<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Tobacco smoking and explain in detail? [/INST] Tobacco smoking is the practice of burning tobacco and ingesting the resulting smoke. The smoke may be inhaled, as is done with cigarettes, or simply released from the mouth, as is generally done with pipes and cigars. The practice is believed to have begun as early as 5000–3000 BC in Mesoamerica and South America. Tobacco was introduced to Eurasia in the late 17th century by European colonists, where it followed common trade routes. The practice encountered criticism from its first import into the Western world onwards but embedded itself in certain strata of a number of societies before becoming widespread upon the introduction of automated cigarette-rolling apparatus.Smoking is the most common method of consuming tobacco, and tobacco is the most common substance smoked. The agricultural product is often mixed with additives and then combusted. The resulting smoke is then inhaled and the active substances absorbed through the alveoli in the lungs or the oral mucosa. Many substances in cigarette smoke trigger chemical reactions in nerve endings, which heighten heart rate, alertness and reaction time, among other things. Dopamine and endorphins are released, which are often associated with pleasure.German scientists identified a link between smoking and lung cancer in the late 1920s, leading to the first anti-smoking campaign in modern history, albeit one truncated by the collapse of Nazi Germany at the end of World War II. In 1950, British researchers demonstrated a clear relationship between smoking and cancer. Evidence continued to mount in the 1960s, which prompted political action against the practice. Rates of consumption since 1965 in the developed world have either peaked or declined. However, they continue to climb in the developing world. As of 2008 to 2010, tobacco is used by about 49% of men and 11% of women aged 15 or older in fourteen low-income and middle-income countries (Bangladesh, Brazil, China, Egypt, India, Mexico, Philippines, Russia, Thailand, Turkey, Ukraine, Uruguay and Vietnam), with about 80% of this usage in the form of smoking. The gender gap tends to be less pronounced in lower age groups.Many smokers begin during adolescence or early adulthood. During the early stages, a combination of perceived pleasure acting as positive reinforcement and desire to respond to social peer pressure may offset the unpleasant symptoms of initial use, which typically include nausea and coughing. After an individual has smoked for some years, the avoidance of withdrawal symptoms and negative reinforcement become the key motivations to continue.
A 2009 study of first smoking experiences of seventh-grade students found out that the most common factor leading students to smoke is cigarette advertisements. Smoking by parents, siblings and friends also encourages students to smoke.

History
Use in ancient cultures
Smokings history dates back to as early as 5000–3000 BC, when the agricultural product began to be cultivated in Mesoamerica and South America; consumption later evolved into burning the plant substance either by accident or with intent of exploring other means of consumption. The practice worked its way into shamanistic rituals. Many ancient civilizations – such as the Babylonians, the Indians, and the Chinese – burnt incense during religious rituals. Smoking in the Americas probably had its origins in the incense-burning ceremonies of shamans but was later adopted for pleasure or as a social tool. The smoking of tobacco and various hallucinogenic drugs was used to achieve trances and to come into contact with the spirit world. Also, to stimulate respiration, tobacco smoke enemas were used.Eastern North American tribes would carry large amounts of tobacco in pouches as a readily accepted trade item and would often smoke it in ceremonial pipes, either in sacred ceremonies or to seal bargains. Adults as well as children enjoyed the practice. It was believed that tobacco was a gift from the Creator and that the exhaled tobacco smoke was capable of carrying ones thoughts and prayers to heaven.Apart from smoking, tobacco had uses as medicine. As a pain killer it was used for earache and toothache and occasionally as a poultice. Smoking was said by the desert Indians to be a cure for colds, especially if the tobacco was mixed with the leaves of the small Desert sage, Salvia dorrii, or the root of Indian balsam or cough root, Leptotaenia multifida, the addition of which was thought to be particularly good for asthma and tuberculosis.

