Carmen Research

8/8/2019 Carmen Research

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Alcohol and Liver DiseaseDrinking too much alcohol can lead to three types of liver conditions - fatty liver, hepatitis, andcirrhosis. You are unlikely to develop these problems if you drink within the recommended safe limits

detailed below. For all types of liver disease caused by alcohol, the main treatment is to stop drinking

completely.

What does the liver do?

The liver is in the upper right part of the abdomen. It has many functions which include:

Storing glycogen, a chemical made from sugars. When required, glycogen is broken down into

glucose which is released into the bloodstream.

Helping to process fats and proteins from digested food.

Making proteins that are essential for blood to clot (clotting factors).

Processing many medicines which you may take.

Helping to remove or process alcohol, poisons and toxins from the body.

Making bile which passes from the liver to the gut and helps to digest fats.

What happens when you drink alcohol?

When you drink alcohol, it is absorbed into the bloodstream from the stomach and intestines. All blood

from the stomach and intestines first goes through the liver before circulating around the whole body.

So, the highest concentration of alcohol is in the blood flowing through the liver.

Liver cells contain enzymes (chemicals) which process (metabolise) alcohol. The enzymes break down

alcohol into other chemicals which in turn are then broken down into water and carbon dioxide. These

are then passed out in the urine and from the lungs.

The liver cells can metabolise only a certain amount of alcohol per hour. So, if you drink alcohol faster

than your liver can deal with it, the level of alcohol in your bloodstream rises.

What are the problems of drinking too much alcohol?

Your liver and body can usually cope with drinking a small amount of alcohol. Indeed, drinking a smallamount of alcohol (1-2 units per day) may help to prevent heart disease and stroke.

However, drinking over the recommended limits (detailed below) can be harmful. If you drink heavily

you have an increased risk of developing: Serious liver problems (alcoholic liver disease).

Some stomach disorders.

Pancreatitis (severe inflammation of the pancreas).

Mental health problems including depression and anxiety.

Sexual difficulties such as impotence.

Muscle and heart muscle disease.

High blood pressure.

Damage to nervous tissue.


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Accidents - drinking alcohol is associated with a much increased risk of accidents. In particular,

injury and death from fire and car crashes. About 1 in 7 road deaths are caused by drinking

alcohol.

Some cancers (mouth, gullet, liver, colon and breast).

Obesity (alcohol has many calories).

Damage to an unborn baby in pregnant women.

Alcohol dependence (addiction).In the UK deaths due to alcohol related diseases (particularly liver disease) have risen considerablyover the last 20 years or so. This is because heavy drinking and binge drinking have become more

common.

The rest of this leaflet is about alcoholic liver disease. See separate leaflets called 'Alcohol and Sensible

Drinking'which deals with general aspects of alcohol, and 'Alcoholism and Problem Drinking'which

includes information on alcohol dependence.

What is alcoholic liver disease?

Drinking too much alcohol can lead to three types of liver conditions - fatty liver, hepatitis, andcirrhosis. Any, or all, of these conditions can occur at the same time in the same person.

Fatty liver

A build-up of fat occurs within liver cells in most people who regularly drink heavily. In itself, fattyliver is not usually serious and does not cause symptoms. Fatty liver will usually reverse if you stop

drinking heavily. However, in some people the fatty liver progresses and develops into hepatitis.

Alcoholic hepatitis

Hepatitis means inflammation of the liver. The inflammation can range from mild to severe.

Mild hepatitis may not cause any symptoms. The only indication of inflammation may be an

abnormal level of liver enzymes in the blood which can be detected by a blood test. However, in

some cases the hepatitis becomes persistent (chronic), which can gradually damage the liver andeventually cause cirrhosis.

A more severe hepatitis tends to cause symptoms such as feeling sick, jaundice (yellowing of

the skin caused by a high level of bilirubin - a chemical normally metabolised in the liver),generally feeling unwell, and sometimes pain over the liver.

A very severe bout of alcoholic hepatitis can quickly lead to liver failure. This can cause deep

jaundice, blood clotting problems, confusion, coma, bleeding into the guts, and is often fatal.

Alcoholic cirrhosis

Cirrhosis is a condition where normal liver tissue is replaced by scar tissue (fibrosis). The scarring

tends to be a gradual process. The scar tissue affects the normal structure and regrowth of liver cells.Liver cells become damaged and die as scar tissue gradually develops. So, the liver gradually loses its

ability to function well. The scar tissue can also affect the blood flow through the liver which can cause

'back pressure' in the blood vessels which bring blood to the liver.

About 1 in 10 heavy drinkers will eventually develop cirrhosis. It tends to occur after 10 or more years


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of heavy drinking. Note: cirrhosis can develop in people who have never had alcoholic hepatitis.

Cirrhosis can happen from many causes other than alcohol. For example, persistent viral hepatitis and

some hereditary and metabolic diseases. If you have another persistent liver disease, and drink heavily,you are likely to increase your risk of developing cirrhosis.

Cirrhosis can lead to end-stage liver disease ('liver failure'). However, in the early stages of thecondition, often there are no symptoms. You can 'get by' with a reduced number of working liver cells.

But, as more and more liver cells die, and more and more scar tissue builds up, symptoms start to

appear. The eventual symptoms and complications are similar to a severe episode of hepatitis (listedabove). However, unlike a bout of severe hepatitis, the symptoms and complications tend to develop

slowly.

See separate leaflet called 'Cirrhosis'for more details.

It is not clear why some people are more prone for their liver cells to be damaged by alcohol and to

develop hepatitis and/or cirrhosis. But, as a rule, the heavier you drink, and the more regularly that youdrink, the more your risk of developing hepatitis and/or cirrhosis.

The scaring and damage of cirrhosis is usually permanent and cannot be reversed. However, recentresearch has led to a greater understanding of cirrhosis. Research suggests that it may be possible to

develop medicines in the future which can reverse the scarring process of cirrhosis.

How is alcoholic liver disease diagnosed?

A doctor may suspect that you have liver problems from your symptoms, and a physical examination.

(For example, they may detect that your liver is enlarged, or that you are retaining fluid.) They may

especially think of liver problems as a cause of your symptoms if you have a history of heavy alcohol

drinking. Some tests may be done: Blood tests may show abnormal liver function. (See separate leaflet called 'Liver Function

Tests'for details.)

An ultrasound scan may show that you have a damaged liver.

To confirm the diagnosis, a biopsy (small sample) of the liver may be taken to be looked at

under the microscope. (See separate leaflet called 'Liver Biopsy'for details.) The scarring of the

liver caused by cirrhosis, or the typical features of liver cells with alcoholic hepatitis can beseen on a biopsy sample.

What is the treatment for alcoholic liver disease?

For all types of liver disease caused by alcohol, you should stop drinking completely. Also, you may bereferred to a dietician to review your diet. This is because many people who drink heavily do not eat

properly and need advice on getting back into eating a healthy diet. Vitamin supplements may be

prescribed for a while.

If you have fatty liver, or alcoholic hepatitis which is not severe, you should fully recover from

these conditions if you stop drinking.

If you have severe hepatitis and require hospital admission, you may require intensive care

treatment. Some people with severe hepatitis will die.


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If you have cirrhosis, stopping drinking can improve your outlook. It depends on how severe the

cirrhosis has become. If cirrhosis is diagnosed when it is not too advanced, and you stop

drinking, the cirrhosis is unlikely to progress. However, the cirrhosis and symptoms will usually

get worse if you continue to drink. In severe cases where the scarring is extensive, and the livercan barely function, then a liver transplant may be the only option.

See separate leaflet called 'Cirrhosis', which provides some details of the treatment of cirrhosis.

