MRI SPECTROSCOPY  [ back to Neuroimaging ]
MRI Spectroscopy applies the same technology as MRI to molecules other than water and protons other than hydrogen. The primary source of energy that drives the chemical reactions needed to produce metabolic activity in the brain is ATP (adenosine triphosphate), which gives up its phosphorous atoms to combine with oxygen. For example, ATP helps drive the sodium pumps in the semi-permeable walls of brain cells needed to clear excess sodium ions from the cell body after the cell has fired and released its neurotransmitter. Application of a powerful magnetic field to phosphorous protons will increase their rate of spin, change their spin axis and spin direction, and lead to emission of a measurable radiofrequency signal as they give off excess energy and relax their spins. Collection, digitization and rapid computer analysis of this data, leads to production of a 3 dimensional spatio-temporal map of energy release in the brain. This contrasts with PET which measures the consumption of glucose by metabolically active areas of the brain which are functioning in response to a given stimulus. PET also subjects the patient to tiny doses of radioactive isotopes, whereas MRI spectroscopy just uses electro-magnetic energy.

MRI spectroscopy is just coming into its own as a tool for detecting subtle TBI and tracking the healing process by taking serial measurements of various brain chemicals that tell us about the structural integrity of brain tissue. While standard MRI covers the whole brain at one time, MRI spectroscopy can target small areas of the brain. Combining the two techniques yields maximum information. Following any TBI, there is an initial brief period of heightened activity (with hyperglycolisis) followed by a lengthy period of metabolic depression; after which the brain shows gradual return to more normal levels of metabolic activity. Neuro-chemical evaluation of brain status after TBI can help predict where the patient is likely to end up. NAA (N-acetylaspartate) is manufactured in the mitochondria of brain cells with ATP. An abnormally low amount of NAA signals neuronal damage or death, both in stroke patients and TBI patients. Elevated levels of lactate signal excito-toxic damage to brain cells with inflammation. Elevated levels of choline compounds signal break up of cell membranes. Depressed levels of ATP show failing mitochrondria - a bad sign, since mitochondria are the source of the brain cell's energy supply. Measuring the ratios of these neuro-chemicals at increasing time intervals from the TBI can give clinicians a window into condition of the healing brain on a cellular level. See, William Brooks et al. "Magnetic Resonance Spectroscopy in Traumatic Brain Injury" J. Head Trauma Rehabilitation; 2001(2):149-164.