Neuronal Dysfunction in Patients with Closed Head Injury Evaluated by In Vivo 1H Magnetic Resonance Spectroscopy

Choe, Bo-Young; Suh, T; Choi, Kyu-Ho; Shinn, Kyung Sub; Park, Chun-Kun; Kang, Joon-Ki

doi:10.1097/00004424-199508000-00008

Cited by 56 publications

(29 citation statements)

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“…NAA may also act as an osmolyte involved in fluid balance in the brain, thus providing protection to neurons (Taylor et al, 1995). Alterations in NAA observed by 1 H-NMR are well described in clinical studies in adults after TBI (Holshouser et al, 2006;Marino et al, 2007;Choe et al, 1995;Garnett et al, 2000;Ross et al, 1998), and reductions were predictive of impairment in cognitive function (Brooks et al, 2000;Friedman et al, 1999). Pediatric TBI studies have described reductions in the NAA/Cr ratio, but few analyses were performed Ͻ72 h after TBI, with a mean time from injury to spectra acquisition of 4-5 days in infants and 6-9 days in children (Ashwal et al, 2000;Brenner et al, 2003).…”

Section: Discussionmentioning

confidence: 96%

Early and Sustained Alterations in Cerebral Metabolism after Traumatic Brain Injury in Immature Rats

Casey

McKenna

Fiskum

et al. 2008

Journal of Neurotrauma

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Although studies have shown alterations in cerebral metabolism after traumatic brain injury (TBI), clinical data in the developing brain is limited. We hypothesized that post-traumatic metabolic changes occur early (Ͻ24 h) and persist for up to 1 week. Immature rats underwent TBI to the left parietal cortex. Brains were removed at 4 h, 24 h, and 7 days after injury, and separated into ipsilateral (injured) and contralateral (control) hemispheres. Proton nuclear magnetic resonance (NMR) spectra were obtained, and spectra were analyzed for N-acetyl-aspartate (NAA), lactate (Lac), creatine (Cr), choline, and alanine, with metabolite ratios determined (NAA/Cr, Lac/Cr). There were no metabolic differences at any time in sham controls between cerebral hemispheres. At 4 and 24 h, there was an increase in Lac/Cr, reflecting increased glycolysis and/or decreased oxidative metabolism. At 24 h and 7 days, there was a decrease in NAA/Cr, indicating loss of neuronal integrity. The NAA/Lac ratio was decreased (ϳ15-20%) at all times (4 h, 24 h, 7 days) in the injured hemisphere of TBI rats. In conclusion, metabolic derangements begin early (Ͻ24 h) after TBI in the immature rat and are sustained for up to 7 days. Evaluation of early metabolic alterations after TBI could identify novel targets for neuroprotection in the developing brain.

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Section: Discussionmentioning

confidence: 96%

Early and Sustained Alterations in Cerebral Metabolism after Traumatic Brain Injury in Immature Rats

Casey

McKenna

Fiskum

et al. 2008

Journal of Neurotrauma

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“…A decrease in NAA (or NAA to total creatine ratio [NAA/tCr], NAA to choline ratio [NAA/ Cho]) has been observed within the first 24 h of injury (Holshouser et al, 1997(Holshouser et al, , 2000Ross et al, 1998), and can remain depressed as long as 8 days after TBI (Brooks et al, 2000;Condon et al, 1998;Holshouser et al, 2005;Ross and Bluml, 2001). While reports of changes in other cerebral metabolites have been less consistent (Brooks et al, 2000;Cecil et al, 1998;Choe et al, 1995;Friedman et al, 1999;Garnett et al, 2000;Marino et al, 2007;Ross et al, 2001;Shutter et al, 2004;Wild et al, 1999;Yeo et al, 2006;Yoon et al, 2005), a few studies on human TBI have shown that the changes in NAA, lactate (Lac), and choline (Cho) are predictive of neurologic outcome 1-25 days post-injury (Brooks et al, 2000;Friedman, 1998Friedman, , 1999Garnett et al, 2000;Ross et al, 1998;Signoretti et al, 2002). However, none of these clinical studies addressed the very early changes following TBI.…”

Section: Introductionmentioning

confidence: 99%

Early Microstructural and Metabolic Changes following Controlled Cortical Impact Injury in Rat: A Magnetic Resonance Imaging and Spectroscopy Study

