Swine Flu : CDC Recommendation

Novel H1N1 Vaccination Recommendations

With the new H1N1 virus continuing to cause illness, hospitalizations and deaths in the US during the normally flu-free summer months and some uncertainty about what the upcoming flu season might bring, CDC's Advisory Committee on Immunization Practices has taken an important step in preparations for a voluntary novel H1N1 vaccination effort to counter a possibly severe upcoming flu season. On July 29, ACIP met to consider who should receive novel H1N1 vaccine when it becomes available.

Novel H1N1 Vaccine

Every flu season has the potential to cause a lot of illness, doctor’s visits, hospitalizations and deaths. CDC is concerned that the new H1N1 flu virus could result in a particularly severe flu season this year. Vaccines are the best tool we have to prevent influenza. CDC hopes that people will start to go out and get vaccinated against seasonal influenza as soon as vaccines become available at their doctor’s offices and in their communities (this may be as early as August for some). The seasonal flu vaccine is unlikely to provide protection against novel H1N1 influenza. However a novel H1N1 vaccine is currently in production and may be ready for the public in the fall. The novel H1N1 vaccine is not intended to replace the seasonal flu vaccine – it is intended to be used along-side seasonal flu vaccine.

CDC’s Advisory Committee on Immunization Practices (ACIP), a

panel made up of medical and public health experts, met July 29, 2009, to make recommendations on who should receive the new H1N1 vaccine when it becomes available. While some issues are still unknown, such as how severe the virus will be during the fall and winter months, the ACIP considered several factors, including current disease patterns, populations most at-risk for severe illness based on current trends in illness, hospitalizations and deaths, how much vaccine is expected to be available, and the timing of vaccine availability.

The groups recommended to receive the novel H1N1 influenza vaccine include:

• Pregnant women because they are at higher risk of complications and can potentially provide protection to infants who cannot be vaccinated;
• Household contacts and caregivers for children younger than 6 months of age because younger infants are at higher risk of influenza-related complications and cannot be vaccinated. Vaccination of those in close contact with infants less than 6 months old might help protect infants by “cocooning” them from the virus;
• Healthcare and emergency medical services personnel because infections among healthcare workers have been reported and this can be a potential source of infection for vulnerable patients. Also, increased absenteeism in this population could reduce healthcare system capacity;
• All people from 6 months through 24 years of age
  • Children from 6 months through 18 years of age because we have seen many cases of novel H1N1 influenza in children and they are in close contact with each other in school and day care settings, which increases the likelihood of disease spread, and
  • Young adults 19 through 24 years of age because we have seen many cases of novel H1N1 influenza in these healthy young adults and they often live, work, and study in close proximity, and they are a frequently mobile population; and,
• Persons aged 25 through 64 years who have health conditions associated with higher risk of medical complications from influenza.

We do not expect that there will be a shortage of novel H1N1 vaccine, but flu vaccine availability and demand can be unpredictable and there is some possibility that initially, the vaccine will be available in limited quantities. So, the ACIP also made recommendations regarding which people within the groups listed above should be prioritized if the vaccine is initially available in extremely limited quantities. For more information see the CDC press release CDC Advisors Make Recommendations for Use of Vaccine Against Novel H1N1.

Once the demand for vaccine for the prioritized groups has been met at the local level, programs and providers should also begin vaccinating everyone from the ages of 25 through 64 years. Current studies indicate that the risk for infection among persons age 65 or older is less than the risk for younger age groups. However, once vaccine demand among younger age groups has been met, programs and providers should offer vaccination to people 65 or older.

Health Hazards of Radiation

Effect Of Hiroshima Bombing
Radiation Induced Health Hazards

Hiroshima Bombing: 6 August 1945

THE ATOMIC BOMBING OF HIROSHIMA
Hiroshima (August 6, 1945)


In the early morning hours of August 6, 1945, a B-29 bomber named Enola Gay took off from the island of Tinian and headed north by northwest toward Japan. The bomber's primary target was the city of Hiroshima, located on the deltas of southwestern Honshu Island facing the Inland Sea. Hiroshima had a civilian population of almost 300,000 and was an important military center, containing about 43,000 soldiers.

The bomber, piloted by the commander of the 509th Composite Group, Colonel Paul Tibbets, flew at low altitude on automatic pilot before climbing to 31,000 feet as it neared the target area. At approximately 8:15 a.m. Hiroshima time the Enola Gay released "Little Boy," its 9,700-pound uranium bomb, over the city. Tibbets immediately dove away to avoid the anticipated shock wave. Forty-three seconds later, a huge explosion lit the morning sky as Little Boy detonated 1,900 feet above the city, directly over a parade field where soldiers of the Japanese Second Army were doing calisthenics. Though already eleven and a half miles away, the Enola Gay was rocked by the blast. At first, Tibbets thought he was taking flak. After a second shock wave (reflected from the ground) hit the plane, the crew looked back at Hiroshima. "The city was hidden by that awful cloud . . . boiling up, mushrooming, terrible and incredibly tall," Tibbets recalled. The yield of the explosion was later estimated at 15 kilotons (the equivalent of 15,000 tons of TNT).

