Neurometabolism of active neuropsychiatric lupus determined with proton MR spectroscopy

• Published in: American journal of neuroradiology : AJNR Vol. 18; no. 7; pp. 1271 - 1277
• Main Authors: Sibbitt, WL, Jr, Haseler, LJ, Griffey, RR, Friedman, SD, Brooks, WM
• Format: Journal Article
• Language: English
• Published: Oak Brook, IL Am Soc Neuroradiology 01-08-1997; American Society of Neuroradiology
• Subjects: Adult; Aspartic Acid - analogs & derivatives; Aspartic Acid - metabolism; Biological and medical sciences; Brain - physiopathology; Brain Damage, Chronic - diagnosis; Brain Damage, Chronic - physiopathology; Brain Ischemia - diagnosis; Brain Ischemia - physiopathology; Brain Mapping; Choline - metabolism; Creatine - metabolism; Energy Metabolism - physiology; Female; Humans; Lactic Acid - metabolism; Lipid Metabolism; Lupus Erythematosus, Systemic - diagnosis; Lupus Erythematosus, Systemic - physiopathology; Magnetic Resonance Spectroscopy; Male; Medical sciences; Middle Aged; Neurocognitive Disorders - diagnosis; Neurocognitive Disorders - physiopathology; Neurons - physiology; Reference Values; Research Support, Non-U.S. Gov't; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Human; Immunopathology; Connective tissue disease; Skin disease; Nervous system diseases; Pathogenesis; Autoimmune disease; Metabolism; NMR spectrometer; Systemic disease; Central nervous system disease; Proton; Mental disorder; Adult; Complication; Lupus erythematosus; Disseminated
• ISSN: 0195-6108; 1936-959X

To determine the neurometabolism of patients with active neuropsychiatric systemic lupus erythematosus (NPSLE) by using proton MR spectroscopy.
Thirty-six patients with SLE and eight control subjects were studied with proton MR spectroscopy to measure brain metabolites. Peaks from N-acetylaspartate (NAA), creatine (Cr), choline (Cho), and at 1.3 parts per million (ppm) lipid, macromolecules, and lactate were measured. Patients were classified as having major NPSLE (seizures, psychosis, major cognitive dysfunction, delirium, stroke, or coma) (n = 15) or minor NPSLE (headache, minor affective disorder, or minor cognitive disorder) (n = 21). Patients with major NPSLE were severely ill and hospitalized.
SLE patients had lower NAA and increased metabolites at 1.3 ppm than did control subjects (NAA/Cr(SLE) = 1.90 +/- 0.35, NAA/Cr(Control) = 2.16 +/- 0.26; 1.3 ppm/Cr(SLE) = 0.49 +/- 0.41, 1.3 ppm/Cr(Control) = 0.27 +/- 0.05). NAA/Cr in patients with current or prior major NPSLE was lower than in patients without major NPSLE. Increased peaks at 1.3 ppm were present in all SLE subgroups, but particularly in patients with major NPSLE. These resonances were not evident at an echo time of 136, indicating that these signals were not lactate.
Major NPSLE, past or present, is associated with decreased levels of NAA. Elevated peaks around 1.3 ppm do not represent lactate even in severely ill patients, indicating that global ischemia is not characteristic of NPSLE. Neurochemical markers determined by MR spectroscopy may be useful for determining activity and degree of brain injury in NPSLE.