Huntington's disease is an inherited disorder that causes the degeneration of brain cells. This results in a progressive loss of the control of movement and mental ability, and changes in personality.
Around 4,800 people in the UK are living with Huntington's disease. It used to be called Huntington's chorea. Chorea means jerky, involuntary movements - a main symptom of the condition.
Huntington's disease usually develops between the ages of 30 and 50, but it can start at any age. Symptoms get worse gradually, sometimes over a period of up to 20 years. At the moment, there is no cure for the disease, but there are ways to help manage the symptoms.
Symptoms
The symptoms of Huntington's disease are sometimes overlooked. This is because they are mild at first and people without the disease can have the same symptoms. People who have Huntington's disease sometimes have problems for a long time before they find out that they have the condition.
Early symptoms include:
* mild tremor
* clumsiness
* lack of concentration and irritability
* difficulty remembering things
* mood changes, including depression
* aggressive antisocial behaviour
Over time the symptoms become progressively worse. Eventually, full-time nursing care will be needed. Later symptoms fall into three categories:
Physical symptoms
Physical symptoms include chorea (involuntary movements of the limbs, face and body). Chorea may lead to difficulty walking, speaking and swallowing. People often lose weight because of difficulty eating and by burning more calories due to the continuous movement. The ability to coordinate movement gets gradually worse as the disease progresses.
Emotional symptoms
Emotional symptoms include depression, not only because of the burden of having a progressive disorder, but as a direct result of the damage to certain brain cells. You may become frustrated at being unable to work or do previously simple tasks. You may behave stubbornly, and have mood swings. People with Huntington's may also become more irritable and antisocial than usual, or have less inhibitions.
Cognitive symptoms
Cognitive symptoms include a loss of drive and initiative. People with Huntington's may appear to be lazy or uninterested in life, spending days doing little or neglecting personal hygiene. You may also lose the ability to organise yourself. This is because planning skills and the ability to do more than one task at once deteriorate. In the later stages, you may get memory loss and be less able to understand speech.
The behavioural changes that occur are often the most distressing for you, your family and your carers. A previously full and active life may be lost with a gradual reduction in independence and mobility. At the same time, your personality can become gradually more self-centred and unmotivated, straining personal relationships.
Causes
Huntington's disease is caused by a faulty gene that runs in families. The gene, which was discovered in 1993, produces a protein called Huntingtin. Scientists are still researching how the faulty gene causes the disease.
Most genes in the body are present in two copies: one from your mother and one from your father. The gene that causes Huntington's disease is dominant. This means that if you inherit a copy of this gene from either parent, you will go on to develop the disease at some point in your life.
If you have one parent with Huntington's disease you have a 50 percent chance of inheriting the faulty gene. The risk is 50 percent for each child. It isn't altered by gender or whether brothers and sisters are affected. Only people who have the faulty gene can pass it on to their children.
Occasionally there is no family history of the condition. This may be because previous generations weren't diagnosed - either because of early death from other causes, or loss of contact through adoption.
Huntington's disease causes progressive damage to cells in areas of your brain called the basal ganglia and cerebral cortex. These areas are involved in the control of movement, planning, motivation and personality.
Juvenile Huntington's disease
A juvenile form of Huntington's disease, which develops before the age of 20, also exists. About five percent of people with Huntington's disease are affected by the condition when this young. The symptoms are similar to those of adult Huntington's, but muscular rigidity is more likely to occur. Epilepsy - which causes fits - is also more common among those with juvenile Huntington's disease compared with adults who have the condition.
Treatment
Although there is currently no cure for Huntington's disease, there are drugs to help manage some of your symptoms. There are medicines that can reduce the involuntary movements, and antidepressant medicines may alleviate depression. Mood stabilisers and antipsychotic drugs can help with some of the emotional disturbances.
Counselling can also be helpful, both for you and your family. Dieticians can advise on adequate calorie and nutrient intake to stop weight loss.
Future promise
Scientists are investigating several drug treatments to slow the progress of Huntington's disease. Some of these have shown promise and are planned to be tested in clinical trials. Examples include the antibiotic minocycline and coenzyme Q10. However, this research is speculative; more work is needed before any recommendations can be made.
Some clinical studies have used stem cells (the most basic form of cells from which others develop) to grow cells that can be transplanted into the brain of people affected by the disease. This approach may eventually improve the outlook for people with Huntington's disease. However, this research is still in the very early stages of development.
Genetic tests
There are tests available to find out whether you have the faulty gene. They fall into three categories: diagnostic, pre-symptomatic and antenatal.
Diagnostic tests
These are carried out if you have symptoms of Huntington's disease and you come from a family where others have the condition. The aim is to confirm the diagnosis.
Pre-symptomatic tests
These tests are carried out if you have no symptoms of Huntington's disease, but you have family members who are affected by it. The test tells you whether you will develop the disease, but not when it will happen.
The decision to take these tests is a serious one and shouldn't be rushed into. A positive result can be devastating since it may tell you that one day you will become severely ill. There are also issues surrounding testing when your parents have themselves not been tested. This is because a positive result means that one of your parents also has the faulty gene.
You should take advice from a genetic counsellor about the implications of taking the test before you go ahead. In the UK you can't have the test if you are under the age of 18.
Antenatal tests
These tests may be carried out early in pregnancy on the unborn children of couples from families affected by Huntington's disease. They can be used to calculate the risk of that child going on to develop the disease in their adult life.
Pre-implantation Genetic Diagnosis (PGD)
If you know that you carry the gene for Huntington's disease, you can opt for PGD. This is a type of in vitro fertilisation (IVF). Only embryos which are not carrying the faulty Huntington gene are used, so the baby is not at risk of having the disease.
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Showing posts with label NEURO-SPINAL. Show all posts
Showing posts with label NEURO-SPINAL. Show all posts
Saturday, February 27, 2010
Friday, January 15, 2010
Alzheimer's Disease
http://www.enotes.com
Definition
Alzheimer's disease (AD) is the most common form of dementia, a neurologic disease characterized by a progressive loss of mental ability severe enough to interfere with normal activities of daily living, lasting at least six months, and not present from birth. AD usually occurs in old age and is marked by a decline in cognitive functions such as remembering, reasoning, and planning.
Description
A person with AD usually has a gradual decline in mental functions, often beginning with slight memory loss, followed by losses in the ability to maintain employment, to plan and execute familiar tasks, and to reason and exercise judgment. Communication ability, mood, and personality may also be affected. Most people who have AD die within eight years of their diagnosis, although that interval may be as short as one year or as long as 20 years. AD is the fourth leading cause of death in adults after heart disease, cancer, and stroke.
In 2001, four million Americans have been diagnosed with AD. That number is expected to grow to as many as 14 million by the middle of the twenty-first century as the baby-boomer population ages. These numbers may be seriously underestimated due to new research that suggests mild cognitive impairment may be early stages of AD.
While a small number of people in their 40s and 50s develop the disease (called early-onset AD), AD predominantly affects the elderly. AD affects about 10% of all people over the age of 65 and nearly half of those over85. Slightly more women than men are affected with AD, since women tend to live longer and occupy a larger proportion of the most affected age groups.
The costs for caring for loved ones with AD is considerable, and has been estimated at approximately $174,000 per person over the course of the disease. More than 70% of people with AD are cared for at home at an estimated annual cost of $196 billion. These costs are not supplemented by outside sources. If patients are cared for by paid home caregivers or are placed in nursing homes, the total annual out-of-pocket costs by families or third party payees account for $83 billion and $32 billion respectively.
Causes and symptoms
Causes
The cause of Alzheimer's disease is unknown. Some strong leads have been found through recent research, however, and these have also given some theoretical support to several new experimental treatments.
AD affects brain cells responsible for learning, reasoning, and memory. Autopsies of people with AD indicate that these regions of the brain become clogged with two abnormal structures, neurofibrillary tangles and senile plaques. Neurofibrillary tangles are twisted masses of protein fibers inside nerve cells (neurons). Senile plaques are composed of parts of neurons surrounding a group of brain proteins called beta-amyloid deposits. While it is not clear exactly how these structures cause problems, some researchers now believe that their formation is responsible for the mental changes of AD, presumably by interfering with the normal communication between neurons in the brain. Drugs approved by the Food and Drug Administration (FDA) increase the level of chemical signaling molecules in the brain, known as neurotransmitters, to make up for this decreased communication ability.
What triggers the formation of plaques and tangles is unknown, although there are several possible candidates. Restriction of blood flow may be part of the problem, perhaps accounting for the beneficial effects of estrogen, which increases blood flow in the brain. However, studies in 2001 do not show estrogen as a protection against the development of AD.
Highly reactive molecular fragments called free radicals damage cells of all kinds, especially brain cells, which have smaller supplies of protective antioxidants thought to protect against free radical damage. Vitamin E is one such antioxidant, and its use in AD is showing some benefit.
Several genes have been implicated in AD, including the gene for amyloid precursor protein (APP) responsible for producing amyloid. Mutations in this gene are linked to some cases of the relatively uncommon earlyonset forms of AD. Other cases of early-onset AD are caused by mutations in the gene for another protein, presenilin. AD eventually affects nearly everyone with Down syndrome, caused by an extra copy of chromosome 21. Other mutations on other chromosomes have been linked to other early-onset cases.
Potentially the most important genetic link was discovered in the early 1990s on chromosome 19. A gene on this chromosome, apoE, codes for a protein involved in transporting lipids into neurons. ApoE occurs in at least three forms: apoE2, apoE3, and apoE4. Each person inherits one apoE from each parent, and therefore can either have one copy of two different forms or two copies of one. Compared to those without ApoE4, people with one copy are about three times as likely to develop lateonset AD, and those with two copies are almost four times as likely to do so. Despite this important link, not everyone with apoE4 develops AD, and people without it can still have the disease. Why apoE4 increases the chances of developing AD is not known.
Promising research in 2001 has discovered a protein, apoptosis-inducing factor, that kills cells by disrupting the genetic material at their cores. This discovery could lead to drugs that could turn off this protein that triggers apoptosis or biologically regulated cell death, which is important in fetal development but is also implicated in stroke, heart disease, and AD. It is thought that this protein runs out of control and shuts off otherwise healthy cells.
There are several risk factors that seem to increase a person's likelihood of developing the disease. The most significant one is, of course, age; older people develop AD at much higher rates than younger ones. Another risk factor is having a family history of AD, Down syndrome, or Parkinson's disease. People who have had head trauma or hypothyroidism may manifest the symptoms of AD sooner.
Many environmental factors have been suspected of contributing to AD, but population studies generally have not borne these out. A study in early 2001, however, showed a specific link between aluminum in drinking water and the incidence of AD. Other suspected risk factors were other pollutants in drinking water, aluminum in any form, and mercury in dental fillings. To date, none of these other factors has been shown to cause AD or to increase its likelihood.
Lifestyle factors, moreover, may prove to be better indicators of risk. Lack of stimulation, mentally and physically, between the ages of 20 and 60 seems linked to the incidence of AD. Studies have not shown, though, that a sedentary lifestyle early in life causes AD or whether it is a marker for the incidence of the disease.
Another study of African Americans and their Nigerian counterparts shows AD appearing more often in the American population than the African one. Researchers suggest that environmental or cultural factors may play a role in the formation of AD. Here, physical activity or diet may play a part.
Symptoms
The symptoms of Alzheimer's disease begin gradually, usually with memory lapses. Occasional memory lapses are common to everyone and do not, by themselves, signify any change in cognitive function. The person with AD may begin with only the routine sort of memory lapse—forgetting where the car keys are—but progresses to more profound or disturbing losses such as forgetting how to even drive a car. Being lost or disoriented on a walk around the neighborhood becomes more likely as the disease progresses. A person with AD may forget the names of family members, or forget what was said at the beginning of a sentence by the end of the sentence.
As AD progresses, other symptoms appear, including inability to perform routine tasks, loss of judgment, and personality or behavior changes. Some patients have trouble sleeping and may suffer from confusion or agitation in the evening, known as sunsetting. In some cases, people with AD repeat the same ideas, movements, words, or thoughts, a behavior known as perseveration. There may be delusional thinking or even hallucinations. In the final stages people may have severe problems with eating, communicating, and controlling their bladder and bowel functions.
The Alzheimer's Association has developed a list of 10 warning signs of AD. A person with several of these symptoms should see a physician for a thorough evaluation:
* memory loss that affects job skills
* difficulty performing familiar tasks
* problems with language, as in word-find problems or inappropriate word substitutions
* disorientation about time and place
* poor or decreased judgment
* problems with abstract thinking
* misplacing things
* changes in mood or behavior
* changes in personality
* loss of initiative
Other types of dementia, including some that are reversible, can cause similar symptoms. It is important for the person with these symptoms to be evaluated by a professional who can weigh the possibility that the symptoms may have another cause. Approximately 20% of those originally suspected of having AD actually have some other disorder; about half of these cases are treatable.
Diagnosis
Diagnosis of Alzheimer's disease is complex and may require visits to several different specialists over several months before a determination can be made. With new diagnostic tools and criteria, it is possible to make a provisional diagnosis that is about 90% accurate. A positive confirmation of these findings can be made only through autopsy.
Early diagnosis is essential in helping the patient and the family make decisions about treatment, long-term care, and financial matters. Finding out that a loved one's behavior is based on a degenerative mental disease can help a family avoid unnecessary anger and feelings of impotence when dealing with the progression of the disease.
There are two diagnoses the clinical team can make for a patient. They are probable AD or possible AD. Probable AD is determined when physicians and psychiatrists rule out all other disorders that might produce similar symptoms. A diagnosis of possible AD is made when AD is considered the primary reason for the symptoms but is complicated with the presence of another disorder that might confuse the general progression of the disease.
Diagnosis for AD begins with the elimination of other physical and psychological causes for the patient's behavior. This is done through a multi-step process that tests for other disorders and measures the amount of deficit the patient is experiencing.
Patient history
A detailed medical history should be taken, noting a list of the patient's medicines (prescription and over the counter), vitamins, and herbs. Since there are many pharmaceuticals that can cause the same mental changes as AD, a careful review of the patient's medication, alcohol, and herbal use is important. If the patient's symptoms are related to any of these, most likely the condition can be reversed through adjustments in the patient's medications or herbal use. Any illicit drugs should also be reported.
Next, the physician should take a detailed report of any changes in the patient's mental functioning and memory. This will determine the mode of onset of symptoms, the progression of the deficits, and the impact of the impairment on daily functioning.
Physical exam and lab tests
AD-like symptoms can also be provoked by other medical conditions, including tumors, infection, thyroid malfunctioning, and dementia caused by mild strokes (multi-infarct dementia). These possibilities must be ruled out through blood screens, urine tests, electroencephalographs (EEGs), and a variety of imaging techniques.
A genetic test for the ApoE4 gene is available, but is not used for diagnosis, since possessing even two copies does not ensure that a person will develop AD.
Cognitive functioning evaluation
Several types of oral and written tests are used in AD diagnosis and disease progression, including tests of mental status, language ability, functional ability, memory, and concentration. In the early stages of the disease, the results of these tests are usually normal. It should be noted that the widely-used Mini-Mental State Examination (MMSE) may not be accurate for highly educated or poorly educated individuals, or cultural minorities.
Neuropsychiatric evaluation
A detailed cognitive evaluation can be done by a psychologist or psychiatrist. These tests of memory and mental functioning provide a quantitative measure of the patient's deficits.
One of the most important parts of the diagnostic process is the evaluation of depression and delirium, since these can be present with AD or may be mistaken for it. (Delirium involves a decreased consciousness or awareness of one's environment.) Depression and memory loss are both common in the elderly, and the combination of the two can often be mistaken for AD. Depression can be treated with drugs, although some antidepressants can worsen dementia if it is present, further complicating both diagnosis and treatment.
Imaging studies
Several imaging techniques can assess brain function and pathology, thus eliminating these as causes of the patient's symptoms. Most frequently used imaging scans are magnetic resonance imaging (MRI) or computed tomography (CT) scans, which detect structural changes in the brain. Brain function can be assessed through MRI, positron emission tomography (PET), and single-photon emission CT (SPECT). These tests help rule out stroke, subdural hematoma, and brain tumor as possible causes for the patient's symptoms.
Treatment
Alzheimer's disease is currently incurable, though a number of pharmaceuticals and home care strategies can mange the disease. The mainstay of AD treatment continues to be good nursing care, providing both physical and emotional support, as the patient gradually is able to do less independently and whose behavior becomes more erratic. Modifications of the home to increase safety are often necessary. Creative strategies to help the patient stay as independent as possible are also indicated. The caregiver also needs support to minimize anger, despair, and burnout.
Drugs
Donepezil hydrochloride (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) have been approved for use in AD treatment. These drugs increase the levels of the neurotransmitter acetylcholine in the brain, thereby increasing the communication ability of the remaining neurons. They do this by inhibiting the enzymes, acetylcholinesterase and butylcholinesterase, which normally break down acetylcholine and butylcholine released by neurons. These drugs modestly increase attention span, concentration, mental acuity, and information processing. Tacrine (Cognex), the first drug used, is no longer used due to the risk of liver toxicity. All cholinesterase inhibitors have mild gastric side effects such as nausea and vomiting.
The antioxidant, vitamin E, is also thought to delay AD onset because it prevents neuron damage caused by free radicals. Vitamin E therapy, in combination with cholinesterase inhibitors, has become a practice standard in the treatment of AD.
Drugs that have been found ineffective are Selegiline (used in the treatment of Parkinson's disease), prednisone, and the anti-inflammatory NSAID diclofenac. Estrogen, once thought to be the keystone in treatment and prevention of AD in women, was found to be ineffective in mitigating symptoms in 2001. There is still some discussion about estrogen's ability to delay the onset of AD.
Depression may be treated with selective serotonin reuptake inhibitors (SSRIs) such as citalopram and sertraline. Physicians may also prescribe typical antipsychotics for agitation, aggression, or hallucinations, such as olanzapine, quetiapine, or risperidone. It should be noted that AD patients have more side effects from most medications, especially psychoactive drugs, and care should be taken in their selection.
Alternative treatment
Several substances are currently being tested for their ability to slow the progress of Alzheimer's disease. Among them are gingko extract, derived from the leaves of the Gingko biloba tree, and huperzine A, from the moss Huperzia serrata. Gingko extract has antioxidant, anti-inflammatory, and neuroprotective effects and has been used for many years in China and is widely prescribed in Europe for treatment of circulatory problems. It has been shown to modestly improve cognitive function. Huperzine A is a natural cholinesterase inhibitor. It is reported to produce greater improvement than the synthetic cholinesterase inhibitors and has few side effects. Since neither herbal is regulated, they may have inconsistent levels of their active ingredients per dosage.
Nursing care and safety
The person with Alzheimer's disease will gradually lose the ability to dress, groom, feed, bathe, or use the toilet without help; in the late stages of the disease, the individual may be unable to move or speak. In addition, the person's behavior becomes increasing erratic. A tendency to wander may make it difficult to leave the patient unattended for even a few minutes, which would make even the home a potentially dangerous place. In addition, some patients may exhibit inappropriate sexual behaviors.
