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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper presents 3 cases of generalized livedo racemosa and cerebral infarction in female patients ages 27, 39, and 42 years. Livedo racemosa is characterized by a broken, irregular pattern on the skin. It is probably caused by patchy impairment of cutaneous arteriolar circulation, resulting in reflectory venous dilation and stasis of blood. Livedo may accompany diseases such as atherosclerosis, diseases with intravascular occlusion, and collagen disorders, indicating a need for a careful search for an underlying condition. These 3 patients demonstrated several risk factors for atherosclerosis: hypertension (1 patient), oral contraceptive use (2 patients), and smoking (2 patients). The clinical findings in these 3 cases provide support to the theory that a chronic endarteritis obliterans of the small and medium-sized arteries is the underlying cause for the skin and neurologic manifestations in livedo racemosa associated with stroke.
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PMID:Livedo racemosa generalisata and stroke. 402 92

Livedo reticularis is a vascular abnormality of the skin resulting in an erythematous reticular rash. The combination of livedo reticularis and stroke-like episodes in adults is known as Sneddon syndrome [Sneddon, IB (1965). Br J Dermatol 77:180-188]. A similar combination of stroke-like episodes and livedo reticularis has been reported to occur in children [Baxter P et al. (1993). Dev Med Child Neuro 35:917-926]. We present here a 7-year-old male with congenital livedo reticularis, obesity, developmental delay, stroke-like episode, hypertension and cystic kidneys. We summarize our patient's findings and family history, and compare his disorder to other possibly related conditions.
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PMID:Livedo reticularis, developmental delay and stroke-like episode in a 7-year-old male. 954 37

A syndrome associating Livedo Reticularis (LR) with Cerebrovascular disease (CVD) was described, in 1965, by Sneddon. It occurs sporadically, but a few familial cases of Sneddon's Syndrome (SS) have been reported, like these 3 cases that represent one of the largest number among siblings. We studied three male brothers, aged 28, 37 and 42 years, with CVD (ischaemic stroke in 2 patients and cerebral haemorrhages in the third) and their sister with no CVD. All patients presented with long lasting Livedo Reticularis, extending beyond the lower limbs. Skin biopsy on the centre of the reticular pattern showed, only in the second patient, partial endothelium detachment in dermo-hypodermic blood vessels. The males also had accesses of Livedoid Vasculitis (LV), in which a skin biopsy showed obliteration of several upper dermal vessels with hialin thrombi and a very scarce inflammatory infiltrate. Complementary studies, with an extensive investigation on pro-coagulation/pro-thrombotic features including antiphospholipid antibodies, were repeatedly negative. Their non-consanguineous parents were not affected, but among these kindred of 9 individuals, apart from the 4 patients reported above, LR and LV were present in two other brothers and also in an aunt and uncle, suggesting autosomal dominant pattern of inheritance, with incomplete penetrance. The relationship between Sneddon's Syndrome and Antiphospholipid Antibody Syndrome is controversial. The present cases, having repeatedly negative antiphospholipid antibodies, support the classification of Sneddon's Syndrome as an independent nosological entity.
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PMID:Familial Sneddon's syndrome. 1280 91

Sneddon syndrome (SS) is an episodic or chronic, slowly progressive disorder and characterized by generalized livedo racemosa (patchy, violaceous, skin discoloration) and recurrent cerebrovascular events. The histopathology of skin and brain is remarkable for a noninflammatory thrombotic vasculopathy involving medium- and small-sized dermal and cerebral arteries, respectively. Approximately 80% of the SS patients are women with a median age of diagnosis at 40 years. However, the onset of the disease during childhood have been reported. Etiopathogenesis of SS is unknown with 2 primary mechanisms proposed - autoimmune/inflammatory versus thrombophilia. SS is primarily classified as antiphospholipid positive or negative type. Neurological manifestations usually occur in 3 phases: (1) prodromal symptoms such as headaches, dizziness, and vertigo, (2) recurrent strokes, and (3) early onset dementia. Livedo racemosa precedes the onset of recurrent strokes by more than 10 years, but in many instances, the significance of the skin lesion is recognized only after the appearance of the stroke. The involvement of the heart valves, systolic labile hypertension, and retinal changes are also commonly associated with this syndrome. Treatment of SS is primarily based on anecdotal reports. Antiplatelet and antithrombotic agents are used for secondary stroke prophylaxis, and a recent study showed a relatively lower stroke recurrence rate with the universal use of antiplatelet/antithrombotic agents. Routine use of anti-inflammatory or immunosuppressive therapies is controversial. Neuropsychiatric prognosis of SS is relatively poor with predominant deficits in the concentration, attention, visual perception, and visuospatial skills.
J Stroke Cerebrovasc Dis 2019 Aug
PMID:Sneddon Syndrome: A Comprehensive Overview. 3116 Feb 19