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Introduction. Sneddon syndrome is determined by the association of two cardinal disorders: one is the presence of livedo racemosa, and the other is the occurrence of strokes, which are often progressive and numerous. This syndrome is closely related to anti-phospholipid syndrome (APS), with which the nosological limitations are not yet clear. Autoimmunity and/or thrombophilia may be present alongside this syndrome, explaining in part its pathophysiology. Observation. We report the case of a 46-year-old female patient, without any notable pathological history, who presented with a lengthy history of neurological symptoms such as headaches and dizziness. She complained of progressive memory problems, which had appeared more recently, as well as paresthesia. She also described experiencing Raynaud’s phenomenon. The clinical examination showed livedo racemosa and arterial hypertension. The test results, particularly the immunology ones (anti-nuclear and anti-phospholipid antibodies), came back negative. Brain MRIs, performed twice, five years apart, revealed progressive cerebral ischemic lesions involving the frontal, parietal, and occipital regions bilaterally. Sneddon syndrome was diagnosed on the basis of clinical, biological, and radiological presumptions. Anti-platelet aggregation and anti-hypertensive treatment was started. The evolution was marked by the disease stabilizing. Conclusion. Since its first description in 1965, Sneddon syndrome has continued to raise etio-pathogenic and nosological questions. Further studies are needed to better understand this disease.