Nursing care required for AD patients is simple enough to learn. The difficulty for many caregivers comes in the constant but unpredictable nature of the demands put on them. Additionally, the personality changes presented in AD can be heartbreaking for family members as a loved one deteriorates, seeming to become a different person. Not all AD patients develop negative behaviors: some become gentle, spending increasing amounts of time in dream-like states.
A loss of grooming skills may be one of the early symptoms of AD. Mismatched clothing, unkempt hair, and decreased interest in personal hygiene become more common. Caregivers, especially spouses, may find these changes socially embarrassing and difficult to cope with. The caregiver will begin to assume more and more grooming duties for the patient as the disease progresses.
Ensuring proper nutrition for the AD patient may require using a colored plate to focus the patient's attention on the food. Finger foods may be preferable to those foods requiring utensils. Later, the caregiver may need to feed the patient. As movement and swallowing become difficult, a feeding tube may be placed into the stomach through the abdominal wall, which will require special attention.
For many caregivers, incontinence becomes the most difficult problem to deal with at home, and is a principal reason for pursuing nursing home care. In the early stages, limiting fluid intake and increasing the frequency of toileting can help. Careful attention to hygiene is important to prevent skin irritation and infection from soiled clothing.
Safety will become of prime importance. In all cases, a person diagnosed with AD should not be allowed to drive, because of the increased potential for accidents and the increased likelihood of wandering far from home while disoriented. In the home, grab bars in the bathroom, bed rails on the bed, and clutter-free passageways can greatly increase safety. Electrical appliances should be unplugged and put away when not in use, and matches, lighters, knives, or weapons should be stored out of reach. The hot water heater temperature should be set lower to prevent accidental scalding. A list of emergency numbers, including the poison control center and the hospital emergency room, should be posted by the phone.
A calm, structured environment with simple orientation aids such as calendars and clocks may reduce anxiety and increase safety. Labeling cabinets and drawers may keep the patient's attention focused. Scheduling meals, bathing, and other activities at regular times and places will provide emotional security and routine, since unfamiliar places and activities can be disorienting for the patient. Sleep disturbances may be minimized by keeping the patient engaged in activities during the day, offering structure and providing physical activities.
Care for the caregiver
Family members or others caring for a person with AD have a difficult and stressful job, which becomes harder still as the disease progresses. It is common for caregivers to develop feelings of anger, resentment, guilt, and hopelessness, in addition to the sorrow they feel for their loved one and for themselves. Depression is an extremely common consequence of being a full-time caregiver for an AD patient. Support groups are an important way to deal with the stress of caregiving. The location and contact numbers for AD caregiver support groups are available from the Alzheimer's Association; they may also be available through a local social service agency, the patient's physician, or pharmaceutical companies that manufacture the drugs used to treat AD. Medical treatment for depression may be an important adjunct to group support.
Outside help, nursing homes, and governmental assistance
Most families eventually need outside help to relieve some of the burden of around-the-clock care for an AD patient. Personal care assistants, either volunteer or paid, may be available through local social service agencies. Adult daycare facilities are becoming increasingly common. Meal delivery, shopping assistance, or respite care may be available as well.
Providing the total care required by a person with late-stage AD can become an overwhelming burden for a family, even with outside help. At this stage, many families consider nursing home care. This decision is often one of the most difficult for the family, since it is often considered an abandonment of the loved one and a failure of the family. Counseling with a physician, clergy, or other trusted adviser may ease the difficulties of this transition. Selecting a nursing home may require a difficult balancing of cost, services, location, and availability. Keeping the entire family involved in the decision may help prevent further stress from developing later on.
Several federal government programs may ease the cost of caring for a person with AD, including Social Security Disability, Medicare, and Supplemental Security Income. Each of these programs provides some assistance for care, medication, or other costs, but none of them will pay for nursing home care indefinitely. Medicaid is a state-funded program that may provide for some or all of the cost of nursing home care, although there are important restrictions. Details of the benefits and eligibility requirements of these programs are available through the local Social Security or Medicaid office, or from local social service agencies. Long-term care insurance can also be another option, if taken out prior to the diagnosis.
Prognosis
Alzheimer's disease can weaken the aging body, making it more susceptible to life-threatening infections such as pneumonia. In the late stages of the disease, autonomic body functions may be impaired, the patient falling into a coma, and death following. In addition, other diseases common in old age—cancer, stroke, and heart disease—may lead to more severe consequences in a person with AD. On average, people with AD live eight years past their diagnosis, with a range from one to 20 years.
Health care team roles
Treatment of AD is a team effort, involving primary care physicians, nurses, imaging and laboratory technicians, gerontology specialists, psychiatrists, psychologists, nursing staff, and caregivers. Physicians order tests that aid in the diagnosis and treatment of AD. These experts must educate the patient and the caregivers in the nature of the disease and its progression, although this burden usually falls on the nursing staff. Nurses are also the first line of access to medical care and support groups. Social workers, counselors, and support group facilitators may also provide emotional support, practical advice, and information about community resources. Special Alzheimer's disease facilities may be used for either respite day care or as permanent long-term care placements.
Prevention
There is currently no proven way to prevent Alzheimer's disease, though some of the drug treatments may delay the development of the disease. The most likely current candidate is estrogen. However, staying active mentally and physically throughout life may be key to prevention.
KEY TERMS
Acetylcholine—One of the substances in the body that helps transmit nerve impulses.
Dementia—Impaired intellectual function that interferes with normal social and work activities.
Donepezil hydrochloride (Aricept)—A drug that increases the brain level of the neurotransmitter acetylcholine, which is given once a day to treat AD.
Ginko—An herb from the Ginko biloba tree that some alternative practitioners recommend for the treatment of AD.
Neurofibrillary tangle—Twisted masses of protein inside nerve cells that develop in the brains of people with AD.
Senile plaque—Structures composed of parts of neurons surrounding brain proteins called beta-amyloid deposits and found in the brains of people with AD.
Sunsetting—Confusion or agitation in the evening.
Tacrine (Cognex)—A drug that may help improve memory in people with mild to moderate cases of AD.
Resources
BOOKS
Castleman, Michael, Dolores Gallagher-Thompson, and Matthew Naythons. There's Still a Person in There: The Complete Guide to Treating and Coping with Alzheimer's. New York: G. P. Putnam's Sons, 1999.
Gray-Davidson, Frena. The Alzheimer's Sourcebook for Caregivers: A Practical Guide for Getting through the Day. Los Angeles: Lowell House, 1999.
Khatchaturian, Zaven S., and M. Marcel Mesulam, eds. Alzheimer's Disease: A Compendium of Current Theories. New York: New York Academy of Sciences, 2000.
Mace, Nancy L., and Peter V. Rabins. The 36-Hour Day. Baltimore: The John Hopkins University Press, 1999.
Tanzi, Rudolph E. Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease. Cambridge, MA: Perseus Publishing, 2000.
PERIODICALS
Glaser, Vicki. "Strategies for Early Diagnosis." Patient Care 35 no. 3 (February 15, 2001): 22.
Hines, Silvia E. "Contemporary Drug Treatment." Patient Care 35 no. 3 (February 15, 2001): 54.
Nichols, Mark. "On the Trail of a Killer: Researchers Discover a Key to the Mystery of Why Cells Die." Maclean's (April 9, 2001): 40.
ORGANIZATIONS
Alzheimer's Association. 919 North Michigan Ave., Suite 1100, Chicago, IL 60611. (800) 272-3900. (312) 335-8700).
National Institute of Aging, Alzheimer's Education, and Referral Center. (800) 438-4380.
OTHER
Alzheimer's Disease Books and Videotapes..
Author unspecified. "Ten Warning Signs." Alzheimer's Association..
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Definition
Alzheimer's disease (AD) is the most common form of dementia, a neurologic disease characterized by a progressive loss of mental ability severe enough to interfere with normal activities of daily living, lasting at least six months, and not present from birth. AD usually occurs in old age and is marked by a decline in cognitive functions such as remembering, reasoning, and planning.
Description
A person with AD usually has a gradual decline in mental functions, often beginning with slight memory loss, followed by losses in the ability to maintain employment, to plan and execute familiar tasks, and to reason and exercise judgment. Communication ability, mood, and personality may also be affected. Most people who have AD die within eight years of their diagnosis, although that interval may be as short as one year or as long as 20 years. AD is the fourth leading cause of death in adults after heart disease, cancer, and stroke.
In 2001, four million Americans have been diagnosed with AD. That number is expected to grow to as many as 14 million by the middle of the twenty-first century as the baby-boomer population ages. These numbers may be seriously underestimated due to new research that suggests mild cognitive impairment may be early stages of AD.
While a small number of people in their 40s and 50s develop the disease (called early-onset AD), AD predominantly affects the elderly. AD affects about 10% of all people over the age of 65 and nearly half of those over85. Slightly more women than men are affected with AD, since women tend to live longer and occupy a larger proportion of the most affected age groups.
The costs for caring for loved ones with AD is considerable, and has been estimated at approximately $174,000 per person over the course of the disease. More than 70% of people with AD are cared for at home at an estimated annual cost of $196 billion. These costs are not supplemented by outside sources. If patients are cared for by paid home caregivers or are placed in nursing homes, the total annual out-of-pocket costs by families or third party payees account for $83 billion and $32 billion respectively.
Causes and symptoms
Causes
The cause of Alzheimer's disease is unknown. Some strong leads have been found through recent research, however, and these have also given some theoretical support to several new experimental treatments.
AD affects brain cells responsible for learning, reasoning, and memory. Autopsies of people with AD indicate that these regions of the brain become clogged with two abnormal structures, neurofibrillary tangles and senile plaques. Neurofibrillary tangles are twisted masses of protein fibers inside nerve cells (neurons). Senile plaques are composed of parts of neurons surrounding a group of brain proteins called beta-amyloid deposits. While it is not clear exactly how these structures cause problems, some researchers now believe that their formation is responsible for the mental changes of AD, presumably by interfering with the normal communication between neurons in the brain. Drugs approved by the Food and Drug Administration (FDA) increase the level of chemical signaling molecules in the brain, known as neurotransmitters, to make up for this decreased communication ability.
What triggers the formation of plaques and tangles is unknown, although there are several possible candidates. Restriction of blood flow may be part of the problem, perhaps accounting for the beneficial effects of estrogen, which increases blood flow in the brain. However, studies in 2001 do not show estrogen as a protection against the development of AD.
Highly reactive molecular fragments called free radicals damage cells of all kinds, especially brain cells, which have smaller supplies of protective antioxidants thought to protect against free radical damage. Vitamin E is one such antioxidant, and its use in AD is showing some benefit.
Several genes have been implicated in AD, including the gene for amyloid precursor protein (APP) responsible for producing amyloid. Mutations in this gene are linked to some cases of the relatively uncommon earlyonset forms of AD. Other cases of early-onset AD are caused by mutations in the gene for another protein, presenilin. AD eventually affects nearly everyone with Down syndrome, caused by an extra copy of chromosome 21. Other mutations on other chromosomes have been linked to other early-onset cases.
Potentially the most important genetic link was discovered in the early 1990s on chromosome 19. A gene on this chromosome, apoE, codes for a protein involved in transporting lipids into neurons. ApoE occurs in at least three forms: apoE2, apoE3, and apoE4. Each person inherits one apoE from each parent, and therefore can either have one copy of two different forms or two copies of one. Compared to those without ApoE4, people with one copy are about three times as likely to develop lateonset AD, and those with two copies are almost four times as likely to do so. Despite this important link, not everyone with apoE4 develops AD, and people without it can still have the disease. Why apoE4 increases the chances of developing AD is not known.
Promising research in 2001 has discovered a protein, apoptosis-inducing factor, that kills cells by disrupting the genetic material at their cores. This discovery could lead to drugs that could turn off this protein that triggers apoptosis or biologically regulated cell death, which is important in fetal development but is also implicated in stroke, heart disease, and AD. It is thought that this protein runs out of control and shuts off otherwise healthy cells.
There are several risk factors that seem to increase a person's likelihood of developing the disease. The most significant one is, of course, age; older people develop AD at much higher rates than younger ones. Another risk factor is having a family history of AD, Down syndrome, or Parkinson's disease. People who have had head trauma or hypothyroidism may manifest the symptoms of AD sooner.
Many environmental factors have been suspected of contributing to AD, but population studies generally have not borne these out. A study in early 2001, however, showed a specific link between aluminum in drinking water and the incidence of AD. Other suspected risk factors were other pollutants in drinking water, aluminum in any form, and mercury in dental fillings. To date, none of these other factors has been shown to cause AD or to increase its likelihood.
Lifestyle factors, moreover, may prove to be better indicators of risk. Lack of stimulation, mentally and physically, between the ages of 20 and 60 seems linked to the incidence of AD. Studies have not shown, though, that a sedentary lifestyle early in life causes AD or whether it is a marker for the incidence of the disease.
Another study of African Americans and their Nigerian counterparts shows AD appearing more often in the American population than the African one. Researchers suggest that environmental or cultural factors may play a role in the formation of AD. Here, physical activity or diet may play a part.
Symptoms
The symptoms of Alzheimer's disease begin gradually, usually with memory lapses. Occasional memory lapses are common to everyone and do not, by themselves, signify any change in cognitive function. The person with AD may begin with only the routine sort of memory lapse—forgetting where the car keys are—but progresses to more profound or disturbing losses such as forgetting how to even drive a car. Being lost or disoriented on a walk around the neighborhood becomes more likely as the disease progresses. A person with AD may forget the names of family members, or forget what was said at the beginning of a sentence by the end of the sentence.
As AD progresses, other symptoms appear, including inability to perform routine tasks, loss of judgment, and personality or behavior changes. Some patients have trouble sleeping and may suffer from confusion or agitation in the evening, known as sunsetting. In some cases, people with AD repeat the same ideas, movements, words, or thoughts, a behavior known as perseveration. There may be delusional thinking or even hallucinations. In the final stages people may have severe problems with eating, communicating, and controlling their bladder and bowel functions.
The Alzheimer's Association has developed a list of 10 warning signs of AD. A person with several of these symptoms should see a physician for a thorough evaluation:
* memory loss that affects job skills
* difficulty performing familiar tasks
* problems with language, as in word-find problems or inappropriate word substitutions
* disorientation about time and place
* poor or decreased judgment
* problems with abstract thinking
* misplacing things
* changes in mood or behavior
* changes in personality
* loss of initiative
Other types of dementia, including some that are reversible, can cause similar symptoms. It is important for the person with these symptoms to be evaluated by a professional who can weigh the possibility that the symptoms may have another cause. Approximately 20% of those originally suspected of having AD actually have some other disorder; about half of these cases are treatable.
Diagnosis
Diagnosis of Alzheimer's disease is complex and may require visits to several different specialists over several months before a determination can be made. With new diagnostic tools and criteria, it is possible to make a provisional diagnosis that is about 90% accurate. A positive confirmation of these findings can be made only through autopsy.
Early diagnosis is essential in helping the patient and the family make decisions about treatment, long-term care, and financial matters. Finding out that a loved one's behavior is based on a degenerative mental disease can help a family avoid unnecessary anger and feelings of impotence when dealing with the progression of the disease.
There are two diagnoses the clinical team can make for a patient. They are probable AD or possible AD. Probable AD is determined when physicians and psychiatrists rule out all other disorders that might produce similar symptoms. A diagnosis of possible AD is made when AD is considered the primary reason for the symptoms but is complicated with the presence of another disorder that might confuse the general progression of the disease.
Diagnosis for AD begins with the elimination of other physical and psychological causes for the patient's behavior. This is done through a multi-step process that tests for other disorders and measures the amount of deficit the patient is experiencing.
Patient history
A detailed medical history should be taken, noting a list of the patient's medicines (prescription and over the counter), vitamins, and herbs. Since there are many pharmaceuticals that can cause the same mental changes as AD, a careful review of the patient's medication, alcohol, and herbal use is important. If the patient's symptoms are related to any of these, most likely the condition can be reversed through adjustments in the patient's medications or herbal use. Any illicit drugs should also be reported.
Next, the physician should take a detailed report of any changes in the patient's mental functioning and memory. This will determine the mode of onset of symptoms, the progression of the deficits, and the impact of the impairment on daily functioning.
Physical exam and lab tests
AD-like symptoms can also be provoked by other medical conditions, including tumors, infection, thyroid malfunctioning, and dementia caused by mild strokes (multi-infarct dementia). These possibilities must be ruled out through blood screens, urine tests, electroencephalographs (EEGs), and a variety of imaging techniques.
A genetic test for the ApoE4 gene is available, but is not used for diagnosis, since possessing even two copies does not ensure that a person will develop AD.
Cognitive functioning evaluation
Several types of oral and written tests are used in AD diagnosis and disease progression, including tests of mental status, language ability, functional ability, memory, and concentration. In the early stages of the disease, the results of these tests are usually normal. It should be noted that the widely-used Mini-Mental State Examination (MMSE) may not be accurate for highly educated or poorly educated individuals, or cultural minorities.
Neuropsychiatric evaluation
A detailed cognitive evaluation can be done by a psychologist or psychiatrist. These tests of memory and mental functioning provide a quantitative measure of the patient's deficits.
One of the most important parts of the diagnostic process is the evaluation of depression and delirium, since these can be present with AD or may be mistaken for it. (Delirium involves a decreased consciousness or awareness of one's environment.) Depression and memory loss are both common in the elderly, and the combination of the two can often be mistaken for AD. Depression can be treated with drugs, although some antidepressants can worsen dementia if it is present, further complicating both diagnosis and treatment.
Imaging studies
Several imaging techniques can assess brain function and pathology, thus eliminating these as causes of the patient's symptoms. Most frequently used imaging scans are magnetic resonance imaging (MRI) or computed tomography (CT) scans, which detect structural changes in the brain. Brain function can be assessed through MRI, positron emission tomography (PET), and single-photon emission CT (SPECT). These tests help rule out stroke, subdural hematoma, and brain tumor as possible causes for the patient's symptoms.
Treatment
Alzheimer's disease is currently incurable, though a number of pharmaceuticals and home care strategies can mange the disease. The mainstay of AD treatment continues to be good nursing care, providing both physical and emotional support, as the patient gradually is able to do less independently and whose behavior becomes more erratic. Modifications of the home to increase safety are often necessary. Creative strategies to help the patient stay as independent as possible are also indicated. The caregiver also needs support to minimize anger, despair, and burnout.
Drugs
Donepezil hydrochloride (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) have been approved for use in AD treatment. These drugs increase the levels of the neurotransmitter acetylcholine in the brain, thereby increasing the communication ability of the remaining neurons. They do this by inhibiting the enzymes, acetylcholinesterase and butylcholinesterase, which normally break down acetylcholine and butylcholine released by neurons. These drugs modestly increase attention span, concentration, mental acuity, and information processing. Tacrine (Cognex), the first drug used, is no longer used due to the risk of liver toxicity. All cholinesterase inhibitors have mild gastric side effects such as nausea and vomiting.
