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Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it is an important consideration because of its potential morbidity. (See Prognosis.) Knowledge of the anatomy of the venous system is essential in evaluating patients with cerebral venous thrombosis (CVT), since symptoms associated with the condition are related to the area of thrombosis. For example, cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue congestion with obstruction. (See Presentation.) Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebri–like picture. Extension into the jugular bulb may cause jugular foramen syndrome, while cranial nerve palsies may be seen in cavernous sinus thrombosis as a compressive phenomenon. Cerebral hemorrhage also may be a presenting feature in patients with venous sinus thrombosis. (See Presentation.) Imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering the opportunity for early therapeutic measures. (See Workup.) Left lateral sinus thrombosis demonstrated on magn Left lateral sinus thrombosis demonstrated on magnetic resonance venography (MRV). This 42-year-old woman presented with sudden onset of headache. Physical examination revealed no neurologic abnormalities. View Media Gallery Axial view of magnetic resonance (MR) venogram dem Axial view of magnetic resonance (MR) venogram demonstrating lack of flow in transverse sinus. View Media Gallery The following guidelines for CVT have been provided by the American Heart Association and the American Stroke Association [1] : In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed. Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment. Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency), antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3-6 months, with a target international normalized ratio of 2.0-3.0. In patients with unprovoked CVT, vitamin K antagonists may be continued for 6-12 months, with a target international normalized ratio of 2.0-3.0. For patients with recurrent CVT, venous thromboembolism (VTE) after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target international normalized ratio of 2.0-3.0. For women with CVT during pregnancy, low-molecular-weight heparin (LMWH) in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target international normalized ratio of 2.0-3.0 should be continued for ≥6 weeks postpartum (for a total minimum duration of therapy of 6 months). It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist or maternal fetal medicine specialist are reasonable. It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than unfractionated heparin. For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is reasonable. Next: Etiology What to Read Next on Medscape Related Conditions and Diseases Quiz: Do You Know the Complications, Proper Workup, and Best Treatment Practices for Ischemic Stroke? Quiz: How Much Do You Know About Hypothyroidism? Quiz: Do You Know the Risk Factors, Symptoms, and Potential Treatments for Alzheimer Disease? Quiz: How Much Do You Know About Hypertension? 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Pediatric febrile seizures, which represent the most common childhood seizure disorder, exist only in association with an elevated temperature. Evidence suggests, however, that they have little connection with cognitive function, so the prognosis for normal neurologic function is excellent in children with febrile seizures. [1] Epidemiologic studies have led to the division of febrile seizures into 3 groups, as follows: Simple febrile seizures Complex febrile seizures Symptomatic febrile seizures Essential update: Starting MMR/MMRV vaccination earlier may reduce seizure risk In a case-series analysis of a cohort of 323,247 US children born from 2004 to 2008, Hambidge et al found that delaying the first dose of measles-mumps-rubella (MMR) or measles-mumps-rubella-varicella (MMRV) vaccine beyond the age of 15 months may more than double the risk of postvaccination seizures in the second year of life. [2, 3] In infants, there was no association between vaccination timing and postvaccination seizures. [3] In the second year of life, however, the incident rate ratio (IRR) for seizures within 7-10 days was 2.65 (95% confidence interval [CI], 1.99-3.55) after first MMR doses at 12-15 months of age, compared with 6.53 (95% CI, 3.15-13.53) after first MMR doses at 16-23 months. For the MMRV vaccine, the IRR for seizures was 4.95 (95% CI, 3.68-6.66) after first doses at 12-15 months, compared with 9.80 (95% CI, 4.35-22.06) for first doses at 16-23 months.
Blind loop syndrome (BLS), commonly referred to in the literature as small intestinal bacterial overgrowth (SIBO) or bacterial overgrowth syndrome (BOS), is a state that occurs when the normal bacterial flora of the small intestine proliferates to numbers that cause significant derangement to the normal physiological ...
Eosinophilic granulomatosis with polyangiitis (EGPA; also known as Churg-Strauss syndrome [CSS] or allergic granulomatosis) is a rare autoimmune condition that causes inflammation of small and medium-sized blood vessels (vasculitis) in persons with a history of airway allergic hypersensitivity (atopy).
Mitral Valve Prolapse and Mitral Regurgitation. Review of mitral valve anatomy and function, including papillary muscle structure and function, with severe mitral valve prolapse and mitral regurgitation due to a flail segment caused by ruptured papillary muscle and chorda tendinae attachment.
An epidural abscess is a collection of pus (infected material) between the outer covering of the brain and spinal cord and the bones of the skull or spine. The abscess causes swelling in the area. Spinal cord abscess (SCA) is a rare condition capable of causing permanent damage to the spinal cord. Abscesses are caused when injured tissue becomes infected. The body's immune system sends white blood cells to help fight off the infection. They begin to fill the damaged tissue, causing pus to build up.
This is part 2 Herbal Medicine. Lecture presented to the International Congress of Pediatric Hepatology Sharm 2009. It is one of a series of lectures discussing the Alternative medicine practices with critical appraisal and measure the evidence.
In this video Erin K, a tubal reversal patient, explains the symptoms she experienced while suffering from Post Tubal Ligation Syndrome (PTLS). After having tubal reversal surgery her symptoms were relieved. Although numerous women suffer from adverse symptoms after having a tubal ligation, many physicians do not believe PTLS exists. In an ongoing study of over 300 patients reporting Post Tubal Ligation symptoms more than 90% have found relief after tubal reversal at Chapel Hill Tubal Reversal Center.