Popularization
In 1612, six years after the settlement of Jamestown, Virginia, John Rolfe was credited as the first settler to successfully raise tobacco as a cash crop. The demand quickly grew as tobacco, referred to as "brown gold", revived the Virginia joint stock company from its failed gold expeditions. In order to meet demands from the Old World, tobacco was grown in succession, quickly depleting the soil. This became a motivator to settle west into the unknown continent, and likewise an expansion of tobacco production. Indentured servitude became the primary labor force up until Bacons Rebellion, from which the focus turned to slavery. This trend abated following the American Revolution as slavery became regarded as unprofitable. However, the practice was revived in 1794 with the invention of the cotton gin.Frenchman Jean Nicot (from whose name the word nicotine is derived) introduced tobacco to France in 1560, and tobacco then spread to England. The first report of a smoking Englishman is of a sailor in Bristol in 1556, seen "emitting smoke from his nostrils". Like tea, coffee and opium, tobacco was just one of many intoxicants that was originally used as a form of medicine. Tobacco was introduced around 1600 by French merchants in what today is modern-day Gambia and Senegal. At the same time, caravans from Morocco brought tobacco to the areas around Timbuktu, and the Portuguese brought the commodity (and the plant) to southern Africa, establishing the popularity of tobacco throughout all of Africa by the 1650s.
Soon after its introduction to the Old World, tobacco came under frequent criticism from state and religious leaders. James VI and I, King of Scotland and England, produced the treatise A Counterblaste to Tobacco in 1604, and also introduced excise duty on the product. Murad IV, sultan of the Ottoman Empire 1623–40 was among the first to attempt a smoking ban by claiming it was a threat to public morals and health. The Chongzhen Emperor of China issued an edict banning smoking two years before his death and the overthrow of the Ming dynasty. Later, the Manchu rulers of the Qing dynasty, would proclaim smoking "a more heinous crime than that even of neglecting archery". In Edo period Japan, some of the earliest tobacco plantations were scorned by the shogunate as being a threat to the military economy by letting valuable farmland go to waste for the use of a recreational drug instead of being used to plant food crops.

Religious leaders have often been prominent among those who considered smoking immoral or outright blasphemous. In 1634, the Patriarch of Moscow forbade the sale of tobacco, and sentenced men and women who flouted the ban to have their nostrils slit and their backs flayed. Pope Urban VIII likewise condemned smoking on holy places in a papal bull of 1624. Despite some concerted efforts, restrictions and bans were largely ignored. When James I of England, a staunch anti-smoker and the author of A Counterblaste to Tobacco, tried to curb the new trend by enforcing a 4000% tax increase on tobacco in 1604 it was unsuccessful, as suggested by the presence of around 7,000 tobacco outlets in London by the early 17th century. From this point on for some centuries, several administrations withdrew from efforts at discouragement and instead turned tobacco trade and cultivation into sometimes lucrative government monopolies.By the mid-17th century most major civilizations had been introduced to tobacco smoking and in many cases had already assimilated it into the native culture, despite some continued attempts upon the parts of rulers to eliminate the practice with penalties or fines. Tobacco, both product and plant, followed the major trade routes to major ports and markets, and then on into the hinterlands. The English language term smoking appears to have entered currency in the late 18th century, before which less abbreviated descriptions of the practice such as drinking smoke were also in use.Growth in the US remained stable until the American Civil War in 1860s, when the primary agricultural workforce shifted from slavery to sharecropping. This, along with a change in demand, accompanied the industrialization of cigarette production as craftsman James Bonsack created a machine in 1881 to partially automate their manufacture.

Social attitudes and public health
In Germany, anti-smoking groups, often associated with anti-liquor groups, first published advocacy against the consumption of tobacco in the journal Der Tabakgegner (The Tobacco Opponent) in 1912 and 1932. In 1929, Fritz Lickint of Dresden, Germany, published a paper containing formal statistical evidence of a lung cancer–tobacco link. During the Great Depression Adolf Hitler condemned his earlier smoking habit as a waste of money, and later with stronger assertions. This movement was further strengthened with Nazi reproductive policy as women who smoked were viewed as unsuitable to be wives and mothers in a German family. In the 20th century, smoking was common. There were social events like the smoke night which promoted the habit.
The anti-tobacco movement in Nazi Germany did not reach across enemy lines during the Second World War, as anti-smoking groups quickly lost popular support. By the end of the Second World War, American cigarette manufacturers quickly reentered the German black market. Illegal smuggling of tobacco became prevalent, and leaders of the Nazi anti-smoking campaign were silenced. As part of the Marshall Plan, the United States shipped free tobacco to Germany; with 24,000 tons in 1948 and 69,000 tons in 1949. Per capita yearly cigarette consumption in post-war Germany steadily rose from 460 in 1950 to 1,523 in 1963. By the end of the 20th century, anti-smoking campaigns in Germany were unable to exceed the effectiveness of the Nazi-era climax in the years 1939–41 and German tobacco health research was described by Robert N. Proctor as "muted".