The antioxidant, vitamin E, is also thought to delay AD onset because it prevents neuron damage caused by free radicals. Vitamin E therapy, in combination with cholinesterase inhibitors, has become a practice standard in the treatment of AD.
Drugs that have been found ineffective are Selegiline (used in the treatment of Parkinson's disease), prednisone, and the anti-inflammatory NSAID diclofenac. Estrogen, once thought to be the keystone in treatment and prevention of AD in women, was found to be ineffective in mitigating symptoms in 2001. There is still some discussion about estrogen's ability to delay the onset of AD.
Depression may be treated with selective serotonin reuptake inhibitors (SSRIs) such as citalopram and sertraline. Physicians may also prescribe typical antipsychotics for agitation, aggression, or hallucinations, such as olanzapine, quetiapine, or risperidone. It should be noted that AD patients have more side effects from most medications, especially psychoactive drugs, and care should be taken in their selection.
Alternative treatment
Several substances are currently being tested for their ability to slow the progress of Alzheimer's disease. Among them are gingko extract, derived from the leaves of the Gingko biloba tree, and huperzine A, from the moss Huperzia serrata. Gingko extract has antioxidant, anti-inflammatory, and neuroprotective effects and has been used for many years in China and is widely prescribed in Europe for treatment of circulatory problems. It has been shown to modestly improve cognitive function. Huperzine A is a natural cholinesterase inhibitor. It is reported to produce greater improvement than the synthetic cholinesterase inhibitors and has few side effects. Since neither herbal is regulated, they may have inconsistent levels of their active ingredients per dosage.
Nursing care and safety
The person with Alzheimer's disease will gradually lose the ability to dress, groom, feed, bathe, or use the toilet without help; in the late stages of the disease, the individual may be unable to move or speak. In addition, the person's behavior becomes increasing erratic. A tendency to wander may make it difficult to leave the patient unattended for even a few minutes, which would make even the home a potentially dangerous place. In addition, some patients may exhibit inappropriate sexual behaviors.
Nursing care required for AD patients is simple enough to learn. The difficulty for many caregivers comes in the constant but unpredictable nature of the demands put on them. Additionally, the personality changes presented in AD can be heartbreaking for family members as a loved one deteriorates, seeming to become a different person. Not all AD patients develop negative behaviors: some become gentle, spending increasing amounts of time in dream-like states.
A loss of grooming skills may be one of the early symptoms of AD. Mismatched clothing, unkempt hair, and decreased interest in personal hygiene become more common. Caregivers, especially spouses, may find these changes socially embarrassing and difficult to cope with. The caregiver will begin to assume more and more grooming duties for the patient as the disease progresses.
Ensuring proper nutrition for the AD patient may require using a colored plate to focus the patient's attention on the food. Finger foods may be preferable to those foods requiring utensils. Later, the caregiver may need to feed the patient. As movement and swallowing become difficult, a feeding tube may be placed into the stomach through the abdominal wall, which will require special attention.
For many caregivers, incontinence becomes the most difficult problem to deal with at home, and is a principal reason for pursuing nursing home care. In the early stages, limiting fluid intake and increasing the frequency of toileting can help. Careful attention to hygiene is important to prevent skin irritation and infection from soiled clothing.
Safety will become of prime importance. In all cases, a person diagnosed with AD should not be allowed to drive, because of the increased potential for accidents and the increased likelihood of wandering far from home while disoriented. In the home, grab bars in the bathroom, bed rails on the bed, and clutter-free passageways can greatly increase safety. Electrical appliances should be unplugged and put away when not in use, and matches, lighters, knives, or weapons should be stored out of reach. The hot water heater temperature should be set lower to prevent accidental scalding. A list of emergency numbers, including the poison control center and the hospital emergency room, should be posted by the phone.
A calm, structured environment with simple orientation aids such as calendars and clocks may reduce anxiety and increase safety. Labeling cabinets and drawers may keep the patient's attention focused. Scheduling meals, bathing, and other activities at regular times and places will provide emotional security and routine, since unfamiliar places and activities can be disorienting for the patient. Sleep disturbances may be minimized by keeping the patient engaged in activities during the day, offering structure and providing physical activities.
Care for the caregiver
Family members or others caring for a person with AD have a difficult and stressful job, which becomes harder still as the disease progresses. It is common for caregivers to develop feelings of anger, resentment, guilt, and hopelessness, in addition to the sorrow they feel for their loved one and for themselves. Depression is an extremely common consequence of being a full-time caregiver for an AD patient. Support groups are an important way to deal with the stress of caregiving. The location and contact numbers for AD caregiver support groups are available from the Alzheimer's Association; they may also be available through a local social service agency, the patient's physician, or pharmaceutical companies that manufacture the drugs used to treat AD. Medical treatment for depression may be an important adjunct to group support.
Outside help, nursing homes, and governmental assistance
Most families eventually need outside help to relieve some of the burden of around-the-clock care for an AD patient. Personal care assistants, either volunteer or paid, may be available through local social service agencies. Adult daycare facilities are becoming increasingly common. Meal delivery, shopping assistance, or respite care may be available as well.
Providing the total care required by a person with late-stage AD can become an overwhelming burden for a family, even with outside help. At this stage, many families consider nursing home care. This decision is often one of the most difficult for the family, since it is often considered an abandonment of the loved one and a failure of the family. Counseling with a physician, clergy, or other trusted adviser may ease the difficulties of this transition. Selecting a nursing home may require a difficult balancing of cost, services, location, and availability. Keeping the entire family involved in the decision may help prevent further stress from developing later on.
Several federal government programs may ease the cost of caring for a person with AD, including Social Security Disability, Medicare, and Supplemental Security Income. Each of these programs provides some assistance for care, medication, or other costs, but none of them will pay for nursing home care indefinitely. Medicaid is a state-funded program that may provide for some or all of the cost of nursing home care, although there are important restrictions. Details of the benefits and eligibility requirements of these programs are available through the local Social Security or Medicaid office, or from local social service agencies. Long-term care insurance can also be another option, if taken out prior to the diagnosis.
Prognosis
Alzheimer's disease can weaken the aging body, making it more susceptible to life-threatening infections such as pneumonia. In the late stages of the disease, autonomic body functions may be impaired, the patient falling into a coma, and death following. In addition, other diseases common in old age—cancer, stroke, and heart disease—may lead to more severe consequences in a person with AD. On average, people with AD live eight years past their diagnosis, with a range from one to 20 years.
Health care team roles
Treatment of AD is a team effort, involving primary care physicians, nurses, imaging and laboratory technicians, gerontology specialists, psychiatrists, psychologists, nursing staff, and caregivers. Physicians order tests that aid in the diagnosis and treatment of AD. These experts must educate the patient and the caregivers in the nature of the disease and its progression, although this burden usually falls on the nursing staff. Nurses are also the first line of access to medical care and support groups. Social workers, counselors, and support group facilitators may also provide emotional support, practical advice, and information about community resources. Special Alzheimer's disease facilities may be used for either respite day care or as permanent long-term care placements.
Prevention
There is currently no proven way to prevent Alzheimer's disease, though some of the drug treatments may delay the development of the disease. The most likely current candidate is estrogen. However, staying active mentally and physically throughout life may be key to prevention.
KEY TERMS
Acetylcholine—One of the substances in the body that helps transmit nerve impulses.
Dementia—Impaired intellectual function that interferes with normal social and work activities.
Donepezil hydrochloride (Aricept)—A drug that increases the brain level of the neurotransmitter acetylcholine, which is given once a day to treat AD.
Ginko—An herb from the Ginko biloba tree that some alternative practitioners recommend for the treatment of AD.
Neurofibrillary tangle—Twisted masses of protein inside nerve cells that develop in the brains of people with AD.
Senile plaque—Structures composed of parts of neurons surrounding brain proteins called beta-amyloid deposits and found in the brains of people with AD.
Sunsetting—Confusion or agitation in the evening.
Tacrine (Cognex)—A drug that may help improve memory in people with mild to moderate cases of AD.
Resources
BOOKS
Castleman, Michael, Dolores Gallagher-Thompson, and Matthew Naythons. There's Still a Person in There: The Complete Guide to Treating and Coping with Alzheimer's. New York: G. P. Putnam's Sons, 1999.
Gray-Davidson, Frena. The Alzheimer's Sourcebook for Caregivers: A Practical Guide for Getting through the Day. Los Angeles: Lowell House, 1999.
Khatchaturian, Zaven S., and M. Marcel Mesulam, eds. Alzheimer's Disease: A Compendium of Current Theories. New York: New York Academy of Sciences, 2000.
Mace, Nancy L., and Peter V. Rabins. The 36-Hour Day. Baltimore: The John Hopkins University Press, 1999.
Tanzi, Rudolph E. Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease. Cambridge, MA: Perseus Publishing, 2000.
PERIODICALS
Glaser, Vicki. "Strategies for Early Diagnosis." Patient Care 35 no. 3 (February 15, 2001): 22.
Hines, Silvia E. "Contemporary Drug Treatment." Patient Care 35 no. 3 (February 15, 2001): 54.
Nichols, Mark. "On the Trail of a Killer: Researchers Discover a Key to the Mystery of Why Cells Die." Maclean's (April 9, 2001): 40.
ORGANIZATIONS
Alzheimer's Association. 919 North Michigan Ave., Suite 1100, Chicago, IL 60611. (800) 272-3900. (312) 335-8700).
National Institute of Aging, Alzheimer's Education, and Referral Center. (800) 438-4380.
OTHER
Alzheimer's Disease Books and Videotapes.
Author unspecified. "Ten Warning Signs." Alzheimer's Association.
Tuesday, December 29, 2009
Cervical Spondylosis and Spondylotic Cervical Myelopathy
merck.com,
Cervical spondylosis is osteoarthritis of the cervical spine causing stenosis of the canal and sometimes cervical myelopathy due to encroachment of bony osteoarthritic growths (osteophytes) on the lower cervical spinal cord, sometimes with involvement of lower cervical nerve roots (radiculomyelopathy).
Cervical spondylosis due to osteoarthritis is common. Occasionally, particularly when the spinal canal is congenitally narrow (< 10 mm), osteoarthritis leads to stenosis of the canal and bony impingement on the cord, causing compression and myelopathy (functional disturbance of the spinal cord). Hypertrophy of the ligamentum flavum can aggravate this effect. Osteophytes in the neural foramina, most commonly between C5 and C6 or C6 and C7, can cause radiculopathy (a nerve root disorder—see also Peripheral Nervous System and Motor Unit Disorders: Nerve Root Disorders). Manifestations vary according to the neural structures involved but commonly include pain.
Symptoms and Signs
Cord compression commonly causes gradual spastic paresis, paresthesias, or both in the hands and feet and may cause hyperreflexia. Neurologic deficits may be asymmetric, nonsegmental, and aggravated by cough or Valsalva maneuvers. After trauma, people with cervical spondylosis may develop central cord syndrome. Eventually, muscle atrophy and flaccid paresis may develop in the upper extremities at the level of the lesion, with spasticity below the level of the lesion.
Nerve root compression commonly causes early radicular pain; later there may be weakness, hyporeflexia, and muscle atrophy.
Diagnosis
*
MRI or CT
Cervical spondylosis is suspected when characteristic neurologic deficits occur in patients who are elderly, have osteoarthritis, or have radicular pain at the C5 or C6 levels. Diagnosis is by MRI or CT.
Treatment
* For radiculopathy only, NSAIDS and soft cervical collar
* For cord involvement or refractory radiculopathy, cervical laminectomy
For patients with cord involvement, cervical laminectomy is usually needed; a posterior approach can relieve the compression but leaves anterior compressive osteophytes and may result in spinal instability and kyphosis. Thus, an anterior approach with spinal fusion is generally preferred. Patients with only radiculopathy may try nonsurgical treatment with NSAIDs and a soft cervical collar; if this approach is ineffective, surgical decompression may be required.
Read More ..
Cervical spondylosis is osteoarthritis of the cervical spine causing stenosis of the canal and sometimes cervical myelopathy due to encroachment of bony osteoarthritic growths (osteophytes) on the lower cervical spinal cord, sometimes with involvement of lower cervical nerve roots (radiculomyelopathy).
Cervical spondylosis due to osteoarthritis is common. Occasionally, particularly when the spinal canal is congenitally narrow (< 10 mm), osteoarthritis leads to stenosis of the canal and bony impingement on the cord, causing compression and myelopathy (functional disturbance of the spinal cord). Hypertrophy of the ligamentum flavum can aggravate this effect. Osteophytes in the neural foramina, most commonly between C5 and C6 or C6 and C7, can cause radiculopathy (a nerve root disorder—see also Peripheral Nervous System and Motor Unit Disorders: Nerve Root Disorders). Manifestations vary according to the neural structures involved but commonly include pain.
Symptoms and Signs
Cord compression commonly causes gradual spastic paresis, paresthesias, or both in the hands and feet and may cause hyperreflexia. Neurologic deficits may be asymmetric, nonsegmental, and aggravated by cough or Valsalva maneuvers. After trauma, people with cervical spondylosis may develop central cord syndrome. Eventually, muscle atrophy and flaccid paresis may develop in the upper extremities at the level of the lesion, with spasticity below the level of the lesion.
Nerve root compression commonly causes early radicular pain; later there may be weakness, hyporeflexia, and muscle atrophy.
Diagnosis
*
MRI or CT
Cervical spondylosis is suspected when characteristic neurologic deficits occur in patients who are elderly, have osteoarthritis, or have radicular pain at the C5 or C6 levels. Diagnosis is by MRI or CT.
Treatment
* For radiculopathy only, NSAIDS and soft cervical collar
* For cord involvement or refractory radiculopathy, cervical laminectomy
For patients with cord involvement, cervical laminectomy is usually needed; a posterior approach can relieve the compression but leaves anterior compressive osteophytes and may result in spinal instability and kyphosis. Thus, an anterior approach with spinal fusion is generally preferred. Patients with only radiculopathy may try nonsurgical treatment with NSAIDs and a soft cervical collar; if this approach is ineffective, surgical decompression may be required.
Read More ..
Saturday, December 5, 2009
Autonomic Dysreflexia
Autonomic Dysreflexia (AD), also known as Hyperreflexia, is a potentially dangerous complication of spinal cord injury (SCI). In AD, an individual's blood pressure may rise to dangerous levels and if not treated can lead to stroke and possibly death. Individuals with SCI at the T-6 level or above are at greater risk. AD usually occurs because of a noxious (irritating) stimulus below the level of the injury. Symptoms include headache, facial flush, perspiration, and a stuffy nose.
AD occurs primarily because of an imbalance in the body systems which control the blood pressure. The human body is an incredibly complicated and beautifully balanced machine. There are balances to each system of the body, including the blood pressure. One of the major ways the body controls blood pressure is by tightening or relaxing little muscles around the blood vessels.
When the muscles contract, the blood vessels get smaller and blood pressure increases. Imagine a garden hose with water streaming through it; when you put your thumb over the opening of the hose, reducing the opening for the water to flow through, the water shoots out at a higher pressure. Similarly, when the blood vessels are smaller, the blood rushes around your body at higher pressure.
When a noxious stimulus occurs, a reflex is initiated that causes the blood vessels to constrict and raises the blood pressure. In an intact spinal cord, this same stimulus also sets in motion another set of reflexes that moderates the constriction of blood vessels. However, in someone who has SCI at the T-6 level or above, the signal which tells the blood vessels to relax cannot get through the spinal cord because of the injury.
Some of the nerves at the T-6 level also control the blood flow to and from the gut, which is a large reservoir of blood. Uncontrolled activity of these nerves may cause the blood from the gut to flow into the rest of the blood system. The result is that blood pressure can increase to dangerous levels and the increase in blood pressure must be controlled by outside means.
What is "Autonomic Dysreflexia"?
Autonomic dysreflexia (AD), in the simplist terms, is the nervous system going crazy. Individuals that have a T-5, or higher, injury are the ones generally subject to suffering from AD. This is a condition that can be life-threatening and can be considered a medical emergency .
What are the indicators for the onset of AD?
* Hypertension (blood pressure greater than 200/100)
* Pounding headache
* Flushed (reddened) face
* Red blotches on the skin above level of spinal injury
* Sweating above level of spinal injury
* Nasal stuffiness
* Nausea (secondary to vagal parasympathetic stimulation)
* Bradycardia - slow pulse <60 beats per minute
* Piloerection ("goose bumps") below level of spinal injury
* Cold, clammy skin below level of spinal injury
What sort of things can precipitate this syndrome?
Irritants, things which would ordinarily cause pain, to areas of body below the level of spinal injury.
Things to consider include:
Bladder (most common) - from overstretch or irritation of bladder wall
* Urinary tract infection (UTI)
* Urinary retention
* Blocked catheter
* Overfilled collection bag
* Non-compliance with intermittent catheterization program
Bowel
* overdistention or irritation
* Constipation / impaction
* Distention during bowel program (digital stimulation)
* Hemorrhoids or anal infections
* Infection or irritation
Skin-related Disorders
* Any direct irritant below the level of injury
* Pressure by object in shoe or chair, cut, bruise, abrasion
* Pressure sores (decubitus ulcer)
* Ingrown toenails
* Burns (eg. - sunburn, burns from using hot water)
* Tight or restrictive clothing or pressure to skin from sitting
Sexual Activity
* Overstimulation during sexual activity
* [stimuli to the pelvic region which would ordinarily be painful if sensation were present]
* Menstrual cramps
* Labor and delivery
Other Causes
* Heterotopic ossification ("Myositis ossificans", "Heterotopic bone")
* Acute abdominal conditions (gastric ulcer, colitis, peritonitis)
* Skeletal fractures
What can be done to manage an episode of autonomic dysreflexia?
The first thing to do is locate and remove the offending stimulus whenever possible. This will often prove successful enough to avoid pharmacological intervention. Once the source of irritation has been removed it will be a good idea to have the individual remain in a sitting up position and take frequent blood pressure checks until the episode has ended.
Typical Causes
Blocked Catheter
The most common cause of AD is a catheter that has become blocked. You will want to check the collection bag, irrigate the catheter and remove any kinks.
Bowel
If symptoms begin while digital stimulation is being performed, stop until symptoms quit. If the individual has impacted stool - begin disimpaction immediately. If digital stimulation continues to bring on the symptoms you may want to consider abdominal massage or commode-based bowel evacuation methods
Skin
Skin irritation, also a common cause of AD, is most often stopped by loosening the clothing. You will was to check for pressure sores and toenail problems.
How can autonomic dysreflexia be prevented?
* Frequent pressure relief in bed/chair
* Avoidance of sun burn/scalds (avoid overexposure, use of #15 sunscreen, watch water temperatures)
* Faithful adherence to bowel program
* Keep catheters clean and remain faithful to catheterization schedule
* Well balanced diet and adequate fluid intake Compliance with medications
Read More ..