Preventing alcoholic liver disease

You are very unlikely to develop liver problems caused by alcohol if you drink within the

recommended safe limits. That is:

Men should drink no more than 21 units of alcohol per week (and no more than four units in

any one day).

Women should drink no more than 14 units of alcohol per week (and no more than three units

in any one day).

Pregnant women. The exact amount that is safe is not known. Therefore, advice from the

Department of Health is that pregnant women and women trying to become pregnant should notdrink at all. If you do chose to drink when you are pregnant then limit it to one or two units,

once or twice a week. And never get drunk.

In general, the more you drink above the safe limits, the more harmful alcohol is likely to be. Andremember, binge drinking can be harmful even though the weekly total may not seem too high. For

example, if you only drink once or twice a week, but when you do you drink 4-5 pints of beer each

time, or a bottle of wine each time, then this is a risk to your health.

One unit of alcohol is 10 ml (1 cl) by volume, or 8 g by weight, of pure alcohol. For example:

One unit of alcohol is about equal to:

half a pint of ordinary strength beer or cider (3-4% alcohol by volume), or

a small pub measure (25 ml) of spirits (40% alcohol by volume), or

a standard pub measure (50 ml) of fortified wine such as sherry or port (20% alcohol by

volume).

There are one and a half units of alcohol in:

a small glass (125 ml) of ordinary strength wine (12% alcohol by volume), or

a standard pub measure (35 ml) of spirits (40% alcohol by volume).

But remember, many wines and beers are stronger than the more traditional 'ordinary' strengths. A more

accurate way of calculating units is as follows. The percentage alcohol by volume (% abv) of a drinkequals the number of units in one litre of that drink. For example:

Strong beer at 6% abv has six units in one litre. If you drink half a litre (500 ml) - just under a

pint - then you have had three units. Wine at 14% abv has 14 units in one litre. If you drink a quarter of a litre (250 ml) - two small

glasses - then you have had three and a half units.

Some other examples

Three pints of beer, three times per week, is at least18-20 units per week. That is nearly the upper

weekly safe limit for a man. However, each drinking session of three pints is at leastsix units, which is

more than the safe limit advised for any one day. Another example: a 750 ml bottle of 12% wine


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contains nine units. If you drink two bottles of 12% wine over a week, that is 18 units. This is above the

upper safe limit for a woman.

But, you should not drink alcohol at all if:

You have already developed early cirrhosis.

You have chronic hepatitis or certain other liver problems. Your doctor will advise for each

specific condition.

Do you need help to stop drinking?

Help and treatment is available if you find that you cannot stop drinking. Counselling and support from

a doctor, nurse, or counsellor is often all that is needed. A 'detoxification' treatment may be advised ifyou are alcohol dependent. Referral for specialist help may be best for some people. See separate

leaflet called 'Alcoholism and Problem Drinking'for more detail.

If you feel that you, or a relative or friend, needs help about alcohol then see your doctor or practice

nurse. Or, contact one of the agencies listed below.

Drinkline - National Alcohol Helpline

Tel: 0800 917 8282

Offers help to callers worried about their own drinking and support to the family and friends of people

who are drinking. Advice to callers on where to go for help.

Alcoholics Anonymous

PO Box 1, 10 Toft Green, York, YO1 7ND

Helpline: 0845 769 7555 Web: www.alcoholics-anonymous.org.uk

There are over 3000 meetings held in the UK each week with over 40,000 members. The onlyrequirement for membership is a desire to stop drinking.

AL-Anon Family Groups

61 Great Dover Street, London, SE1 4YF

Tel: 020 7403 0888 Web: www.al-anonuk.org.uk

Support for families and friends of alcoholics whether the drinker is still drinking or not.

Diabetes mellitus, often simply referred to as diabetesis a group of metabolic diseases in which a

person has highblood sugar, either because the body does not produce enoughinsulin, or because cells

do not respond to the insulin that is produced. This high blood sugar produces the classical symptomsofpolyuria (frequent urination),polydipsia (increased thirst) andpolyphagia (increased hunger).

There are three main types of diabetes:

Type 1 diabetes: results from the body's failure to produce insulin, and presently requires the

person to inject insulin. (Also referred to as insulin-dependentdiabetes mellitus,IDDMfor

short, andjuvenile diabetes.)

Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use insulin

properly, sometimes combined with an absolute insulin deficiency.
http://www.alcoholics-anonymous.org.uk/http://www.al-anonuk.org.uk/http://wiki/Blood_sugarhttp://wiki/Insulinhttp://wiki/Insulinhttp://wiki/Insulinhttp://wiki/Polyuriahttp://wiki/Polydipsiahttp://wiki/Polyphagiahttp://wiki/Diabetes_mellitus_type_1http://wiki/Diabetes_mellitus_type_2http://wiki/Insulin_resistancehttp://www.alcoholics-anonymous.org.uk/http://www.al-anonuk.org.uk/http://wiki/Blood_sugarhttp://wiki/Insulinhttp://wiki/Polyuriahttp://wiki/Polydipsiahttp://wiki/Polyphagiahttp://wiki/Diabetes_mellitus_type_1http://wiki/Diabetes_mellitus_type_2http://wiki/Insulin_resistance


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Gestational diabetes: is when pregnant women, who have never had diabetes before, have a

high blood glucose level during pregnancy. It may precede development of type 2 DM.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin

secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids,and several forms ofmonogenic diabetes.

All forms of diabetes have been treatable sinceinsulinbecame available in 1921, and type 2 diabetes

may be controlled with medications. Both type 1 and 2 arechronic conditions that usually cannot be

cured.Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass surgeryhas been successful in many with morbid obesity and type 2 DM. Gestational diabetes usually resolves

after delivery. Diabetes without proper treatments can cause many complications.Acute complications

include hypoglycemia, diabetic ketoacidosis, ornonketotic hyperosmolar coma. Serious long-term

complications includecardiovascular disease, chronic renal failure,retinal damage. Adequate treatmentof diabetes is thus important, as well asblood pressure control and lifestyle factors such as smoking

cessation and maintaining a healthybody weight.

As of 2000 at least 171 million people worldwide suffer from diabetes, or 2.8% of the population.[2]

Type 2 diabetes is by far the most common, affecting 90 to 95% of the U.S. diabetes population.[3]

Definition

The term diabetes, without qualification, usually refers to diabetes mellitus, which roughly translates to

excessive sweet urine (known as "glycosuria"). Several rare conditions are also named diabetes. The

most common of these is diabetes insipidus in which large amounts of urine are produced (polyuria),which is not sweet (insipidus meaning "without taste" in Latin).

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes,

juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2

diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes,and non-insulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-

upon standard nomenclature. Various sources have defined "type 3 diabetes" as: gestational diabetes,[4]

insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to requireinjected insulin, and latent autoimmune diabetes of adults (or LADA or "type 1.5" diabetes)[5]

Classification

Most cases of diabetes mellitus fall into three broad categories:type 1,type 2, and gestational diabetes.A few other types are described.

Type 1 diabetes

Main article:Diabetes mellitus type 1

Type 1 diabetes mellitus is characterized by loss of the insulin-producingbeta cells of the islets of

Langerhans in the pancreas leading to insulin deficiency. This type of diabetes can be further classified

as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature,
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where beta cell loss is a T-cell mediated autoimmune attack.[6] There is no known preventive measure

against type 1 diabetes, which causes approximately 10% of diabetes mellitus cases in North America

and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs.

Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it

represents a majority of the diabetes cases in children.

Type 2 diabetes

Main article:Diabetes mellitus type 2

Type 2 diabetes mellitus is characterized byinsulin resistance which may be combined with relatively

reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involvetheinsulin receptor. However, the specific defects are not known. Diabetes mellitus due to a known

defect are classified separately. Type 2 diabetes is the most common type.

