Neurovascular Consequences of Systemic Disease: Lupus and Primary Hyperparathyroidism

Abstract

Cognitive dysfunction is a common feature in systemic lupus erythematosus (SLE) patients, with a prevalence of ranging from 55–80% in SLE patients (Ainiala et al., Arthritis Rheum 45:419–423, 2001; Brey et al., Neurology 58:1214–1220, 2002; Hanly et al., J Rheumatol 31:2156–2162, 2004; Sanna et al., J Rheumatol 30:985–992, 2003; Sibbitt et al., J Rheumatol 29:1536–1542, 2002). Cognitive impairment often involves the subcortical brain, causing difficulties with working memory as well as a reduction in information-processing and executive functioning, such as planning, organizing, or multi-tasking (Leritz et al., J Int Neuropsychol Soc 6:821–825, 2000). The etiology of cognitive dysfunction in SLE is still under investigation, with current studies demonstrating that cognitive dysfunction cannot be fully explained by SLE disease activity or treatments or prior strokes (Brey et al., Neurology 58:1214–1220, 2002; Rivest et al., J Rheumatol 27:680–684, 2000). Alternative explanations, such as infection, malignancy, medication adverse effect (e.g. steroid-induced psychosis), metabolic disturbances (e.g. uremia) need to be aggressively evaluated and excluded (“The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes,” Arthritis Rheum, 42:599–608, 1999; Futrell et al., Neurology 42:1649–1657, 1992; West et al., Am J Med 99:153–163, 1995).