AD occurs primarily because of an imbalance in the body systems which control the blood pressure. The human body is an incredibly complicated and beautifully balanced machine. There are balances to each system of the body, including the blood pressure. One of the major ways the body controls blood pressure is by tightening or relaxing little muscles around the blood vessels.
When the muscles contract, the blood vessels get smaller and blood pressure increases. Imagine a garden hose with water streaming through it; when you put your thumb over the opening of the hose, reducing the opening for the water to flow through, the water shoots out at a higher pressure. Similarly, when the blood vessels are smaller, the blood rushes around your body at higher pressure.
When a noxious stimulus occurs, a reflex is initiated that causes the blood vessels to constrict and raises the blood pressure. In an intact spinal cord, this same stimulus also sets in motion another set of reflexes that moderates the constriction of blood vessels. However, in someone who has SCI at the T-6 level or above, the signal which tells the blood vessels to relax cannot get through the spinal cord because of the injury.
Some of the nerves at the T-6 level also control the blood flow to and from the gut, which is a large reservoir of blood. Uncontrolled activity of these nerves may cause the blood from the gut to flow into the rest of the blood system. The result is that blood pressure can increase to dangerous levels and the increase in blood pressure must be controlled by outside means.
What is "Autonomic Dysreflexia"?
Autonomic dysreflexia (AD), in the simplist terms, is the nervous system going crazy. Individuals that have a T-5, or higher, injury are the ones generally subject to suffering from AD. This is a condition that can be life-threatening and can be considered a medical emergency .
What are the indicators for the onset of AD?
* Hypertension (blood pressure greater than 200/100)
* Pounding headache
* Flushed (reddened) face
* Red blotches on the skin above level of spinal injury
* Sweating above level of spinal injury
* Nasal stuffiness
* Nausea (secondary to vagal parasympathetic stimulation)
* Bradycardia - slow pulse <60 beats per minute
* Piloerection ("goose bumps") below level of spinal injury
* Cold, clammy skin below level of spinal injury
What sort of things can precipitate this syndrome?
Irritants, things which would ordinarily cause pain, to areas of body below the level of spinal injury.
Things to consider include:
Bladder (most common) - from overstretch or irritation of bladder wall
* Urinary tract infection (UTI)
* Urinary retention
* Blocked catheter
* Overfilled collection bag
* Non-compliance with intermittent catheterization program
Bowel
* overdistention or irritation
* Constipation / impaction
* Distention during bowel program (digital stimulation)
* Hemorrhoids or anal infections
* Infection or irritation
Skin-related Disorders
* Any direct irritant below the level of injury
* Pressure by object in shoe or chair, cut, bruise, abrasion
* Pressure sores (decubitus ulcer)
* Ingrown toenails
* Burns (eg. - sunburn, burns from using hot water)
* Tight or restrictive clothing or pressure to skin from sitting
Sexual Activity
* Overstimulation during sexual activity
* [stimuli to the pelvic region which would ordinarily be painful if sensation were present]
* Menstrual cramps
* Labor and delivery
Other Causes
* Heterotopic ossification ("Myositis ossificans", "Heterotopic bone")
* Acute abdominal conditions (gastric ulcer, colitis, peritonitis)
* Skeletal fractures
What can be done to manage an episode of autonomic dysreflexia?
The first thing to do is locate and remove the offending stimulus whenever possible. This will often prove successful enough to avoid pharmacological intervention. Once the source of irritation has been removed it will be a good idea to have the individual remain in a sitting up position and take frequent blood pressure checks until the episode has ended.
Typical Causes
Blocked Catheter
The most common cause of AD is a catheter that has become blocked. You will want to check the collection bag, irrigate the catheter and remove any kinks.
Bowel
If symptoms begin while digital stimulation is being performed, stop until symptoms quit. If the individual has impacted stool - begin disimpaction immediately. If digital stimulation continues to bring on the symptoms you may want to consider abdominal massage or commode-based bowel evacuation methods
Skin
Skin irritation, also a common cause of AD, is most often stopped by loosening the clothing. You will was to check for pressure sores and toenail problems.
How can autonomic dysreflexia be prevented?
* Frequent pressure relief in bed/chair
* Avoidance of sun burn/scalds (avoid overexposure, use of #15 sunscreen, watch water temperatures)
* Faithful adherence to bowel program
* Keep catheters clean and remain faithful to catheterization schedule
* Well balanced diet and adequate fluid intake Compliance with medications
Read More ..
Wednesday, December 2, 2009
CAUDA EQUINA
http://www.emedicinehealth.com
Cauda Equina Syndrome Overview
The spinal cord extends from the brain down through the spinal canal inside the vertebral column. Nerves that branch off of the spinal cord (also called nerve roots) are an extension of the spinal cord and are responsible for sending signals to and from the muscles and other structures throughout the body. These signals allow the brain to interpret information from the body including pain, touch, and sense of position. Outgoing signals allow the brain to control actions of the organs and muscle movements.
The spinal cord ends near the first lumbar vertebra in the lower back, forming the conus medullaris. The fibrous extension of the spinal cord is the filum terminale. The bundle of nerve roots below the conus medullaris is named the cauda equina
Compression or inflammation of the nerve roots can cause symptoms of pain, altered reflexes, decreased strength, and decreased sensation. Although these symptoms can become severe, and in some cases disabling, most are self-limiting and respond to conservative care.
An extreme version of nerve compression or inflammation is cauda equina syndrome. Cauda equina syndrome is a serious condition caused by compression of the nerves in the lower portion of the spinal canal (see Multimedia File 2). Cauda equina syndrome is considered a surgical emergency because if left untreated it can lead to permanent loss of bowel and bladder control and paralysis of the legs.
Cauda Equina Syndrome Causes
Cauda equina syndrome is caused by significant narrowing of the spinal canal that compresses the nerve roots below the level of the spinal cord. Numerous causes of cauda equina syndrome have been reported, including traumatic injury, disk herniation, spinal stenosis, spinal tumors (neoplasms), such as metastatic tumors, meningiomas, schwannomas, and ependymomas, inflammatory conditions, infectious conditions, and accidental causes by medical intervention (iatrogenic causes).
Trauma
* Traumatic events leading to fracture or partial dislocation (subluxation) of the low back (lumbar spine) result in compression of the cauda equina.
* A collection of blood surrounding the nerves following trauma (epidural hematoma) in the low back area can lead to compression of the cauda equina.
* Penetrating trauma (gunshot or stab wounds) can cause damage or compression of the cauda equina.
* A rare complication of spinal manipulation is partial dislocation (subluxation) of the low back (lumbar spine) that can cause cauda equina syndrome.
Herniated Disk
* Most disk herniations will improve on their own (are self-limiting) and respond well to conservative treatment, including antiinflammatory medications, physical therapy, and short periods of rest (one to two days).
* Cauda equina syndrome results from a herniated lumbar disk in 1-15% of cases.
* Of lumbar disk herniations, 90% occur either at the vertebral levels L4-L5 or L5-S1.
* Seventy percent of cases of herniated disks leading to cauda equina syndrome occur in people with a history of chronic low back pain, and 30% develop cauda equina syndrome as the first symptom of lumbar disk herniation.
* Males in their 30s and 40s are most prone to cauda equina syndrome caused by disk herniation.
* Most cases of cauda equina syndrome caused by disk herniation involve large particles of disk material that have completely separated from the normal disk and compress the nerves (extruded disk herniations). In most cases, the disk material takes up at least one-third of the canal diameter.
Spinal Stenosis
* Spinal stenosis is any narrowing of the normal front to back distance (diameter) of the spinal canal.
* Narrowing of the spinal canal can be caused by a developmental abnormality or degenerative process.
* The abnormal forward slip of one vertebral body on another is called spondylolisthesis. Severe cases can cause a narrowing of the spinal canal and lead to cauda equina syndrome (see Multimedia File 3).
Tumors (Neoplasms)
* Cauda equina syndrome can be caused by isolated tumors (primary neoplasms) or from tumors that have spread to the spine from other parts of the body (metastatic spinal neoplasms). Metastatic spine tumors are most commonly from the prostate or lung in males and from the lung and breast in females.
* The most common initial symptom of people with cauda equina syndrome caused by a tumor (spinal neoplasm) is severe low back and leg pain.
* Later findings include lower extremity weakness.
* Loss of feeling in the legs (sensory loss) and loss of bowel or bladder control (sphincter dysfunction) are also common.
Inflammatory Conditions
* Long-lasting inflammatory conditions of the spine, including Paget disease and ankylosing spondylitis, can cause a narrowing of the spinal canal and lead to cauda equina syndrome.
Infectious Conditions
* Infections in the spinal canal (spinal epidural abscess) can cause deformity of the nerve roots and spinal column.
* Symptoms generally include severe back pain and rapidly worsening muscle weakness.
Accidental Medical Causes (Iatrogenic Causes)
* Poorly positioned screws placed in the spine can compress and injure nerves and cause cauda equina syndrome.
* Continuous spinal anesthesia has been linked to cases of cauda equina syndrome.
* Lumbar puncture (spinal tap) can cause a collection of blood in the spinal canal (spontaneous spinal epidural hematoma) in patients receiving medication to thin the blood (anticoagulation therapy). This collection of blood can compress the nerves and cause cauda equina syndrome.
Cauda Equina Syndrome Symptoms
Symptoms of cauda equina syndrome include the following:
* Low back pain
* Pain in one leg (unilateral) or both legs (bilateral) that starts in the buttocks and travels down the back of the thighs and legs (sciatica)
* Numbness in the groin or area of contact if sitting on a saddle (perineal or saddle paresthesia)
* Bowel and bladder disturbances
* Lower extremity muscle weakness and loss of sensations
* Reduced or absent lower extremity reflexes
Low back pain can be divided into local and radicular pain.
* Local pain is generally a deep, aching pain resulting from soft tissue and vertebral body irritation.
* Leg pain (radicular pain) is generally a sharp, stabbing pain resulting from compression of the nerve roots. Radicular pain projects along the specific areas controlled by the compressed nerve (known as a dermatomal distribution).
Bladder disturbance (urinary manifestations) related to cauda equina syndrome include the following:
* Inability to urinate (urinary retention)
* Difficulty initiating urination (urinary hesitancy)
* Decreased sensation when urinating (decreased urethral sensation)
* Inability to stop or control urination (incontinence)
Bowel disturbances may include the following:
* Inability to stop or feel a bowel movement (incontinence)
* Constipation
* Loss of anal tone and sensation
When to Seek Medical Care
Cauda equina syndrome is a surgical emergency. Persons should seek immediate medical care or go to the emergency department if they believe they have symptoms of cauda equina syndrome. Some of the early symptoms related to cauda equina syndrome, including low back pain and muscle weakness, are more often caused by simple disk herniation, which does not require urgent attention. However, if you develop severe pain or loss of sensation or bowel or bladder disturbances, you should contact your physician immediately.
Your chances of regaining normal function and having a positive outcome are related to how long you have had symptoms of cauda equina syndrome. Most experts agree that people with cauda equina syndrome should undergo surgery to make more space for the nerves (lumbar decompression) within 48 hours in order to have the best chance for complete recovery.
Exams and Tests
The initial diagnosis of cauda equina syndrome is made based on findings from the individual's history, symptoms, and physical exam. The physical exam includes testing muscle strength of the lower extremities, evaluating sensation to touch and pain, especially around the groin (perineum), checking the lower extremity reflexes, and evaluating rectal tone, sensation, and reflex.
Imaging studies helpful in the diagnosis include plain x-ray films of the lower back to assess for evidence of trauma or severe arthritis (degenerative changes). MRI with and without contrast provides a detailed look at tumors, infection, intervertebral disks, and nerve roots. This study allows the doctor to determine if the nerves are being compressed, to what degree, and by what structures. Findings from these studies help the surgeon plan the appropriate treatment.
Not all people with back pain and/or leg pain and changes in bowel or bladder function have cauda equina syndrome. More common causes of bladder changes are urinary tract infections, which can be identified by a simple urine test, and diabetes, which can be identified with blood tests.
People with symptoms suggesting a possible infection or tumor should be further evaluated with blood and other tests to identify any abnormalities.
Cauda Equina Syndrome Treatment
Self-Care at Home
Cauda equina syndrome is a surgical emergency. Self-care at home is not appropriate for this condition.
Medical Treatment
Medical treatment options are useful in certain persons, depending on the underlying cause of the cauda equina syndrome. Antiinflammatory agents, such as ibuprofen (Advil, Motrin), and corticosteroids, such as methylprednisolone (Solu-Medrol, Depo-Medrol), can be effective in people with inflammatory processes, including ankylosing spondylitis.
People with cauda equina syndrome caused by an infection should receive appropriate antibiotic therapy. People with spinal tumors (neoplasms) should be evaluated for chemotherapy and radiation therapy.
Caution should be used in any medical management of cauda equina syndrome. Any person with cauda equina syndrome with symptoms of groin numbness (saddle anesthesia) and/or weakness or both legs or loss of bowel or bladder control should wait no more than 24 hours before seeking initial medical management. If no relief of symptoms is achieved during this period, immediate surgical decompression is often recommended to minimize the chances of permanent nerve injury.
Medications
People with infections or tumors (infectious or neoplastic causes) causing cauda equina syndrome should receive the appropriate antibiotics or chemotherapy for treatment of the underlying cause.
In most cases, treatment with medications alone is not indicated because of a need for emergent release of the nerve compression (surgical decompression) of the spinal canal.
Surgery
In many cases of cauda equina syndrome, emergency decompression of the spinal canal is the best treatment option. The goal is to relieve pressure on the nerves of the cauda equina by removing the compressing structures and increasing the space available for the nerves in the spinal canal. Traditionally, cauda equina syndrome has been considered a surgical emergency, with surgical decompression considered necessary within 48 hours of the onset of symptoms.
For people with a herniated disk as the cause of cauda equina syndrome, removal of a portion of the bone surrounding the nerves (laminectomy) is performed and the disk material compressing the nerves is removed (discectomy). Many clinical and experimental reports have presented data on the functional outcome based on the timing of surgical decompression. Some investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression. Even with these findings, however, most investigators recommend surgical decompression as soon as possible following onset of symptoms to offer the greatest chances of complete neurologic recovery.
Many clinical and experimental studies have investigated patient outcomes in relation to the timing of surgical decompression. Some investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression. Even with these findings, however, most investigators recommend surgical decompression as soon as possible following the onset of symptoms to offer the greatest chances of complete neurologic recovery.
Investigators have attempted to identify specific criteria that can aid in predicting the outcome of persons with cauda equina syndrome.
* People with pain in both legs (bilateral sciatica) have less chance or full recovery than persons with single leg pain (unilateral sciatica).
* People with complete groin numbness (perineal anesthesia) are more likely to have permanent paralysis of the bladder.
* The extent of groin numbness (perineal or saddle sensory deficit) is the most important predictor of recovery.
Follow-up
Persons with cauda equina syndrome should have close follow-up with their surgeon to monitor any changes in function. Early surgery gives the patient the best chance for complete recovery from cauda equina syndrome.
Prevention
Prevention of cauda equina syndrome is focused on early diagnosis by identifying the symptoms described above. While low back pain with leg pain and/or weakness is a common complaint that affects many people, cauda equina syndrome is a rare complication. Doctors should be vigilant in identifying these cases. People should be educated on signs and symptoms that could suggest possible cauda equina syndrome, including change in bowel or bladder function and loss of sensation in the groin.
Read More ..
Cauda Equina Syndrome Overview
The spinal cord extends from the brain down through the spinal canal inside the vertebral column. Nerves that branch off of the spinal cord (also called nerve roots) are an extension of the spinal cord and are responsible for sending signals to and from the muscles and other structures throughout the body. These signals allow the brain to interpret information from the body including pain, touch, and sense of position. Outgoing signals allow the brain to control actions of the organs and muscle movements.
The spinal cord ends near the first lumbar vertebra in the lower back, forming the conus medullaris. The fibrous extension of the spinal cord is the filum terminale. The bundle of nerve roots below the conus medullaris is named the cauda equina
Compression or inflammation of the nerve roots can cause symptoms of pain, altered reflexes, decreased strength, and decreased sensation. Although these symptoms can become severe, and in some cases disabling, most are self-limiting and respond to conservative care.
An extreme version of nerve compression or inflammation is cauda equina syndrome. Cauda equina syndrome is a serious condition caused by compression of the nerves in the lower portion of the spinal canal (see Multimedia File 2). Cauda equina syndrome is considered a surgical emergency because if left untreated it can lead to permanent loss of bowel and bladder control and paralysis of the legs.
Cauda Equina Syndrome Causes
Cauda equina syndrome is caused by significant narrowing of the spinal canal that compresses the nerve roots below the level of the spinal cord. Numerous causes of cauda equina syndrome have been reported, including traumatic injury, disk herniation, spinal stenosis, spinal tumors (neoplasms), such as metastatic tumors, meningiomas, schwannomas, and ependymomas, inflammatory conditions, infectious conditions, and accidental causes by medical intervention (iatrogenic causes).
Trauma
* Traumatic events leading to fracture or partial dislocation (subluxation) of the low back (lumbar spine) result in compression of the cauda equina.
* A collection of blood surrounding the nerves following trauma (epidural hematoma) in the low back area can lead to compression of the cauda equina.
* Penetrating trauma (gunshot or stab wounds) can cause damage or compression of the cauda equina.
* A rare complication of spinal manipulation is partial dislocation (subluxation) of the low back (lumbar spine) that can cause cauda equina syndrome.
Herniated Disk
* Most disk herniations will improve on their own (are self-limiting) and respond well to conservative treatment, including antiinflammatory medications, physical therapy, and short periods of rest (one to two days).
* Cauda equina syndrome results from a herniated lumbar disk in 1-15% of cases.
* Of lumbar disk herniations, 90% occur either at the vertebral levels L4-L5 or L5-S1.
* Seventy percent of cases of herniated disks leading to cauda equina syndrome occur in people with a history of chronic low back pain, and 30% develop cauda equina syndrome as the first symptom of lumbar disk herniation.
* Males in their 30s and 40s are most prone to cauda equina syndrome caused by disk herniation.
* Most cases of cauda equina syndrome caused by disk herniation involve large particles of disk material that have completely separated from the normal disk and compress the nerves (extruded disk herniations). In most cases, the disk material takes up at least one-third of the canal diameter.
Spinal Stenosis
* Spinal stenosis is any narrowing of the normal front to back distance (diameter) of the spinal canal.
* Narrowing of the spinal canal can be caused by a developmental abnormality or degenerative process.
* The abnormal forward slip of one vertebral body on another is called spondylolisthesis. Severe cases can cause a narrowing of the spinal canal and lead to cauda equina syndrome (see Multimedia File 3).
Tumors (Neoplasms)
* Cauda equina syndrome can be caused by isolated tumors (primary neoplasms) or from tumors that have spread to the spine from other parts of the body (metastatic spinal neoplasms). Metastatic spine tumors are most commonly from the prostate or lung in males and from the lung and breast in females.
