Chronological Positron Emission Tomographic Study of Severe Diffuse Brain Injury in the Chronic Stage

Yamaki, Takashi; Yoshino, Eiji; Fujimoto, Masahito; Ohmori, Yasuhiro; Imahori, Yoshio; Ueda, Satoshi

doi:10.1097/00005373-199601000-00010

Cited by 26 publications

(10 citation statements)

References 14 publications

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“…All participants were between the ages of 18 and 55, had normal or corrected-to-normal vision, were right handed, and were native speakers of English. The people with TBI were 1-3 years post-injury to ensure sampling of people in the chronic phase (Yamaki, Yoshino, Fujimoto, Ohmori, Imahori, & Ueda, 1996), and they had a definitive diagnosis of TBI as defined by the TBI Model Systems National…”

Section: Methods 221 Participantsmentioning

confidence: 99%

Hemispheric and executive influences on low-level language processing after traumatic brain injury

Russell

Arenth

Scanlon³

et al. 2012

Brain Injury

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Section: Methods 221 Participantsmentioning

confidence: 99%

Hemispheric and executive influences on low-level language processing after traumatic brain injury

Russell

Arenth

Scanlon³

et al. 2012

Brain Injury

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“…Cross-sectional studies using 18 F-FDG PET in humans at various times after severe traumatic brain injury (TBI) suggest a triphasic pattern of perturbations in metabolic brain function (1)(2)(3). Acutely after TBI, an elevated metabolic state occurs.…”

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confidence: 99%

Progressive Metabolic and Structural Cerebral Perturbations After Traumatic Brain Injury: An In Vivo Imaging Study in the Rat

Liu¹,

Cardamone²,

Hogan³

et al. 2010

J Nucl Med

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Traumatic brain injury (TBI) has a high incidence of long-term neurologic and neuropsychiatric morbidity. Metabolic and structural changes in rat brains were assessed after TBI using serial 18 F-FDG PET and 3-dimensional MRI in vivo. Methods: Rats underwent lateral fluid percussion injury (FPI; n 5 16) or a sham procedure (n 5 11). PET and MR images were acquired at 1 wk and at 1, 3, and 6 mo after injury. Morphologic changes were assessed using MRI-based regions of interest, and hippocampal shape changes were assessed with large-deformation highdimensional mapping. Metabolic changes were assessed using region-of-interest analysis and statistical parametric mapping with the flexible factorial analysis. Anxiety-like behavior and learning were assessed at 1, 3, and 6 mo after injury. Results: PET analyses showed widespread hypometabolism in injured rats, in particular involving the ipsilateral cortex, hippocampus, and amygdalae, present at 1 wk after FPI, most prominent at 1 mo, and then decreasing. Compared with the sham group, rats in the FPI group had decreased structural volume which progressively increased over 3-6 mo, occurring in the ipsilateral cortex, hippocampus, and ventricles after FPI (P , 0.05). Largedeformation high-dimensional mapping showed evolving hippocampal shape changes across the 6 mo after FPI. Injured rats displayed increased anxiety-like behavior (P , 0.05), but there were no direct correlations between the severity of the behavior abnormalities and functional or structural imaging changes. Conclusion: In selected brain structures, FPI induces early hypometabolism and delayed progressive atrophic changes that are dynamic and continue to evolve for months. These findings have implications for the understanding of the pathophysiology and evolution of long-term neurologic morbidity following TBI, and indicate an extended window for targeted neuroprotective interventions.

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“…Cerebral metabolic (glucose and oxygen) depression is a common finding after many types of experimental brain injury, including fluid percussion (Dietrich et al, 1994;Ginsberg et al, 1997;Hovda et al, 1991;Jiang et al, 1999Jiang et al, , 2000Moore et al, 2000;Yoshino et al, 1991Yoshino et al, , 1992, as well as after human traumatic brain injury (TBI; Bergsneider et al, 2000;Yamaki et al, 1996). Specifically, after a lateral fluid percussion injury (LFPI) in the rat, the brain exhibits a prolonged decrease in glucose utilization as well as a reduction in the capacity to use oxygen lasting for up to 10 days (Ginsberg et al, 1997;Hovda et al, 1991;Yoshino et al, 1991).…”

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confidence: 99%

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

Zanier

Moore

et al. 2003

J Cereb Blood Flow Metab

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Summary: During the prolonged metabolic depression after traumatic brain injury (TBI), neurons are less able to respond metabolically to peripheral stimulation. Because this decreased responsiveness has been attributed to circuit dysfunction, the present study examined the metabolic, neurochemical, and histologic responses to direct cortical stimulation after lateral fluid percussion injury (LFPI). This study addressed three specific hypotheses: that neurons, if activated after LFPI, will increase their utilization of glucose even during a period of posttraumatic metabolic depression; that this secondary activation results in an increase in the production of lactate and a depletion of extracellular glucose; and that because cells are known to be in a state of energy crisis after traumatic brain injury, additional energy demands resulting from activation can result in their death. The results indicate that stimulating to levels eliciting a vibrissa twitch resulted in an increase in the cerebral metabolic rate for glucose (CMR glc ; mol·100 g ) of 34% to 61% in the sham-operated, 1-hour LFPI, and 7-day LFPI groups.However, in the 1-day LFPI group, stimulation induced a 161% increase in CMR glc and a 35% decrease in metabolic activation volume. Extracellular lactate concentrations during stimulation significantly increased from 23% in the sham-injured group to 55% to 63% in the 1-day and 7-day LFPI groups. Extracellular glucose concentrations during stimulation remained unchanged in the sham-injured and 7-day LFPI groups, but decreased 17% in the 1-day LFPI group. The extent of cortical degeneration around the stimulating electrode in the 1-day LFPI group nearly doubled when compared with controls. These results indicate that at 1 day after LFPI, the cortex can respond to stimulation with an increase in anaerobic glycolysis; however, this metabolic response to levels eliciting a vibrissa response via direct cortical stimulation appears to constitute a secondary injury in the TBI brain.

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Chronological Positron Emission Tomographic Study of Severe Diffuse Brain Injury in the Chronic Stage

Cited by 26 publications

References 14 publications

Hemispheric and executive influences on low-level language processing after traumatic brain injury

Hemispheric and executive influences on low-level language processing after traumatic brain injury

Progressive Metabolic and Structural Cerebral Perturbations After Traumatic Brain Injury: An In Vivo Imaging Study in the Rat

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

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