In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity. At this

stage hyperglycemia can be reversed by a variety of measures and medications that improve insulinsensitivity or reduce glucose production by the liver.

Gestational diabetes

Main article:Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving acombination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%5% of

allpregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but

requires careful medical supervision throughout the pregnancy. About 20%50% of affected womendevelop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or

mother. Risks to the baby includemacrosomia (high birth weight), congenital cardiac and centralnervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetalsurfactant production and cause respiratory distress syndrome.Hyperbilirubinemia may result from red

blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor

placental perfusion due to vascular impairment. Labor inductionmay be indicated with decreasedplacental function. Acesarean section may be performed if there is marked fetal distress or an increased

risk of injury associated with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that more American women are entering pregnancy with

preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past6 years.[7] This is particularly problematic as diabetes raises the risk of complications during

pregnancy, as well as increasing the potential that the children of diabetic mothers will also become

diabetic in the future.

Other types

Pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher than

normal but not high enough for a diagnosis of type 2 diabetes. Many people destined to develop type 2diabetes spend many years in a state of pre-diabetes which has been termed "America's largest

healthcare epidemic."[8]:1011
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Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when

insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon.

Genetic mutations (autosomal ormitochondrial) can lead to defects in beta cell function. Abnormal

insulin action may also have been genetically determined in some cases. Any disease that causesextensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic

fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause

diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulinsecretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity,

malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the

World Health Organization when the current taxonomy was introduced in 1999.[9]

Following is a comprehensive list of other causes of diabetes:[10]

Genetic defects of -cell Function

Maturity onset diabetes of the young

(MODY)

Mitochondrial DNA mutations

Genetic defects in insulin processing or

insulin action

Defects in proinsulin conversion

Insulin gene mutations

Insulin receptor mutations

Exocrine Pancreatic Defects

Chronic pancreatitis

Pancreatectomy

Pancreatic neoplasia

Cystic fibrosis

Hemochromatosis

Fibrocalculous pancreatopathy

Endocrinopathies

Growth hormone excess

(acromegaly)

Cushing syndrome

Hyperthyroidism

Pheochromocytoma

Glucagonoma

Infections

Cytomegalovirus infection

Coxsackievirus B

Drugs

Glucocorticoids

Thyroid hormone

-adrenergic agonists

Signs and symptoms

Overview of the most significant symptoms of diabetes.

The classical symptoms of diabetes arepolyuria(frequent urination),polydipsia (increased thirst) and
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polyphagia (increased hunger).[11]Symptoms may develop rapidly (weeks or months) in type 1

diabetes while in type 2 diabetes they usually develop much more slowly and may be subtle or absent.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the

lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns thelens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1

should always be suspected in cases of rapid vision change, whereas with type 2 change is generally

more gradual, but should still be suspected.

People (usually with type 1 diabetes) may also present with diabetic ketoacidosis, a state of metabolicdysregulation characterized by the smell ofacetone; a rapid, deep breathing known as Kussmaul

breathing; nausea; vomiting and abdominal pain; and an altered states of consciousness.

A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in

type 2 diabetes and is mainly the result of dehydration. Often, the patient has been drinking extremeamounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.

A number of skin rashes can occur in diabetes that are collectively known asdiabetic dermadromes.

CausesThe cause of diabetes depends on the type. Type 2 diabetes is due primarily to lifestyle factors and

genetics.[12]

Type 1 diabetes is also partly inherited and then triggered by certain infections, with some evidence

pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of thesetriggers which has been traced to particularHLAgenotypes(i.e., the genetic "self" identifiers relied

upon by the immune system). However, even in those who have inherited the susceptibility, type 1

diabetes mellitus seems to require an environmental trigger.

Pathophysiology

The fluctuation of blood sugar (red) and the sugar-lowering hormone insulin (blue) in humans during

the course of a day with three meals. One of the effects of asugar-rich vs a starch-rich meal is

highlighted.

Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less

constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending

release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbableglucose. The chief trigger is a rise in blood glucose levels after eating

Insulin is the principal hormone that regulates uptake ofglucose from the blood into most cells

(primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or

the insensitivity of itsreceptors plays a central role in all forms of diabetes mellitus.

Humans are capable of digesting some carbohydrates, in particular those most common in food; starch,

and some disaccharides such as sucrose, are converted within a few hours to simpler forms most

notably themonosaccharideglucose, the principal carbohydrate energy source used by the body. The
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most significant exceptions are fructose, most disaccharides (exceptsucrose and in some people

lactose), and all more complex polysaccharides, with the outstanding exception ofstarch. The rest are

passed on for processing by gut flora largely in the colon. Insulin is released into the blood by beta cells

(-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of bloodglucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose

from the blood for use as fuel, for conversion to other needed molecules, or for storage.

Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage inliver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from thebeta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly

controlled by the hormone glucagon which acts in the opposite manner to insulin. Glucose thus forcibly

produced from internal liver cell stores (as glycogen) re-enters the bloodstream; muscle cells lack thenecessary export mechanism. Normally liver cells do this when the level of insulin is low (which

normally correlates with low levels of blood glucose).

Higher insulin levels increase some anabolic ("building up") processes such as cell growth and

duplication,protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in convertingmany of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice

versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning

metabolic phase).

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulininsensitivity orresistance), or if the insulin itself is defective, then glucose will not have its usual effect

so that glucose will not be absorbed properly by those body cells that require it nor will it be stored

appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poorprotein synthesis, and other metabolic derangements, such asacidosis.

When the glucose concentration in the blood is raised beyond itsrenal threshold(about 10 mmol/L,

although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the

proximal renal tubuli is incomplete, and part of the glucose remains in theurine(glycosuria). Thisincreases theosmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in

increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replacedosmotically from water held in body cells and other body compartments, causing dehydration and

increased thirst.

Diagnosis

See also: Glycosylated hemoglobin and Glucose tolerance test

2006 WHO Diabetes criteria[13] edit

Condition 2 hour glucose Fasting glucose

mmol/l(mg/dl) mmol/l(mg/dl)

Normal


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Glycated hemoglobin (Hb A1C) 6.5%.[14]

A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any

of the above-listed methods on a different day. It is preferable to measure a fasting glucose level

because of the ease of measurement and the considerable time commitment of formal glucose tolerancetesting, which takes two hours to complete and offers no prognostic advantage over the fasting test. [15]

According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L)

is considered diagnostic for diabetes mellitus.

People with fasting glucose levels from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) are considered to haveimpaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not

over 200 mg/dL (11.1 mmol/L), two hours after a 75 g oral glucose load are considered to have

impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor

for progression to full-blown diabetes mellitus as well as cardiovascular disease.[16]

Management

Main article:Diabetes management

Diabetes mellitus is a chronic diseasewhich is difficult to cure. Management concentrates on keepingblood sugar levels as close to normal ("euglycemia") as possible without presenting undue patient

danger. This can usually be with close dietary management, exercise, and use of appropriate

medications (insulin only in the case of type 1 diabetes mellitus. Oral medications may be used in thecase of type 2 diabetes, as well as insulin).

Patient education, understanding, and participation is vital since the complications of diabetes are far

less common and less severe in people who have well-managed blood sugar levels.[17] [18] Wider

health problems may accelerate the deleterious effects of diabetes. These includesmoking, elevatedcholesterol levels,obesity, high blood pressure, and lack of regularexercise.

Lifestyle modificationsMain article:Diabetic diet

There are roles for patient education, dietetic support, sensible exercise, with the goal of keeping both

short-term and long-term blood glucose levels within acceptable bounds. In addition, given the

associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control

blood pressure[19].

