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Introduction Neuropsychiatric manifestations in systemic lupus erythematosus (SLE) occur in about half of the patients; however, movement disorders like Parkinsonism are rare. We describe a case of SLE who presented solely with features of Parkinsonism. Case report 50-year-old female presented with global slowing of movements and slowing of speech since 2 months. On examination, she had mask-like facies with a faint malar rash sparing the nasolabial folds, hard palate ulcer, cog-wheel rigidity, and proximal muscle weakness. Lab evaluation revealed lymphopenia, high ESR, elevated lactate dehydrogenase, creatinine phosphokinase, AST, and ALT levels. She had high anti-dsDNA levels with low complements. Urinalysis showed proteinuria and hematuria. ANA was positive at a titer of 1:320, and she had positive anti-ribosomal-P antibody. She had severe flare with a SLEDAI of 33. She was treated with pulse IV methylprednisolone followed by cyclophosphamide (NIH protocol). At 4 weeks follow-up, she had dramatic improvement in her Parkinsonian symptoms and her proximal muscle weakness. Discussion The prevalence of movement disorders in cases of neuropsychiatric SLE is very low at 0.7%, with chorea being most frequent and Parkinsonism rare. The pathogenesis is multifactorial including anti-dopaminergic antibodies or associated anti-phospholipids causing microvascular thrombosis or vasculitis of the thalamostriatal arteries or disease activity itself. As in our case, immunosuppression and optimal treatment of active lupus reverts symptoms in most cases. Conclusion A high index of suspicion needs to be exercised in cases of SLE presenting with Parkinsonism as adequate immunosuppression translates to near-complete recovery.

Inflammatory rheumatic disorders come with their plethora of complications including accelerated ovarian aging and the associated adversities which could be a consequence of disease itself or treatment with immunosuppressants. While aiming for treat-to-target in these patients, its effect on the ovaries takes a backseat. This review focusses on this underexplored avenue of effect of inflammation, inflamm-aging and the associated complications that come with early menopause, in the context of autoimmune rheumatic diseases (AIRDs). Some autoimmune diseases like lupus have a major role of estrogen in their causation and tend to be less severe when the onset is after menopause, while in other inflammatory arthritis like rheumatoid arthritis (RA), estrogen may have some anti-inflammatory potential. Inflamm-aging that is associated with the AIRDs also leads to early menopause and premature ovarian insufficiency in some patients, which adds-on to the morbidity and sometimes, mortality. With early ovarian aging and precipitous decline in circulating estrogen, there is accelerated reduction in the bone mass and early set-in of osteoporosis. Long-term steroids, on-going inflammation and RA itself are major risk factors. The high risk of detrimental fragility fractures in these patients with a consequential reduction in the quality of life with higher loss of disability adjusted life years (DALY) and poorer functional outcomes, contributes to long-term morbidity. While remission induction and maintenance are a major part of treatment, physicians should exercise a keen eye towards recognizing early menopause and its adversities and inculcate measures for osteo-protection and prevent adding on to the morbidity. Future prospects would include attempts at delaying ovarian aging by targeting mTOR/S6 kinase pathways and preservation of ovarian tissue.