%0 Journal Article
%T Diffuse Leukoencephalopathy and Subacute Parkinsonism as an Early Manifestation of Systemic Lupus Erythematosus
%A Gary G. Tse
%A Alberto S. Santos-Ocampo
%A Dominic C. Chow
%A Aaron M. McMurtray
%A Beau K. Nakamoto
%J Case Reports in Neurological Medicine
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/367185
%X Parkinsonism in SLE is rare. Diffuse leukoencephalopathy is equally uncommon and is associated with a poor prognosis. We present a single case of a 50-year-old Filipino man who presented with a generalized discoid rash after starting lisinopril. The rash persisted despite discontinuation of lisinopril, and over the next three months, he developed rapidly progressive parkinsonism. Brain MRI showed symmetric confluent T2-hyperintensities involving the white matter and basal ganglia. Four of the 11 American College of Rheumatology criteria for the classification of SLE were met. A rheumatologist made a diagnosis of SLE with cutaneous and central nervous system involvement. Significant neurologic and radiologic improvement occurred following treatment with IV steroids followed by a prolonged taper. This report highlights a case of subacute parkinsonism with a diffuse leukoencephalopathy as an early manifestation of SLE which resulted in a good recovery following treatment with only immunosuppressive therapy. 1. Introduction Central nervous system (CNS) involvement is present in up to 70% of individuals with systemic lupus erythematosus (SLE) and can present with an acute confusional state, demyelinating syndrome, stroke, seizures, or cognitive dysfunction [1]. Radiologic abnormalities associated with CNS lupus include demyelinating plaques, myelitis, ischemic or hemorrhagic stroke, dural venous sinus thrombosis, rhombencephalitis, and cerebral atrophy [2]. We report a single case of subacute parkinsonism with a diffuse leukoencephalopathy on brain MRI as an early manifestation of SLE. 2. Report of a Case A 50-year-old Filipino male with a history of hypertension developed a discoid, photosensitive, and hyperpigmented rash on sun-exposed areas of his face, arms, and legs in March 2012 shortly after starting lisinopril. Lisinopril was discontinued in April 2012 without resolution of the rash, prompting consultation with a dermatologist who suspected discoid lupus and ordered screening lupus labs. Complete blood count (CBC) was normal. Erythrocyte sedimentation rate (ESR) was 76£¿mm/hour, anti-nuclear antibody (ANA) 1£¿:£¿320 in a homogenous and fine speckled pattern, anti-histone and anti-RNP antibodies were positive, and complement C50, C3, and C4 were low. Anti-double-stranded DNA (anti-ds DNA) and anti-smith (anti-Sm) antibodies were negative. Initial impression was drug-induced lupus. In July 2012, he was admitted for recurrent falls. Neurological examination was notable for reduced degree of facial expression (hypomimia), weak and soft speech (hypophonia),
%U http://www.hindawi.com/journals/crinm/2013/367185/