RADIOGRAPHIC FEATURES:

CNS lupus has a non-specific radiographic presentation. 

A normal brain is seen in 40-50% of MRI conventional sequences.

¤ Cerebrovascular disease:

1. Small vessel disease and cerebral atrophy: 

- Frontal and parietal lobes predilection. Fig. 1. 

- Anterior to posterior gradient, different from multiple sclerosis.

• Lacunar infarcts.
• Small cortical infarctions. Fig. 2. 
• Microbleeds. Fig. 3.
• Cortical atrophy. Fig. 4, Fig. 5.

2. Large vessel/Ischemic stroke: mainly in the middle cerebral artery territory.  Fig. 6, Fig. 7.

3. Intracerebral hemorrhage. Fig. 8.

4. Dural venous sinus thrombosis. Fig. 9.

5. Cerebral vasculitis (lupus angiitis).

¤ Inflammatory-type lesions.

¤ Myelopathy:

• Transverse myelitis.
• Optic neuritis.

¤ Other manifestations:

• Aseptic meningitis.
• Posterior reversible encephalopathy syndrome (PRES). Fig. 10.
• Brain abscess. Fig. 11.
• Anti-NMDA receptor encephalitis. 
• Intraparenquimatous calcifications. Fig. 12.

SUMMARY:

¤ Cranial MRI findings:

• Normal (25–60%).
• Small subcortical hyperintensity/white-matter lesions (30–75%).
• Cerebral atrophy (15–20%).
• Infarct larger than 10mm.

¤ Spine MRI findings:

• Increased signal intensity.
• Diffuse edema in the cervical cord.

ADVANCED MRI SEQUENCES:

¤  Voxel-based morphometry (VBM):

It allows the assessment of tissue-specific atrophy. 

It is frequently performed for examining differences between populations. 

SLE patients compared to healthy controls present decreased whole brain volume with increased lateral ventricle volume and both global gray and white matter atrophy.

Atrophy evolves over a short period of time. 

Selective cortical atrophy is the measure with the best correlation with the presence of NPSLE, and it is more important for mediating brain damage in NPSLE patients than the micro- or macrostructural damage in the white matter. 

Some authors compared cohorts of NPSLE with SLE and controls. 

• The NPSLE group exhibited decreased cortical thickness in left frontal and parietal lobes as well as in right parietal and occipital lobes compared to controls. 
• Both SLE and NPSLE groups exhibited comparable thinning in frontal and temporal lobes.

Automated morphometric methods were also used for segmenting white matter lesions in patients with SLE, which could give a more precise quantification of the focal injuries.

¤ Diffusion-tensor imaging (DTI): 

It is based on the measurement of water diffusion through cellular compartments and it provides better resolution than conventional sequences regarding white matter microstructure. White matter presents higher anisotropy, with preferential diffusion along the length of the axon, and this anisotropy is due to the well-structured axonal membranes and their myelin sheaths. 

The diffusion can be quantified by the following parameters:

• Apparent diffusion coefficient (ADC).
• Fractional anisotropy (FA)*: measure of myelination and axonal integrity.
• Mean diffusivity (MD)*: a measure of molecular motion.
  A High FA and low MD suggest greater myelination and axonal integrity.
• Radial diffusivity (RD).
• Axial diffusivity (AD).

In patients with SLE, white matter injury in frontal lobes, corpus callosum, and thalamus has been found. 

In NPSLE patients:

• FA values are lower.
• MD values are higher.
• AD values are higher. 

¤ Magnetization transfer imaging (MTI): 

• It is based on the interaction between free water protons and bound protons. The differences in proton mobility in various macromolecules and tissues are used to generate differences in the image signals. A study showed MTI histogram parameters in different subjects:
   - The magnetization transfer ratio histograms in the group of SLE without NPSLE and the group of healthy controls were similar, whereas those in chronic NPSLE and multiple sclerosis groups were flatter. 
   - The active NPSLE group showed also a flattening of the histograms, but with a higher magnetization transfer ratio. 
  This suggests that MTI could be able to differentiate active NPSLE. 
• It is also believed that MTI might be a good method for monitoring treatment trials in NPSLE. 

¤ Magnetic resonance spectroscopy (MRS): 

It allows the analysis of brain metabolites. Different proton groups have different magnetic fields in relation to their valence electrons. As a result, they resonate at different frequencies of the magnetic field, which can be demonstrated by MRS, as peaks that correspond to different metabolites. 

• N-acetyl aspartate (NAA)* is one of the main markers assessed on MRS and is found in higher concentrations in neurons. Thus, it is a marker of neuronal viability. 
• Glutamate* is the most important excitatory neurotransmitter and, prolonged neuron excitation by glutamate can be toxic to neurons.
  *NAA and glutamine-glutamate changes were demonstrated in normal-appearing brain in SLE patients, before neurologic and imaging manifestations became apparent, which suggests that these markers might predict the early cerebral involvement of SLE. 
• Myo-inositol is a marker of gliosis.

SLE and NPSLE patients have:

• Lower NAA ratios.
• Increased Myo-inositol.
  Both are suggested as poor prognosis markers in NPSLE. 

¤ Perfusion imaging:

3 techniques:

• With administration of gadolinium:
   - Dynamic susceptibility contrast imaging.
   - Dynamic contrast-enhanced imaging.

• Without contrast administration:
   - Arterial spin-labeled imaging. 

Few prospective studies analyzed brain perfusion in SLE patients:

• Some authors showed that perfusion in SLE patients was not different from healthy controls.
• Others reported a pattern of hypoperfusion in both SLE and NPSLE or even hyperperfusion in the posterior cingulate gyrus in patients with active disease.