On the ground moments before the blast it was a calm and sunny Monday morning. An air raid alert from earlier that morning had been called off after only a solitary aircraft was seen (the weather plane), and by 8:15 the city was alive with activity -- soldiers doing their morning calisthenics, commuters on foot or on bicycles, groups of women and children working outside to clear firebreaks. Those closest to the explosion died instantly, their bodies turned to black char. Nearby birds burst into flames in mid-air, and dry, combustible materials such as paper instantly ignited as far away as 6,400 feet from ground zero. The white light acted as a giant flashbulb, burning the dark patterns of clothing onto skin (right) and the shadows of bodies onto walls. Survivors outdoors close to the blast generally describe a literally blinding light combined with a sudden and overwhelming wave of heat. (The effects of radiation are usually not immediately apparent.) The blast wave followed almost instantly for those close-in, often knocking them from their feet. Those that were indoors were usually spared the flash burns, but flying glass from broken windows filled most rooms, and all but the very strongest structures collapsed. One boy was blown through the windows of his house and across the street as the house collapsed behind him. Within minutes 9 out of 10 people half a mile or less from ground zero were dead.

People farther from the point of detonation experienced first the flash and heat, followed seconds later by a deafening boom and the blast wave. Nearly every structure within one mile of ground zero was destroyed, and almost every building within three miles was damaged. Less than 10 percent of the buildings in the city survived without any damage, and the blast wave shattered glass in suburbs twelve miles away. The most common first reaction of those that were indoors even miles from ground zero was that their building had just suffered a direct hit by a bomb. Small ad hoc rescue parties soon began to operate, but roughly half of the city's population was dead or injured. In those areas most seriously affected virtually no one escaped serious injury. The numerous small fires that erupted simultaneously all around the city soon merged into one large firestorm, creating extremely strong winds that blew towards the center of the fire. The firestorm eventually engulfed 4.4 square miles of the city, killing anyone who had not escaped in the first minutes after the attack. One postwar study of the victims of Hiroshima found that less than 4.5 percent of survivors suffered leg fractures. Such injuries were not uncommon; it was just that most who could not walk were engulfed by the firestorm.

Even after the flames had subsided, relief from the outside was slow in coming. For hours after the attack the Japanese government did not even know for sure what had happened. Radio and telegraph communications with Hiroshima had suddenly ended at 8:16 a.m., and vague reports of some sort of large explosion had begun to filter in, but the Japanese high command knew that no large-scale air raid had taken place over the city and that there were no large stores of explosives there. Eventually a Japanese staff officer was dispatched by plane to survey the city from overhead, and while he was still nearly 100 miles away from the city he began to report on a huge cloud of smoke that hung over it. The first confirmation of exactly what had happened came only sixteen hours later with the announcement of the bombing by the United States. Relief workers from outside the city eventually began to arrive and the situation stabilized somewhat. Power in undamaged areas of the city was even restored on August 7th, with limited rail service resuming the following day. Several days after the blast, however, medical staff began to recognize the first symptoms of radiation sickness among the survivors. Soon the death rate actually began to climb again as patients who had appeared to be recovering began suffering from this strange new illness. Deaths from radiation sickness did not peak until three to four weeks after the attacks and did not taper off until seven to eight weeks after the attack. Long-range health dangers associated with radiation exposure, such as an increased danger of cancer, would linger for the rest of the victims' lives, as would the psychological effects of the attack.

No one will ever know for certain how many died as a result of the attack on Hiroshima. Some 70,000 people probably died as a result of initial blast, heat, and radiation effects. This included about twenty American airmen being held as prisoners in the city. By the end of 1945, because of the lingering effects of radioactive fallout and other after effects, the Hiroshima death toll was probably over 100,000. The five-year death total may have reached or even exceeded 200,000, as cancer and other long-term effects took hold.

At 11:00 a.m., August 6 (Washington D.C. time), radio stations began playing a prepared statement from President Truman (right) informing the American public that the United States had dropped an entirely new type of bomb on the Japanese city of Hiroshima -- an "atomic bomb." Truman warned that if Japan still refused to surrender unconditionally, as demanded by the Potsdam Declaration of July 26, the United States would attack additional targets with equally devastating results. Two days later, on August 8, the Soviet Union declared war on Japan and attacked Japanese forces in Manchuria, ending American hopes that the war would end before Russian entry into the Pacific theater. By August 9th, American aircraft were showering leaflets all over Japan informing its people that "We are in possession of the most destructive explosive ever devised by man. A single one of our newly developed atomic bombs is actually the equivalent in explosive power to what 2,000 of our giant B-29s can carry on a single mission. This awful fact is one for you to ponder and we solemnly assure you it is grimly accurate. We have just begun to to use this weapon against your homeland. If you still have any doubt, make inquiry as to what happened to Hiroshima when just one atomic bomb fell on that city." Meanwhile, Tibbets's bomber group was simply waiting for the weather to clear in order to drop its next bomb, the plutonium weapon nicknamed "Fat Man" (right) that was destined for the city of Nagasaki.

Neurocysticercosis: Tanea Solium

Tanea Solium: Devastaiting effect.

Introduction
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease. Tanae Solium.

Clinical Features:
History
NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.



•Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
•The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:

◦Epilepsy
■Epilepsy is the most common presentation (70%)
■Seizures secondary to NCC may be generalized or partial.

◦Headache
■Chronic headaches associated with nausea and vomiting (simulating migraines)
■Headaches associated with intracranial hypertension and indicative of hydrocephalus
■Headaches due to meningitis

◦Intracranial hypertension
■Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
■These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.

◦Strokes5
■Ischemic cerebrovascular complications of NCC include lacunar infarcts6 and large cerebral infarcts due to occlusion or vascular damage.
■Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
■Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.

◦Neuropsychiatric disturbances
■These range from poor performance on neuropsychological tests to severe dementia.
■These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.

◦Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.

◦Hydrocephalus
■Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
■Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
•Other forms of neurocysticercosis

◦Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.

◦Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.