In 1950, Richard Doll published research in the British Medical Journal showing a close link between smoking and lung cancer. Beginning in December 1952, the magazine Readers Digest published "Cancer by the Carton", a series of articles that linked smoking with lung cancer.In 1954, the British Doctors Study, a prospective study of some 40 thousand doctors for about 2.5 years, confirmed the suggestion, based on which the government issued advice that smoking and lung cancer rates were related. In January 1964, the United States Surgeon Generals Report on Smoking and Health likewise began suggesting the relationship between smoking and cancer.As scientific evidence mounted in the 1980s, tobacco companies claimed contributory negligence as the adverse health effects were previously unknown or lacked substantial credibility. Health authorities sided with these claims up until 1998, from which they reversed their position. The Tobacco Master Settlement Agreement, originally between the four largest US tobacco companies and the Attorneys General of 46 states, restricted certain types of tobacco advertisement and required payments for health compensation; which later amounted to the largest civil settlement in United States history.Social campaigns have been instituted in many places to discourage smoking, such as Canadas National Non-Smoking Week.
From 1965 to 2006, rates of smoking in the United States declined from 42% to 20.8%. The majority of those who quit were professional, affluent men. Although the per-capita number of smokers decreased, the average number of cigarettes consumed per person per day increased from 22 in 1954 to 30 in 1978. This paradoxical event suggests that those who quit smoked less, while those who continued to smoke moved to smoke more light cigarettes. The trend has been paralleled by many industrialized nations as rates have either leveled-off or declined. In the developing world, however, tobacco consumption continues to rise at 3.4% in 2002. In Africa, smoking is in most areas considered to be modern, and many of the strong adverse opinions that prevail in the West receive much less attention. Today Russia leads as the top consumer of tobacco followed by Indonesia, Laos, Ukraine, Belarus, Greece, Jordan, and China.As a result of public pressure and the FDA, Walmart and Sams club announced that they were raising the minimum age to purchase tobacco products, including all e-cigarettes, to 21 starting  1 July 2019.

Consumption
Methods
Tobacco is an agricultural product processed from the fresh leaves of plants in the genus Nicotiana. The genus contains several species, of which Nicotiana tabacum is the most commonly grown. Nicotiana rustica follows second, containing higher concentrations of nicotine. The leaves are harvested and cured to allow the slow oxidation and degradation of carotenoids in tobacco leaf. This produces certain compounds in the tobacco leaves which can be attributed to sweet hay, tea, rose oil, or fruity aromatic flavors. Before packaging, the tobacco is often combined with other additives in order to increase the addictive potency, shift the products pH, or improve the effects of smoke by making it more palatable. In the United States these additives are regulated to 599 substances. The product is then processed, packaged, and shipped to consumer markets.

Beedi
Beedis are thin South Asian cigarettes filled with tobacco flakes and wrapped in a tendu leaf tied with a string at one end. They produce higher levels of carbon monoxide, nicotine, and tar than cigarettes typical in the United States.
Cigars
Cigars are tightly rolled bundles of dried and fermented tobacco which are ignited so that smoke may be drawn into the smokers mouth. They are generally not inhaled because of the high alkalinity of the smoke, which can quickly become irritating to the trachea and lungs. The prevalence of cigar smoking varies depending on location, historical period, and population surveyed, and prevalence estimates vary somewhat depending on the survey method. The United States is the top consuming country by far, followed by Germany and the United Kingdom; the US and Western Europe account for about 75% of cigar sales worldwide. As of 2005 it is estimated that 4.3% of men and 0.3% of women smoke cigars in the USA.Cigarettes
Cigarettes, French for "small cigar", are a product consumed through smoking and manufactured out of cured and finely cut tobacco leaves and reconstituted tobacco, often combined with other additives, which are then rolled or stuffed into a paper-wrapped cylinder. Cigarettes are ignited and inhaled, usually through a cellulose acetate filter, into the mouth and lungs.

