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of abstracts from every available medical article about
Sneddon's Syndrome. At this early stage we can offer
collections of abstracts on the following topics:
2. The Sneddon's Patient's Optimal INR as 3 - 4
4. Sneddon's and the Eyes
5. Sneddon's and Headache
6. Sneddon's and Tests for Antiphospholipid Antibodies
On Warfarin as the Most Effective Treatment for Sneddon’s
1. 1. Sneddon's
syndrome is a thrombotic vasculopathy: neuropathologic and neuroradiologic
evidence. Neurology. 1995 Mar;45(3 Pt 1):557-60. Comment in: Neurology. 1996 Jun;46(6):1781-2. Geschwind DH, FitzPatrick M, Mischel PS, Cummings JL. Department of
Neurology, UCLA School of Medicine 90024. We report the
first case of pathologic findings from brain biopsy in a patient with Sneddon's
syndrome. The observations suggest that Sneddon's syndrome is not a vasculitis
but is more comparable to the autoimmune vasculopathies such as the
antiphospholipid antibody syndrome. Vascular thrombosis and emboli from cardiac
sources are the likely causes of stroke in most cases. The success of warfarin
in the treatment of antiphospholipid syndromes and the failure of
immunosuppression and aspirin in the treatment of Sneddon's syndrome argue that
warfarin anticoagulation may be the most appropriate intervention currently
available. PMID: 7898716 2. 2. Sneddon and
antiphospholipid antibody syndromes causing bilateral thalamic infarction. Pediatr Neurol. 1994 May;10(3):262-3. Department of
Neurology, Vanderbilt University School of Medicine, Nashville, TN 37212-3375. A child suffered
bilateral thalamic infarction secondary to Sneddon and antiphospholipid
antibody syndromes. Her initial findings of hypersomnolence, mood disturbance,
and amnesia are characteristic of bilateral thalamic infarction. Clinical and
laboratory evaluation confirmed the diagnosis of both Sneddon and
antiphospholipid antibody syndromes as the cause of her unusual stroke. The
treatment of this patient, based on experience with adult patients, was
long-term, high-intensity warfarin anticoagulation. PMID: 8060434 3. 3. Perioperative
management of a patient with Sneddon syndrome--a case report Anaesthesiol
Reanim. 2003;28(3):74-8. Vagts DA, Arndt M, Nöldge-Schomburg GF. Sneddon's syndrome is a rare combination of
generalised livedo reticularis and cerebrovascular accidents. Its clinical
presentation varies widely and its aetiology is still not known. 60 to 80% of
patients are female. First symptoms of the syndrome are mostly repetitive
cerebral strokes, but reduced perfusion of the skin, seen as blue or red-brown
mottling, precedes the strokes. The vascular disease is generalised and often
accompanied by arteriosclerosis, systemic arterial hypertension, valvular heart
disease and the presence of antiphospholipid antibodies. The diagnostic
procedures are complicated and have to exclude other autoimmunological
diseases. Therapeutic options are anticoagulatory therapy with warfarin, ASS or
heparin, reduction of endothelial proliferation with ACE-inhibitors, and
improvement of microvascular perfusion with prostaglandine. The increased
anaesthesiological risk with these patients is due to the acute risk of
thromboembolism and ischaemic cerebral and cardiovascular insults. The
anaesthetic management must provide stable perfusion pressures for cerebral and
myocardial arteries and avoid increasing risk factors for thromboembolism such
as increased blood viscosity or stasis due to improper positioning of the
patient. The choice of anaesthetic drugs is dependent on good controllability
for haemodynamic stability. The high risk of patients with Sneddon's syndrome
justifies a more invasive haemodynamic monitoring and postoperative
surveillance on an intensive care unit. This case report describes the
anaesthesiological considerations for, and management of, a patient with
Sneddon's syndrome who was admitted to hospital for vaginal hysterectomy. PMID: 12872540 4. 4. Aspirin
and antiphospholipid syndrome [Article in French] Rev Med Interne. 2000 Mar;21 Suppl
1:83s-88s. Hachulla E, Piette AM, Hatron PY, Blétry O. Service de médecine interne, hôpital Huriez, CHRU,
Lille, France. INTRODUCTION: Antiphospholipid syndrome is the most
frequent cause of acquired thrombophilia. Aspirin may have some indications.
CURRENT KONWLEDGE AND KEY POINTS: The usefulness of low doses of aspirin is now
well demonstrated in the prevention of obstetric complications associated with
antiphospholipid antibodies (especially pregnancy loss). When heparin is
combined with low-dose aspirin, the recurrent rate of fetal loss is lower than
30%. In patients with arterial or venous thrombosis, there is a high rate of
recurrence during the two first years except if high-dose warfarin was used
(i.e., INR > or = 3). The association warfarin-aspirin in secondary
prevention of thrombosis may be evaluated in prospective studies. It is not so clear in the literature and in our
experience that warfarin is superior to aspirin in stroke recurrence prevention
in patients with antiphospholipid antibodies, except in Sneddon's syndrome. There are no guidelines in primary
thrombosis prevention in patients with antiphospholipid antibodies. In lupus
patients, aspirin may not be sufficient after many years of follow-up in
preventing a first episode of thrombosis. Prospective studies may be
undertaken. Atherosclerotic patients with antiphospholipid antibodies are
particularly exposed to the risk of thrombosis after revascularisation or
angioplasty and stent implantation. Aspirin may have a place in those patients
but these must be evaluated. FUTUR PROSPECTS AND PROJECTS: Except in prevention
of obstetric complications, the usefulness of aspirin in patients with
antiphospholipid antibodies must be evaluated in prospective studies. PMID: 10763209 Eur Neurol. 2002;48(3):126-32. Flöel A, Imai T, Lohmann H, Bethke F, Sunderkötter C, Droste DW. Department of Neurology, University of Münster,
Münster, Germany. [email protected] We report the case of a young woman with
progressive cognitive decline and epilepsy. She showed ischemic cerebrovascular
disease and proximal livedo racemosa. Antiphospholipid antibody (aPL) could not
be detected and there were no microemboli on continuous transcranial Doppler
ultrasonography monitoring. Histology of cerebral vessels showed intimal
hyperplasia in small leptomeningeal venous vessels and micronecrosis of grey
and white matter. We subsequently made the diagnosis of aPL-negative Sneddon
Syndrome (SNS). Anticoagulation with warfarin could not be initiated because of
a drug-resistant epilepsy with the risk of falls and subsequent bleeding;
immunosuppression with steroids and azathioprine was ineffective, as was
initial antiplatelet therapy with clopidogrel alone. However, when we
intensified antiplatelet therapy by combining clopidogrel and ASS, a slowing of
disease progression, as assessed by neuropsychological testing and magnetic
resonance imaging, was noted on a follow-up after 6 months. Therapeutic options
in SNS in both aPL-positive and aPL-negative patients with SNS are discussed.
Copyright 2002 S. Karger AG, Basel PMID: 12373028 6. 6. Sneddon's
syndrome: a case report. Cutis. 2001 Mar;67(3):211-4, 220. Review. Lahti J, Yu T, Burnett JW, Lutz L, LaMonte MP, Gunawardane R. 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. PMID: 11270293 7. 7. Warfarin in
Sneddon's syndrome. Neurology. 1996 Jun;46(6):1781-2. Dupont S, Fénelon G, Saiag P, Sirmai J. No abstract available. PMID: 8649599