Physical
Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:

•Cognitive decline
•Dysarthria
•Extraocular movement palsy or paresis
•Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
•Hemisensory loss
•Movement disorders
•Hyper/hyporeflexia
•Gait disturbances
•Meningeal signs

Causes
NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.

Laboratory Studies
•CSF analysis
◦Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.

•Stool examination
◦Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
◦Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.

•Immunological tests
◦Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.

Imaging Studies
•CT scan

•MRI

considering biopsy.

Medical Care
Treatment of neurocysticercosis depends upon the viability of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite.

•If the parasite is dead, the treatment is directed primarily against the symptoms (eg, anticonvulsants for management of seizures). Monotherapy is usually sufficient. Duration of the treatment remains undefined, and depends neither on the type of seizure at presentation nor on other risk factors for recurrence, such as age at onset and number of seizures before diagnosis. Calcification remains an epileptogenic focus. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice.
•If the parasite is viable or active and the patient has vasculitis, arachnoiditis, or encephalitis, a course of steroids or immunosuppressants is recommended before the use of anticysticercal drugs. Antiparasitic treatment8 with albendazole is also useful in cysticercosis of the racemose type. If only parenchymal, subarachnoid, or spinal cysts are present without the complications mentioned, anticysticercal treatment can be considered, with the concomitant use of steroids, even in patients with massive brain infection. Reports indicate that multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts.
•A recent double-blind, placebo-controlled study has shown that in patients with seizures due to viable parenchymal cysts, antiparasitic therapy decreases the burden of parasites and is safe and effective, at least in reducing the number of seizures with generalization.

Surgical Care
•In the presence of hydrocephalus due to intraventricular cyst, placement of a ventricular shunt is recommended, followed by surgical extirpation of the cyst and subsequent medical treatment.
•In cases of multiple cysts in the subarachnoid space (ie, the racemose form), surgical extirpation, on an urgent basis, is recommended.
•If the obstruction is due to arachnoiditis, placement of a ventricular shunt should be followed by administration of steroids and subsequent medical therapy.
•Because of frequent shunt dysfunctions due to entry of inflammatory tissue as well as parasitic debris inside the ventricular cavities, Sotelo designed a device that functions at a constant flow without the valvular mechanism of Pudenz-type shunts.
•Neuroendoscopy is a new tool with great potential for use in the management of ventricular cysticercosis.
•Surgical treatment in the particular case of medically refractory epilepsy due to a single lesion has been reported. Evaluation in an epilepsy center is indicated.

Alzeimer's Disease or just a poor Memroy?

Alzheimer's Disease Fact Sheet

Alzheimer’s disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks. In most people with AD, symptoms first appear after age 60.

AD is the most common cause of dementia among older people. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—to such an extent that it interferes with a person’s daily life and activities. According to recent estimates, as many as 2.4 to 4.5 million Americans are living with AD.

AD is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles). Plaques and tangles in the brain are two of the main features of AD. The third is the loss of connections between nerve cells (neurons) in the brain.

Changes in the Brain in AD

Although we still don’t know what starts the AD process, we do know that damage to the brain begins as many as 10 to 20 years before any problems are evident. Tangles begin to develop deep in the brain, in an area called the entorhinal cortex, and plaques form in other areas. As more and more plaques and tangles form in particular brain areas, healthy neurons begin to work less efficiently. Then, they lose their ability to function and communicate with each other, and eventually they die. This damaging process spreads to a nearby structure, called the hippocampus, which is essential in forming memories. As the death of neurons increases, affected brain regions begin to shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly.

Very Early Signs and Symptoms

Memory problems are one of the first signs of AD. Some people with memory problems have a condition called amnestic mild cognitive impairment (MCI). People with this condition have more memory problems than normal for people their age, but their symptoms are not as severe as those with AD. More people with MCI, compared with those without MCI, go on to develop AD.

Other changes may also signal the very early stages of AD. For example, recent research has found links between some movement difficulties and MCI. Researchers also have seen links between some problems with the sense of smell and cognitive problems. Brain imaging and biomarker studies of people with MCI and those with a family history of AD are beginning to detect early changes in the brain like those seen in AD. These findings will need to be confirmed by other studies but appear promising. Such findings offer hope that some day, we may have tools that could help detect AD early, track the course of the disease, and monitor response to treatments.

Mild AD

As AD progresses, memory loss continues and changes in other cognitive abilities appear. Problems can include getting lost, trouble handling money and paying bills, repeating questions, taking longer to complete normal daily tasks, poor judgment, and mood and personality changes. People often are first diagnosed in this stage.

Moderate AD

In this stage, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion increase, and people begin to have problems recognizing family and friends. They may be unable to learn new things, carry out tasks that involve multiple steps (such as getting dressed), or cope with new situations. They may have hallucinations, delusions, and paranoia, and may behave impulsively.

Severe AD

By the final stage, plaques and tangles have spread throughout the brain and brain tissue has shrunk significantly. People with severe AD cannot communicate and are completely dependent on others for their care. Near the end, the person may be in bed most or all of the time as the body shuts down.

What Causes AD

Scientists don’t yet fully understand what causes AD, but it is clear that it develops because of a complex series of events that take place in the brain over a long period of time. It is likely that the causes include genetic, environmental, and lifestyle factors. Because people differ in their genetic make-up and lifestyle, the importance of these factors for preventing or delaying AD differs from person to person.

The Basics of AD

Scientists are conducting studies to learn more about plaques, tangles, and other features of AD. They can now visualize plaques by imaging the brains of living individuals. They are also exploring the very earliest steps in the disease process. Findings from these studies will help them understand the causes of AD.

