Janna Trovato Biology Lab 1615 Term Paper

Neuropsychiatric Lupus: Development in Diagnosis and Treatment

The autoimmune disease Systemic Lupus Erythematosus (SLE) is a systemic disease with the potential to involve multiple organ systems simultaneously (Morrison et al, 2014). There is no specific trend or order as to which organ SLE will attack. Specifically, disease attacks on the brain can lead to Neuropsychiatric Lupus (NL). This involvement causes morbidity and mortality caused by the disease or associated infections (Zirkzee et al, 2014). A confirmative diagnostic tool for neuropsychiatric SLE is yet to be developed (Lee et al, 2012). Therefore, the early detection and treatment of brain involvement in SLE is of utmost importance.

Neuropsychiatric Lupus (NL) is a diagnosis that is both untreatable and unrelated to Systemic Lupus Erythematosus (SLE) disease activity (Diamond and Volpe, 2006). Symptoms include: headache, seizures, and mood disorders (Lee et al, 2012). New research developments show due to SLE inflammation can occur throughout the body including the Central Nervous System (CNS) which can cause neurological effects diagnosed as NL (Diamond and Volpe, 2006). NL is similar to other autoimmune disorders in that it can progress or remit. Possibly can contract NL if diagnosed with a number of disease syndromes in which anti-neuronal antibodies are causing damage to the CNS (Diamond and Volpe, 2006). Higher antibody accumulation leads to

greater SLE activity index, causing symptom increase (Hanaoka et al, 2012). NL is a form of SLE causing negative neurological effects.

The diagnosis of NL is minimal, as there is no way to track the state of symptom complexes and lack knowledge of pathophysiology (Diamond & Volpe, 2006). Furthermore, damage accumulates at a higher rate in patients with more active disease (Eder et al, 2013). Reiterating the importance of prompt disease manifestation control, which is unattainable without correct diagnosis and treatment. New clinical reports show 30%-50% of SLE patients carry these antibodies prevalent in NL (Diamond and Volpe, 2006). Although NL diagnosis time period doesnt greatly effect survival rate there is a need for more study into NL, the antibodies responsible, and possible treatments (Zirkzee et al, 2014).

Research and further observation of Neuropsychiatric Lupus has increased disease education. Antibodies studied with new magnetic resonance imaging technique to find use of apparent diffusion co-efficiency (ADC) (Diamond and Volpe, 2006). During the technique ADCs measures water molecules movement systematically modified in circumstances of chronic, acute, and sub-acute tissue inflammation, destruction, and injury. Two published studies use ADC measurements on patients with SLE. In conclusion 37 patients with NL had strokes, cognitive dysfunction, confused states, mood or anxiety disorders, psychosis, neuropathy, myelopathy, or headache syndromes (Diamond and Volpe, 2006). Separate study performed in 2012 concluded most common neuropsychiatric manifestation was headache (45%), followed by seizure (20%) and mood disorder (20%) (Lee et al, 2012). In January 2014, prescribed antiplatelet therapy in treatment of NL led to decreased mortality risk (Zirkzee et al, 2014).

Intravenous immunoglobulin also found to treat NL when symptoms do not remit and other toxic therapies are refused (Milstone et al, 2005). Research is performed, but still requires more information to improve NL diagnosis and treatment.

The new advanced imaging techniques displayed measurable evidence of Neuropsychiatric Lupus (NL) and are low risk to patients (Diamond and Volpe, 2006). Research supports possible beneficial treatment options. Evidence shows possible cause of NL thus helping efficient diagnosis. Advancement in this research will improve diagnosis of NL in patients with Systemic Lupus Erythematosus reducing current dilemma for lack of treatment.

References: Diamond B, Volpe B T. (Dec2006). Antibodies and Brain Disease: A Convergence of Immunology and Physiology. PLOS Medicine; Vol3 Issue12 Eder L, Urowitz, MB, Gladman DD. (Oct2013). Damage in lupus patients- what have we learned so far? Lupus; Vol22 Issue12. p1225-1231. Hanoakla H, Okazaki Y, Satoh T, Kaneko Y, Yasuoka H, Seta N, Kuwana M. (Oct2012). Circulating anti-double-stranded DNA antibody-secreting cells in patients with systemic lupus erythematosus: a novel biomarker for disease activity. Lupus; Vol21 Issue12. p1284-1293. Lee SW, Park MC, Lee SK, Park YB. (2012). The efficacy of brain 18F-fluorodeoxyglucose positron emission tomography in neuropsychiatric lupus patients with normal brain magnetic resonance imaging findings. Lupus; Vol21 Issue12. p1531-1537.

Milstone AM, Meyers K, Elia J. (Aug2005). Treatment of acute neuropsychiatric lupus with intravenous immunoglobulin (IVIG): a case report and review of the literature. Clinical Rheumatology; Vol24 Issue4. p394-397. Morrison E, Carpentier S, Shaw E, Doucette S, Hanly JG. (Apr2014). Neuropsychiatric systemic lupus erythematosus: association with global disease activity. Lupus; Vol23 Issue4. p370377. Zirkzee EJM, Huizinga TWJ, Bollen ELEM, Cuchem MA van, Middelkoop HAM, Wee NJA van der, Cessie S le, Steup-Beekman GM. (Jan2014). Mortality in neuropsychiatric systemic lupus erythematosus (NPSLE). Lupus; Vol23 Issue 1. p31-38.