Cerebral aging is a complex and heterogeneous process that is associated with a high degree of inter-individual variability and characterized by a pattern of selective loss and preservation. Magnetic resonance imaging (MRI) makes in vivo characterization of brain alterations occurring with advancing age possible. The use of MRI allows thorough characterization of non-disease-related brain aging and facilitates the study of anatomical alterations that contribute to the cognitive and affective symptoms of late-life psychiatric illnesses. This review will focus on the results of MRI studies of white matter changes that occur with normal aging and the relationship of age-associated changes in white matter to age-related declines in cognitive abilities.

Aging of cerebral white matter: a review of MRI findings.

The functional neuroanatomy of mood disorders.

Proton MR spectroscopy (MRS) studies have found both decreased N-acetylaspartate (NAA) and increased myo-inositol in the occipital, temporal, parietal, and frontal regions of patients with AD, even at the early stages of the disease. This diffuse NAA decline is independent of regional atrophy and probably reflects a decrease in neurocellular viability. Reports of such metabolite changes are now emerging in the mild cognitive impairment prodrome and in investigation of the medial temporal lobe. In vivo quantitation of neural choline in AD has been inconclusive because of poor test-retest repeatability. Less robust evidence using phosphorous MRS has shown significant phosphocreatine decline and increments in the cell membrane phosphomonoesters in the early, and possibly asymptomatic, stages of the disease. These phosphorous metabolite disturbances normalize with disease progression. Phosphodiester concentration has been found to correlate strongly with AD plaque counts. MRS of AD has therefore introduced new pathophysiologic speculations. Studies of automated MRS for AD diagnosis have reported high sensitivity and moderate specificity, but are yet to test prospective samples and should be extended to include at least two MRS regions of interest. MRS has promise for predicting cognitive status and monitoring pharmacologic efficacy, and can assess cortical and subcortical neurochemical change.

Magnetic resonance spectroscopy in AD

BACKGROUND AND PURPOSE: Current imaging does not permit quantification of neural injury after traumatic brain injury (TBI) and therefore limits both the development of new treatments and the appropriate counseling of patients concerning prognosis. We evaluated the utility of magnetization transfer ratio (MTR) and proton MR spectroscopy in identifying patients with neuronal injury after TBI. METHODS: Thirty patients with TBI (21–77 years old; mean age, 42 years; admission Glasgow Coma Scale (GOS) scores 3–15; mean score, 11) were studied on a 1.5-T system with magnetization transfer imaging and MR spectroscopy of the splenium. Magnetization transfer imaging was also performed in the brain stem in all patients, and other areas of the brain were sampled in one patient. The splenium of the corpus callosum and brain stem were studied because these are often affected by diffuse axonal injury. Scans were obtained 2 to 1129 days after injury (median, 41 days). MTR was considered abnormal if it was more than 2 SD below normal. Proton MR spectroscopy was used to calculate the N-acetylaspartate (NAA)/creatine (Cr) ratio. GOS was determined at least 3 months after injury. RESULTS: In 10 patients with a GOS of 1 to 4, the mean NAA/Cr was 1.24 ± 0.28; two of these patients had abnormal MTR in normal-appearing white matter (NAWM). In 20 patients with a GOS of 5, the mean NAA/Cr was 1.53 ± 0.37 (P CONCLUSION: MTR and MR spectroscopy can quantify damage after TBI, and NAA levels may be a sensitive indicator of the neuronal damage that results in a worse clinical outcome.

http://www.ajnr.org/content/ajnr/22/1/143.full.pdf

Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury.

Quantitative localized 1H MR spectroscopy for clinical use

In the elderly, asymptomatic white matter hyperintensities are common on T2-weighted magnetic resonance imaging (MRI). In symptomatic patients, such MRI appearances correlate with varied postmortem findings including demyelination or stroke. What structural correlates underlie the T2 hyperintensities in patients whose lesions are asymptomatic is controversial. Therefore, in order to investigate the underlying metabolism and perfusion in white matter lesions (exhibiting T2 hyperintensity), 13 patients underwent proton magnetic resonance spectroscopy and dynamic gadolinium-DTPA perfusion-weighted MR imaging. N-acetyl aspartate (NA) levels were reduced in the lesions compared with age-matched controls (P = 0.031), implying neuronal/axonal loss. Creatine levels were also reduced (P = 0.001). Choline levels were unchanged in the lesions. Lactate was identified in the lesions of 5 of the 13 patients. Although not statistically significant, perfusion studies exhibited a trend toward lower cerebral blood volumes in patients with high grade extracranial carotid stenosis and lactate-containing lesions. These findings suggest that neuronal/axonal loss underlies the majority of T2-weighted asymptomatic lesions in the older population, and in many cases these changes may be due to chronic ischemia.

T. J. Preziosi

Papers

Proton Magnetic Resonance Spectroscopy and Gadolinium‐DTPA Perfusion Imaging of Asymptomatic MRI White Matter Lesions