* The most common initial symptom of people with cauda equina syndrome caused by a tumor (spinal neoplasm) is severe low back and leg pain.
* Later findings include lower extremity weakness.
* Loss of feeling in the legs (sensory loss) and loss of bowel or bladder control (sphincter dysfunction) are also common.
Inflammatory Conditions
* Long-lasting inflammatory conditions of the spine, including Paget disease and ankylosing spondylitis, can cause a narrowing of the spinal canal and lead to cauda equina syndrome.
Infectious Conditions
* Infections in the spinal canal (spinal epidural abscess) can cause deformity of the nerve roots and spinal column.
* Symptoms generally include severe back pain and rapidly worsening muscle weakness.
Accidental Medical Causes (Iatrogenic Causes)
* Poorly positioned screws placed in the spine can compress and injure nerves and cause cauda equina syndrome.
* Continuous spinal anesthesia has been linked to cases of cauda equina syndrome.
* Lumbar puncture (spinal tap) can cause a collection of blood in the spinal canal (spontaneous spinal epidural hematoma) in patients receiving medication to thin the blood (anticoagulation therapy). This collection of blood can compress the nerves and cause cauda equina syndrome.
Cauda Equina Syndrome Symptoms
Symptoms of cauda equina syndrome include the following:
* Low back pain
* Pain in one leg (unilateral) or both legs (bilateral) that starts in the buttocks and travels down the back of the thighs and legs (sciatica)
* Numbness in the groin or area of contact if sitting on a saddle (perineal or saddle paresthesia)
* Bowel and bladder disturbances
* Lower extremity muscle weakness and loss of sensations
* Reduced or absent lower extremity reflexes
Low back pain can be divided into local and radicular pain.
* Local pain is generally a deep, aching pain resulting from soft tissue and vertebral body irritation.
* Leg pain (radicular pain) is generally a sharp, stabbing pain resulting from compression of the nerve roots. Radicular pain projects along the specific areas controlled by the compressed nerve (known as a dermatomal distribution).
Bladder disturbance (urinary manifestations) related to cauda equina syndrome include the following:
* Inability to urinate (urinary retention)
* Difficulty initiating urination (urinary hesitancy)
* Decreased sensation when urinating (decreased urethral sensation)
* Inability to stop or control urination (incontinence)
Bowel disturbances may include the following:
* Inability to stop or feel a bowel movement (incontinence)
* Constipation
* Loss of anal tone and sensation
When to Seek Medical Care
Cauda equina syndrome is a surgical emergency. Persons should seek immediate medical care or go to the emergency department if they believe they have symptoms of cauda equina syndrome. Some of the early symptoms related to cauda equina syndrome, including low back pain and muscle weakness, are more often caused by simple disk herniation, which does not require urgent attention. However, if you develop severe pain or loss of sensation or bowel or bladder disturbances, you should contact your physician immediately.
Your chances of regaining normal function and having a positive outcome are related to how long you have had symptoms of cauda equina syndrome. Most experts agree that people with cauda equina syndrome should undergo surgery to make more space for the nerves (lumbar decompression) within 48 hours in order to have the best chance for complete recovery.
Exams and Tests
The initial diagnosis of cauda equina syndrome is made based on findings from the individual's history, symptoms, and physical exam. The physical exam includes testing muscle strength of the lower extremities, evaluating sensation to touch and pain, especially around the groin (perineum), checking the lower extremity reflexes, and evaluating rectal tone, sensation, and reflex.
Imaging studies helpful in the diagnosis include plain x-ray films of the lower back to assess for evidence of trauma or severe arthritis (degenerative changes). MRI with and without contrast provides a detailed look at tumors, infection, intervertebral disks, and nerve roots. This study allows the doctor to determine if the nerves are being compressed, to what degree, and by what structures. Findings from these studies help the surgeon plan the appropriate treatment.
Not all people with back pain and/or leg pain and changes in bowel or bladder function have cauda equina syndrome. More common causes of bladder changes are urinary tract infections, which can be identified by a simple urine test, and diabetes, which can be identified with blood tests.
People with symptoms suggesting a possible infection or tumor should be further evaluated with blood and other tests to identify any abnormalities.
Cauda Equina Syndrome Treatment
Self-Care at Home
Cauda equina syndrome is a surgical emergency. Self-care at home is not appropriate for this condition.
Medical Treatment
Medical treatment options are useful in certain persons, depending on the underlying cause of the cauda equina syndrome. Antiinflammatory agents, such as ibuprofen (Advil, Motrin), and corticosteroids, such as methylprednisolone (Solu-Medrol, Depo-Medrol), can be effective in people with inflammatory processes, including ankylosing spondylitis.
People with cauda equina syndrome caused by an infection should receive appropriate antibiotic therapy. People with spinal tumors (neoplasms) should be evaluated for chemotherapy and radiation therapy.
Caution should be used in any medical management of cauda equina syndrome. Any person with cauda equina syndrome with symptoms of groin numbness (saddle anesthesia) and/or weakness or both legs or loss of bowel or bladder control should wait no more than 24 hours before seeking initial medical management. If no relief of symptoms is achieved during this period, immediate surgical decompression is often recommended to minimize the chances of permanent nerve injury.
Medications
People with infections or tumors (infectious or neoplastic causes) causing cauda equina syndrome should receive the appropriate antibiotics or chemotherapy for treatment of the underlying cause.
In most cases, treatment with medications alone is not indicated because of a need for emergent release of the nerve compression (surgical decompression) of the spinal canal.
Surgery
In many cases of cauda equina syndrome, emergency decompression of the spinal canal is the best treatment option. The goal is to relieve pressure on the nerves of the cauda equina by removing the compressing structures and increasing the space available for the nerves in the spinal canal. Traditionally, cauda equina syndrome has been considered a surgical emergency, with surgical decompression considered necessary within 48 hours of the onset of symptoms.
For people with a herniated disk as the cause of cauda equina syndrome, removal of a portion of the bone surrounding the nerves (laminectomy) is performed and the disk material compressing the nerves is removed (discectomy). Many clinical and experimental reports have presented data on the functional outcome based on the timing of surgical decompression. Some investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression. Even with these findings, however, most investigators recommend surgical decompression as soon as possible following onset of symptoms to offer the greatest chances of complete neurologic recovery.
Many clinical and experimental studies have investigated patient outcomes in relation to the timing of surgical decompression. Some investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression. Even with these findings, however, most investigators recommend surgical decompression as soon as possible following the onset of symptoms to offer the greatest chances of complete neurologic recovery.
Investigators have attempted to identify specific criteria that can aid in predicting the outcome of persons with cauda equina syndrome.
* People with pain in both legs (bilateral sciatica) have less chance or full recovery than persons with single leg pain (unilateral sciatica).
* People with complete groin numbness (perineal anesthesia) are more likely to have permanent paralysis of the bladder.
* The extent of groin numbness (perineal or saddle sensory deficit) is the most important predictor of recovery.
Follow-up
Persons with cauda equina syndrome should have close follow-up with their surgeon to monitor any changes in function. Early surgery gives the patient the best chance for complete recovery from cauda equina syndrome.
Prevention
Prevention of cauda equina syndrome is focused on early diagnosis by identifying the symptoms described above. While low back pain with leg pain and/or weakness is a common complaint that affects many people, cauda equina syndrome is a rare complication. Doctors should be vigilant in identifying these cases. People should be educated on signs and symptoms that could suggest possible cauda equina syndrome, including change in bowel or bladder function and loss of sensation in the groin.
Read More ..
Monday, November 9, 2009
MULTIPLE SCLEROSIS
Overview
Multiple sclerosis (MS) is an inflammatory, chronic, degenerative disorder that affects nerves in the brain and spinal cord. Myelin, the fatty substance that surrounds and insulates nerves and facilitates the conduction of nerve impulses is the initial target of inflammatory destruction in multiple sclerosis.
MS is characterized by intermittent damage to myelin , called demyelination. Demyelination causes scarring and hardening (sclerosis) of nerve tissue in the spinal cord, brain, and optic nerves. Demyelination slows conduction of nerve impulses, which results in weakness, numbness, pain, and vision loss. CLICK HERE FOR DETAILS
CLICK HERE TO DOWNLOAD ALL IMAGE
CLICK HERE TO DOWNLOAD POWER POINT FILE. Power point file contains some videos. You must download the video to view power point file. Click here to download video1, video 2, video 3, video 4, video 5, video 6
Read More ..
Friday, October 23, 2009
Alzheimer's disease
Definition
Alzheimer's disease is the most common cause of dementia — the loss of intellectual and social abilities severe enough to interfere with daily functioning. In Alzheimer's disease, healthy brain tissue degenerates, causing a steady decline in memory and mental abilities.
Alzheimer's disease is not a part of normal aging, but the risk of the disorder increases with age. About 5 percent of people between the ages of 65 and 74 have Alzheimer's disease, while nearly half the people over the age of 85 have Alzheimer's.
Although there's no cure, treatments may improve the quality of life for people with Alzheimer's disease. Those with Alzheimer's — as well as those who care for them — need support and affection from friends and family to cope.
Symptoms
Alzheimer's disease may start with slight memory loss and confusion, but it eventually leads to irreversible mental impairment that destroys a person's ability to remember, reason, learn and imagine.
Memory loss
Everyone has occasional lapses in memory. It's normal to forget where you put your car keys or to blank on the names of people whom you rarely see. But the memory problems associated with Alzheimer's disease persist and worsen. People with Alzheimer's may:
* Repeat things
* Often forget conversations or appointments
* Routinely misplace things, often putting them in illogical locations
* Eventually forget the names of family members and everyday objects
Problems with abstract thinking
People with Alzheimer's may initially have trouble balancing their checkbook, a problem that progresses to trouble recognizing and dealing with numbers.
Difficulty finding the right word
It may be a challenge for those with Alzheimer's to find the right words to express thoughts or even follow conversations. Eventually, reading and writing also are affected.
Disorientation
People with Alzheimer's disease often lose their sense of time and dates, and may find themselves lost in familiar surroundings.
Loss of judgment
Solving everyday problems, such as knowing what to do if food on the stove is burning, becomes increasingly difficult, eventually impossible. Alzheimer's is characterized by greater difficulty in doing things that require planning, decision making and judgment.
Difficulty performing familiar tasks
Once-routine tasks that require sequential steps, such as cooking, become a struggle as the disease progresses. Eventually, people with advanced Alzheimer's may forget how to do even the most basic things.
Personality changes
People with Alzheimer's may exhibit:
* Mood swings
* Distrust in others
* Increased stubbornness
* Social withdrawal
* Depression
* Anxiety
* Aggressiveness
Causes
No one factor appears to cause Alzheimer's disease. Instead, scientists believe that it may take a combination of genetic, lifestyle and environmental factors to trigger the onset of symptoms. While the causes of Alzheimer's are poorly understood, its effect on brain tissue is clear. Alzheimer's disease damages and kills brain cells.
Two types of brain cell (neuron) damage are common in people who have Alzheimer's:
* Plaques. Clumps of a normally harmless protein called beta-amyloid may interfere with communication between brain cells. Although the ultimate cause of neuron death in Alzheimer's isn't known, mounting evidence suggests that the abnormal processing of beta-amyloid protein may be the culprit.
* Tangles. The internal support structure for brain cells depends on the normal functioning of a protein called tau. In people with Alzheimer's, threads of tau protein undergo alterations that cause them to become twisted. Many researchers believe this may seriously damage neurons, causing them to die.
Risk factors
Age
Alzheimer's usually affects people older than 65, but can, rarely, affect those younger than 40. Less than 5 percent of people between 65 and 74 have Alzheimer's. For people 85 and older, that number jumps to nearly 50 percent.
Heredity
Your risk of developing Alzheimer's appears to be slightly higher if a first-degree relative — parent, sister or brother — has the disease. Although the genetic mechanisms of Alzheimer's among families remain largely unexplained, researchers have identified several genetic mutations that greatly increase risk in some families.
Sex
Women are more likely than men are to develop the disease, in part because they live longer.
Mild cognitive impairment
People who have mild cognitive impairment have memory problems that are worse than what might be expected for people of their age, yet not bad enough to be classified as dementia. Many of those who have this condition go on to develop Alzheimer's disease.
Lifestyle
The same factors that put you at risk of heart disease may also increase the likelihood that you'll develop Alzheimer's disease. Examples include:
* High blood pressure
* High cholesterol
* Poorly controlled diabetes
And keeping your body fit isn't your only concern — you've got to exercise your mind as well. Some studies have suggested that remaining mentally active throughout your life, especially in your later years, reduces the risk of Alzheimer's disease.
Education levels
Studies have found an association between less education and the risk of Alzheimer's. But the precise reason why this occurs is unknown. Some researchers theorize that the more you use your brain, the more synapses you create, which provides a greater reserve as you age. But it may simply be harder to detect Alzheimer's in people who exercise their minds frequently or who have more education.
Complications
In advanced Alzheimer's disease, people may lose all ability to care for themselves. This can make them more prone to additional health problems such as:
* Pneumonia. Difficulty swallowing food and liquids may cause people with Alzheimer's to inhale (aspirate) some of what they eat and drink into their airways and lungs, which can lead to pneumonia.
* Infections. Urinary incontinence may require the placement of a urinary catheter, which increases the risk of urinary tract infections. Untreated urinary tract infections can lead to more-serious, life-threatening infections.
* Injuries from falls. People with Alzheimer's may become disoriented, increasing their risk of falls. Falls can lead to fractures. In addition, falls are a common cause of serious head injuries, such as bleeding in the brain.
Tests and diagnosis
Doctors can accurately diagnose 90 percent of Alzheimer's cases. Alzheimer's disease can be diagnosed with complete accuracy only after death, when microscopic examination of the brain reveals plaques and tangles.
To help distinguish Alzheimer's disease from other causes of memory loss, doctors typically rely on the following types of tests.
Lab tests
Blood tests may be done to help doctors rule out other potential causes of the dementia, such as thyroid disorders or vitamin deficiencies.
Neuropsychological testing
Sometimes doctors undertake a more extensive assessment of thinking and memory skills. This type of testing, which can take several hours to complete, is especially helpful in trying to detect Alzheimer's and other dementias at an early stage.
Brain scans
By looking at images of the brain, doctors may be able to pinpoint any visible abnormalities — such as clots, bleeding or tumors — that may be causing signs and symptoms. Positron emission tomography (PET) can reveal areas of the brain that may be less active and the density of amyloid plaques.
* Magnetic resonance imaging (MRI). An MRI machine uses radio waves and a strong magnetic field to produce detailed images of your brain. You lie on a narrow table that slides into the tube-shaped MRI machine, which makes loud banging noises during scans. The entire procedure can take an hour or more. MRIs are painless, but some people feel claustrophobic in the machine.
* Computerized tomography (CT). For a CT scan, you lie on a narrow table that slides into a small chamber. X-rays pass through your body from various angles, and a computer uses this information to create cross-sectional images, or slices, of your brain. The test is painless and takes about 20 minutes.
* Positron emission tomography (PET). During a PET scan, you'll be injected with a low-level radioactive material, which binds to chemicals that travel to the brain. You lie on a table while an overhead scanner tracks the radioactive material. This helps show which parts of your brain aren't functioning properly. The test is painless and can be particularly useful in distinguishing between different types of dementia.
Treatments and drugs
Currently, there's no cure for Alzheimer's disease. Doctors sometimes prescribe drugs to improve signs and symptoms that often accompany Alzheimer's, including sleeplessness, wandering, anxiety, agitation and depression. But only two varieties of medications have been proved to slow the cognitive decline associated with Alzheimer's.
Cholinesterase inhibitors
This group of medications — which includes donepezil (Aricept), rivastigmine (Exelon) and galantamine (Razadyne) — works by improving the levels of neurotransmitters in the brain. But cholinesterase inhibitors don't work for everyone. As many as half the people who take these drugs show no improvement. Other people may choose to stop taking the drugs because of the side effects, which include diarrhea, nausea and vomiting.
Memantine (Namenda)
The first drug approved to treat moderate to severe stages of Alzheimer's, memantine protects brain cells from damage caused by the chemical messenger glutamate. It sometimes is used in combination with a cholinesterase inhibitor. Memantine's most common side effect is dizziness, although it also appears to increase agitation and delusional behavior in some people.
Lifestyle and home remedies
A healthy lifestyle may help prevent or postpone the development of Alzheimer's disease. Because Alzheimer's is most common in people over the age of 80, delaying the onset of the disease would increase the probability that people will die of other causes before Alzheimer's has a chance to develop.
Eat your veggies
Maintaining a healthy weight and eating a healthy diet appears to reduce the risk of developing Alzheimer's disease. Your doctor may suggest:
* Lots of fruits and vegetables
* Fish or poultry, instead of red meat
* Whole-grain breads and cereals
* Alternate sources of proteins, such as beans, nuts and seeds
* More olive oil and less saturated fat
Exercise your body
Higher levels of physical activity have been associated with a lower incidence of Alzheimer's disease.
Exercise your brain, too
Maintaining mental fitness may delay onset of dementia. Some researchers believe that lifelong mental exercise and learning may promote the growth of additional synapses, the connections between neurons, and delay the onset of dementia.
Carry a reminder calendar.
Record not just upcoming events, but things that happen and activities you need to complete on a daily basis. And check off those activities when done. If you can make this process a habit before your memory problems worsen, you'll be more likely to retain this skill as the disease progresses. If you can't remember if you took your pills or who called that morning, you can check your journal.
Alternative medicine
Vitamin E
Some studies have shown that vitamin E can slow the progression of Alzheimer's disease, while other studies have shown no benefit. Doctors now warn people against taking large dosages of vitamin E, because it can increase your risk of cardiovascular death.
Ginkgo
Some people believe that extracts from the leaves of the ginkgo biloba tree may help slow the progression of memory problems associated with Alzheimer's disease. But a recent large-scale study showed no benefit. Be aware that these preparations can interact with blood-thinning medications and cause bleeding.
Huperzine A
Made from Chinese club moss, Huperzine A appears to work in ways similar to prescription cholinesterase inhibitors. Because of the increased risk of toxic side effects, you shouldn't take Huperzine A if you're also taking a drug like donepezil (Aricept).
Coping and support
People with Alzheimer's disease often experience a mixture of emotions — confusion, frustration, anger, fear, uncertainty, grief and depression.
You can help a person cope with the disease by being there to listen, reassuring the person that life can still be enjoyed, providing unconditional love, and doing your best to help the person retain dignity and self-respect.
A calm and stable home environment reduces behavior problems. New situations, noise, large groups of people, being rushed or pressed to remember, or being asked to do complicated tasks can cause anxiety. As a person with Alzheimer's becomes upset, the ability to think clearly declines even more.