One of the great mysteries of AD is why it largely strikes older adults. Research on how the brain changes normally with age is shedding light on this question. For example, scientists are learning how age-related changes in the brain may harm neurons and contribute to AD damage. These age-related changes include inflammation and the production of unstable molecules called free radicals.

Genetics

In a very few families, people develop AD in their 30s, 40s, and 50s. These people have a mutation, or permanent change, in one of three genes that they inherited from a parent. We know that these gene mutations cause AD in these “early-onset” familial cases.

However, most people with AD have “late-onset” AD, which usually develops after age 60. Many studies have linked a gene called APOE to late-onset AD. This gene has several forms. One of them, APOE ε4, increases a person’s risk of getting the disease. About 40 percent of all people who develop late-onset AD carry this gene. However, carrying the APOE ε4 form of the gene does not necessarily mean that a person will develop AD, and people carrying no APOE ε4 forms can also develop AD.

Lifestyle Factors

A nutritious diet, exercise, social engagement, and mentally stimulating pursuits can all help people stay healthy. New research suggests the possibility that these factors also might help to reduce the risk of cognitive decline and AD. Scientists are investigating associations between cognitive decline and heart disease, high blood pressure, diabetes, and obesity. Understanding these relationships and testing them in clinical trials will help us understand whether reducing risk factors for these diseases may help with AD as well.

How AD Is Diagnosed

AD can be definitively diagnosed only after death by linking clinical course with an examination of brain tissue and pathology in an autopsy. But doctors now have several methods and tools to help them determine fairly accurately whether a person who is having memory problems has “possible AD” (the symptoms may be due to another cause) or “probable AD” (no other cause for the symptoms can be found). To diagnose AD, doctors:

• ask questions about the person’s overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality
• conduct tests of memory, problem solving, attention, counting, and language
• carry out medical tests, such as tests of blood, urine, or spinal fluid
• perform brain scans, such as a computerized tomography (CT) scan or a magnetic resonance imaging (MRI) test

These tests may be repeated to give doctors information about how the person’s memory is changing over time.

Early diagnosis is beneficial for several reasons. Having an early diagnosis and starting treatment in the early stages of the disease can help preserve function for months to years, even though the underlying AD process cannot be changed. Having an early diagnosis also helps families plan for the future, make living arrangements, take care of financial and legal matters, and develop support networks.

In addition, an early diagnosis can provide greater opportunities for people to get involved in clinical trials. In a clinical trial, scientists test drugs or treatments to see which are most effective and for whom they work best. (See the box, below, for more information.)

How AD Is Treated

AD is a complex disease, and no single “magic bullet” is likely to prevent or cure it. That’s why current treatments focus on several different aspects, including helping people maintain mental function; managing behavioral symptoms; and slowing, delaying, or preventing AD.

Helping People with AD Maintain Mental Function

Four medications are approved by the U.S. Food and Drug Administration to treat AD. Donepezil (Aricept®), rivastigmine (Exelon®), and galantamine (Razadyne®) are used to treat mild to moderate AD (donepezil can be used for severe AD as well). Memantine (Namenda®) is used to treat moderate to severe AD. These drugs work by regulating neurotransmitters (the chemicals that transmit messages between neurons). They may help maintain thinking, memory, and speaking skills, and help with certain behavioral problems. However, these drugs don’t change the underlying disease process and may help only for a few months to a few years.

Managing Behavioral Symptoms

Common behavioral symptoms of AD include sleeplessness, agitation, wandering, anxiety, anger, and depression. Scientists are learning why these symptoms occur and are studying new treatments—drug and non-drug—to manage them. Treating behavioral symptoms often makes people with AD more comfortable and makes their care easier for caregivers.

Slowing, Delaying, or Preventing AD

AD research has developed to a point where scientists can look beyond treating symptoms to think about addressing the underlying disease process. In ongoing AD clinical trials, scientists are looking at many possible interventions, such as cardiovascular treatments, antioxidants, immunization therapy, cognitive training, and physical activity.

Supporting Families and Caregivers

Caring for a person with AD can have high physical, emotional, and financial costs. The demands of day-to-day care, changing family roles, and difficult decisions about placement in a care facility can be hard to handle. Researchers are learning a lot about AD caregiving, and studies are helping experts develop new ways to support caregivers.

Becoming well-informed about AD is one important long-term strategy. Programs that teach families about the various stages of AD and about flexible and practical strategies for dealing with difficult caregiving situations provide vital help to those who care for people with AD.

Developing good coping skills and a strong support network of family and friends also are important ways that caregivers can help themselves handle the stresses of caring for a loved one with AD. For example, staying physically active provides physical and emotional benefits. Some AD caregivers have found that participating in an AD support group is a critical lifeline. These support groups allow caregivers to find respite, express concerns, share experiences, get tips, and receive emotional comfort. The Alzheimer’s Association, Alzheimer’s Disease Centers, and many other organizations sponsor in-person and online AD support groups across the country. There are a growing number of groups for people in the early stage of AD and their families. Support networks can be especially valuable when caregivers face the difficult decision of whether and when to place a loved one in a nursing home.

House, MD: Season 5

Season 5 of House MD began airing on September 16, 2008. From September to December 2008, it aired every Tuesday at 8.00 PM EST. House MD was moved to Monday 8.00 PM EST starting January 19, 2009. The season finale “Both Sides Now” was shown last May 11, 2009. The season finale was really a cliffhanger. House thought all along that he slept with Cuddy. But the fact is Cuddy never went home with him and he spent the night popping Vicodin instead of detoxing.

