Long-term declarative memory deficits in diffuse TBI: Correlations with cortical thickness, white matter integrity and hippocampal volume

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• 作者：Eva M. Palacios^a ; ^b ; Roser Sala-Llonch^a ; ^b ; Carme Junque^a ; ^b ; ^{cjunque@ub.edu} ; Davinia Fernandez-Espejo^c ; Teresa Roig^d ; Jose M. Tormos^d ; Nuria Bargallo^e ; Pere Vendrell^a ; ^b
• 关键词：Traumatic brain injury ; Declarative memory ; Cortical thickness ; Diffusion tensor imaging ; Hippocampus
• 刊名：Cortex
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：49
• 期：3
• 页码：646-657
• 全文大小：1829 K

文摘

We investigated structural brain damage in subjects who had suffered severe and diffuse traumatic brain injury (TBI), and examined its relationship with declarative memory impairment. Cortical thickness, diffusion tensor imaging (DTI), and volumetric and shape data of the hippocampus were assessed in a group of 26 adults with severe TBI in the chronic stage and 22 healthy matched controls. Declarative memory was evaluated by Rey¡¯s Auditory Verbal Learning Test (RAVLT). TBI patients performed significantly worse than controls on all RAVLT measures. The group comparison for cortical thickness and DTI revealed a pattern of widespread atrophy in TBI patients. In the TBI group DTI measures correlated with cortical thickness in the prefrontal and parietal regions, including the precuneus. Declarative memory correlated with both cortical thickness and DTI measures. However, although hippocampal volume was significantly decreased in TBI patients, no correlations were found. Multiple regression analysis of all the structural measures revealed that decreases in Fractional anisotropy (FA) and thinning of the left parietal region were the best predictors of memory impairment. In conclusion, cortical thickness reductions in the left hemisphere and a lack of white matter integrity are the main contributors to long-term impairment in declarative memory among patients suffering from severe and diffuse TBI. In this study the hippocampus did not make a significant contribution to memory dysfunctions, suggesting that damage to this structure is compensated for by other regions, with the definitive sequelae being mainly explained by alterations in cortico-subcortical connectivity.