Fornix and Hippocampal Atrophy in Traumatic Brain Injury

Tate, David F.; Bigler, Erin D.

doi:10.1101/lm.33000

Cited by 166 publications

(96 citation statements)

References 26 publications

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“…Further, longitudinal results indicate that both of these effects emerge relatively early after injury, with hypersynchrony progressing from a uni-to a bilateral phenomenon. These findings fit with previous literature documenting structural hippocampal anomalies 77,78 and episodic memory impairment 79-81 after brain trauma. Critically, our results show that the connectivity profiles of the hippocampi do not seem to ''recover'' with greater time postinjury.…”

Section: Development Of Hippocampal Connectivity Alterationssupporting

confidence: 82%

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Venkatesan

Dennis

Hillary

2015

Journal of Neurotrauma

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Whereas traumatic brain injury (TBI) results in widespread disruption of neural networks, changes in regional resting-state functional connectivity patterns after insult remain unclear. Specifically, little is known about the chronology of emergent connectivity alterations and whether they persist after a critical recovery window. We used resting-state functional magnetic resonance imaging and seed-voxel correlational analyses in both cross-sectional and longitudinal designs to probe intrinsic connectivity patterns involving the posterior cingulate cortex (PCC) and hippocampi, regions shown to be important in the default mode network (DMN) and vulnerable to neuropathology. A total of 22 participants in the chronic stage of moderateto-severe TBI and 18 healthy controls were included for cross-sectional study. Longitudinal analyses included 13 individuals in the TBI group for whom data approximately 3 months after injury (subacute) were available. Overall, results indicated dissociable connectivity trajectories of the PCC and hippocampi during recovery from TBI, with PCC alterations characterized by early hypersynchrony with the anterior DMN that is gradually reduced, and hippocampal changes marked by increasing synchrony with proximal cortex and subcortex. The PCC also showed increasing antiphase synchrony with posterior attentional regions, and the hippocampi showed decreasing antiphase synchrony with frontal attentional regions. Antiphase synchrony of the hippocampus and dorsolateral prefrontal cortex at the subacute stage of TBI was positively associated with attentional performance on neuropsychological tests at both the subacute and chronic stages. Our findings highlight the heterogeneity of regional whole-brain connectivity changes after TBI, and suggest that residual connectivity alterations exist in the clinically stable phase of TBI. Parallels between the chronicity of the observed effects and findings in neurodegenerative disease are discussed in the context of potential long-term outcomes of TBI.

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Section: Development Of Hippocampal Connectivity Alterationssupporting

confidence: 82%

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Venkatesan

Dennis

Hillary

2015

Journal of Neurotrauma

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“…Blumbergs et al (1995) in a follow-up study demonstrated that the microscopic pathology was on a continuum from mild (GCS of 13-15) to severe (GCS of 3-8), again demonstrating the susceptibility of the fornix. As shown by Viano et al (2005b), the fornix is distinctly vulnerable to the stress0strain effects of concussion and is a common area of damage in moderate-to-severe TBI, as visualized using MRI (Gale et al, 1995;Tate & Bigler, 2000;Tomaiuolo et al, 2004), where the degree of atrophy is related to severity of injury Tate & Bigler, 2000;Tomaiuolo et al, 2004;Wilde et al, 2006b). Because the fornix is a white matter structure containing projecting axons from the hippocampus, disruption in fornix integrity likely relates to the concussive effects of disrupted short-term memory, at least transiently.…”

Section: Is Brain Injury On a Continuum: Concussion R Severe Tbi?mentioning

confidence: 99%

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Bigler

2007

J Int Neuropsychol Soc

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359

248

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On the mild end of the acquired brain injury spectrum, the terms concussion and mild traumatic brain injury (mTBI) have been used interchangeably, where persistent post-concussive syndrome (PPCS) has been a label given when symptoms persist for more than three months post-concussion. Whereas a brief history of concussion research is overviewed, the focus of this review is on the current status of PPCS as a clinical entity from the perspective of recent advances in the biomechanical modeling of concussion in human and animal studies, particularly directed at a better understanding of the neuropathology associated with concussion. These studies implicate common regions of injury, including the upper brainstem, base of the frontal lobe, hypothalamic-pituitary axis, medial temporal lobe, fornix, and corpus callosum. Limitations of current neuropsychological techniques for the clinical assessment of memory and executive function are explored and recommendations for improved research designs offered, that may enhance the study of long-term neuropsychological sequelae of concussion. (JINS, 2008, 14, 1-22.)

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“…Volumetric magnetic resonance imaging (MRI) studies of chronic TBI (Sidaros et al, 2009;Trivedi et al, 2007;Levin et al, 2000;Tate and Bigler, 2000;Verger et al, 2001;Yount et al, 2002) have reported that global and regional brain atrophy occurs over a period ranging from months to years after the injury. This atrophy seems to be dependent on the extent of the initial injury, can involve important structures such as the hippocampus, and correlates with deficits in long-term cognitive performance (Wilde et al, 2005;Levine et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Early Nonischemic Oxidative Metabolic Dysfunction Leads to Chronic Brain Atrophy in Traumatic Brain Injury

McArthur

Alger

et al. 2009

J Cereb Blood Flow Metab

101

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Chronic brain atrophy after traumatic brain injury (TBI) is a well-known phenomenon, the causes of which are unknown. Early nonischemic reduction in oxidative metabolism is regionally associated with chronic brain atrophy after TBI. A total of 32 patients with moderate-to-severe TBI prospectively underwent positron emission tomography (PET) and volumetric magnetic resonance imaging (MRI) within the first week and at 6 months after injury. Regional lobar assessments comprised oxidative metabolism and glucose metabolism. Acute MRI showed a preponderance of hemorrhagic lesions with few irreversible ischemic lesions. Global and regional chronic brain atrophy occurred in all patients by 6 months, with the temporal and frontal lobes exhibiting the most atrophy compared with the occipital lobe. Global and regional reduction in cerebral metabolic rate of oxygen (CMRO 2 ), cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of glucose were observed. The extent of metabolic dysfunction was correlated with the total hemorrhage burden on initial MRI (r = 0.62, P = 0.01). The extent of regional brain atrophy correlated best with CMRO 2 and CBF. Lobar values of OEF were not in the ischemic range and did not correlate with chronic brain atrophy. Chronic brain atrophy is regionally specific and associated with regional reductions in oxidative brain metabolism in the absence of irreversible ischemia.

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Fornix and Hippocampal Atrophy in Traumatic Brain Injury

Cited by 166 publications

References 26 publications

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Early Nonischemic Oxidative Metabolic Dysfunction Leads to Chronic Brain Atrophy in Traumatic Brain Injury

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