Kutner appeared, presumably for the last time, as part of House’s hallucination. The hallucination arc has been on going for three episodes and the finale is the best among the hallucination story arc.

No explanation on Kutner’s suicide. I guess the writers would just leave it as that. Kutner’s suicide is really a blow to all House MD fans. House checked in a rehab facility and I guess this is where Season 6 would begin.

The link for the Season 5 finale is up. Again thanks to Simon of HouseMDVideos.com for providing excellent online links to all the House MD episodes. We would have to wait for at least 4 more months for Season 6. But until then, catch all the Season 5 episodes below.

Season 5: September 16, 2008 to present

1. Dying Changes Everything
2. Not Cancer
3. Adverse Events
4. Birthmarks
5. Lucky Thirteen
6. Joy
7. The Itch
8. Emancipation
9. Last Resort
10. Let Them Eat Cake
11. Joy to the World
12. Painless
13. Big Baby
14. The Greater Good
15. Unfaithful
16. The Softer Side
17. The Social Contract
18. Here Kitty
19. Locked In
20. Simple Explanation
21. Saviors
22. House Divided
23. Under My Skin
24. Both Sides Now

Acromegaly: Know it Before it Know you

Acromegaly

Acromegaly is the Greek word for "extremities" and "enlargement." When the pituitary gland produces excess growth hormones, this results in excessive growth - called acromegaly. The excessive growth occurs first in the hands and feet, as soft tissue begins to swell. Acromegaly affects mostly middle-aged adults. Untreated, the disease can lead to severe illness and death.

symptoms

Symptoms of acromegaly vary depending on how long the patient has had the disease. The following are the most common symptoms of acromegaly. However, each individual may experience symptoms differently. Symptoms may include:

• swelling of the hands and feet
• facial features become coarse as bones grow
• body hair becomes coarse as the skin thickens and/or darkens
• increased perspiration accompanied with body odor
• protruding jaw
• voice deepening
• enlarged lip, nose, and tongue
• thickened ribs (creating a barrel chest)
• joint pain
• degenerative arthritis
• enlarged heart
• enlargement of other organs
• strange sensations and weakness in arms and legs
• snoring
• fatigue and weakness
• headaches
• loss of vision
• irregular menstrual cycles in women
• breast milk production in women
• impotence in men

The symptoms of acromegaly may resemble other conditions or medical problems. Always consult your physician for a diagnosis.

diagnosis

Due to the subtlety of the symptoms, acromegaly is often not diagnosed until years later. In addition to a complete medical history and medical examination, diagnostic procedures for acromegaly may include:

• serial photos taken over the years (to observe physical changes in the patient)
• x-rays (to detect bone thickening)
• blood tests (to check the growth hormone level)

Treatment for acromegaly:

Specific treatment for acromegaly will be determined by your physician based on:

• your age, overall health, and medical history
• extent of the disease
• your tolerance for specific medications, procedures, or therapies
• expectations for the course of the disease
• your opinion or preference

Treatment of acromegaly depends on the cause of the disease. Ninety percent of acromegaly cases are caused by benign tumors on the pituitary gland. Because the tumor is compressing the pituitary gland, the hormone production can be altered. Some other acromegaly cases are caused by tumors of the pancreas, lungs, or adrenal glands.

The goal of treatment is to restore the pituitary gland to normal function, producing normal levels of growth hormone.

Treatment may include removal of the tumor, radiation therapy, and injection of a growth hormone blocking drug.

Left untreated, acromegaly can lead to diabetes mellitus and hypertension. The disease also increases a patient's risk for cardiovascular disease and colon polyps that may lead to cancer.

Anencephaly: Newborn Deformity

ANENCEPHALY
is a neural tube defect (a disorder involving incomplete development of the brain, spinal cord, and/or their protective coverings). The neural tube is a narrow sheath that folds and closes between the 3rd and 4th weeks of pregnancy to form the brain and spinal cord of the embryo. Anencephaly occurs when the "cephalic" or head end of the neural tube fails to close, resulting in the absence of a major portion of the brain, skull, and scalp. Infants with this disorder are born without both a forebrain (the front part of the brain) and a cerebrum (the thinking and coordinating area of the brain). The remaining brain tissue is often exposed--not covered by bone or skin. The infant is usually blind, deaf, unconscious, and unable to feel pain. Although some individuals with anencephaly may be born with a rudimentary brain stem, the lack of a functioning cerebrum permanently rules out the possibility of ever gaining consciousness. Reflex actions such as respiration (breathing) and responses to sound or touch may occur. The cause of anencephaly is unknown. Although it is believed that the mother's diet and vitamin intake may play a role, scientists believe that many other factors are also involved.

treatment

There is no cure or standard treatment for anencephaly. Treatment is supportive.

prognosis

The prognosis for individuals with anencephaly is extremely poor. If the infant is not stillborn, then he or she will usually die within a few hours or days after birth. [Editor's Note: The unborn child may have been diagnosed as having anencephaly, but be born with a less severe form of the disease, allowing the infant to live for years or more

Gullain Barre Syndrome and Miller Fisher

Guillain-Barré syndrome

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy (AIDP), an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infectious process. It is included in the wider group of peripheral neuropathies. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, AIDP. It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment by plasmapheresis or intravenous immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present.