Medications

Oral medications

Main article:Anti-diabetic drug

Routine use ofaspirin has not been found to improve outcomes in uncomplicated diabetes.[20]

Insulin

Main article:Insulin therapy

Type 1 treatments usually include combinations of regular or NPH insulin, and/or synthetic insulin

analogs.
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Support

In countries using a general practitionersystem, such as theUnited Kingdom, care may take place

mainly outside hospitals, with hospital-based specialist care used only in case of complications,

difficult blood sugar control, or research projects. In other circumstances, general practitioners andspecialists share care of a patient in a team approach. Optometrists,podiatrists/chiropodists, dietitians,

physiotherapists, nursing specialists (e.g., DSNs (Diabetic Specialist Nurse)), nurse practitioners, or

Certified Diabetes Educators, may jointly provide multidisciplinary expertise. In countries wherepatients must provide for their own health care (e.g. in the US, and in much of the undeveloped world).

Peer support links people living with diabetes. Within peer support, people with a common illness share

knowledge and experience that others, including many health workers, do not have. Peer support is

frequent, ongoing, accessible and flexible and can take many formsphone calls, text messaging,

group meetings, home visits, and even grocery shopping. It complements and enhances other healthcare services by creating the emotional, social and practical assistance necessary for managing disease

and staying healthy.

Prognosis

Main article:Prognosis of diabetes mellitus

Diabetes doubles the risk of vascular problems, includingcardiovascular disease.[21]

According to one study, women with high blood pressure (hypertension) were three times more likely

to develop type 2 diabetes as compared with women with optimal BP after adjusting for various factorssuch as age, ethnicity, smoking, alcohol intake, body mass index (BMI), exercise, family history of

diabetes, etc.[22] The study was conducted by researchers from theBrigham and Womens Hospital,

Harvard Medical School and the Harvard School of Public Health, USA, who followed over 38,000female health professionals for ten years.

Except in the case of type 1 diabetes, which always requires insulin replacement, the way type 2

diabetes is managed may change with age. Insulin production decreases because of age-relatedimpairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss oflean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue

sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of

type 2 diabetes and postchallenge hyperglycemia in the older population.[23] Age-related glucoseintolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are

similar to those of younger people.[24] Treatment goals for older patients with diabetes vary with the

individual, and take into account health status, as well as life expectancy, level of dependence, andwillingness to adhere to a treatment regimen.[25]Glycated hemoglobin is better thanfasting glucose

for determining risks of cardiovascular disease and death from any cause.[26]

[edit] Seizure types

Seizure types are organized firstly according to whether the source of the seizure within the brain is

localized (partialorfocalonset seizures) or distributed (generalizedseizures). Partial seizures are

further divided on the extent to which consciousness is affected. If it is unaffected, then it is asimple

partialseizure; otherwise it is a complex partial(psychomotor) seizure. A partial seizure may spread

within the brain - a process known assecondary generalization. Generalized seizures are divided

according to the effect on the body but all involve loss of consciousness. These includeabsence (petit

mal), myoclonic,clonic, tonic, tonic-clonic (grand mal) andatonic seizures.
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Children may exhibit behaviors that are easily mistaken for epileptic seizures but are not caused by

epilepsy. These include:

Inattentive staring

Benign shudders (among children younger than age 2, usually when they are tired or excited)

Self-gratification behaviors (nodding, rocking, head banging)

Conversion disorder(flailing and jerking of the head, often in response to severe personal stress

such as physical abuse)

Conversion disorder can be distinguished from epilepsy because the episodes never occur during sleepand do not involve incontinence or self-injury.[11]

[edit] Epilepsy syndromes

There are over 40 different types of epilepsy, including: Absence seizures, atonic seizures, benignRolandic epilepsy, childhood absence, clonic seizures, complex partial seizures,frontal lobe epilepsy,

Febrile seizures,Infantile spasms, Juvenile Myoclonic Epilepsy,Juvenile Absence Epilepsy,Hot Water

Epilepsy, Lennox-Gastaut syndrome,Landau-Kleffner syndrome , myoclonic seizures,MitochondrialDisorders,Progressive Myoclonic Epilepsies, Psychogenic Seizures , Reflex Epilepsy, Rasmussen's

Syndrome, Simple Partial seizures, Secondarily Generalized Seizures, Temporal Lobe Epilepsy,Tonic-clonic seizures, Tonic seizures,Psychomotor Seizures,Limbic Epilepsy, Partial-Onset Seizures,

generalised-onset seizures,Status Epilepticus,Abdominal Epilepsy,Akinetic Seizures,Autonomicseizures,Massive Bilateral Myoclonus, Catamenial epilepsy,Drop seizures,Emotional seizures,Focal

seizures,Gelastic seizures,Jacksonian March,Lafora Disease,Motor seizures,Multifocal seizures,

Neonatal seizures,Nocturnal seizures,Photosensitive epilepsy,Pseudo seizures,Sensory seizures,Subtle seizures, Sylvan Seizures, Withdrawal seizures, Visual Reflex Seizures amongst others.[12]

Each type of epilepsy presents with its own unique combination of seizure type, typical age of onset,

EEG findings, treatment, and prognosis. The most widespread classification of the epilepsies[9]

divides epilepsy syndromes by location or distribution of seizures (as revealed by the appearance of the

seizures and by EEG) and by cause. Syndromes are divided into localization-related epilepsies,generalized epilepsies, or epilepsies of unknown localization.

Localization-related epilepsies, sometimes termed partial or focal epilepsies, arise from an epileptic

focus, a small portion of the brain that serves as the irritant driving the epileptic response. Generalized

epilepsies, in contrast, arise from many independent foci (multifocal epilepsies) or from epileptic

circuits that involve the whole brain.Epilepsies of unknown localization remain unclear whether they

arise from a portion of the brain or from more widespread circuits.

Epilepsy syndromes are further divided by presumptive cause: idiopathic, symptomatic, andcryptogenic.Idiopathic epilepsies are generally thought to arise from genetic abnormalities that lead to

alteration of basic neuronal regulation. Symptomatic epilepsies arise from the effects of an epileptic

lesion, whether that lesion is focal, such as a tumor, or a defect in metabolism causing widespreadinjury to the brain. Cryptogenic epilepsies involve a presumptive lesion that is otherwise difficult or

impossible to uncover during evaluation.

The genetic component to epilepsy is receiving particular interest from the scientific community.

Conditions such asRing chromosome 20 syndrome (r(20))are gaining acknowledgment, and althoughonly 60 cases have been reported in the literature since 1976, "more widespread cytogenetic

chromosomal karyotyping in non-etiological cases of epilepsy" is likely. http://www.ring20.org/what-

