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Category: Viruses and Viral Pathogenesis
Magnetic Resonance Spectroscopy in HIV-Associated Brain Injury, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555815691/9781555813697_Chap20-1.gif /docserver/preview/fulltext/10.1128/9781555815691/9781555813697_Chap20-2.gifAbstract:
This chapter describes the different methods used to perform magnetic resonance spectroscopy (MRS) studies of patients with HIV infection, reviews the major findings from the studies, and identifies future directions for clinical studies that may further elucidate the pathophysiology of HIV-associated brain injury, as well as discusses issues to consider in treatment monitoring. MRS studies have been performed in both adult and pediatric patients with HIV infection, using localized MRS and MRS imaging (MRSI) techniques and long TEs and short TEs, and before or after antiretroviral treatment. The majority of the studies used localized spectroscopy techniques (either point resolved spectroscopy (PRESS) technique or the stimulated echo acquisition method) and evaluated one to three brain regions. Limited by magnetic-susceptibility problems in evaluating the frontal brain regions, many of the earlier localized MRS studies evaluated the parietal or the occipital brain regions. Improvements in MRS techniques, such as adjustments of the slice order, allow the assessment of the frontal lobe and subcortical brain regions. Prior to highly active antiretroviral therapy (HAART), several longitudinal MRS studies reported changes in metabolite ratios or levels in HIV patients during antiretroviral treatment. Levels of inflammatory markers, such as the chemokine macrophage chemoattractant protein 1 (MCP-1), were found to be higher in patients with HIV-associated dementia than in those who were neuroasymptomatic. Additionally, both in vivo and ex vivo MRS studies in animal models of AIDS (e.g., simian immunodeficiency virus (SIV) and feline immunodeficiency virus (FIV)) should provide additional insights into the pathophysiology of HIV-associated dementia.
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Typical 1H-MR spectra acquired from a 1.5-T (left) and a 4-T (right) MR scanner; both used PRESS (TR/TE = 3,000/30 ms). The major metabolite peaks include an NA peak (2.02 ppm), glutamate and glutamine (Glx) (2.1 to 2.7 ppm), total CR (3.0 ppm), CHO (3.2 ppm), and occasional lactate (Lac) (1.3 ppm). Note that the MI peak(s) appears as a characteristic “pseudosinglet” at 1.5 T and as a multiplet at 4 T (insets); the difference demonstrates the better separation of the spectral peaks at higher magnetic-field strengths.
Selected 31P-MR spectra from the cerebellum in an HIV-infected patient (a) and a healthy volunteer (b), both acquired with a 4.1-T MR scanner. Each spectrum was selected in an 11.5-ml spectroscopic imaging voxel. PCr was used as an internal reference and was assigned a chemical shift of 0.0 ppm. The chemical shift of Pi versus PCr was used for pH determination. The spectra are shown with baseline correction. (Figure from Patton et al., 2001 .)
Metabolite changes dependent on ADC stages. Note that there is decreased NA only at stage 3 (ADC = 3) (severe dementia) and a relatively normal level of NA during the earlier stages of dementia. Note also the gradual increases in CR, CHO, and MI concentrations. All MR spectra were acquired on a 4-T MR scanner (PRESS sequence, TR/TE = 3,000/30 ms; 64 averages).
Characteristic metabolite maps from MRSI of two patients with HIV. The patient with mild cognitive motor disorder and a higher CD4 count had mildly elevated CHO in the frontal white-matter region with relatively normal NAA (top row), while the patient with ADC and a lower CD4 count had further elevation of CHO and decreased NAA in the frontal brain region. MRS images were acquired with a 1.5-T MR scanner; PRESS, TR/TE = 2 300/272 ms. (Courtesy of Peter Barker; modified from data presented in Barker et al., 1995 .)