Clinical Image Madame F, 55 years old with a story; four miscarriages and two fetal deaths in utero. At 40 years old, she had a brutal motor deficit in the left lower limb and then in the homolateral upper limb associated with left hemifacialparaesthesia with complete recovery 10 years ago. She was readmitted for the installation of a left hemiplegia, a left central facial paralysis, a dysarthria with a NIH score of 9 associated with a livemedracemosis, branched, with large irregular open meshes, asymmetric diffusion affecting the legs; thighs, legs and feet. The brain scan shows an infarction of the superficial territory of the right Sylvian artery. On the balance sheet a negative determination of anti-phospholipid antibodies. The diagnosis of Sneddon syndrome is retained, the NIH score rose to 2 under curative anticoagulation followed by secondary prevention. Sneddon syndrome is a rare disease of unknown cause. Its frequency is difficult to estimate and seems underestimated [1]. It is characterized by the association of reticular and cerebrovascular accidents, sometimes responsible for deficits. The other neurological manifestations are polymorphic: headache, epilepsy, paraesthesia, dizziness, facial paralysis, pseudo-bulbar syndrome, long-term dementia. Biologically, antiphospholipid antibodies (APL) are found in 40% of cases [2]. The occurrence of a stroke in young people, especially in the presence of a racemosalivedo, should suggest the diagnosis of Sneddon syndrome (Figure 1). Conflicts of Interest Author declares that there is no conflict of interest.
A 20-year-old woman with a history of contact with animals. She has had a rash for 2 years. Clinical examination revealed an eruption of non-follicular papules and micropustules from the trunk and upper limbs, on the scalp of alopecic plaques with floury dander and a sign of positive traction. The rest of the examination showed cervical lymphadenopathy with no other abnormalities. The applied dermocorticoid and the administered griseofulvin are taken at a dose of 20 mg/kg/day for eight weeks. Dermatophytides are type IV delayed hypersensitivity reactions, secondary to opsonization, by antibodies directed against dermophyte antigens released at the site of infection. They occur in the acute phase of an infection between the 10th and 15th day or after 13 days of introduction of an antifungal treatment [1-3]. Several clinical pictures have been reported and the etiologies are diverse. Clinically, they manifest as rashes, itching [4-6]. The combination of oral corticosteroid therapy with antifungal therapy in the management of inflammatory ringworm is controversial and very little studied, the doses are from 0.5 mg/kg/day to 1 mg/kg/day of prednisone [7,8]. Clinical improvement with regression of lesions has been favored by dermocorticoids. It is important to know this clinical presentation in order to adopt the best therapeutic strategy (Figure 1).
Submission of an original paper with copyright agreement and authorship responsibility.I (corresponding author) certify that I have participated sufficiently in the conception and design of this work and the analysis of the data (wherever applicable), as well as the writing of the manuscript, to take public responsibility for it. I believe the manuscript represents valid work. I have reviewed the final version of the manuscript and approve it for publication. Neither has the manuscript nor one with substantially similar content under my authorship been published nor is being considered for publication elsewhere, except as described in an attachment. Furthermore I attest that I shall produce the data upon which the manuscript is based for examination by the editors or their assignees, if requested.Thanking you.
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