is-r20.php

Some epileptic syndromes are difficult to fit within this classification scheme and fall in the unknown
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ersion_disorderhttp://w/index.php?title=Epilepsy&action=edit&section=3http://wiki/Absence_seizureshttp://wiki/Atonic_seizureshttp://wiki/Rolandic_epilepsyhttp://w/index.php?title=Childhood_absence&action=edit&redlink=1http://wiki/Clonic_seizureshttp://wiki/Complex_partial_seizureshttp://wiki/Frontal_lobe_epilepsyhttp://wiki/Febrile_seizureshttp://wiki/Infantile_spasmshttp://w/index.php?title=Juvenile_Myoclonic_Epilepsy&action=edit&redlink=1http://w/index.php?title=Juvenile_Absence_Epilepsy&action=edit&redlink=1http://w/index.php?title=Hot_Water_Epilepsy&action=edit&redlink=1http://w/index.php?title=Hot_Water_Epilepsy&action=edit&redlink=1http://wiki/Lennox-Gastaut_syndromehttp://wiki/Landau-Kleffner_syndromehttp://wiki/Myoclonic_seizureshttp://w/index.php?title=Mitochondrial_Disorders&action=edit&redlink=1http://w/index.php?title=Mitochondrial_Disorders&action=edit&redlink=1http://w/index.php?title=Progressive_Myoclonic_Epilepsies&action=edit&redlink=1http://w/index.php?title=Psychogenic_Seizures&action=edit&redlink=1http://w/index.php?title=Reflex_Epilepsy&action=edit&redlink=1http://w/index.php?title=Rasmussen%27s_Syndrome&action=edit&redlink=1http://w/index.php?title=Rasmussen%27s_Syndrome&action=edit&redlink=1http://w/index.php?title=Simple_Partial_seizures&action=edit&redlink=1http://w/index.php?title=Secondarily_Generalized_Seizures&action=edit&redlink=1http://wiki/Temporal_Lobe_Epilepsyhttp://wiki/Tonic-clonic_seizureshttp://wiki/Tonic-clonic_seizureshttp://w/index.php?title=Tonic_seizures&action=edit&redlink=1http://w/index.php?title=Psychomotor_Seizures&action=edit&redlink=1http://w/index.php?title=Limbic_Epilepsy&action=edit&redlink=1http://w/index.php?title=Partial-Onset_Seizures&action=edit&redlink=1http://w/index.php?title=Generalised-onset_seizures&action=edit&redlink=1http://w/index.php?title=Status_Epilepticus&action=edit&redlink=1http://w/index.php?title=Abdominal_Epilepsy&action=edit&redlink=1http://w/index.php?title=Akinetic_Seizures&action=edit&redlink=1http://w/index.php?title=Autonomic_seizures&action=edit&redlink=1http://w/index.php?title=Autonomic_seizures&action=edit&redlink=1http://w/index.php?title=Massive_Bilateral_Myoclonus&action=edit&redlink=1http://wiki/Catamenial_epilepsyhttp://wiki/Drop_seizureshttp://w/index.php?title=Emotional_seizures&action=edit&redlink=1http://wiki/Focal_seizureshttp://wiki/Focal_seizureshttp://w/index.php?title=Gelastic_seizures&action=edit&redlink=1http://w/index.php?title=Jacksonian_March&action=edit&redlink=1http://w/index.php?title=Lafora_Disease&action=edit&redlink=1http://w/index.php?title=Motor_seizures&action=edit&redlink=1http://w/index.php?title=Multifocal_seizures&action=edit&redlink=1http://w/index.php?title=Neonatal_seizures&action=edit&redlink=1http://w/index.php?title=Nocturnal_seizures&action=edit&redlink=1http://wiki/Photosensitive_epilepsyhttp://w/index.php?title=Pseudo_seizures&action=edit&redlink=1http://w/index.php?title=Sensory_seizures&action=edit&redlink=1http://w/index.php?title=Subtle_seizures&action=edit&redlink=1http://w/index.php?title=Sylvan_Seizures&action=edit&redlink=1http://w/index.php?title=Withdrawal_seizures&action=edit&redlink=1http://w/index.php?title=Visual_Reflex_Seizures&action=edit&redlink=1http://wiki/EEGhttp://wiki/Cryptogenichttp://wiki/Ring_chromosome_20_syndromehttp://www.ring20.org/what-is-r20.phphttp://www.ring20.org/what-is-r20.php


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localization/etiology category. People who only have had a single seizure, or those with seizures that

occur only after specific precipitants ("provoked seizures"), have "epilepsies" that fall into this

category. Febrile convulsions are an example of seizures bound to a particular precipitant. Landau-

Kleffner syndrome is another epilepsy which, because of its variety ofEEG distributions, falls uneasilyin clear categories. More confusingly, certain syndromes likeWest syndrome featuring seizures such as

Infantile spasms can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can

arise from both focal or generalized epileptic lesions.Below are some common seizure syndromes:

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an idiopathic

localization-related epilepsy that is an inherited epileptic disorder that causes seizures during

sleep. Onset is usually in childhood. These seizures arise from the frontal lobes and consist of

complex motor movements, such as hand clenching, arm raising/lowering, and knee bending.Vocalizations such as shouting, moaning, or crying are also common. ADNFLE is often

misdiagnosed as nightmares. ADNFLE has a genetic basis[13]. These genes encode various

nicotinic acetylcholine receptors.

Benign centrotemporal lobe epilepsy of childhood orBenign rolandic epilepsy is an

idiopathic localization-related epilepsy that occurs in children between the ages of 3 and 13years with peak onset in prepubertal late childhood. Apart from their seizure disorder, these

patients are otherwise normal. This syndrome features simple partial seizures that involve facialmuscles and frequently cause drooling. Although most episodes are brief, seizures sometimes

spread and generalize. Seizures are typically nocturnal and confined to sleep. The EEG may

demonstrate spike discharges that occur over the centrotemporal scalp over the central sulcus ofthe brain (the Rolandic sulcus) that are predisposed to occur during drowsiness or light sleep.

Seizures cease near puberty.[14]Seizures may requireanticonvulsant treatment, but sometimes

are infrequent enough to allow physicians to defer treatment.

Benign occipital epilepsy of childhood (BOEC) is an idiopathic localization-related epilepsyand consists of an evolving group of syndromes. Most authorities include two subtypes, an early

subtype with onset between 35 years and a late onset between 710 years. Seizures in BOECusually feature visual symptoms such as scotoma or fortifications (brightly colored spots or

lines) or amaurosis (blindness or impairment of vision). Convulsions involving one half thebody, hemiconvulsions, or forced eye deviation or head turning are common. Younger patients

typically experience symptoms similar to migraine with nausea and headache, and older patients

typically complain of more visual symptoms. The EEG in BOEC shows spikes recorded fromthe occipital (back of head) regions. The EEG and genetic pattern suggest an autosomal

dominant transmission as described by Ruben Kuznieckyet al.[15] Lately, a group of epilepsies

termedPanayiotopoulos syndrome[16] that share some clinical features of BOEC but have awider variety of EEG findings are classified by some as BOEC.

Catamenial epilepsy (CE) is when seizures cluster around certain phases of a woman's

menstrual cycle.
http://wiki/Febrile_convulsionshttp://wiki/Landau-Kleffner_syndromehttp://wiki/Landau-Kleffner_syndromehttp://wiki/EEGhttp://wiki/EEGhttp://wiki/West_syndromehttp://wiki/West_syndromehttp://wiki/Infantile_spasmshttp://wiki/Autosomal_dominant_nocturnal_frontal_lobe_epilepsyhttp://wiki/Nicotinic_acetylcholine_receptorhttp://wiki/Benign_rolandic_epilepsyhttp://wiki/Benign_rolandic_epilepsyhttp://wiki/EEGhttp://wiki/Anticonvulsanthttp://wiki/Anticonvulsanthttp://wiki/EEGhttp://wiki/Ruben_Kuznieckyhttp://wiki/Ruben_Kuznieckyhttp://wiki/Panayiotopoulos_syndromehttp://wiki/Panayiotopoulos_syndromehttp://wiki/Febrile_convulsionshttp://wiki/Landau-Kleffner_syndromehttp://wiki/Landau-Kleffner_syndromehttp://wiki/EEGhttp://wiki/West_syndromehttp://wiki/Infantile_spasmshttp://wiki/Autosomal_dominant_nocturnal_frontal_lobe_epilepsyhttp://wiki/Nicotinic_acetylcholine_receptorhttp://wiki/Benign_rolandic_epilepsyhttp://wiki/EEGhttp://wiki/Anticonvulsanthttp://wiki/EEGhttp://wiki/Ruben_Kuznieckyhttp://wiki/Panayiotopoulos_syndrome


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Childhood absence epilepsy (CAE) is an idiopathic generalized epilepsy that affects children

between the ages of 4 and 12 years of age, although peak onset is around 56 years old. These

patients have recurrentabsence seizures, brief episodes of unresponsive staring, sometimes with

minor motor features such as eye blinking or subtle chewing. The EEG finding in CAE isgeneralized 3 Hz spike and wave discharges. Some go on to develop generalized tonic-clonic

seizures. This condition carries a good prognosis because children do not usually show

cognitive decline or neurological deficits, and the seizures in the majority cease spontaneouslywith onging maturation.

