Acute metabolic brain changes following traumatic brain injury and their relevance to clinical severity and outcome

Abstract

Background: Conventional MRI can provide critical information for care of patients with traumatic brain injury (TBI), but MRI abnormalities rarely correlate to clinical severity and outcome. Previous magnetic resonance spectroscopy studies have reported clinically relevant brain metabolic changes in patients with TBI. However, these changes were often assessed a few to several days after the trauma, with a consequent variation of the metabolic pattern due to temporal changes. Methods: Proton magnetic resonance spectroscopic imaging ( 1 H-MRSI) examinations were performed in 10 patients with TBI 48-72 h after the trauma, to obtain early measurements of central brain levels of Nacetylaspartate (NAA), choline (Cho), creatine (Cr) and lactate (La). Metabolite values were expressed as ratios to (1) a metabolic pattern, given by the sum of the resonance intensities of all metabolites detected in the same voxel and (2) intravoxel Cr. Results: NAA ratios were found to be significantly lower in patients with TBI than in normal controls. In contrast, Cho ratios were significantly higher in patients with TBI than in normal controls. Increased La levels were found in 5 of 10 patients with TBI. Both NAA and La values correlated closely with those of the Glasgow Coma Scale at presentation (r = 0.73 and 20.62, respectively; p,0.01 for both) and the Glasgow Outcome Scale at 3 months (r = 20.79 and 0.79, respectively; p,0.01 for both). Conclusion: Spectroscopic measures of neuro-axonal damage occurring soon after a brain trauma are clinically relevant. Significant increases in cerebral La level also may be detected when 1 H-MRSI is performed early after the trauma and, at this stage, can represent a reliable index of injury severity and disease outcome in patients with TBI.

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

“…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).…”

“…Regardless of the sources of lactate, increases in this metabolite have been associated with poor neurologic outcome in human TBI studies using 1 H spectroscopy (Marino et al, 2007;Brooks et al, 2001;Ashwal et al, 1997;Holshouser et al, 1997;Ross et al, 1998). Pediatric studies showed that the detection of lactate in the uninjured tissue was strongly correlated with poor neurologic outcome up to several years after injury (Ashwal et al, 2000;Brenner et al, 2003).…”

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

“…The combination of these two techniques may be useful. Other people showed that NAA/Cr and NAA/all metabolites ratios to be significantly lower in the medial cortex of patients with TBI than in normal controls, whereas the La/Cr and La/all metabolites ratios were increased (Marino et al, 2007). Both NAA and La ratios correlated with GOS score.…”

“…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 ).…”

Imaging of Traumatic Brain Injury

“…It shows promise as an imaging technique sensitive to detecting effects of TBI including changes in neural integrity (reduced NAA levels -an amino acid synthesized in mitochondria, that decreases with neuronal and axonal loss or dysfunction), brain energy metabolism (creatine), and membrane integrity/synthesis/repair (choline -primarily consisting of phosphoryl and glycerophosphoryl choline) [44]. To date much of the study of 1H MRS in TBI has been in adolescents [44,45], and in more severe injury populations [46,47]. There have been fewer investigations of 1H MRS in populations with mild and moderate TBI (MTBI) and the results have been less clear cut, in part related to the different methodologies and Figure 2: Surface-rendered projection on a representative atlas brain (SPM99) of areas of activation while performing a working memory task (n back) with variable processing load demands for mild TBI (n =18) and control (n =12) groups.…”