Pathophysiology

All forms of Guillain-Barré syndrome are due to an immune response to foreign antigens (such as infectious agents) that are mistargeted at host nerve tissues instead (a form of antigenic mimicry). The targets of such immune attack are thought to be gangliosides, which are complex glycosphingolipids present in large quantities on human nerve tissues, especially in the nodes of Ranvier. An example is the GM1 ganglioside, which can be affected in as many as 20-50% of cases, especially in those preceded by Campylobacter jejuni infections. Another example is the GQ1b ganglioside, which is the target in the Miller Fisher syndrome variant

The most common antecedent infection is Campylobacter jejuni. However, 60% of cases do not have a known cause.

The end result of such autoimmune attack on the peripheral nerves is inflammation of myelin and conduction block, leading to a muscle paralysis that may be accompanied by sensory or autonomic disturbances.

Serum sickness can rarely manifest as the Guillain-Barre syndrome (GBS)

Signs and symptoms

1. weakness which affects the lower limbs first, and rapidly progresses in an ascending fashion.
   
2. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness, (oropharyngeal dysphagia, that is difficulty with swallowing, drooling, and/or maintaining an open airway) and respiratory difficulties.
3. Most patients require hospitalization and about 30% require ventilatory assistance.
   
4. Facial weakness is also commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant
   
5. Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of GBS.
   
6. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising.
   
7. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disorder should be suspected.
8. Fever should not be present, and if it is, another cause should be suspected.
9. In severe cases of GBS, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension, and cardiac arrhythmias.

Six different subtypes of Guillain-Barre syndrome (GBS) exist:

• Acute inflammatory demyelinating polyneuropathy (AIDP)
  

• Miller Fisher syndrome (MFS)
  

• Acute motor axonal neuropathy (AMAN)

• Acute motor sensory axonal neuropathy (AMSAN)
  

• Acute panautonomic neuropathy

• Bickerstaff’s brainstem encephalitis (BBE)

Diagnosis

The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. CSF and ECD is used almost every time to verify symptoms, but because of the acute nature of the disorder, they may not become abnormal until after the first week of onset of signs and symptoms.

There currently is no cure for Guillain-Barre syndrome. However, treatments have been proven effective against this syndrome.

• CSF

Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100 - 1000 mg/dL), without an accompanying pleocytosis (increased cell count). A sustained pleocytosis may indicate an alternative diagnosis such as infection.

Electrodiagnostics

Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.

Diagnostic criteria

Required

• Progressive, relatively symmetrical weakness of 2 or more limbs due to neuropathy
• Areflexia
• Disorder course <>
• Exclusion of other causes (see below)

Supportive

• relatively symmetric weakness accompanied by numbness and/or tingling
• mild sensory involvement
• facial nerve or other cranial nerve involvement
• absence of fever
• typical CSF findings obtained from lumbar puncture
• electrophysiologic evidence of demyelination from electromyogram

Treatment

Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm.

Early intubation should be considered in any patient with a vital capacity (VC) <20>2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.

Once the patient is stabilized, treatment of the underlying condition should be initiated as soon as possible.

Either high-dose intravenous immunoglobulins (IVIg) at 400 mg/kg for 5 days or

plasmapheresis

Appendicectomy Video: Watch it

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic Lateral Sclerosis (ALS)

Pop Star Jason beckeris surviving it.

Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig's disease, is a disease that attacks the nerve cells (motor neurons) that control muscles. It gets worse over time (is progressive). Motor neurons carry messages about movement from the brain to the muscles, but in ALS the motor neurons degenerate and die; therefore, the messages to move no longer get to the muscles. When muscles aren't used for a long time, they weaken, waste away (atrophy), and twitch under the skin (fasciculate).
Eventually, all the muscles that a person can control (voluntary muscles) are affected. People with ALS lose the ability to move their arms, legs, mouth, and body. It may get to the point that the muscles used for breathing are affected, and the person might need a respirator (ventilator) in order to breathe. People with ALS can live 3 to 10 years or more after diagnosis.

Mental changesFor a long time it was believed that ALS only affected muscles. It is now known that one-third to one-half of individuals with ALS experience some changes in thinking (cognition). The disease can also cause changes in personality and behavior.

Who gets it?

People are most commonly diagnosed with ALS between the ages of 40 and 70, but younger people can also develop it. ALS affects people all over the world, in all ethnic backgrounds. Men are affected more often than women. About 90-95% of ALS cases appear at random, meaning no one in the person's family has the disorder. In about 5-10% of cases, a family member also has the disorder.

What causes it?

The exact cause of ALS is not known. In 1991, researchers identified a link between ALS and Chromosome 21. Two years later, a particular gene, SOD1, was identified as being associated with about 20% of the inherited cases in families. SOD1 controls an enzyme that breaks down free radicals, harmful particles that attacks cells from the inside and cause their death. Since not all inherited cases are connected to this gene, and some people are the only ones in their families with ALS, other genetic causes must exist.

Symptoms and diagnosis

Usually ALS comes on slowly, starting out as weakness in one or more muscles. Only one leg or arm may be affected. People notice that they stumble, having trouble lifting things, or have trouble with using their hands. As the disease progresses, the person with ALS will not be able to stand or walk, have trouble moving around, and trouble talking and swallowing. The diagnosis of ALS is based on the symptoms and signs the physician observes, as well as tests eliminating all the other possibilities, such as multiple sclerosis, post-polio syndrome, or infectious diseases.

Treatment

There is as yet no cure for ALS. Treatments are designed to relieve the symptoms and improve the quality of life for people with the disorder. Medications can help reduce fatigue, ease muscle cramps, and lessen pain. There is also a specific medication for ALS, called Rilutek (riluzole). It does not repair the damage already done to the body, but appears to be modestly effective in prolonging the survival of people with ALS. Through physical therapy, special equipment, and speech therapy, people with ALS can remain mobile and able to communicate.

