Surface coil spectroscopic imaging: Time and spatial evolution of lactate production following fluid percussion brain injury

Abstract

Detailed temporal and spatial distributions of lactate production are presented for graded fluid-percussion brain injury in the rat. A one-dimensional proton spin-echo spectroscopic imaging (1D SESI) technique, performed with a surface coil, is presented and evaluated. This technique, which represents a practical compromise, provides spatially localized proton nuclear magnetic resonance (NMR) brain spectra from a series of small voxels (less than 0.15 cm3) in less than 10 min, thus enabling both spatial and temporal monitoring of lactate production. These high-resolution lactate maps are correlated with hyperintense regions observed in T2-weighted images taken 10 h after impact, which, in turn, correlate with histology. The data demonstrate that, following severe trauma there is delayed production and propagation of lactate to regions of the brain that are remote from the trauma site. The extent of lactate production depends on the severity of impact. More significantly, the data show that following severe trauma, local lactate concentrations exceed 15 mumol/g, the concentration that has been claimed as the threshold for brain injury. Therefore high lactate levels cannot be ruled out a priori as a possible factor in brain injury following severe head trauma.

Nuclear magnetic resonance characterization of secondary mechanisms following traumatic brain injury

“…Moreover, animals demonstrating significantly different neurological outcomes showed no significant differences in brain lactic acid concentration, suggesting that brain lactate accumulation per se is not related to injury outcome. Subsequent studies have shown that the lactic acid may diffuse from the injured tissue into the noninjured hemisphere (Cohen et al, 1991) and into the cerebrospinal fluid (Inao et al, 1988;Yoshida and Marmarou, 1991), The latter study also demonstrated that lactic acid in cerebrospinal fluid may also derive from systemic sources.…”

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

“…Increases in cerebral lactate after TBI typically begin early (minutes to hours) after injury in adult animal models of both fluid percussion (Cohen et al, 1991;Inao et al, 1988;McIntosh et al, 1987) and CCI (Brooks et al, 2001;Schuhmann et al, 2003). Increased lactate can result from several potential mechanisms, such as post-injury increases in glycolysis (Kawamata et al, 1995;Yoshino et al, 1991) and reduced oxidative metabolism, with oxidative injury to key metabolic enzymes (Bogaert et al, 2000;Kochanek et al, 2006;Martin et al, 2005;Opii et al, 2007;Richards et al, 2006;Robertson et al, 2007).…”

Stability of Brain Intracellular Lactate and 3P-Metabolite Levels at Reduced Intracellular pH during Prolonged Hypercapnia in Rats

“…Additional studies were conducted to verify that the inverted lH signal at 1.32 ppm was from lactate in brain. First, one-dimensional spectroscopic imaging experi-ments were performed with the same surface coil using a pulse sequence recently described by our group (Cohen et al, 1989). The spectroscopic imaging sequence permitted concomitant acquisition of signals from a series of slices, 1 mm thick, through the head.…”