Caring for the caregiver
Providing care for a person with Alzheimer's disease is physically and emotionally demanding. Feelings of anger and guilt, frustration and discouragement, worry and grief, and social isolation are common. If you're a caregiver for someone with Alzheimer's disease, you can help yourself by:
* Asking friends or other family members for help when you need it
* Taking care of your health
* Learning as much about the disease as you can
* Asking questions of doctors, social workers and others involved in the care of your loved one
* Joining a support group
Many people with Alzheimer's and their families benefit from counseling or local support groups. Contact your local Alzheimer's Association affiliate to get connected with support groups, doctors, resources and referrals, home care agencies, supervised living facilities, a telephone help line, and educational seminars.
Prevention
Right now, there's no proven way to prevent the onset of Alzheimer's disease. Human trials of a promising vaccine against Alzheimer's had to be stopped several years ago because some of the people who received the vaccine developed a serious inflammation of the brain.
However, you may be able to reduce your risk of Alzheimer's disease by reducing your risk of heart disease. Many of the same factors that increase your risk of heart disease can also increase your risk of dementia. The main players appear to be blood pressure, cholesterol and blood glucose levels.
Keeping active — physically, mentally and socially — also seems to reduce the risk of Alzheimer's disease.
Read More ..
Alzheimer's disease is the most common cause of dementia — the loss of intellectual and social abilities severe enough to interfere with daily functioning. In Alzheimer's disease, healthy brain tissue degenerates, causing a steady decline in memory and mental abilities.
Alzheimer's disease is not a part of normal aging, but the risk of the disorder increases with age. About 5 percent of people between the ages of 65 and 74 have Alzheimer's disease, while nearly half the people over the age of 85 have Alzheimer's.
Although there's no cure, treatments may improve the quality of life for people with Alzheimer's disease. Those with Alzheimer's — as well as those who care for them — need support and affection from friends and family to cope.
Symptoms
Alzheimer's disease may start with slight memory loss and confusion, but it eventually leads to irreversible mental impairment that destroys a person's ability to remember, reason, learn and imagine.
Memory loss
Everyone has occasional lapses in memory. It's normal to forget where you put your car keys or to blank on the names of people whom you rarely see. But the memory problems associated with Alzheimer's disease persist and worsen. People with Alzheimer's may:
* Repeat things
* Often forget conversations or appointments
* Routinely misplace things, often putting them in illogical locations
* Eventually forget the names of family members and everyday objects
Problems with abstract thinking
People with Alzheimer's may initially have trouble balancing their checkbook, a problem that progresses to trouble recognizing and dealing with numbers.
Difficulty finding the right word
It may be a challenge for those with Alzheimer's to find the right words to express thoughts or even follow conversations. Eventually, reading and writing also are affected.
Disorientation
People with Alzheimer's disease often lose their sense of time and dates, and may find themselves lost in familiar surroundings.
Loss of judgment
Solving everyday problems, such as knowing what to do if food on the stove is burning, becomes increasingly difficult, eventually impossible. Alzheimer's is characterized by greater difficulty in doing things that require planning, decision making and judgment.
Difficulty performing familiar tasks
Once-routine tasks that require sequential steps, such as cooking, become a struggle as the disease progresses. Eventually, people with advanced Alzheimer's may forget how to do even the most basic things.
Personality changes
People with Alzheimer's may exhibit:
* Mood swings
* Distrust in others
* Increased stubbornness
* Social withdrawal
* Depression
* Anxiety
* Aggressiveness
Causes
No one factor appears to cause Alzheimer's disease. Instead, scientists believe that it may take a combination of genetic, lifestyle and environmental factors to trigger the onset of symptoms. While the causes of Alzheimer's are poorly understood, its effect on brain tissue is clear. Alzheimer's disease damages and kills brain cells.
Two types of brain cell (neuron) damage are common in people who have Alzheimer's:
* Plaques. Clumps of a normally harmless protein called beta-amyloid may interfere with communication between brain cells. Although the ultimate cause of neuron death in Alzheimer's isn't known, mounting evidence suggests that the abnormal processing of beta-amyloid protein may be the culprit.
* Tangles. The internal support structure for brain cells depends on the normal functioning of a protein called tau. In people with Alzheimer's, threads of tau protein undergo alterations that cause them to become twisted. Many researchers believe this may seriously damage neurons, causing them to die.
Risk factors
Age
Alzheimer's usually affects people older than 65, but can, rarely, affect those younger than 40. Less than 5 percent of people between 65 and 74 have Alzheimer's. For people 85 and older, that number jumps to nearly 50 percent.
Heredity
Your risk of developing Alzheimer's appears to be slightly higher if a first-degree relative — parent, sister or brother — has the disease. Although the genetic mechanisms of Alzheimer's among families remain largely unexplained, researchers have identified several genetic mutations that greatly increase risk in some families.
Sex
Women are more likely than men are to develop the disease, in part because they live longer.
Mild cognitive impairment
People who have mild cognitive impairment have memory problems that are worse than what might be expected for people of their age, yet not bad enough to be classified as dementia. Many of those who have this condition go on to develop Alzheimer's disease.
Lifestyle
The same factors that put you at risk of heart disease may also increase the likelihood that you'll develop Alzheimer's disease. Examples include:
* High blood pressure
* High cholesterol
* Poorly controlled diabetes
And keeping your body fit isn't your only concern — you've got to exercise your mind as well. Some studies have suggested that remaining mentally active throughout your life, especially in your later years, reduces the risk of Alzheimer's disease.
Education levels
Studies have found an association between less education and the risk of Alzheimer's. But the precise reason why this occurs is unknown. Some researchers theorize that the more you use your brain, the more synapses you create, which provides a greater reserve as you age. But it may simply be harder to detect Alzheimer's in people who exercise their minds frequently or who have more education.
Complications
In advanced Alzheimer's disease, people may lose all ability to care for themselves. This can make them more prone to additional health problems such as:
* Pneumonia. Difficulty swallowing food and liquids may cause people with Alzheimer's to inhale (aspirate) some of what they eat and drink into their airways and lungs, which can lead to pneumonia.
* Infections. Urinary incontinence may require the placement of a urinary catheter, which increases the risk of urinary tract infections. Untreated urinary tract infections can lead to more-serious, life-threatening infections.
* Injuries from falls. People with Alzheimer's may become disoriented, increasing their risk of falls. Falls can lead to fractures. In addition, falls are a common cause of serious head injuries, such as bleeding in the brain.
Tests and diagnosis
Doctors can accurately diagnose 90 percent of Alzheimer's cases. Alzheimer's disease can be diagnosed with complete accuracy only after death, when microscopic examination of the brain reveals plaques and tangles.
To help distinguish Alzheimer's disease from other causes of memory loss, doctors typically rely on the following types of tests.
Lab tests
Blood tests may be done to help doctors rule out other potential causes of the dementia, such as thyroid disorders or vitamin deficiencies.
Neuropsychological testing
Sometimes doctors undertake a more extensive assessment of thinking and memory skills. This type of testing, which can take several hours to complete, is especially helpful in trying to detect Alzheimer's and other dementias at an early stage.
Brain scans
By looking at images of the brain, doctors may be able to pinpoint any visible abnormalities — such as clots, bleeding or tumors — that may be causing signs and symptoms. Positron emission tomography (PET) can reveal areas of the brain that may be less active and the density of amyloid plaques.
* Magnetic resonance imaging (MRI). An MRI machine uses radio waves and a strong magnetic field to produce detailed images of your brain. You lie on a narrow table that slides into the tube-shaped MRI machine, which makes loud banging noises during scans. The entire procedure can take an hour or more. MRIs are painless, but some people feel claustrophobic in the machine.
* Computerized tomography (CT). For a CT scan, you lie on a narrow table that slides into a small chamber. X-rays pass through your body from various angles, and a computer uses this information to create cross-sectional images, or slices, of your brain. The test is painless and takes about 20 minutes.
* Positron emission tomography (PET). During a PET scan, you'll be injected with a low-level radioactive material, which binds to chemicals that travel to the brain. You lie on a table while an overhead scanner tracks the radioactive material. This helps show which parts of your brain aren't functioning properly. The test is painless and can be particularly useful in distinguishing between different types of dementia.
Treatments and drugs
Currently, there's no cure for Alzheimer's disease. Doctors sometimes prescribe drugs to improve signs and symptoms that often accompany Alzheimer's, including sleeplessness, wandering, anxiety, agitation and depression. But only two varieties of medications have been proved to slow the cognitive decline associated with Alzheimer's.
Cholinesterase inhibitors
This group of medications — which includes donepezil (Aricept), rivastigmine (Exelon) and galantamine (Razadyne) — works by improving the levels of neurotransmitters in the brain. But cholinesterase inhibitors don't work for everyone. As many as half the people who take these drugs show no improvement. Other people may choose to stop taking the drugs because of the side effects, which include diarrhea, nausea and vomiting.
Memantine (Namenda)
The first drug approved to treat moderate to severe stages of Alzheimer's, memantine protects brain cells from damage caused by the chemical messenger glutamate. It sometimes is used in combination with a cholinesterase inhibitor. Memantine's most common side effect is dizziness, although it also appears to increase agitation and delusional behavior in some people.
Lifestyle and home remedies
A healthy lifestyle may help prevent or postpone the development of Alzheimer's disease. Because Alzheimer's is most common in people over the age of 80, delaying the onset of the disease would increase the probability that people will die of other causes before Alzheimer's has a chance to develop.
Eat your veggies
Maintaining a healthy weight and eating a healthy diet appears to reduce the risk of developing Alzheimer's disease. Your doctor may suggest:
* Lots of fruits and vegetables
* Fish or poultry, instead of red meat
* Whole-grain breads and cereals
* Alternate sources of proteins, such as beans, nuts and seeds
* More olive oil and less saturated fat
Exercise your body
Higher levels of physical activity have been associated with a lower incidence of Alzheimer's disease.
Exercise your brain, too
Maintaining mental fitness may delay onset of dementia. Some researchers believe that lifelong mental exercise and learning may promote the growth of additional synapses, the connections between neurons, and delay the onset of dementia.
Carry a reminder calendar.
Record not just upcoming events, but things that happen and activities you need to complete on a daily basis. And check off those activities when done. If you can make this process a habit before your memory problems worsen, you'll be more likely to retain this skill as the disease progresses. If you can't remember if you took your pills or who called that morning, you can check your journal.
Alternative medicine
Vitamin E
Some studies have shown that vitamin E can slow the progression of Alzheimer's disease, while other studies have shown no benefit. Doctors now warn people against taking large dosages of vitamin E, because it can increase your risk of cardiovascular death.
Ginkgo
Some people believe that extracts from the leaves of the ginkgo biloba tree may help slow the progression of memory problems associated with Alzheimer's disease. But a recent large-scale study showed no benefit. Be aware that these preparations can interact with blood-thinning medications and cause bleeding.
Huperzine A
Made from Chinese club moss, Huperzine A appears to work in ways similar to prescription cholinesterase inhibitors. Because of the increased risk of toxic side effects, you shouldn't take Huperzine A if you're also taking a drug like donepezil (Aricept).
Coping and support
People with Alzheimer's disease often experience a mixture of emotions — confusion, frustration, anger, fear, uncertainty, grief and depression.
You can help a person cope with the disease by being there to listen, reassuring the person that life can still be enjoyed, providing unconditional love, and doing your best to help the person retain dignity and self-respect.
A calm and stable home environment reduces behavior problems. New situations, noise, large groups of people, being rushed or pressed to remember, or being asked to do complicated tasks can cause anxiety. As a person with Alzheimer's becomes upset, the ability to think clearly declines even more.
Caring for the caregiver
Providing care for a person with Alzheimer's disease is physically and emotionally demanding. Feelings of anger and guilt, frustration and discouragement, worry and grief, and social isolation are common. If you're a caregiver for someone with Alzheimer's disease, you can help yourself by:
* Asking friends or other family members for help when you need it
* Taking care of your health
* Learning as much about the disease as you can
* Asking questions of doctors, social workers and others involved in the care of your loved one
* Joining a support group
Many people with Alzheimer's and their families benefit from counseling or local support groups. Contact your local Alzheimer's Association affiliate to get connected with support groups, doctors, resources and referrals, home care agencies, supervised living facilities, a telephone help line, and educational seminars.
Prevention
Right now, there's no proven way to prevent the onset of Alzheimer's disease. Human trials of a promising vaccine against Alzheimer's had to be stopped several years ago because some of the people who received the vaccine developed a serious inflammation of the brain.
However, you may be able to reduce your risk of Alzheimer's disease by reducing your risk of heart disease. Many of the same factors that increase your risk of heart disease can also increase your risk of dementia. The main players appear to be blood pressure, cholesterol and blood glucose levels.
Keeping active — physically, mentally and socially — also seems to reduce the risk of Alzheimer's disease.
Read More ..
Tuesday, September 22, 2009
DEMENTIA
Written by Christian Nordqvist
The word dementia comes from the Latin de meaning "apart" and mens from the genitive mentis meaning "mind". Dementia is the progressive deterioration in cognitive function - the ability to process thought (intelligence).
Progressive means the symptoms will gradually get worse. The deterioration is more than might be expected from normal aging and is due to damage or disease. Damage could be due to a stroke, while an example of a disease might be Alzheimer's.
Dementia is a set of signs and symptoms
Dementia is a non-specific syndrome in which affected areas of brain function may be affected, such as memory, language, problem solving and attention. Dementia, unlike Alzheimer's, is not a disease in itself. When dementia appears the higher mental functions of the patient are involved initially. Eventually, in the later stages, the person may not know what day of the week, month or year it is, he may not know where he is, and might not be able to identify the people around him.
Dementia is significantly more common among elderly people. However, it can affect adults of any age.
What are the symptoms of dementia?
* Memory loss - the patient may forget his way back home from the shops. He may forget names and places. He may find it hard to remember what happened earlier on during the day.
* Moodiness - the patient may become more and more moody as parts of the brain that control emotion become damaged. Moods may also be affected by fear and anxiety - the patient is frightened about what is happening to him.
* Communicative difficulties - the affected person finds it harder to talk read and/or write.
As the dementia progresses, the patient's ability to carry out everyday tasks diminishes and he may not be able to look after himself.
Diseases that cause dementia
# Alzheimer's disease - This is by far the most common cause of dementia. The chemistry and structure of the brain of a person with Alzheimer's disease changes and his brain cells die prematurely.
# Stroke (Vascular problems) - this means problems with blood vessels (veins and arteries). Our brain needs a good supply of oxygen-rich blood. If this supply is undermined in any way our brain cells could die - causing symptoms of vascular dementia. Symptoms may appear suddenly, or gradually. A major stroke will cause symptoms to appear suddenly while a series of mini strokes will not.
# Dementia with Lewy bodies - spherical structures develop inside nerve cells. Brain cells are nerve cells; they form part of our nervous system. These spherical structures in the brain damage brain tissue. The patient's memory, concentration and ability to speak are affected. Dementia with Lewy bodies is sometimes mistaken for Parkinson's disease because the symptoms are fairly similar.
# Fronto-temporal dementia - this includes Pick's disease. The front part of the brain is damaged. The patient's behavior and personality are affected first, later his memory changes.
# Other diseases - progressive supranuclear palsy, Korsakoff's syndrome, Binswanger's disease, HIV and AIDS, and Creutzfeldt-Jakob disease (CJD). Dementia is also more common among patients who suffer from Parkinson's disease, Huntington's disease, Motor Neurone disease and Multiple Sclerosis. People who suffer from AIDS sometimes go on to develop cognitive impairment.
There are two main categories of dementia
According to most experts, there are two main categories of dementia - cortical and subcortical dementias.
* Cortical Dementia - The cerebral cortex is affected. This is the outer layer of the brain. The cerebral cortex is vital for cognitive processes, such as language and memory. Alzheimer's disease is a form of cortical dementia, as is CJD (Creutzfeldt-Jakob disease).
* Subcortical Dementia - A part of the brain beneath the cortex (deeper inside) becomes affected or damaged. Language and memory are not usually affected. A patient with subcortical dementia will usually experience changes in his personality, his thinking may slow down, and his attention span may be shortened. Dementias which sometimes result from Parkinson's disease are subcortical dementias, as are those caused by AIDS and Huntington's disease.
A patient with multi-infarct dementia will have both the cortical and subcortical parts of the brain affected or damaged.
Diagnosis of dementia
Although there are some brief tests, a more reliable diagnosis needs to be carried out by a specialist, such as a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist.
The following tests are commonly used:
* AMTS (Abbreviated Mental Test Score) A score lower than six out of ten suggests a need for further evaluation.
* MMSE (Mini Mental State Examination) A score lower than twenty-four out of thirty suggests a need for further evaluation)
* 3MS (Modified Mini-Mental State Examination)
* CASI (Cognitive Abilities Screening Instrument)
It is important that the patient's score is interpreted in context with his socio-economic, educational and cultural background. The tester must also factor in the patient's present physical and mental state - does the patient suffer from depression, is he in great pain?
What is the treatment for dementia?
In the majority of cases dementia is incurable. Researchers are making inroads into treatments that may slow down dementia's progress. Cholinestaerase inhibitors are frequently administered during the early stages. Cognitive and behavioral therapies may also be useful. Several studies have found that music therapy helps patients with dementia. It is important to remember that the patient's caregiver also needs training and emotional support.
In the USA, Tacrine (Cognex), donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon) have been approved for the treatment of dementia caused by Alzheimer's disease - some physicians prescribe these drugs for vascular dementia as well. Selegiline, which is used for treating Parkinson's disease, has been found to slow down the progress of dementia.
In Canada, a country where two languages are spoken, English and French, researchers found that bilingual people who develop dementia do so four years later than monolingual people who develop dementia. The four year difference prevails even after factoring for such variables as cultural differences, education, employment, gender and immigration.
How common is dementia?
* United Kingdom - According to a report by the Alzheimer's Society (UK), approximately 700,000 people in the United Kingdom have dementia, out of a total population of about 61 million. Your chances of having dementia are 1 in 100 during your late 60s, this rises to 6 in 100 in your late 70s, and 20 in 100 in your late 80s. As people live longer experts predict dementia will rise significantly. According to predictions, there will be 940,000 people with dementia in the United Kingdom by 2021.
* Worldwide - According to a study published in The Lancet, approximately 24.3 million people had dementia worldwide in 2005, with 4.6 new cases every year. The number of people with dementia will double every two decades and reach 81.1 million by 2040. The rate of increase is expected to be faster in developing countries which have rapidly-growing life expectancies. (Lancet. 2005 Dec 17;366(9503):2112-7)
Sources - The Alzheimer's Society (UK), NIH, Wikipedia, The Lancet
Read More ..
The word dementia comes from the Latin de meaning "apart" and mens from the genitive mentis meaning "mind". Dementia is the progressive deterioration in cognitive function - the ability to process thought (intelligence).
Progressive means the symptoms will gradually get worse. The deterioration is more than might be expected from normal aging and is due to damage or disease. Damage could be due to a stroke, while an example of a disease might be Alzheimer's.
Dementia is a set of signs and symptoms
Dementia is a non-specific syndrome in which affected areas of brain function may be affected, such as memory, language, problem solving and attention. Dementia, unlike Alzheimer's, is not a disease in itself. When dementia appears the higher mental functions of the patient are involved initially. Eventually, in the later stages, the person may not know what day of the week, month or year it is, he may not know where he is, and might not be able to identify the people around him.