LeaRN ABOUT bECKER AT www.xyzmusic.blogspot.com

Uterovaginal Prolapse: Types and Causes

Uterovaginal Prolapse Is a form of Hernia in which the uterus and Vagina protrudes down out of their normal confinement.

Types
I. Vaginal
a. Anterior wall
-Cystocele( Uriary bladder prolapse)
-Urethrocele( Urethra)
-Combined
b.Posterior wall
-Relaxed perinium
-Rectocele
-Vault prolapse

II. Uterine
Uterovaginal
Congenital

Causes Of Prolapse

Preciptating factors
I. Acquired
a. Overstretching of mackenrodth and Uterosacral Ligaments due to
Premature bear down
Application of forceps when cervix not fully dilated
down pressure on fundus to deliver placents
Precipitate labour
b. Overstretching of endopelvic fascial sheath of vagina
Degree of distension during delivery and duration
c.Subinvolution
ill nourished mother
early resumption of work
perisitent overfilling of bladder
repeated childbirth
d.Over stretching of perinium

Congenital
Spina Bifida occulta
Neurological disorders.

II. Aggravating factors.
a Increased abd pressure.
cough, constipation
b. bulky uterus, fibroid.
c.post menopausal atrophy
d.Asthenia and undernutrition



Overstretchin of perinium

Rhinophyma: Cosmetic Issue

Rhinophyma

Rhinophyma (an advanced type of rosacea) is characterized by an enlarged, bulbous, and red nose resulting from enlargement of the oil-producing glands beneath the surface of the skin on the nose. Depending on the severity of rhinophyma, doctors may begin treatment with topical or oral rosacea treatment.



What Is Rhinophyma?
To understand what rhinophyma is, it's important to first have a basic understanding of rosacea. Rosacea is a chronic disease that affects the skin. The disease is characterized by redness, pimples, and, in advanced stages, thickened skin. When rosacea reaches this advanced stage, rhinophyma may develop. The most common characteristic of rhinophyma is an enlarged, bulbous, and red nose. Rhinophyma is associated with the sebaceous (oil-producing) glands beneath the surface of the skin on the nose. The condition is more common in men than women.


Symptoms of Rhinophyma
Rhinophyma is characterized by an enlarged, bulbous, and red nose resulting from the enlargement of the sebaceous (oil-producing) glands beneath the surface of the skin on the nose.


What Causes Rhinophyma?
Doctors do not know the exact cause of rhinophyma.


Diagnosing Rhinophyma
Dermatologists usually diagnose rhinophyma by its appearance and associated symptoms because there are no tests that can diagnose this disease. However, on rare occasions, skin biopsies can pinpoint rhinophyma. Doctors will usually diagnose a patient with rhinophyma if the patient has rhinophyma symptoms and a family history of rhinophyma.


Current Treatment of Rhinophyma
Depending on the severity of the rhinophyma, doctors may begin treatment with topical or oral rosacea medications. Rhinophyma that does not respond to medications may be treated with:

Electrosurgery
Laser treatment
Dermabrasion
Resculpturing

ALOPECIA: HAIR LOSS causes

Hair loss

loss of hair is called alopecia.

Facts:
Hair loss usually develops gradually and may be patchy or diffuse (all over).

Roughly 100 hairs are lost from your head every day.

The average scalp contains about 100,000 hairs.
Each individual hair survives for an average of 4-1/2 years, during which time it grows about half an inch a month. Usually in its 5th year, the hair falls out and is replaced within 6 months by a new one.

Genetic baldness is caused by the body's failure to produce new hairs and not by excessive hair loss.
Both men and women tend to lose hair thickness and amount as they age. Inherited or "pattern baldness" affects many more men than women. About 25% of men begin to bald by the time they are 30 years old, and about two-thirds are either bald or have a balding pattern by age 60.

male pattern baldness involves a receding hairline and thinning around the crown with eventual bald spots. Ultimately, you may have only a horseshoe ring of hair around the sides. In addition to genes, male-pattern baldness seems to require the presence of the male hormone testosterone . Men who do not produce testosterone (because of genetic abnormalities or castration) do not develop this pattern of baldness.

Some women also develop a particular pattern of hair loss due to genetics, age, and male hormones that tend to increase in women after menopause. The pattern is different from that of men. Female pattern baldness involves a thinning throughout the scalp while the frontal hairline generally remains intact.

Common Causes:
Baldness is not usually caused by a disease, but is related to aging, heredity, and testosterone. In addition to the common male and female patterns from a combination of these factors, other possible causes of hair loss, especially if in an unusual pattern, include:
Alopecia areata -- bald patches that develop on the scalp, beard, and, possibly, eyebrows. Eyelashes may fall out as well.
Autoimmune conditions such as lupus
Burns
Certain infectious diseases such as syphilis
Chemotherapy
Emotional or physical stress
Excessive shampooing and blow-drying
Fever
Hormonal changes -- for example, thyroid disease , childbirth, or use of birth control pills
Nervous habits such as continual hair pulling or scalp rubbing
Radiation therapy
Tinea capitis (ringworm of the scalp)
Tumor of the ovary or adrenal glands

The Largest Physics experiment : Hoax of Doomsday ??