Dravet's syndrome Severe myoclonic epilepsy of infancy (SMEI). This syndrome was

described by Charlotte Dravet, French psychiatrist and epileptologist (born July 14, 1936).

Dravet described this syndrome while working at the Centre Saint Paul at the University ofMarseille. At Centre Saint Paul one of her supervisors was Henri Gastauts who described the

Lennox-Gastaut syndrome. She described this condition in 1978 [17] The condition is

considered to be rare with approximately 450 cases described worldwide in 2005 (A review in1992 found only 172 published cases.) This syndrome was renamed severe myoclonic epilepsy

in infancy in 1981. Defining clinical criteria were established in 1984. The condition is due

either to mutations in the alpha subunit of the voltage dependent sodium channel or mutations in

the gamma subunit of the GABA A receptor. Nosologically it is located in group 3 of the 1989international classification of epilepies - the epileptic syndromes without a focal determination

or which are generalised. The incidence is probably less than one in 40,000 population.

Severe myoclonic epilepsy in infancy is distinguished from benign myoclonic epilepsy by its severity

and must be differentiated from the Lennox-Gastaut syndrome and Dooses myoclonic-astatic epilepsy.Onset is in the first year of life and symptoms peak at about 5 months of age with febrile hemiclonic or

generalized status epilepticus. Boys are twice as often affected as girls. Prognosis is poor. Most cases

are sporadic. Family history of epilepsy and febrile convulsions is present in around 25 percent of thecases.[18]

Frontal lobe epilepsy, usually a symptomatic or cryptogenic localization-related epilepsy,

arises from lesions causing seizures that occur in the frontal lobes of the brain. These epilepsiescan be difficult to diagnose because the symptoms of seizures can easily be confused withnonepileptic spells and, because of limitations of the EEG, be difficult to "see" with standard

scalp EEG.

Juvenile absence epilepsy is an idiopathic generalized epilepsy with later onset that CAE,

typically in prepubertal adolescence, with the most frequent seizure type being absence seizures.Generalized tonic-clonic seizures can occur. 3 Hz spike-wave or multiple spike discharges can

be seen on EEG. Prognosis is mixed, with some patients going on to a syndrome that is poorly

distinguishable from JME.

Juvenile myoclonic epilepsy (JME) is an idiopathic generalized epilepsy that occurs in patientsaged 8 to 20 years. Patients have normal cognition and are otherwise neurologically intact. The

most common seizures are myoclonic jerks, although generalized tonic-clonic seizures and

absence seizures may occur as well. Myoclonic jerks usually cluster in the early morning afterawakening. The EEG reveals generalized 46 Hz spike wave discharges or multiple spike

discharges. Interestingly, these patients are often first diagnosed when they have their first

generalized tonic-clonic seizure later in life when they experience sleep deprivation (e.g.,freshman year in college after staying up late to study for exams). Alcohol withdrawal can also

be a major contributing factor inbreakthrough seizuresas well. The risk of the tendency to have

seizures is lifelong; however, the majority have well-controlled seizures with anticonvulsant

medication and avoidance of seizure precipitants.
http://wiki/Childhood_absence_epilepsyhttp://wiki/Absence_seizureshttp://wiki/Absence_seizureshttp://wiki/Dravet%27s_syndromehttp://wiki/Marseillehttp://wiki/Lennox-Gastaut_syndromehttp://wiki/Frontal_lobe_epilepsyhttp://wiki/Frontal_lobe_epilepsyhttp://wiki/EEGhttp://wiki/Juvenile_myoclonic_epilepsyhttp://wiki/Breakthrough_seizurehttp://wiki/Breakthrough_seizurehttp://wiki/Childhood_absence_epilepsyhttp://wiki/Absence_seizureshttp://wiki/Dravet%27s_syndromehttp://wiki/Marseillehttp://wiki/Lennox-Gastaut_syndromehttp://wiki/Frontal_lobe_epilepsyhttp://wiki/EEGhttp://wiki/Juvenile_myoclonic_epilepsyhttp://wiki/Breakthrough_seizure


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Lennox-Gastaut syndrome (LGS) is a generalized epilepsy that consists of a triad of

developmental delay or childhood dementia, mixed generalized seizures, and EEG

demonstrating a pattern of approximately 2 Hz "slow" spike-wave. Onset occurs between 218

years. As in West syndrome, LGS result from idiopathic, symptomatic, or cryptogenic causes,and many patients first haveWest syndrome. Authorities emphasize different seizure types as

important in LGS, but most have astatic seizures (drop attacks), tonic seizures, tonic-clonic

seizures, atypical absence seizures, and sometimes, complex partial seizures. Anticonvulsantsare usually only partially successful in treatment.

Ohtahara Syndrome is a rare but severe form of epilepsy syndrome combined with cerebral

palsy and characterised with frequent seizures which typically start in the first few days of life.

Sufferers trend to be severely disabled and their lives very short (they are unlikely to reachadulthood).

Primary reading epilepsy is a reflex epilepsy classified as an idiopathic localization-related

epilepsy. Reading in susceptible individuals triggers characteristic seizures.[19]

Progressive myoclonic epilepsies define a group of symptomatic generalized epilepsies

characterized by progressive dementiaand myoclonic seizures. Tonic-clonic seizures may occur

as well. Diseases usually classified in this group are Unverricht-Lundborg disease, myoclonusepilepsy with ragged red fibers (MERRF syndrome), Lafora disease, neuronal ceroid

lipofucinosis, and sialdosis.

Rasmussen's encephalitis is a symptomatic localization-related epilepsy that is a progressive,inflammatory lesion affecting children with onset before the age of 10. Seizures start as separate

simple partial or complex partial seizures and may progress to epilepsia partialis continuata

(simple partial status epilepticus). Neuroimaging shows inflammatory encephalitis on one sideof the brain that may spread if not treated. Dementia and hemiparesis are other problems. The

cause is hypothesized to involve an immulogical attack against glutamate receptors, a common

neurotransmitter in the brain.[20]

Symptomatic localization-related epilepsies Symptomatic localization-related epilepsies aredivided by the location in the brain of the epileptic lesion, since the symptoms of the seizures

are more closely tied to the brain location rather than the cause of the lesion. Tumors,

atriovenous malformations, cavernous malformations, trauma, and cerebral infarcts can all becauses of epileptic foci in different brain regions.

Temporal lobe epilepsy (TLE), a symptomatic localization-related epilepsy, is the most

common epilepsy of adults who experience seizures poorly controlled with anticonvulsant

medications. In most cases, the epileptogenic region is found in the midline (mesial) temporalstructures (e.g., the hippocampus, amygdala, andparahippocampal gyrus). Seizures begin in late

childhood and adolescence. Most of these patients have complex partial seizures sometimes

preceded by an aura, and some TLE patients also suffer from secondary generalizedtonic-clonic

seizures. If the patient does not respond sufficiently to medical treatment, epilepsy surgery maybe considered.