Dementia is significantly more common among elderly people. However, it can affect adults of any age.
What are the symptoms of dementia?
* Memory loss - the patient may forget his way back home from the shops. He may forget names and places. He may find it hard to remember what happened earlier on during the day.
* Moodiness - the patient may become more and more moody as parts of the brain that control emotion become damaged. Moods may also be affected by fear and anxiety - the patient is frightened about what is happening to him.
* Communicative difficulties - the affected person finds it harder to talk read and/or write.
As the dementia progresses, the patient's ability to carry out everyday tasks diminishes and he may not be able to look after himself.
Diseases that cause dementia
# Alzheimer's disease - This is by far the most common cause of dementia. The chemistry and structure of the brain of a person with Alzheimer's disease changes and his brain cells die prematurely.
# Stroke (Vascular problems) - this means problems with blood vessels (veins and arteries). Our brain needs a good supply of oxygen-rich blood. If this supply is undermined in any way our brain cells could die - causing symptoms of vascular dementia. Symptoms may appear suddenly, or gradually. A major stroke will cause symptoms to appear suddenly while a series of mini strokes will not.
# Dementia with Lewy bodies - spherical structures develop inside nerve cells. Brain cells are nerve cells; they form part of our nervous system. These spherical structures in the brain damage brain tissue. The patient's memory, concentration and ability to speak are affected. Dementia with Lewy bodies is sometimes mistaken for Parkinson's disease because the symptoms are fairly similar.
# Fronto-temporal dementia - this includes Pick's disease. The front part of the brain is damaged. The patient's behavior and personality are affected first, later his memory changes.
# Other diseases - progressive supranuclear palsy, Korsakoff's syndrome, Binswanger's disease, HIV and AIDS, and Creutzfeldt-Jakob disease (CJD). Dementia is also more common among patients who suffer from Parkinson's disease, Huntington's disease, Motor Neurone disease and Multiple Sclerosis. People who suffer from AIDS sometimes go on to develop cognitive impairment.
There are two main categories of dementia
According to most experts, there are two main categories of dementia - cortical and subcortical dementias.
* Cortical Dementia - The cerebral cortex is affected. This is the outer layer of the brain. The cerebral cortex is vital for cognitive processes, such as language and memory. Alzheimer's disease is a form of cortical dementia, as is CJD (Creutzfeldt-Jakob disease).
* Subcortical Dementia - A part of the brain beneath the cortex (deeper inside) becomes affected or damaged. Language and memory are not usually affected. A patient with subcortical dementia will usually experience changes in his personality, his thinking may slow down, and his attention span may be shortened. Dementias which sometimes result from Parkinson's disease are subcortical dementias, as are those caused by AIDS and Huntington's disease.
A patient with multi-infarct dementia will have both the cortical and subcortical parts of the brain affected or damaged.
Diagnosis of dementia
Although there are some brief tests, a more reliable diagnosis needs to be carried out by a specialist, such as a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist.
The following tests are commonly used:
* AMTS (Abbreviated Mental Test Score) A score lower than six out of ten suggests a need for further evaluation.
* MMSE (Mini Mental State Examination) A score lower than twenty-four out of thirty suggests a need for further evaluation)
* 3MS (Modified Mini-Mental State Examination)
* CASI (Cognitive Abilities Screening Instrument)
It is important that the patient's score is interpreted in context with his socio-economic, educational and cultural background. The tester must also factor in the patient's present physical and mental state - does the patient suffer from depression, is he in great pain?
What is the treatment for dementia?
In the majority of cases dementia is incurable. Researchers are making inroads into treatments that may slow down dementia's progress. Cholinestaerase inhibitors are frequently administered during the early stages. Cognitive and behavioral therapies may also be useful. Several studies have found that music therapy helps patients with dementia. It is important to remember that the patient's caregiver also needs training and emotional support.
In the USA, Tacrine (Cognex), donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon) have been approved for the treatment of dementia caused by Alzheimer's disease - some physicians prescribe these drugs for vascular dementia as well. Selegiline, which is used for treating Parkinson's disease, has been found to slow down the progress of dementia.
In Canada, a country where two languages are spoken, English and French, researchers found that bilingual people who develop dementia do so four years later than monolingual people who develop dementia. The four year difference prevails even after factoring for such variables as cultural differences, education, employment, gender and immigration.
How common is dementia?
* United Kingdom - According to a report by the Alzheimer's Society (UK), approximately 700,000 people in the United Kingdom have dementia, out of a total population of about 61 million. Your chances of having dementia are 1 in 100 during your late 60s, this rises to 6 in 100 in your late 70s, and 20 in 100 in your late 80s. As people live longer experts predict dementia will rise significantly. According to predictions, there will be 940,000 people with dementia in the United Kingdom by 2021.
* Worldwide - According to a study published in The Lancet, approximately 24.3 million people had dementia worldwide in 2005, with 4.6 new cases every year. The number of people with dementia will double every two decades and reach 81.1 million by 2040. The rate of increase is expected to be faster in developing countries which have rapidly-growing life expectancies. (Lancet. 2005 Dec 17;366(9503):2112-7)
Sources - The Alzheimer's Society (UK), NIH, Wikipedia, The Lancet
Read More ..
Sunday, August 16, 2009
The Neurological Assessment
A neurological assessment includes several exams, tests and procedures which are used to make the diagnosis of nervous system diseases. So what can you expect when undergoing neurological evaluations? Every condition is different and therefore the assessment will vary considerable. However, there are some general tests and exams which many neuro patients will undergo. Here is an overview of some of these common parts of a neuro assessment.
The Neuro Assessment
A neurological evaluation is a clinical assessment of the nervous system aimed at detecting any abnormalities which may be related to a nervous system disease. An initial neurological assessment may be conducted by a primary care physician such as an internal medicine doctor or family practitioner, but a complete and thorough assessment is generally conducted by a specialist in the area of neurological disorders such as a neurologist or neurosurgeon, depending on the disorder in question.
The neurological evaluation is a complete assessment of the nervous system but may be focused on parts of the nervous system related to symptoms with which the patient is presenting. For example, a patient presenting with back pain and leg symptoms may have a focused neurological assessment which spends more time evaluating the legs and back while a patient presenting with facial weakness and difficulty with hearing may have a quite different assessment.
An evaluation of the nervous system for nervous system diseases can include three general components, a subjective review of the patient's presenting complaints and medical history, a neurological exam and diagnostic testing focused on the nervous system.
The review of the complaint and medical history is common to all medical assessments. The patient is questioned by their physician about all aspects of their complaint or symptoms as well as details of their past medical history, family history, medications, allergies, social history and a review of other symptoms. This helps the physician understand the complaint as well as other medical conditions and other aspects of the patient's history which may impact the current problem in one way or another.
The neurological exam is a physical examination which is focused on the nervous system. It is aimed at determining any signs or symptoms related to the nervous system or its function. The complete nervous system examination is quite detailed with several areas of the body examined. We will not list every physical exam test and maneuver here but the general sections of the complete neurological exam are described on the neurological exam page.
Finally, after these assessments by the physician, diagnostic testing is used in some cases to help detect a suspected or concerning pathology. This varies from patient to patient and from disease to disease. However, common tests or studies used to help diagnose nervous system diseases include x-rays, MRI scans, and CT scans of the head and/or spine. Additionally, nerve conduction studies, electromyelography (EMG), eletroencephalograms (EEG), blood tests, lumbar puncture (spinal tap) can also be used in some select instances. There are other tests, procedures or studies which are performed in more specific examples. For example, in a patient with a tumor, a biopsy or removal of the tumor is sometimes required to make the definitive diagnosis.
All of these parts of the neurological evaluation can help the physician to determine the most likely diagnosis as well as the most appropriate course of action. Determination of prognosis and treatment for the disease rely on this evaluation and the data it supplies. Every patient and disease is different and the specific aspects of one patient's evaluation may differ somewhat from another.
A neurological exam is a physical examination conducted by a health care provider which is focused on the nervous system. It is a common part of a complete neurological assessment as may be conducted by various physicians, most commonly a neurologist or neurosurgeon. The goal of the examination is to detect any signs or symptoms related to the nervous system and its functioning.
The neurological exam can be conducted by anyone, including primary care providers such as family practitioners and internal medicine doctors. However, it is most commonly part of a neurological evaluation by a physician specializing in diseases of the nervous system, such as a neurologist or a neurosurgeon.
What Are the Parts of a Typical Neurological Exam?
* Behavioral, Cognitive and Mental Status: This part of the neurological evaluation helps to determine the higher functioning of a patient's brain. It is an assessment of their mental status, or level of alertness and consciousness, as well as their higher functions of memory, reasoning, logic and general behavior. While some of this overlaps with a psychological assessment, it is, at least in part, a part of the complete neurological examination.
* Head and Neck Exam: Because the brain and spinal cord are in the head and neck, a general examination of the head and neck for malformations, abnormal anatomy, masses and other findings is often undertaken.
* Cranial Nerve Exam: There are 12 cranial nerves which are nerves that originate in the head, coming off the brain and brain stem. The examination of these nerves and their functions is complex but includes areas such as smell, vision and eye movements, facial sensation, reflexes and movement, hearing, taste, tongue and palate movements and even movements of the head, neck and shoulders.
* Motor Exam: This part of the examination tests the motor function, or movement, of the major muscle groups, most notably in the shoulders, arms, hips and legs. The muscles are tested for mass, muscle tone, and strength.
* Reflex Exam: Various reflexes are tested throughout the body. While these can indicate problems with sensation and/or motor function, they can also reveal other aspects of nervous system dysfunction as well.
* Coordination and Gait: Coordination testing and evaluating a patient's gait reveal much about various aspects of their nervous system. While they involve motor function they also reveal aspects of other more subtle components of brain function which controls these things.
* Sensory Exam: Finally, the sensory exam part of the neurological exam evaluates the sensation of the patient. This includes not just normal touch but also pain and temperature and sensation of limb position and movement.
The neuro exam is just one part of a complete neurological assessment. While in some patients the complete neurological exam is undertaken, in others a focused exam is used to evaluate only those aspects of the nervous system which are most concerning because of the patient's presenting complaints or symptoms. While some diagnoses can be made simply on the basis of the physical examination, most require further testing or studies, such as a CT scan or MRI scan, to make or confirm the diagnosis.
CAT Scan (CT Scan or Computed Axial Tomography)
A CAT scan, or Computed Axial Tomography or CT scan, is an imaging study which uses x-rays to produce images of the internal parts of the body. It is commonly used to visualize the brain and other structures in the head to investigate diseases of the brain. They can be used to visualize other body parts as well, including the chest, abdomen and pelvis.
A CT scanner, like a brain MRI scanner, is a large donut-shaped device that the patient is place into on a moving table. Rather than a plain x-ray machine which shoots a single burst of x-rays through a body part, a CAT scan rotates around the patient while using x-rays to take several radial images. Through computer manipulation, these multiple images are recombined into cross-sectional images of the inside of the body which gives much more subtle and detailed information than a plain x-ray alone. These images can then be viewed by a radiologist or other physician to interpret.
X-rays are high energy photons (the energy "packets" of electromagnetic energy, similar to light but not in a visible wavelength) similar to gamma rays that pass through the body. More dense tissues such as bone block most x-rays while softer tissues let more x-rays pass completely through. Therefore, the image produced by an x-ray and CT scan is based on the density of tissues. Bones show up brightest while air is the darkest.
Because a CAT scan brain scan uses x-rays, the patient is exposed to some radiation. However, because most patients are not exposed to many over a lifetime and because the exposure is small, they are generally considered very safe for general use. They do not cause any pain or discomfort but some patients complain of claustrophobia while in the round scanner. However, most CT scans are very fast, faster than a typical MRI scan.
Occasionally a brain CT scan is performed with an injection of a contrast agent. Contrast is basically a dye that is injected into a vein which is very dense and therefore shows up brightly on the CT scan. It can help to visualize blood vessels and may make some diagnoses, such as some brain tumors, easier to see.
What Is It Used For?
CT brain scans produced a quick and relatively inexpensive, compared to MRI, image of the brain and surrounding structures. It does not have the high resolution and special imaging types that MRI is capable of but it has advantages over MRI in a couple areas.
For one, CT is very good at showing detail of bone anatomy and pathology. Therefore, for identifying fractures and bony spine abnormalities it is superior to MRI.
CT is also very good at demonstrating acute bleeding. It can clearly show bleeding associated with trauma, rupture of an intracranial aneurysm or other causes. Therefore, CT is often used in the setting of trauma and some other hemorrhagic conditions.
For other pathologies, like ischemic stroke and brain tumors for example, generally MRI is preferred for its better anatomic detail and resolution. However, in some centers MRI is not as easily available or CT will be performed first because it is cheaper and faster as a basic screening test.
While MRI is generally better for most types of spinal disease, CT can be helpful in demonstrating bony abnormalities in spine disease.
Brain MRI Scan (Magnetic Resonance Imaging)
A Brain MRI (alternately called a brain scan, MRI scan, or magnetic resonance imaging) is a neurological test which produces a high-resolution image of the contents of the head. It is a commonly used study to evaluate patients with neurological complaints to investigate for diseases of the brain. MRI scans can be performed for other parts of the body as well, including the spine, extremities and chest.
Magnetic resonance imaging, the scientific term behind a brain MRI, is a relatively new technique which uses the quantum mechanical characteristics of protons in your body tissues to create an image. The specific details of the science behind an MRI is quite complex. In general, the patient is placed in a large magnet which aligns all their protons into the same spin. A radiofrequency pulse stimulates these protons, most abundant in water, and an electrical coil around the head detects the signals that result. In the end, the computer uses complex mathematics to convert these signals into an image which the physicians read and interpret.
The appearance of an MRI scanner is similar to a CT Scan in that it is a large donut-shaped tube. The patient's lays on a table while their head is inside the "donut". Unlike a CT scan, no x-rays are used to produce a brain MRI so there is no exposure to radiation. The patient does not feel anything during the performance of the study although some patients complain of claustrophobia while in the scanner.
Sometimes a brain MRI is performed with injection of a contract agent. This is basically a dye that is injected into the blood which shows up brightly on the MRI scan. It can help to make some diagnoses more clearly visible, such as many brain tumors.
What Is It Used For?
As mentioned above, an MRI produces a high-resolution image of the internal parts of the body. There are several different types of MRI imaging which focus on different characteristics of the tissues. By interpreting these various images that are produced, a radiologist or other physicians can help to make diagnoses of medical conditions.
Not all medical conditions have specific findings on MRI. For example, a patient in coma due to uncontrolled diabetes would typically show nothing abnormal in their brain. Rather, brain MRI is good at showing structural changes in or around the brain. For example, MRI is excellent at detecting tumors of the nervous system. They can also show changes in the tissue of the brain consistent with stroke and hemorrhage, or bleeding into the brain.
MRI is more expensive and slower to perform than CT scan, so they are not used for every patient. Pathologies which can be easily diagnosed quickly on a CAT scan, such as acute head trauma and bone pathology, will use that type of brain scan. MRI however is more versatile and shows better resolution of subtle details than a CT scan so it is used frequently for stroke, tumors, spinal disease and other pathology.
Cerebral Angiogram
A cerebral angiogram is a neurological test which evaluates the blood vessels that supply the brain.
Normally, on x-ray the blood vessels are relatively invisible. However, when injected with a radio-opaque dye, the blood vessels show up clearly on an x-ray. This technique is used to visualize the brain blood vessels in a cerebral angiogram but is also used in other parts of the body, such as in a coronary angiogram of the heart.
For a standard angiogram, a small catheter is placed into the blood vessels that supply the brain, the carotid arteries and the vertebral arteries. The catheter is placed through the femoral artery in the thigh and maneuvered up to the head with x-ray guidance. When the catheter is in place, dye is injected into the blood stream while x-rays are taken to allow clear visualization of the blood vessels. X-rays are taken at several time points and from several angles to visualize both the arteries and the venous system in the head.
Some centers now have 3-dimensional angiography machines that rotate around the head while the dye is injected to create a 3D model of the blood vessels. Additionally, some CT scanners have the capability of producing a 3D image of the blood vessels called a CT Angiogram. This has the advantage that no catheter is placed into the artery as the dye can be injected into the general circulation through a standard intravenous catheter (an IV).
In general a cerebral angiogram is safe, but it does have some risks. The catheter in the artery can occasionally cause injury to the artery leading either to bleeding or an arterial dissection and subsequent clotting. This can lead to stroke in rare cases. Additionally, the site of catheter insertion in the leg can be prone to hematoma formation and/or infection. These insertion site complications are generally well tolerated and easily treated in the great majority of patients.
What Is It Used For?
An angiogram is an excellent test to evaluate the blood vessels of the brain and any abnormalities or pathologies that involve them. Common examples of blood vessel abnormalities which can be demonstrated on a cerebral angiogram include cerebral aneurysm, arteriovenous malformation, and Moyamoya disease.
Angiograms are also commonly performed to evaluate blockages of the blood vessels to the brain as in acute stroke or vasospasm.
In addition to being a diagnostic test for these various pathologies and others, some procedures are performed through the catheter while performing an angiogram. These endovascular procedures, usually performed by an interventional neuroradiologist or neurosurgeon, include coiling of aneurysms, embolization of arteriovenous malformations, angioplasty or stenting of obstructed arteries and retrieval of clots during acute stroke. In some types of brain tumors, such as meningiomas, the blood vessels supplying the tumor are embolized prior to surgical removal of the tumor.
Electroencephalogram (EEG)
An electroencephalogram (EEG) is a neurological test which records the electrical activity at the surface of the brain by way of electrodes placed on or in the scalp.
The EEG is performed by placing electrodes on the scalp. Generally, these are superficial stickers which are attached to wires which carry information to the monitor which displays the results. In some cases where a continuous EEG is to be taken for a prolonged period of time, such as in a comatose head trauma victim, the electrodes can be implanted in the scalp as tiny needles.
The electrodes record electrical activity from the surface of the brain which is converted to a trace on the electroencephalogram output, traditionally wiggly lines on a sheet of paper although nowadays they are often simply displayed on a computer screen. The shape, frequency, amplitude and other characteristics of the trace from various regions of the brain are interpreted by a physician, usually a neurologist, and can reveal changes in the electrical activity of the brain.
Evaluation with an EEG varies depending on the clinical situation. In some patients a short EEG will be taken while in others a prolonged EEG overnight or even longer may be required. Patients with epilepsy will often undergo prolonged EEG monitoring in the attempt to catch a seizure on the EEG so that physicians can determine the location it originated from and other characteristics which may help in treatment.
What Is It Used For?
Because the EEG reveals changes in the electrical activity of the neurons in the brain, it can aid in the diagnosis of various pathologies. Traditionally, besides general nervous system research, the EEG has been used to evaluate patients with epilepsy. Seizures, either generalized to the whole brain or focal, can often be seen as a characteristic rhythmic activity on the EEG which is quite different from the normal, seemingly random activity. Therefore, the electroencephalogram is often used to diagnose and work-up patients who present with seizures or activity which is suspicious for epilepsy.