Hookah
Hookah are a single or multi-stemmed (often glass-based) water pipe for smoking. Originally from India. The hookah was a symbol of pride and honor for the landlords, kings and other such high class people.  Now, the hookah has gained immense popularity, especially in the Middle East. A hookah operates by water filtration and indirect heat. It can be used for smoking herbal fruits, tobacco, or cannabis.
Kretek
Kretek are cigarettes made with a complex blend of tobacco, cloves and a flavoring "sauce". It was first introduced in the 1880s in Kudus, Java, to deliver the medicinal eugenol of cloves to the lungs. The quality and variety of tobacco play an important role in kretek production, from which kretek can contain more than 30 types of tobacco. Minced dried clove buds weighing about one-third of the tobacco blend are added to add flavoring. In 2004 the United States prohibited cigarettes from having a "characterizing flavor" of certain ingredients other than tobacco and menthol, thereby removing kretek from being classified as cigarettes.
Pipe smoking
Pipe smoking is done with a tobacco pipe, typically consisting of a small chamber (the bowl) for the combustion of the tobacco to be smoked and a thin stem (shank) that ends in a mouthpiece (the bit). Shredded pieces of tobacco are placed into the chamber and ignited.
Roll-your-own
Roll-your-own or hand-rolled cigarettes, often called "rollies", "cigi" or "Roll-ups", are very popular particularly in European countries and the UK. These are prepared from loose tobacco, cigarette papers, and filters all bought separately. They are usually much cheaper than ready-made cigarettes and small contraptions can be bought making the process easier.
Vaporizer
A vaporizer is a device used to sublimate the active ingredients of plant material. Rather than burning the herb, which produces potentially irritating, toxic, or carcinogenic by-products; a vaporizer heats the material in a partial vacuum so that the active compounds contained in the plant boil off into a vapor. This method is often preferable when medically administrating the smoke substance, as opposed to directly pyrolyzing the plant material.

Physiology
The active substances in tobacco, especially cigarettes, are administered by burning the leaves and inhaling the vaporized gas that results. This quickly and effectively delivers substances into the bloodstream by absorption through the alveoli in the lungs. The lungs contain some 300 million alveoli, which amounts to a surface area of over 70 m2 (about the size of a tennis court). This method is not completely efficient as not all of the smoke will be inhaled, and some amount of the active substances will be lost in the process of combustion, pyrolysis. Pipe and Cigar smoke are not inhaled because of its high alkalinity, which are irritating to the trachea and lungs. However, because of its higher alkalinity (pH 8.5) compared to cigarette smoke (pH 5.3), non-ionized nicotine is more readily absorbed through the mucous membranes in the mouth. Nicotine absorption from cigar and pipe, however, is much less than that from cigarette smoke. Nicotine and cocaine activate similar patterns of neurons, which supports the existence of common substrates among these drugs.The absorbed nicotine mimics nicotinic acetylcholine which when bound to nicotinic acetylcholine receptors prevents the reuptake of acetylcholine thereby increasing that neurotransmitter in those areas of the body. These nicotinic acetylcholine receptors are located in the central nervous system and at the nerve-muscle junction of skeletal muscles; whose activity increases heart rate, alertness, and faster reaction times. Nicotine acetylcholine stimulation is not directly addictive. However, since dopamine-releasing neurons are abundant on nicotine receptors, dopamine is released; and, in the nucleus accumbens, dopamine is associated with motivation causing reinforcing behavior. Dopamine increase, in the prefrontal cortex, may also increase working memory.When tobacco is smoked, most of the nicotine is pyrolyzed. However, a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. There is also a formation of harmane (an MAO inhibitor) from the acetaldehyde in tobacco smoke. This may play a role in nicotine addiction, by facilitating a dopamine release in the nucleus accumbens as a response to nicotine stimuli. Using rat studies, withdrawal after repeated exposure to nicotine results in less responsive nucleus accumbens cells, which produce dopamine responsible for reinforcement.

