Systemic Lupus Erythematosus

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Involvement of the CNS occurs in 14-75% of patients with systemic lupus erythematosus (SLE) [4]. Pathologically, microinfarcts and small vessel vasculopathy are the most common. Vasculopathy affects predominantly the arterioles and capillaries, resulting in vessel tortuosity, vascular hyalinization, endothelial proliferation and perivascular inflammation or gliosis.

Spectrum of CNS vasculopathy. (Modified from [10])

Arteriolar Hyalinization

Figure 7.12 a-d

Systemic lupus erythematosus in a 39-year-old woman with recurrent episodes of stroke, who presented with fever and disturbance of consciousness. a T2-weighted image shows hyperintense lesions in the right thalamus, internal capsule, putamen, subcortical white matter, and the left internal capsule (arrows). b Gadolinium-enhanced T1-weighted image reveals marked enhancement of the lesion in the right side,suggesting blood-brain barrier breakdown (arrows). c DW image shows a slightly hyperintense lesion in the right thalamus but an isointense lesion in the right putamen and white matter (arrows). There is a linear hyperintense lesion in the right internal capsule (long thin arrow). A subtle hyperintense lesion in the left internal capsule is also seen (arrowhead). d The ADC map shows increased ADC of the lesion in the right side (short thick arrows), representing vasogenic edema. Increased ADC of the lesion in the left internal capsule (arrowhead) represents an old infarct. Decreased ADC is seen in the lesion in the right internal capsule (long thin arrow), presumably representing acute microinfarcts. (From [51])

Shwartzman Phenomenon

True vasculitis is very rare (0-7%). This vasculopathy may be related to both acute inflammation and ischemia [28]. In recent reports,the mechanism of vas-culopathy in CNS involvement of SLE has been attributed to intravascular activation of a complement, which leads to adhesion between neutrophils and/or platelets and endothelium, resulting in leukothrom-bosis in the microvasculature (Shwartzman phenomenon) [29].

In this vasculopathy, despite widespread microvascular occlusions, parenchymal damage is minimal and potentially reversible. Sibbit et al. reported that up to 38% of CNS lesions in SLE were potentially reversible on MR imaging [30]. MR angiography and conventional angiography may provide additional information concerning vascular abnormalities. DW imaging shows primarily two patterns of parenchymal lesions with acute or subacute CNS symptoms: one is an acute or subacute infarction, and the other is vasogenic edema with or without mi-croinfarcts (Fig. 7.12) [5]. CNS involvement in SLE is also due to associated uremia, hypertension, infection, Libman-Sacks endocarditis, and corticosteroid or immunosuppressive therapy.

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