Persistent metabolic sequelae of severe head injury in humansin vivo

Publisher Website
Google Scholar
Abstract
Six patients who had suffered severe non-penetrating high velocity head injuries were investigated with phosphorus (31P) magnetic resonance spectroscopy (MRS) to determine, non-invasively, long-term alteration in intracellular biochemistry. The normal subjects were found to have a constant intracellular pH (pHi, 7.03±0.03) with depth into the brain. The adenosine triphosphate (ATP, 3.46±0.66mmol/L of brain tissue), inorganic phosphate (Pi, 1.15±0.41 mmol/L) and phosphomonester (PME, 2.76±1.0 mmol/L) tissue concentrations did not alter significantly with depth into normal brain. The phosphocreatine (PCr, 2 cm = 5.21±1.25, 5 cm=4.85±1.49 mmol/L) was slightly reduced, whilst phosphodiesters (PDE, 2 cm=9.53 ±2.6, 5 cm=14.41±4.2 mmol/L) rose significantly between tissue comprising mainly of gray (2 cm) and white matter (5 cm). In comparison the contra-lateral hemisphere to the side of worst spasticity showed significant changes a considerable time after injury (6–18 months). The intracellular metabolite tissue concentrations were all reduced by 30% (ATP 2.53±1.0 mmol/L, PCr 3.44±0.8 mmol/L) with PDE reduced most significantly at depth (5 cm=8.4±3.4 mmol/L), compatible with the cerebral atrophy seen in these patients. In white matter the pHi also decreased with depth (2 cm=7.03±0.03, 5 cm=6.89±0.05). The reduction in pHi so long after injury is difficult to explain in these steady-state conditions. A structural abnormality, such as a disorder in the blood brain barrier or accumulation of large acidic lysosomes, could cause these pHi changes. There may also be a failure in blood flow regulation, with near critical fluctuations in blood flow both with time and space.