PURPOSE: This study aimed to examine memory dysfunction in relation to the hippocampal magnetic resonance spectroscopy (MRS) neurometabolites N-acetylaspartate (NAA), glutamate (Glu), glutamine (Gln), and myo-inositol (mI) in SLE patients without prior or overt neuropsychiatric symptoms.
METHODS: Subjects included 19 SLE patients with a mean age of 38.1 (SD=7.5), mean education of 14.9 years (SD=2.3), mean length of SLE diagnosis of 78.6 months (SD=43.1), and mean SLEDAI of 5.4 (SD=7.8). Cognitive function was assessed by administration of the ACR-SLE neuropsychological battery. Specific scores for verbal learning, verbal delayed recall, immediate nonverbal recall, and delayed nonverbal recall were analyzed. The four scores were converted to t-scores using demographically corrected normative data; t-scores less than 40 were considered impaired. The memory impairment index (MII), which is the sum of the above four scores, ranges from 0 to 4 (no impairment to severe impairment). MR spectra were obtained from the hippocampal region using a 3.0T GE whole body scanner and the PRESS pulse sequence. These results were analyzed using LCModel software and the results expressed as ratios to creatine (Cr).
RESULTS: Twenty-six percent of the SLE patients had no memory impairment, with a score of 0 on the MII. Twenty-six percent of the patients had a score of 1; 21% had a score of 2; 11% had a score of 3; 16% had a score of 4 on the MII. We performed a Pearson’s correlation analysis and results indicated that higher MII was associated with lower right hippocampal Glu+Gln/Cr (r=-0.56, p=0.01), lower right hippocampal NAA/Cr (r=-0.57, p=0.01), lower left hippocampal mI/Cr (r=-0.48, p=0.04), and a trend towards lower right hippocampal Glu/Cr (r=-0.42, p=0.07).CONCLUSIONS: SLE patients without prior histories of neurological or psychiatric symptoms demonstrate high levels of memory impairment associated with abnormalities in neurometabolites within the hippocampal region. Patients with very mild SLE who do not exhibit over CNS changes demonstrate specific abnormalities in glutamate and myo-inositol, suggesting biological mechanisms associated with learning and memory problems.
METHODS: Subjects included 19 SLE patients with a mean age of 38.1 (SD=7.5), mean education of 14.9 years (SD=2.3), mean length of SLE diagnosis of 78.6 months (SD=43.1), and mean SLEDAI of 5.4 (SD=7.8). Cognitive function was assessed by administration of the ACR-SLE neuropsychological battery. Specific scores for verbal learning, verbal delayed recall, immediate nonverbal recall, and delayed nonverbal recall were analyzed. The four scores were converted to t-scores using demographically corrected normative data; t-scores less than 40 were considered impaired. The memory impairment index (MII), which is the sum of the above four scores, ranges from 0 to 4 (no impairment to severe impairment). MR spectra were obtained from the hippocampal region using a 3.0T GE whole body scanner and the PRESS pulse sequence. These results were analyzed using LCModel software and the results expressed as ratios to creatine (Cr).
RESULTS: Twenty-six percent of the SLE patients had no memory impairment, with a score of 0 on the MII. Twenty-six percent of the patients had a score of 1; 21% had a score of 2; 11% had a score of 3; 16% had a score of 4 on the MII. We performed a Pearson’s correlation analysis and results indicated that higher MII was associated with lower right hippocampal Glu+Gln/Cr (r=-0.56, p=0.01), lower right hippocampal NAA/Cr (r=-0.57, p=0.01), lower left hippocampal mI/Cr (r=-0.48, p=0.04), and a trend towards lower right hippocampal Glu/Cr (r=-0.42, p=0.07).CONCLUSIONS: SLE patients without prior histories of neurological or psychiatric symptoms demonstrate high levels of memory impairment associated with abnormalities in neurometabolites within the hippocampal region. Patients with very mild SLE who do not exhibit over CNS changes demonstrate specific abnormalities in glutamate and myo-inositol, suggesting biological mechanisms associated with learning and memory problems.
E. Kozora, None; D. Arciniegas, None; M. Brown, None; M.D. Devore, None; C.M. Filley, None; A. Grimm, None; D. Miller, None; L. Zhang, None; C. Wingrove, None; S. West, None.
See more of: SLE: Clinical Aspects and Treatment I
See more of: ACR Abstract Submission Poster Sessions
See more of: ACR Abstract Submission Poster Sessions
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