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

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