West syndrome is a triad of developmental delay, seizures termed infantile spasms, and EEG

demonstrating a pattern termed hypsarrhythmia. Onset occurs between 3 months and 2 years,

with peak onset between 89 months. West syndrome may arise from idiopathic, symptomatic,or cryptogenic causes. The most common cause istuberous sclerosis. The prognosis varies with

the underlying cause. In general most surviving patients remain with significant cognitive

impairment and continuing seizures and may evolve to another eponymic syndrome,Lennox-Gastaut syndrome.
http://wiki/EEGhttp://wiki/West_syndromehttp://wiki/West_syndromehttp://wiki/Cerebral_palsyhttp://wiki/Cerebral_palsyhttp://wiki/Reflex_epilepsyhttp://wiki/Dementiahttp://wiki/Dementiahttp://wiki/Unverricht-Lundborg_diseasehttp://wiki/MERRF_syndromehttp://wiki/Lafora_diseasehttp://wiki/Lafora_diseasehttp://wiki/Rasmussen%27s_encephalitishttp://wiki/Temporal_lobe_epilepsyhttp://wiki/Anticonvulsanthttp://wiki/Mesialhttp://wiki/Hippocampushttp://wiki/Amygdalahttp://wiki/Parahippocampal_gyrushttp://wiki/Aura_(symptom)http://wiki/Tonic-clonic_seizureshttp://wiki/Tonic-clonic_seizureshttp://wiki/Tonic-clonic_seizureshttp://wiki/West_syndromehttp://wiki/Infantile_spasmshttp://wiki/EEGhttp://wiki/Hypsarrhythmiahttp://wiki/Tuberous_sclerosishttp://wiki/Tuberous_sclerosishttp://wiki/Lennox-Gastaut_syndromehttp://wiki/Lennox-Gastaut_syndromehttp://wiki/Lennox-Gastaut_syndromehttp://wiki/EEGhttp://wiki/West_syndromehttp://wiki/Cerebral_palsyhttp://wiki/Cerebral_palsyhttp://wiki/Reflex_epilepsyhttp://wiki/Dementiahttp://wiki/Unverricht-Lundborg_diseasehttp://wiki/MERRF_syndromehttp://wiki/Lafora_diseasehttp://wiki/Rasmussen%27s_encephalitishttp://wiki/Temporal_lobe_epilepsyhttp://wiki/Anticonvulsanthttp://wiki/Mesialhttp://wiki/Hippocampushttp://wiki/Amygdalahttp://wiki/Parahippocampal_gyrushttp://wiki/Aura_(symptom)http://wiki/Tonic-clonic_seizureshttp://wiki/Tonic-clonic_seizureshttp://wiki/West_syndromehttp://wiki/Infantile_spasmshttp://wiki/EEGhttp://wiki/Hypsarrhythmiahttp://wiki/Tuberous_sclerosishttp://wiki/Lennox-Gastaut_syndromehttp://wiki/Lennox-Gastaut_syndrome


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[edit] Causes

The diagnosis of epilepsy usually requires that the seizures occur spontaneously. Nevertheless, certain

epilepsy syndromes require particular precipitants or triggers for seizures to occur. These are termed

reflex epilepsy. For example, patients withprimary reading epilepsy have seizures triggered by reading.Photosensitive epilepsy can be limited to seizures triggered by flashing lights. Other precipitants can

trigger an epileptic seizure in patients who otherwise would be susceptible to spontaneous seizures. For

example, children with childhood absence epilepsy may be susceptible tohyperventilation. In fact,flashing lights andhyperventilation are activating procedures used in clinical EEG to help trigger

seizures to aid diagnosis. Finally, other precipitants can facilitate, rather than obligately trigger, seizures

in susceptible individuals. Emotional stress, sleep deprivation, sleep itself, heat stress, alcohol andfebrile illness are examples of precipitants cited by patients with epilepsy. Notably, the influence of

various precipitants varies with the epilepsy syndrome.[21]. Likewise, themenstrual cyclein women

with epilepsy can influence patterns of seizure recurrence. Catamenial epilepsy is the term denoting

seizures linked to themenstrual cycle.[22]

There are different causes of epilepsy that are common in certain age groups.

During the neonatal period and early infancy the most common causes include hypoxic-

ischemic encephalopathy, CNS infections, trauma, congenital CNS abnormalities, andmetabolic disorders.

During late infancy and early childhood, febrile seizures are fairly common. These may be

caused by many different things, some thought to be things such as CNS infections and trauma.

During childhood, well-defined epilepsy syndromes are generally seen.

During adolescence and adulthood, the causes are more likely to be secondary to any CNSlesion. Further, idiopathic epilepsy is less common. Other causes associated with these age

groups are stress, trauma, CNS infections, brain tumors, illicit drug use and alcohol withdrawal.

In older adults, cerebrovascular disease is a very common cause. Other causes are CNS tumors,head trauma, and other degenerative diseases which are common in the older age group, such as

dementia.

[23]

[edit] Pathophysiology

Mutations in several genes have been linked to some types of epilepsy. Several genes that code for

protein subunits ofvoltage-gated andligand-gatedion channels have been associated with forms ofgeneralized epilepsy and infantile seizure syndromes.[24]Several ligand-gated ion channels have been

linked to some types of frontal and generalized epilepsies. One speculated mechanism for some forms

of inherited epilepsy are mutations of the genes which code for sodium channel proteins; these

defective sodium channels stay open for too long thus making the neuron hyper-excitable. Glutamate,

an excitatory neurotransmitter, may thereby be released from these neurons in large amounts whichby binding with nearby glutamatergic neuronstriggers excessive calcium (Ca2+) release in these post-synaptic cells. Such excessive calcium release can be neurotoxic to the affected cell. The hippocampus,

which contains a large volume of just such glutamanergic neurons (and NMDA receptors, which are

permeable to Ca2+ entry after binding of both sodium and glutamate), is especially vulnerable to

epileptic seizure, subsequent spread of excitation, and possible neuronal death. Another possible

mechanism involves mutations leading to ineffective GABA (the brain's most common inhibitory

neurotransmitter) action. Epilepsy-related mutations in some non-ion channel genes have also beenidentified.
http://w/index.php?title=Epilepsy&action=edit&section=4http://wiki/Reflex_epilepsyhttp://w/index.php?title=Primary_reading_epilepsy&action=edit&redlink=1http://w/index.php?title=Primary_reading_epilepsy&action=edit&redlink=1http://wiki/Photosensitive_epilepsyhttp://wiki/Childhood_absence_epilepsyhttp://wiki/Hyperventilationhttp://wiki/Hyperventilationhttp://wiki/Hyperventilationhttp://wiki/Hyperventilationhttp://wiki/Hyperventilationhttp://wiki/EEGhttp://wiki/Menstrual_cyclehttp://wiki/Menstrual_cyclehttp://wiki/Menstrual_cyclehttp://wiki/Menstrual_cyclehttp://wiki/Menstrual_cyclehttp://w/index.php?title=Epilepsy&action=edit&section=5http://wiki/Mutationhttp://wiki/Genehttp://wiki/Proteinhttp://wiki/Voltage-gated_ion_channelhttp://wiki/Ligand-gated_ion_channelhttp://wiki/Ligand-gated_ion_channelhttp://wiki/Ion_channelhttp://wiki/Ion_channelhttp://w/index.php?title=Epilepsy&action=edit&section=4http://wiki/Reflex_epilepsyhttp://w/index.php?title=Primary_reading_epilepsy&action=edit&redlink=1http://wiki/Photosensitive_epilepsyhttp://wiki/Childhood_absence_epilepsyhttp://wiki/Hyperventilationhttp://wiki/Hyperventilationhttp://wiki/EEGhttp://wiki/Menstrual_cyclehttp://wiki/Menstrual_cyclehttp://w/index.php?title=Epilepsy&action=edit&section=5http://wiki/Mutationhttp://wiki/Genehttp://wiki/Proteinhttp://wiki/Voltage-gated_ion_channelhttp://wiki/Ligand-gated_ion_channelhttp://wiki/Ion_channel


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Epileptogenesis is the process by which a normal brain develops epilepsy after an insult. One

interesting finding in animals is that repeated low-level electrical stimulation to some brain sites can

lead to permanent increases in seizure susceptibility: in other words, a permanent decrease in seizure

"threshold." This phenomenon, known as kindling (by analogy with the use of burning twigs to start alarger fire) was discovered by Dr. Graham Goddard in 1967. It is important to note that these "kindled"

animals do not experience spontaneous seizures. Chemical stimulation can also induce seizures;

repeated exposures to some pesticides have been shown to induce seizures in both humans and animals.One mechanism proposed for this is called excitotoxicity. The roles of kindling and excitotoxicity, if

any, in human epilepsy are currently hotly debated.

