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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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symptoms of kidney dysfunction. I find kidney dysfunction in my patients very frequently. Lower back pain is a common indicator that the kidneys are starting to become irritated. Yes, lower back pain can come from many different areas, but one of the areas I always rule out is kidney congestion.
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The word enuresis is derived from a Greek word (enourein) that means “to void urine.” It can occur either during the day or at night (though some restrict the term to bedwetting that occurs at night). Enuresis can be divided into primary and secondary forms.
This title in the new Surgical Techniques Atlas series presents state-of-the-art updates on the full range of pediatric surgical techniques performed today. Expand your repertoire and hone your clinical skills thanks to the expert advice, procedural videos, and online access at expertconsult.com. For more information, please visit http://www.us.elsevierhealth.com/product.jsp?sid=EHS_US_BS-SPE-59&isbn=9781416046899&dmnum=null&elsca1=CriticalCare&elsca2=soc_med&elsca3=null&elsca4=youtube_ELSpromovideos
There are twelve cranial nerves in total. The olfactory nerve (CN I) and optic nerve (CN II) originate from the cerebrum. Cranial nerves III – XII arise from the brain stem (Figure 1). They can arise from a specific part of the brain stem (midbrain, pons or medulla), or from a junction between two parts: Midbrain – the trochlear nerve (IV) comes from the posterior side of the midbrain. It has the longest intracranial length of all the cranial nerves. Midbrain-pontine junction – oculomotor (III). Pons – trigeminal (V). Pontine-medulla junction – abducens, facial, vestibulocochlear (VI-VIII). Medulla Oblongata – posterior to the olive: glossopharyngeal, vagus, accessory (IX-XI). Anterior to the olive: hypoglossal (XII). The cranial nerves are numbered by their loca
How are seizures and epilepsy treated? What should I do if someone has a seizure? When seizure medications don't work, what else can be tried? These are just a few of the questions that you'll find answered here. Some treatment goals are common to everyone. Everyone should know what to do when a person is having a seizure. All people with seizures and their families should know that the real goal of treating epilepsy is to stop seizures or control them as best as possible. But you are more than just a seizure and how epilepsy affects you and your family may be different from someone else. Don't forget the most important goal of the Epilepsy Foundation - helping people with seizures and their families lead full and unrestricted lives according to their own wishes. Patient and doctor discussing treatment options"No seizures, no side effects" is the motto for epilepsy treatment. Not every person will reach that goal right now, but research and getting the "right care at the right time" can help more people achieve it each year. You may learn things here that can help you right away or later on. While seizure medicines are the mainstay of epilepsy treatment, there are other approaches to think about too. We hope these sections will help you learn about different treatments and get the help you need. Learn about the basics of Treatment 101 to help you get started. Look at Receiving Quality Care to see what to expect when you have just been diagnosed or after you have already started treatment. Then learn about specific treatments, what to do if seizures don't stop, and how to develop your health care team. You'll also find tools to help you manage your epilepsy or learn about research studies in other sections, so don't stop here!