The EEG is also used to evaluate other general changes in the activity of the brain. For example, patients in coma are sometimes followed with EEG both to rule out subclinical seizures but also to evaluate for signs of recovery or brain death. In fact, determination of brain death sometimes utilizes EEG to determine if there is any normal brain activity. While the diagnosis of brain death does not require an EEG, it sometimes helps physicians feel confident that their is no normal brain activity.
Electromyogram (EMG)
An electromyogram (EMG) is a neurological test, usually performed by a neurologist, which evaluates the responses of muscles and the nerves that supply them. It is performed by inserting small needles into various muscles that act as stimulating and recording electrodes. Through these electrodes the muscle is stimulated and the EMG can record the responses that occur in the muscle.
An EMG is often performed along with a nerve conduction study as part of a neurological assessment for various diseases that affect the muscles and/or nervous system.
What Is It Used For?
The EMG provides the physician with information about the functioning of both the muscle and the nerves that supply that muscle. This can be used to help diagnose various diseases that affect these structures. For example, EMG may be used as part of the work-up for diseases of the muscle such as muscular dystrophies. Additionally, along with a nerve conduction study, it may be used to evaluate disease of the peripheral nerves such as peripheral nerve tumors, neuropathies, traumatic nerve injuries, nerve entrapments (such as carpal tunnel syndrome) and various diseases of the spine which involve the nerves as the enter or leave the spinal cord.
Nerve Conduction Study
A nerve conduction study is a neurological test, usually performed by a neurologist and often along with an electromyogram, which evaluates the conduction of electrical impulses down peripheral nerves. Because nerves conduct signals at a standard speed and amplitude, diseases of the nerves which may alter these impulses can be detected by measurement of these signals.
The nerve conduction study is performed by placing surface electrodes over nerves, usually in the arms and/or legs. The electrodes are used to stimulate the nerves and then record the conduction of the signal down the nerve to some other point. This can be done in several positions to help determine the site of nerve injury or disease which may be causing the patient's symptoms.
What Is It Used For?
The nerve conduction test provides physicians with information about the functioning of the peripheral nerves including both the type of dysfunction and the likely location of its cause. This can be used to help diagnose various diseases that impact the nerves. Some pathologies of the peripheral nerves for which work-up can include a nerve conduction test include peripheral nerve tumors, neuropathies, traumatic nerve injuries, nerve entrapments (such as carpal tunnel syndrome) and various diseases of the spine which involve the nerves as the enter or leave the spinal cord.
The information supplied by the test can aid in the diagnosis of these disorders and in some cases can help direct treatment as well. For example, it may direct a surgeon to the likely site of injury of the nerve so that their treatment can be focused on the correct area.
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The Neuro Assessment
A neurological evaluation is a clinical assessment of the nervous system aimed at detecting any abnormalities which may be related to a nervous system disease. An initial neurological assessment may be conducted by a primary care physician such as an internal medicine doctor or family practitioner, but a complete and thorough assessment is generally conducted by a specialist in the area of neurological disorders such as a neurologist or neurosurgeon, depending on the disorder in question.
The neurological evaluation is a complete assessment of the nervous system but may be focused on parts of the nervous system related to symptoms with which the patient is presenting. For example, a patient presenting with back pain and leg symptoms may have a focused neurological assessment which spends more time evaluating the legs and back while a patient presenting with facial weakness and difficulty with hearing may have a quite different assessment.
An evaluation of the nervous system for nervous system diseases can include three general components, a subjective review of the patient's presenting complaints and medical history, a neurological exam and diagnostic testing focused on the nervous system.
The review of the complaint and medical history is common to all medical assessments. The patient is questioned by their physician about all aspects of their complaint or symptoms as well as details of their past medical history, family history, medications, allergies, social history and a review of other symptoms. This helps the physician understand the complaint as well as other medical conditions and other aspects of the patient's history which may impact the current problem in one way or another.
The neurological exam is a physical examination which is focused on the nervous system. It is aimed at determining any signs or symptoms related to the nervous system or its function. The complete nervous system examination is quite detailed with several areas of the body examined. We will not list every physical exam test and maneuver here but the general sections of the complete neurological exam are described on the neurological exam page.
Finally, after these assessments by the physician, diagnostic testing is used in some cases to help detect a suspected or concerning pathology. This varies from patient to patient and from disease to disease. However, common tests or studies used to help diagnose nervous system diseases include x-rays, MRI scans, and CT scans of the head and/or spine. Additionally, nerve conduction studies, electromyelography (EMG), eletroencephalograms (EEG), blood tests, lumbar puncture (spinal tap) can also be used in some select instances. There are other tests, procedures or studies which are performed in more specific examples. For example, in a patient with a tumor, a biopsy or removal of the tumor is sometimes required to make the definitive diagnosis.
All of these parts of the neurological evaluation can help the physician to determine the most likely diagnosis as well as the most appropriate course of action. Determination of prognosis and treatment for the disease rely on this evaluation and the data it supplies. Every patient and disease is different and the specific aspects of one patient's evaluation may differ somewhat from another.
A neurological exam is a physical examination conducted by a health care provider which is focused on the nervous system. It is a common part of a complete neurological assessment as may be conducted by various physicians, most commonly a neurologist or neurosurgeon. The goal of the examination is to detect any signs or symptoms related to the nervous system and its functioning.
The neurological exam can be conducted by anyone, including primary care providers such as family practitioners and internal medicine doctors. However, it is most commonly part of a neurological evaluation by a physician specializing in diseases of the nervous system, such as a neurologist or a neurosurgeon.
What Are the Parts of a Typical Neurological Exam?
* Behavioral, Cognitive and Mental Status: This part of the neurological evaluation helps to determine the higher functioning of a patient's brain. It is an assessment of their mental status, or level of alertness and consciousness, as well as their higher functions of memory, reasoning, logic and general behavior. While some of this overlaps with a psychological assessment, it is, at least in part, a part of the complete neurological examination.
* Head and Neck Exam: Because the brain and spinal cord are in the head and neck, a general examination of the head and neck for malformations, abnormal anatomy, masses and other findings is often undertaken.
* Cranial Nerve Exam: There are 12 cranial nerves which are nerves that originate in the head, coming off the brain and brain stem. The examination of these nerves and their functions is complex but includes areas such as smell, vision and eye movements, facial sensation, reflexes and movement, hearing, taste, tongue and palate movements and even movements of the head, neck and shoulders.
* Motor Exam: This part of the examination tests the motor function, or movement, of the major muscle groups, most notably in the shoulders, arms, hips and legs. The muscles are tested for mass, muscle tone, and strength.
* Reflex Exam: Various reflexes are tested throughout the body. While these can indicate problems with sensation and/or motor function, they can also reveal other aspects of nervous system dysfunction as well.
* Coordination and Gait: Coordination testing and evaluating a patient's gait reveal much about various aspects of their nervous system. While they involve motor function they also reveal aspects of other more subtle components of brain function which controls these things.
* Sensory Exam: Finally, the sensory exam part of the neurological exam evaluates the sensation of the patient. This includes not just normal touch but also pain and temperature and sensation of limb position and movement.
The neuro exam is just one part of a complete neurological assessment. While in some patients the complete neurological exam is undertaken, in others a focused exam is used to evaluate only those aspects of the nervous system which are most concerning because of the patient's presenting complaints or symptoms. While some diagnoses can be made simply on the basis of the physical examination, most require further testing or studies, such as a CT scan or MRI scan, to make or confirm the diagnosis.
CAT Scan (CT Scan or Computed Axial Tomography)
A CAT scan, or Computed Axial Tomography or CT scan, is an imaging study which uses x-rays to produce images of the internal parts of the body. It is commonly used to visualize the brain and other structures in the head to investigate diseases of the brain. They can be used to visualize other body parts as well, including the chest, abdomen and pelvis.
A CT scanner, like a brain MRI scanner, is a large donut-shaped device that the patient is place into on a moving table. Rather than a plain x-ray machine which shoots a single burst of x-rays through a body part, a CAT scan rotates around the patient while using x-rays to take several radial images. Through computer manipulation, these multiple images are recombined into cross-sectional images of the inside of the body which gives much more subtle and detailed information than a plain x-ray alone. These images can then be viewed by a radiologist or other physician to interpret.
X-rays are high energy photons (the energy "packets" of electromagnetic energy, similar to light but not in a visible wavelength) similar to gamma rays that pass through the body. More dense tissues such as bone block most x-rays while softer tissues let more x-rays pass completely through. Therefore, the image produced by an x-ray and CT scan is based on the density of tissues. Bones show up brightest while air is the darkest.
Because a CAT scan brain scan uses x-rays, the patient is exposed to some radiation. However, because most patients are not exposed to many over a lifetime and because the exposure is small, they are generally considered very safe for general use. They do not cause any pain or discomfort but some patients complain of claustrophobia while in the round scanner. However, most CT scans are very fast, faster than a typical MRI scan.
Occasionally a brain CT scan is performed with an injection of a contrast agent. Contrast is basically a dye that is injected into a vein which is very dense and therefore shows up brightly on the CT scan. It can help to visualize blood vessels and may make some diagnoses, such as some brain tumors, easier to see.
What Is It Used For?
CT brain scans produced a quick and relatively inexpensive, compared to MRI, image of the brain and surrounding structures. It does not have the high resolution and special imaging types that MRI is capable of but it has advantages over MRI in a couple areas.
For one, CT is very good at showing detail of bone anatomy and pathology. Therefore, for identifying fractures and bony spine abnormalities it is superior to MRI.
CT is also very good at demonstrating acute bleeding. It can clearly show bleeding associated with trauma, rupture of an intracranial aneurysm or other causes. Therefore, CT is often used in the setting of trauma and some other hemorrhagic conditions.
For other pathologies, like ischemic stroke and brain tumors for example, generally MRI is preferred for its better anatomic detail and resolution. However, in some centers MRI is not as easily available or CT will be performed first because it is cheaper and faster as a basic screening test.
While MRI is generally better for most types of spinal disease, CT can be helpful in demonstrating bony abnormalities in spine disease.
Brain MRI Scan (Magnetic Resonance Imaging)
A Brain MRI (alternately called a brain scan, MRI scan, or magnetic resonance imaging) is a neurological test which produces a high-resolution image of the contents of the head. It is a commonly used study to evaluate patients with neurological complaints to investigate for diseases of the brain. MRI scans can be performed for other parts of the body as well, including the spine, extremities and chest.
Magnetic resonance imaging, the scientific term behind a brain MRI, is a relatively new technique which uses the quantum mechanical characteristics of protons in your body tissues to create an image. The specific details of the science behind an MRI is quite complex. In general, the patient is placed in a large magnet which aligns all their protons into the same spin. A radiofrequency pulse stimulates these protons, most abundant in water, and an electrical coil around the head detects the signals that result. In the end, the computer uses complex mathematics to convert these signals into an image which the physicians read and interpret.
The appearance of an MRI scanner is similar to a CT Scan in that it is a large donut-shaped tube. The patient's lays on a table while their head is inside the "donut". Unlike a CT scan, no x-rays are used to produce a brain MRI so there is no exposure to radiation. The patient does not feel anything during the performance of the study although some patients complain of claustrophobia while in the scanner.
Sometimes a brain MRI is performed with injection of a contract agent. This is basically a dye that is injected into the blood which shows up brightly on the MRI scan. It can help to make some diagnoses more clearly visible, such as many brain tumors.
What Is It Used For?
As mentioned above, an MRI produces a high-resolution image of the internal parts of the body. There are several different types of MRI imaging which focus on different characteristics of the tissues. By interpreting these various images that are produced, a radiologist or other physicians can help to make diagnoses of medical conditions.
Not all medical conditions have specific findings on MRI. For example, a patient in coma due to uncontrolled diabetes would typically show nothing abnormal in their brain. Rather, brain MRI is good at showing structural changes in or around the brain. For example, MRI is excellent at detecting tumors of the nervous system. They can also show changes in the tissue of the brain consistent with stroke and hemorrhage, or bleeding into the brain.
MRI is more expensive and slower to perform than CT scan, so they are not used for every patient. Pathologies which can be easily diagnosed quickly on a CAT scan, such as acute head trauma and bone pathology, will use that type of brain scan. MRI however is more versatile and shows better resolution of subtle details than a CT scan so it is used frequently for stroke, tumors, spinal disease and other pathology.
Cerebral Angiogram
A cerebral angiogram is a neurological test which evaluates the blood vessels that supply the brain.
Normally, on x-ray the blood vessels are relatively invisible. However, when injected with a radio-opaque dye, the blood vessels show up clearly on an x-ray. This technique is used to visualize the brain blood vessels in a cerebral angiogram but is also used in other parts of the body, such as in a coronary angiogram of the heart.
For a standard angiogram, a small catheter is placed into the blood vessels that supply the brain, the carotid arteries and the vertebral arteries. The catheter is placed through the femoral artery in the thigh and maneuvered up to the head with x-ray guidance. When the catheter is in place, dye is injected into the blood stream while x-rays are taken to allow clear visualization of the blood vessels. X-rays are taken at several time points and from several angles to visualize both the arteries and the venous system in the head.
Some centers now have 3-dimensional angiography machines that rotate around the head while the dye is injected to create a 3D model of the blood vessels. Additionally, some CT scanners have the capability of producing a 3D image of the blood vessels called a CT Angiogram. This has the advantage that no catheter is placed into the artery as the dye can be injected into the general circulation through a standard intravenous catheter (an IV).
In general a cerebral angiogram is safe, but it does have some risks. The catheter in the artery can occasionally cause injury to the artery leading either to bleeding or an arterial dissection and subsequent clotting. This can lead to stroke in rare cases. Additionally, the site of catheter insertion in the leg can be prone to hematoma formation and/or infection. These insertion site complications are generally well tolerated and easily treated in the great majority of patients.
What Is It Used For?
An angiogram is an excellent test to evaluate the blood vessels of the brain and any abnormalities or pathologies that involve them. Common examples of blood vessel abnormalities which can be demonstrated on a cerebral angiogram include cerebral aneurysm, arteriovenous malformation, and Moyamoya disease.
Angiograms are also commonly performed to evaluate blockages of the blood vessels to the brain as in acute stroke or vasospasm.
In addition to being a diagnostic test for these various pathologies and others, some procedures are performed through the catheter while performing an angiogram. These endovascular procedures, usually performed by an interventional neuroradiologist or neurosurgeon, include coiling of aneurysms, embolization of arteriovenous malformations, angioplasty or stenting of obstructed arteries and retrieval of clots during acute stroke. In some types of brain tumors, such as meningiomas, the blood vessels supplying the tumor are embolized prior to surgical removal of the tumor.
Electroencephalogram (EEG)
An electroencephalogram (EEG) is a neurological test which records the electrical activity at the surface of the brain by way of electrodes placed on or in the scalp.
The EEG is performed by placing electrodes on the scalp. Generally, these are superficial stickers which are attached to wires which carry information to the monitor which displays the results. In some cases where a continuous EEG is to be taken for a prolonged period of time, such as in a comatose head trauma victim, the electrodes can be implanted in the scalp as tiny needles.
The electrodes record electrical activity from the surface of the brain which is converted to a trace on the electroencephalogram output, traditionally wiggly lines on a sheet of paper although nowadays they are often simply displayed on a computer screen. The shape, frequency, amplitude and other characteristics of the trace from various regions of the brain are interpreted by a physician, usually a neurologist, and can reveal changes in the electrical activity of the brain.
Evaluation with an EEG varies depending on the clinical situation. In some patients a short EEG will be taken while in others a prolonged EEG overnight or even longer may be required. Patients with epilepsy will often undergo prolonged EEG monitoring in the attempt to catch a seizure on the EEG so that physicians can determine the location it originated from and other characteristics which may help in treatment.
What Is It Used For?
Because the EEG reveals changes in the electrical activity of the neurons in the brain, it can aid in the diagnosis of various pathologies. Traditionally, besides general nervous system research, the EEG has been used to evaluate patients with epilepsy. Seizures, either generalized to the whole brain or focal, can often be seen as a characteristic rhythmic activity on the EEG which is quite different from the normal, seemingly random activity. Therefore, the electroencephalogram is often used to diagnose and work-up patients who present with seizures or activity which is suspicious for epilepsy.
The EEG is also used to evaluate other general changes in the activity of the brain. For example, patients in coma are sometimes followed with EEG both to rule out subclinical seizures but also to evaluate for signs of recovery or brain death. In fact, determination of brain death sometimes utilizes EEG to determine if there is any normal brain activity. While the diagnosis of brain death does not require an EEG, it sometimes helps physicians feel confident that their is no normal brain activity.
Electromyogram (EMG)
An electromyogram (EMG) is a neurological test, usually performed by a neurologist, which evaluates the responses of muscles and the nerves that supply them. It is performed by inserting small needles into various muscles that act as stimulating and recording electrodes. Through these electrodes the muscle is stimulated and the EMG can record the responses that occur in the muscle.
An EMG is often performed along with a nerve conduction study as part of a neurological assessment for various diseases that affect the muscles and/or nervous system.
What Is It Used For?
The EMG provides the physician with information about the functioning of both the muscle and the nerves that supply that muscle. This can be used to help diagnose various diseases that affect these structures. For example, EMG may be used as part of the work-up for diseases of the muscle such as muscular dystrophies. Additionally, along with a nerve conduction study, it may be used to evaluate disease of the peripheral nerves such as peripheral nerve tumors, neuropathies, traumatic nerve injuries, nerve entrapments (such as carpal tunnel syndrome) and various diseases of the spine which involve the nerves as the enter or leave the spinal cord.
Nerve Conduction Study
A nerve conduction study is a neurological test, usually performed by a neurologist and often along with an electromyogram, which evaluates the conduction of electrical impulses down peripheral nerves. Because nerves conduct signals at a standard speed and amplitude, diseases of the nerves which may alter these impulses can be detected by measurement of these signals.
The nerve conduction study is performed by placing surface electrodes over nerves, usually in the arms and/or legs. The electrodes are used to stimulate the nerves and then record the conduction of the signal down the nerve to some other point. This can be done in several positions to help determine the site of nerve injury or disease which may be causing the patient's symptoms.
What Is It Used For?
The nerve conduction test provides physicians with information about the functioning of the peripheral nerves including both the type of dysfunction and the likely location of its cause. This can be used to help diagnose various diseases that impact the nerves. Some pathologies of the peripheral nerves for which work-up can include a nerve conduction test include peripheral nerve tumors, neuropathies, traumatic nerve injuries, nerve entrapments (such as carpal tunnel syndrome) and various diseases of the spine which involve the nerves as the enter or leave the spinal cord.
The information supplied by the test can aid in the diagnosis of these disorders and in some cases can help direct treatment as well. For example, it may direct a surgeon to the likely site of injury of the nerve so that their treatment can be focused on the correct area.
Read More ..
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