Other causes of epilepsy are brain lesions, where there is scar tissue or another abnormal mass of tissue

in an area of the brain.

The complexity of understanding what seizures are have led to considerable efforts to usecomputational models of epilepsy to both interpret experimental and clinical data, as well as guide

strategies for therapy.

[edit] Management

Epilepsy is usually treated withmedication prescribed by aphysician;primary caregivers,neurologists,

and neurosurgeons all frequently care for people with epilepsy. However, it has been stressed thataccurate differentiation between generalized and partial seizures is especially important in determining

the appropriate treatment.[25]In some cases the implantation of a stimulator of the vagus nerve, or a

special diet can be helpful. Neurosurgical operations for epilepsy can bepalliative, reducing the

frequency or severity of seizures; or, in some patients, an operation can be curative.

[edit] Responding to a seizure

In most cases, the proper emergency response to a generalized tonic-clonic epileptic seizureis simplyto prevent the patient from self-injury by moving him or her away from sharp edges, placing something

soft beneath the head, and carefully rolling the person into the recovery position to avoid asphyxiation.

In some cases the person may seem to start snoringloudly following a seizure, before coming to. This

merely indicates that the person is beginning to breathe properly and does not mean he or she issuffocating. Should the person regurgitate, the material should be allowed to drip out the side of the

person's mouth by itself. If a seizure lasts longer than 5 minutes, or if the seizures begin coming in

'waves' one after the other - then Emergency Medical Services should be contacted immediately.Prolonged seizures may develop intostatus epilepticus, a dangerous condition requiring hospitalization

and emergency treatment.

Objects should never be placed in a person's mouth by anybody - including paramedics - during a

seizure as this could result in serious injury to either party. Despite commonfolklore, it is not possible

for a person to swallow their own tongue during a seizure. However, it is possible that the person willbite their own tongue, especially if an object is placed in the mouth.

With other types of seizures such as simple partial seizures andcomplex partial seizures where the

person is not convulsing but may be hallucinating, disoriented, distressed, or unconscious, the personshould be reassured, gently guided away from danger, and sometimes it may be necessary to protect the

person from self-injury, but physical force should be used only as a last resort as this could distress the

person even more. In complex partial seizures where the person is unconscious, attempts to rouse theperson should not be made as the seizure must take its full course. After a seizure, the person may pass

into a deep sleep or otherwise they will be disoriented and often unaware that they have just had a
http://wiki/Epileptogenesishttp://wiki/Kindling_modelhttp://wiki/Excitotoxicityhttp://wiki/Excitotoxicityhttp://www.scholarpedia.org/article/Models_of_epilepsyhttp://w/index.php?title=Epilepsy&action=edit&section=6http://wiki/Medicationhttp://wiki/Medicationhttp://wiki/Physicianhttp://wiki/Primary_carehttp://wiki/Neurologisthttp://wiki/Neurologisthttp://wiki/Neurologisthttp://wiki/Neurosurgeonhttp://wiki/Vagus_nervehttp://wiki/Palliativehttp://wiki/Palliativehttp://w/index.php?title=Epilepsy&action=edit&section=7http://wiki/Tonic-clonic_seizurehttp://wiki/Tonic-clonic_seizurehttp://wiki/Head_(anatomy)http://wiki/Head_(anatomy)http://wiki/Recovery_positionhttp://wiki/Asphyxiationhttp://wiki/Asphyxiationhttp://wiki/Snoringhttp://wiki/Snoringhttp://wiki/Emergency_Medical_Serviceshttp://wiki/Status_epilepticushttp://wiki/Mouthhttp://wiki/Folklorehttp://wiki/Folklorehttp://wiki/Tonguehttp://wiki/Simple_partial_seizureshttp://wiki/Complex_partial_seizureshttp://wiki/Complex_partial_seizureshttp://wiki/Epileptogenesishttp://wiki/Kindling_modelhttp://wiki/Excitotoxicityhttp://www.scholarpedia.org/article/Models_of_epilepsyhttp://w/index.php?title=Epilepsy&action=edit&section=6http://wiki/Medicationhttp://wiki/Physicianhttp://wiki/Primary_carehttp://wiki/Neurologisthttp://wiki/Neurosurgeonhttp://wiki/Vagus_nervehttp://wiki/Palliativehttp://w/index.php?title=Epilepsy&action=edit&section=7http://wiki/Tonic-clonic_seizurehttp://wiki/Head_(anatomy)http://wiki/Recovery_positionhttp://wiki/Asphyxiationhttp://wiki/Snoringhttp://wiki/Emergency_Medical_Serviceshttp://wiki/Status_epilepticushttp://wiki/Mouthhttp://wiki/Folklorehttp://wiki/Tonguehttp://wiki/Simple_partial_seizureshttp://wiki/Complex_partial_seizures


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seizure, as amnesia is common with complex partial seizures. The person should remain observed until

they have completely recovered, as with a tonic-clonic seizure.

After a seizure, it is typical for a person to be exhausted and confused (this is known as post-ictal state).

Often the person is not immediately aware that they have just had a seizure. During this time oneshould stay with the person - reassuring and comforting them - until they appear to act as they normally

would. Seldom during seizures do people lose bladder or bowel control. In some instances the person

mayvomit after coming to. People should not be allowed to wander about unsupervised until they havereturned to their normal level of awareness. Many patients will sleep deeply for a few hours after aseizure - this is common for those having just experienced a more violent type of seizure such as a

tonic-clonic. In about 50% of people with epilepsy, headaches may occur after a seizure. These

headaches share many features with migraines, and respond to the same medications.

It is helpful if those present at the time of a seizure make note of how long and how severe the seizurewas. It is also helpful to note any mannerisms displayed during the seizure. For example, the individual

may twist the body to the right or left, may blink, might mumble nonsense words, or might pull at

clothing. Any observed behaviors, when relayed to a neurologist, may be of help in diagnosing the typeof seizure which occurred.

[edit] Pharmacologic treatment

Main article:Anticonvulsant

The mainstay of treatment of epilepsy is anticonvulsant medications. Often, anticonvulsant medication

treatment will be lifelong and can have major effects on quality of life. The choice among

anticonvulsants and their effectiveness differs by epilepsy syndrome. Mechanisms, effectiveness for

particular epilepsy syndromes, and side effects differ among the individual anticonvulsant medications.Some general findings about the use of anticonvulsants are outlined below.

Availability- Currently there are 20 medications approved by the Food and Drug Administration for the

use of treatment of epileptic seizures in the US:carbamazepine (common US brand name Tegretol),

clorazepate(Tranxene), clonazepam (Klonopin), ethosuximide (Zarontin), felbamate(Felbatol),fosphenytoin (Cerebyx), gabapentin (Neurontin), lacosamide(Vimpat),lamotrigine (Lamictal),

levetiracetam(Keppra),oxcarbazepine (Trileptal),phenobarbital (Luminal),phenytoin (Dilantin),

pregabalin (Lyrica),primidone (Mysoline), tiagabine (Gabitril), topiramate (Topamax), valproatesemisodium (Depakote), valproic acid (Depakene), and zonisamide

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