Sneddon's syndrome: a case report.
We report a case of Sneddon's syndrome with the triad of livedo reticularis, hypertension, and neurologic symptoms. The procedures for diagnosis and the tests to delineate clotting abnormalities are examined.
Biomedical subjects
Publications and source records attributed to M P LaMonte.
We report a case of Sneddon's syndrome with the triad of livedo reticularis, hypertension, and neurologic symptoms. The procedures for diagnosis and the tests to delineate clotting abnormalities are examined.
STUDY OBJECTIVES: To review the randomized, controlled, multicenter trials of intravenous thrombolytic therapy for ischemic stroke. METHODS: Studies of ischemic stroke confirmed by computed tomography (CT) and randomization of more than 100 patients are reviewed. Streptokinase studies are the MAST-I, the MAST-E, and the ASK Trial. Studies using tissue plasminogen activator (tPA) are the NINDS Stroke Study, ECASS I, ECASS II, and ATLANTIS. One study using ancrod is STAT. We discuss significant factors common to each study, including thrombolytic agent used, CT scan interpretation, time of therapy administration in relation to stroke onset, thrombolytic dose, ancillary medication administration, safety, and neurologic outcomes. RESULTS: All streptokinase studies were stopped early because of increased mortality in the treated groups. Initial results of the STAT study are promising; publication of full study details is awaited. The ATLANTIS study was terminated early because of nonstatistical efficacy at interim analysis. The NINDS and the ECASS trials were completed; only the NINDS study demonstrated significant increase in the percentage of patients with complete recovery or minimal deficit at 3 months, without significant difference in mortality in the treated group. CONCLUSION: This review supports the use of intravenous thrombolytic therapy for ischemic stroke using tPA at a dose of.9 mg/kg body weight and a "golden window" treatment time of 3 hours. Administration without strict adherence to protocol, even within this time frame, may shift the benefit/risk profile of tPA. We recommend the treating physician have rapid access to CT scanning and to collaboration with individuals experienced in the evaluation of stroke and CT interpretation.
BACKGROUND: Williams syndrome is a genetic disorder characterized by a high incidence of heart disease, arterial stenosis, and hypertension. Despite these features, cerebrovascular accidents have been described only recently and only in association with stenoses of the cerebral vasculature. CASE DESCRIPTION: A 19-year-old girl with Williams syndrome developed an acute-onset hemiparesis. MRI demonstrated an infarct involving the internal capsule and putamen. No stenotic areas were seen on angiography. CONCLUSIONS: Stroke should be considered as a possible consequence of Williams syndrome, even in the absence of stenoses of the cerebral vasculature. Comparison of this case with those previously reported in the literature emphasizes the multiplicity of features in Williams syndrome that can contribute to the risk of stroke.
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