Volumetric and cognitive findings in transient global amnesia: results of the FORGOT cohort

Abstract

AbstractBackgroundTransient global amnesia (TGA) is a sudden onset syndrome of episodic amnesia with unclear pathophysiology. Although expected to last less than 24 hours, different studies described persistent cognitive impairment primarily in memory and executive functions. We aim to analyze the cognitive performance and cortical volume of patients after a TGA as contributing factors to its pathophysiology.MethodCase‐control study of matched TGA subjects (n = 50) and normal controls (NC) (n = 50). All were studied with brain MRI with volumetric T1 sequences (in TGA subjects performed 1.4 months after the episode (SD±3.4)). Voxel‐based morphometry (VBM), region‐based morphometry (RBM) and surface‐based morphometry (SBM) steps were performed using an extension of the software package SPM12. All subjects were evaluated with a modified UDS3 neuropsychological battery. TGA patients were assesed 3 months after the event to avoid confusors. A deficit in each cognitive domain was diagnosed when individuals scored below ‐1.5 SD for normal values for age, sex and education. Anxiety, depression and cognitive complaints were also assessed. For VBM and RBM, a two‐sample independent t‐test was modeled and estimated with TIV, sex, and age as covariates. For SBM, a two‐sample independent t‐test without covariates was modeled and estimated. We applied the FDR method for multiple comparison corrections and defined a p<.05 threshold for statistical significance.ResultAmong 50 patients with TGA, 54% were female. Mean age was 66 (±9). No significant differences were found in VBM analysis. In the RBM test, we observed reduced volume in the left accumbens nucleus (figure 1) and in SBM, reduced cortical thickness on the right temporal pole and ventromedial visual area 2 (figure 2). No differences were found among cognitive performance between TGA and control patients (table 1).ConclusionThe absence of abnormalities in cortical volume and cognitive failure beyond three months of the event affirms the transient nature of the episode and dispells the association with a neurodegenerative disease as a predisposing factor. SBM abnormalities in distant regions may suggest a network disruption beyond the hippocampus.