely known that amnesia affects the content of memories, few studies focused on the consequences of an impairment of EAM on the subjective self, also called the I-self. In the present study, we explored the I-self in two puzzling disorders that affect EAM: functional amnesia, which has an impact on autobiographical memory, and transient global amnesia (TGA), which only affects episodic memory. I-self was assessed through an original measure of self-integration in autobiographical narratives, namely the use of general or personal pronouns. Results showed that patients with functional amnesia tended to use general pronouns, whereas patients with TGA preferentially used the first person. The link between I-self and depersonalization-derealisation tendencies was also explored, showing dissociative tendencies in patients with functional amnesia but not in patients with TGA. We discuss these results from a combined neuropsychological and psychopathological perspective, with a view to proposing an explanatory model of the links between self-awareness and the episodic component of autobiographical memory.


Sign in / Sign up

Export Citation Format

Share Document