1. When u attack the most difficult and fundamental questions [in science] you get a wide range of innovations, from MRI scanners to Facebook
   

"f you destroy particle physics and astronomy you will not produce more scientists working on carbon capture, you will just produce fewer scientists. "
Professor David L Wark

"The most powerful physics experiment ever built, the Large Hadron Collider will re-create the conditions just after the Big Bang in an attempt to answer fundamental questions of science and the universe itself. "

For More http://news.bbc.co.uk/2/hi/science/nature/7567926.stm

10 September,

News of Suicide by a Girl in India:

The Fear of Doomsday, Hoax made by Indian Cheap News Channels Like AAjtak, has lead to suicide of a Girl in Bhopal.

Since last 7-8 days the channels have been making a hoax of a doomsday resulting from this experiment, creating fear in the minds of the viewers. even my friends got scared... like these were the last few days to live...

Is it right to make such kinda publicites just to increase TPR of TV channels.?

Please leave you valuable coments>>>>

Birth defects Gallery

DOWN SYNDROME

HYDROCEPHALUS

ANENCEPHALY

Top Medical sites 2008

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Chest Pain Differential Diagnosis

Myocardial Ischaemic Pain

The main feature of myocardial ischaemia (impending infarction) is usually prolonged chest pain. Typical characteristics of the pain include:
Duration usually over 20 minutes
Located in the retrosternal area, possibly radiating to the arms (usually to the left arm), back, neck, or the lower jaw
The pain is described as pressing or heavy or as a sensation of a tight band around the chest; breathing or changing posture does not notably influence the severity of the pain.
The pain is continuous, and its intensity does not alter
The symptoms (pain beginning in the upper abdomen, nausea) may resemble the symptoms of acute abdomen. Nausea and vomiting are sometimes the main symptoms, especially in inferoposterior wall ischaemia.
In inferoposterior wall ischaemia, vagal reflexes may cause bradycardia and hypotension, presenting as dizziness or fainting.
Electrocardiogram (ECG) is the key examination during the first 4 hours after pain onset, but normal ECG does not rule out an imminent infarction.
Markers of myocardial injury (cardiac troponins T and I, creatine kinase-MB mass) start to rise about 4 hours after pain onset. An increase of these markers is diagnostic of myocardial infarction irrespective of ECG findings.
Minor signs of myocardial infarction in ECG, see Table 1 in the original guideline document
Nonischaemic Causes of Chest Pain

Illness/condition Differentiating symptoms and signs
Reflux oesophagitis, oesophageal spasm
No ECG changes
Heartburn
Worse in recumbent position, but also while straining, like angina pectoris
The most common cause of chest pain

Pulmonary embolism
Tachypnoea, hypoxaemia, hypocarbia
No pulmonary congestion on chest x-ray
Clinical presentation may resemble hyperventilation.
Both arterial oxygen pressure (PaO2) and partial arterial pressure of carbon dioxide (PaCO2) decreased.
Pain is not often marked.
D-dimer assay positive

Hyperventilation
Hyperventilation Syndrome

The main symptom is dyspnoea, as in pulmonary embolism.
Often a young patient
Tingling and numbness of the limbs, dizziness
PaCO2 decreased, PaO2 increased or normal
Secondary Hyperventilation

Attributable to an organic illness/cause; acidosis, pulmonary embolism, pneumothorax, asthma, infarction, etc.

Spontaneous pneumothorax
Dyspnoea is the main symptom.
Auscultation and chest x-ray

Aortic dissection
Severe pain with changing localization
Type A dissection sometimes obstructs the origin of a coronary artery (usually the right) with signs of impending inferoposterior infarction
Pulses may be asymmetrical
Sometimes broad mediastinum on chest x-ray
New aortic valve regurgitation

Pericarditis
Change of posture and breathing influence the pain.
A friction sound may be heard.
ST-elevation but no reciprocal ST depression

Pleuritis
A stabbing pain when breathing. The most common cause of stabbing pain is, however, caused by prolonged cough

Costochondral pain
Palpation tenderness, movements of chest influence the pain
Might also be an insignificant incidental finding

Early herpes zoster
No ECG changes, rash
Localized paraesthesia before rash

Ectopic beats
Transient, in the area of the apex

Peptic ulcer, cholecystitis, pancreatitis
Clinical examination (inferior wall ischaemia may resemble acute abdomen)

Depression
Continuous feeling of heaviness in the chest, no correlation to exercise
ECG normal

Alcohol-related
A young male patient in a casualty department, inebriated


ST changes resembling those of acute ischaemia
ST segment elevation
Early repolarization in V1–V3. Seen particularly in athletic men ("athlete's heart")
Acute myopericarditis in all leads except V1, aVR. Not resolved with a beta-blocker.
Pulmonary embolism – in inferior leads
Hyperkalaemia
Hypertrophic cardiomyopathy



ECG
ST segment depression
Sympathicotonia
Hyperventilation
Pulmonary embolism
Hypokalaemia
Digoxin
Antiarrhythmics
Psychiatric medication
Hypertrophic cardiomyopathy
Reciprocal ST depression of an inferior infarction in leads V2–V3–V4
Circulatory shock

QRS changes resembling those of Q wave infarction
Hypertrophic cardiomyopathy
Wolff-Parkinson-White (WPW) syndrome
Myocarditis
Blunt cardiac injury
Massive pulmonary embolism (QS in leads V1–V3)
Pneumothorax
Cardiac amyloidosis
Cardiac tumours
Progressing muscular dystrophy
Friedreich's ataxia

ST changes resembling those of a non-Q wave infarction
Increased intracranial pressure – subarachnoid bleed – skull injury
Hyperventilation syndrome
Post-tachyarrhythmia state
Circulatory shock – haemorrhage – sepsis
Acute pancreatitis
Myopericarditis

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