Demographics
As of 2000, smoking was practiced by around 1.22 billion people. At current rates of smoker replacement and market growth, this may reach around 1.9 billion in 2025.Smoking may be up to five times more prevalent among men than women in some communities, although the gender gap usually declines with younger age. In some developed countries smoking rates for men have peaked and begun to decline, while for women they continue to climb.As of 2002, about twenty percent of young teenagers (13–15) smoked worldwide. 80,000 to 100,000 children begin smoking every day, roughly half of whom live in Asia. Half of those who begin smoking in adolescent years are projected to go on to smoke for 15 to 20 years. As of 2019 in the United States, roughly 800,000 high school students smoke.The World Health Organization (WHO) states that "Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor". Of the 1.22 billion smokers, 1 billion of them live in developing or transitional economies. Rates of smoking have leveled off or declined in the developed world. In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.The WHO in 2004 projected 58.8 million deaths to occur globally, from which 5.4 million are tobacco-attributed, and 4.9 million as of 2007. As of 2002, 70% of the deaths are in developing countries. As of 2017, smoking causes one in ten deaths worldwide, with half of those deaths in the US, China, India and Russia.

Psychology
Takeup
Most smokers begin smoking during adolescence or early adulthood. Some studies also show that smoking can also be linked to various mental health complications. Smoking has elements of risk-taking and rebellion, which often appeal to young people. The presence of peers that smoke and media featuring high-status models smoking may also encourage smoking. Because teenagers are influenced more by their peers than by adults, attempts by parents, schools, and health professionals at preventing people from trying cigarettes are often unsuccessful.Children of smoking parents are more likely to smoke than children with non-smoking parents. Children of parents who smoke are less likely to quit smoking. One study found that parental smoking cessation was associated with less adolescent smoking, except when the other parent currently smoked. A current study tested the relation of adolescent smoking to rules regulating where adults are allowed to smoke in the home. Results showed that restrictive home smoking policies were associated with lower likelihood of trying smoking for both middle and high school students.Behavioural research generally indicates that teenagers begin their smoking habits due to peer pressure, and cultural influence portrayed by friends. However, one study found that direct pressure to smoke cigarettes played a less significant part in adolescent smoking, with adolescents also reporting low levels of both normative and direct pressure to smoke cigarettes. Mere exposure to tobacco retailers may motivate smoking behaviour in adults. A similar study suggested that individuals may play a more active role in starting to smoke than has previously been thought and that social processes other than peer pressure also need to be taken into account. Another studys results indicated that peer pressure was significantly associated with smoking behavior across all age and gender cohorts, but that intrapersonal factors were significantly more important to the smoking behavior of 12- to 13-year-old girls than same-age boys. Within the 14- to 15-year-old age group, one peer pressure variable emerged as a significantly more important predictor of girls than boys smoking. It is debated whether peer pressure or self-selection is a greater cause of adolescent smoking.
Psychologist Hans Eysenck (who later was questioned for nonplausible results
 and unsafe publications) developed a personality profile for the typical smoker. Extraversion is the trait that is most associated with smoking, and smokers tend to be sociable, impulsive, risk taking, and excitement seeking individuals.

Persistence
The reasons given by some smokers for this activity have been categorized as addictive smoking, pleasure from smoking, tension reduction/relaxation, social smoking, stimulation, habit/automatism, and handling. There are gender differences in how much each of these reasons contribute, with females more likely than males to cite tension reduction/relaxation, stimulation and social smoking.Some smokers argue that the depressant effect of smoking allows them to calm their nerves, often allowing for increased concentration. However, according to the Imperial College London, "Nicotine seems to provide both a stimulant and a depressant effect, and it is likely that the effect it has at any time is determined by the mood of the user, the environment and the circumstances of use. Studies have suggested that low doses have a depressant effect, while higher doses have stimulant effect."

Patterns
A number of studies have established that cigarette sales and smoking follow distinct time-related patterns. For example, cigarette sales in the United States of America have been shown to follow a strongly seasonal pattern, with the high months being the months of summer, and the low months being the winter months.Similarly, smoking has been shown to follow distinct circadian patterns during the waking day—with the high point usually occurring shortly after waking in the morning, and shortly before going to sleep at night.

Impact
Health
Tobacco smoking is the leading cause of preventable death and a global public health concern. There are 1.1 billion tobacco users in the world. One person dies every six seconds from a tobacco related disease.

