Vol. 2, Article 3 Neurographics logo Hart et al.

 

Diffuse Brain Damage

Many SLE patients have significant neuropsychiatric problems without focal lesions demonstrable on CT or MRI. It is clear that diffuse brain damage can occur in SLE. The underlying pathological basis of this damage is not yet clear. Generalized neuronal cell loss, decreased neuronal density, and bland vasculopathy may occur. CT and MRI can demonstrate atrophy, and steroid administration does not account entirely for this observation. In addition, special imaging techniques demonstrate diffuse or regional injury to the brain. For example, SPECT and PET have been utilized in SLE patients and found to demonstrate patchy areas of hypoperfusion and focal defects in oxygen uptake. Quantitative T2 measurements have shown a diffusely increased T2 signal intensity in the frontal gray matter of SLE patients compared with controls, indicating increased water content that may reflect subtle edema not visible to qualitative observation (6). (Fig. 8) Volumetric magnetization transfer imaging has shown differences between NPSLE patients and controls and may separate active from chronic NPSLE (7). Magnetic resonance spectroscopy can also document diffuse brain damage in SLE (8, 9). (Figure 9) NAA levels in patients with NPSLE are decreased relative to controls, and choline levels can be elevated. The latter may correspond to active disease and inflammatory changes.

(Fig 8)

Figure 8. Segmented T2-weighted image in SLE showing (a) frontal gray matter - pixels resulting from partial volume CSF are excluded; pure gray matter is retained, (b) CSF of ventricles and sulci, and (c) lesions. T2 values of gray matter were specifically elevated, as were focal lesions.

(Fig 9
A. B.

Figure 9. Magnetic resonance spectroscopy in SLE. T2-weighted image of a NPSLE patient with multiple lesions showing the locations of spectroscopic voxels. A) normal-appearing white, B) normal-appearing gray, C) and D) hyperintense lesions. Right: Spectra from voxels A, B, C, and D, demonstrating decreased NAA and increased Cho. These abnormalities are accentuated in the lesions (C and D) that demonstrate different spectroscopic patterns relative to NAA, Cre, and Cho, indicating considerable metabolic heterogeneity within the population of focal lesions.

 



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