Zhuo

Racz

et al. 2011

Journal of Neurotrauma

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Understanding tissue alterations at an early stage following traumatic brain injury (TBI) is critical for injury management and limiting severe consequences from secondary injury. We investigated the early microstructural and metabolic profiles using in vivo diffusion tensor imaging (DTI) and proton magnetic resonance spectroscopy ((1)H MRS) at 2 and 4 h following a controlled cortical impact injury in the rat brain using a 7.0 Tesla animal MRI system and compared profiles to baseline. Significant decrease in mean diffusivity (MD) and increased fractional anisotropy (FA) was found near the impact site (hippocampus and bilateral thalamus; p<0.05) immediately following TBI, suggesting cytotoxic edema. Although the DTI parameters largely normalized on the contralateral side by 4 h, a large inter-individual variation was observed with a trend towards recovery of MD and FA in the ipsilateral hippocampus and a sustained elevation of FA in the ipsilateral thalamus (p<0.05). Significant reduction in metabolite to total creatine ratios of N-acetylaspartate (NAA, p=0.0002), glutamate (p=0.0006), myo-inositol (Ins, p=0.04), phosphocholine and glycerophosphocholine (PCh+GPC, p=0.03), and taurine (Tau, p=0.009) were observed ipsilateral to the injury as early as 2 h, while glutamine concentration increased marginally (p=0.07). These metabolic alterations remained sustained over 4 h after TBI. Significant reductions of Ins (p=0.024) and Tau (p=0.013) and marginal reduction of NAA (p=0.06) were also observed on the contralateral side at 4 h after TBI. Overall our findings suggest significant microstructural and metabolic alterations as early as 2 h following injury. The tendency towards normalization at 4 h from the DTI data and no further metabolic changes at 4 h from MRS suggest an optimal temporal window of about 3 h for interventions that might limit secondary damage to the brain. Results indicate that early assessment of TBI patients using DTI and MRS may provide valuable information on the available treatment window to limit secondary brain damage.

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“…Four phases may be distinguished: an acute phase, which lasts 24 h after TBI; an early subacute phase, from the day 1 to 13; a late subacute phase, from days 14 to 20; and a chronic phase, which starts on day 21 (Weiss et al, 2007). Among these MRS studies, two included patients at the acute phase (Marino et al, 2007;Ross et al, 1998), two from the early subacute phase to the first month (Carpentier et al, 2006;Garnett et al, 2000), one at the late subacute phase up to 11 months (Choe et al, 1995), and four at the chronic phase from 3 weeks to 8 months after TBI (Friedman et al, 1999;Ricci et al, 1997;Sinson et al, 2001;Uzan et al, 2003). In a retrospective study using DTI, comatose patients were excluded if the time delay between trauma and MRI exceeded 7 days to avoid the various changes in anisotropic diffusion related to secondary tissue injury ).…”

Section: Comatose Patients Assessmentmentioning

confidence: 99%

“…To our knowledge, Choe et al (1995) performed the first assessment of patient with closed head injury using in vivo proton MRS to evaluate neuronal and axonal dysfunction. The main result in this case-control study was a significant decrease of NAA/Cr ratio compared with normal controls.…”

Section: Magnetic Resonance Spectroscopymentioning

confidence: 99%

Magnetic resonance spectroscopy and diffusion tensor imaging in coma survivors: promises and pitfalls

Tshibanda

Vanhaudenhuyse

Galanaud

et al. 2009

Progress in Brain Research

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The status of comatose patient is currently established on the basis of the patient-exhibited behaviors. Clinical assessment is subjective and, in 40% of patients, fails to distinguish vegetative state (VS) from minimally conscious states (MCS). The technologic advances of magnetic resonance imaging (MRI) have dramatically improved our understanding of these altered states of consciousness. The role of neuroimaging in coma survivors has increased beyond the simple evaluation of morphological abnormalities. The development of 1H-MR spectroscopy (MRS) and diffusion tensor imaging (DTI) provide opportunity to evaluate processes that cannot be approached by current morphologic MRI sequences. They offer potentially unique insights into the histopathology of VS and MCS. The MRS is a powerful noninvasive imaging technique that enables the in vivo quantification of certain chemical compound or metabolites as N-acetylaspartate (NAA), Choline (Cho), and Creatine (Cr). These biomarkers explore neuronal integrity (NAA), cell membrane turnover (Cho), and cell energetic function (Cr). DTI is an effective and proved quantitative method for evaluating tissue integrity at microscopic level. It provides information about the microstructure and the architecture of tissues, especially the white matter. Various physical parameters can be extracted from this sequence: the fractional anisotropy (FA), a marker of white matter integrity; mean diffusivity (MD); and the apparent diffusion coefficient (ADC) which can differentiate cytotoxic and vasogenic edema. The most prominent findings with MRS and DTI performed in traumatic brain-injured (TBI) patients in subacute phase are the reduction of the NAA/Cr ratio in posterior pons and the decrease of mean infratentorial and supratentorial FA except in posterior pons that enables to predict unfavorable outcome at 1 year from TBI with up to 86% sensitivity and 97% specificity. This review will focus on the interest of comatose patients MRI multimodal assessment with $ Luaba Tshibanda and Audrey Vanhaudenhuyse contributed equally to this work.

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Neuronal Dysfunction in Patients with Closed Head Injury Evaluated by In Vivo 1H Magnetic Resonance Spectroscopy

Cited by 56 publications

References 0 publications

Early and Sustained Alterations in Cerebral Metabolism after Traumatic Brain Injury in Immature Rats

Early and Sustained Alterations in Cerebral Metabolism after Traumatic Brain Injury in Immature Rats

Early Microstructural and Metabolic Changes following Controlled Cortical Impact Injury in Rat: A Magnetic Resonance Imaging and Spectroscopy Study

Magnetic resonance spectroscopy and diffusion tensor imaging in coma survivors: promises and pitfalls

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