Dr. Jeffrey Ojemann, director of epilepsy surgery at Seattle Children's Hospital, explains a cutting-edge treatment for epilepsy: minimally invasive MRI-guided laser ablation surgery. Laser ablation surgery is much safer and more precise than other treatments, with fewer side effects.

A special thanks to patient Keoni Giauque.

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External cephalic version, or version, is a procedure used to turn a fetus from a breech position or side-lying (transverse) position into a head-down (vertex) position before labor begins. When successful, version makes it possible for you to try a vaginal birth.

The majority of fetuses are in a breech presentation early in pregnancy. By week 38th week of gestation, however, the fetus normally turns to a cephalic presentation. Although the fetal head is the widest single diameter, the fetus’s buttocks [ breech], plus the lower extremities, actually takes up more space. The fundus, being the largest part of the uterus, probably accounts for the fact that in approximately 97% of all pregnancies, the fetus turns so that the buttocks and lower extremities are in the fundus. Vaginal delivery of a breech presentation requires great skill if the fetus is not to be damaged. With the low rate of vaginal breech deliveries in the developed world, experience is being lost. 6% of women with breech presentation still have a vaginal breech delivery as they present too late - so units need to retain a high level of preparedness. Types of breech presentation: I. Complete breech [ flexed breech]: The fetal attitude is one of complete flexion, with hips and knees both flexed and the feet tucked in beside the buttocks. The presenting part consists of two buttocks, external genitalia and two feet. It is commonly present in multiparae. II. Incomplete breech: This is due to varying degrees of extension of thighs or legs at podalic pole. Three varieties are possible; - Breech with extended legs [ frank breech ]: The breech presents with the hips flexed and legs extended on the abdomen. 70% of breech presentations are of this type and it is particularly common in primigravidae whose good uterine muscle tone inhibits flexion of the legs and free turning of the fetus. - Footling breech: This is rare. One or both feet present because neither hips nor knees are fully flexed. The feet are lower than the buttocks, which distinguishes it from the complete breech. - Knee presentation: This is very rare. Thighs are extended but the knees are flexed, bringing the knees down to present at the brim.

LBD is not a rare disease. It affects an estimated 1.4 million individuals and their families in the United States. Because LBD symptoms can closely resemble other more commonly known diseases like Alzheimer’s and Parkinson’s, it is currently widely underdiagnosed. Many doctors or other medical professionals still are not familiar with LBD. LBD is an umbrella term for two related diagnoses. LBD refers to both Parkinson’s disease dementia and dementia with Lewy bodies. The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. While it may take more than a year or two for enough symptoms to develop for a doctor to diagnose LBD, it is critical to pursue a formal diagnosis. Early diagnosis allows for important early treatment that may extend quality of life and independence. LBD is a multisystem disease and typically requires a comprehensive treatment approach. This approach involves a team of physicians from different specialties who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms. Many people with LBD enjoy significant improvement of their symptoms with a comprehensive approach to treatment, and some can have remarkably little change from year to year. Some people with LBD are extremely sensitive or may react negatively to certain medications used to treat Alzheimer’s or Parkinson’s in addition to certain over-the-counter medications.

Fifth disease is a mild rash illness caused by parvovirus B19. This disease, also called erythema infectiosum, got its name because it was fifth in a list of historical classifications of common skin rash illnesses in children. It is more common in children than adults. A person usually gets sick with fifth disease within 4 to 14 days after getting infected with parvovirus B19.

The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.

Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently. Not all conditions that lead to heart failure can be reversed, but treatments can improve the signs and symptoms of heart failure and help you live longer. Lifestyle changes — such as exercising, reducing salt in your diet, managing stress and losing weight — can improve your quality of life. One way to prevent heart failure is to control conditions that cause heart failure, such as coronary artery disease, high blood pressure, diabetes or obesity.