Tobacco use leads most commonly to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), emphysema, and various types and subtypes of cancers (particularly lung cancer, cancers of the oropharynx, larynx, and mouth, esophageal and pancreatic cancer). Cigarette smoking increases the risk of Crohns disease as well as the severity of the course of the disease. It is also the number one cause of bladder cancer. Cigarette smoking has also been associated with sarcopenia, the age-related loss of muscle mass and strength. The smoke from tobacco elicits carcinogenic effects on the tissues of the body that are exposed to the smoke. Regular cigar smoking is known to carry serious health risks, including increased risk of developing various types and subtypes of cancers, respiratory diseases, cardiovascular diseases, cerebrovascular diseases, periodontal diseases and teeth loss, and malignant diseases.Tobacco smoke is a complex mixture of over 7,000 toxic chemicals, 98 of which are associated with an increased risk of cardiovascular disease and 69 of which are known to be carcinogenic. The most important chemicals causing cancer are those that produce DNA damage, since such damage appears to be the primary underlying cause of cancer. Cunningham et al. combined the microgram weight of the compound in the smoke of one cigarette with the known genotoxic effect per microgram to identify the most carcinogenic compounds in cigarette smoke: acrolein, formaldehyde, acrylonitrile, 1,3-butadiene, acetaldehyde, ethylene oxide, and isoprene. In addition to the aforementioned toxic chemicals, flavored tobacco contains flavorings which upon heating release toxic chemicals and carcinogens such as carbon monoxide (CO), polycyclic aromatic hydrocarbons (PAHs), furans, phenols, aldehydes (such as acrolein), and acids, in addition to nitrogenous carcinogens, alcohols, and heavy metals, all of which are dangerous to human health. A comparison of 13 common hookah flavors found that melon flavors are the most dangerous, with their smoke containing four classes of hazards in high concentrations.The World Health Organization estimates that tobacco caused 5.4 million deaths in 2004 and 100 million deaths over the course of the 20th century. Similarly, the United States Centers for Disease Control and Prevention describes tobacco use as "the single most important preventable risk to human health in developed countries and an important cause of premature death worldwide." Although 70% of smokers state their intention to quit only 3–5% are actually successful in doing so.The probabilities of death from lung cancer before age 75 in the United Kingdom are 0.2% for men who never smoked (0.4% for women), 5.5% for male former smokers (2.6% in women), 15.9% for current male smokers (9.5% for women) and 24.4% for male "heavy smokers" defined as smoking more than 5 cigarettes per day (18.5% for women). Tobacco smoke can combine with other carcinogens present within the environment in order to produce elevated degrees of lung cancer.
The risk of lung cancer decreases almost from the first day someone quits smoking. Healthy cells that have escaped mutations grow and replace the damaged ones in the lungs. In the research dated December 2019, 40% of cells in former smokers looked like those of people who had never smoked.Rates of smoking have generally leveled-off or declined in the developed world. Smoking rates in the United States have dropped by half from 1965 to 2006, falling from 42% to 20.8% in adults. In the developing world, tobacco consumption is rising by 3.4% per year.Smoking alters the transcriptome of the lung parenchyma; the expression levels of a panel of seven genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) are increased in the lung tissue of smokers.Passive smoking is the inhalation of tobacco smoke by individuals who are not actively smoking. This smoke is known as second-hand smoke (SHS) or environmental tobacco smoke (ETS) when the burning end is present, and third-hand smoke after the burning end has been extinguished. Because of its negative implications, exposure to SHS has played a central role in the regulation of tobacco products. Six hundred thousand deaths were attributed to SHS in 2004. It also has been known to produce skin conditions such as freckles and dryness.In 2015, a meta-analysis found that smokers were at greater risk of developing psychotic disorder. Tobacco has also been described an anaphrodisiac due to its propensity for causing erectile dysfunction. There is a correlation between tobacco smoking and a reduced risk of Parkinsons disease.

Economic
In countries where there is a universally funded healthcare system, the government covers the cost of medical care for smokers who become ill through smoking in the form of increased taxes. Two broad debating positions exist on this front, the "pro-smoking" argument suggesting that heavy smokers generally do not live long enough to develop the costly and chronic illnesses which affect the elderly, reducing societys healthcare burden, and the "anti-smoking" argument suggests that the healthcare burden is increased because smokers get chronic illnesses younger and at a higher rate than the general population.  Data on both positions has been contested. The Centers for Disease Control and Prevention published research in 2002 claiming that the cost of each pack of cigarettes sold in the United States was more than $7 in medical care and lost productivity. The cost may be higher, with another study putting it as high as $41 per pack, most of which however is on the individual and his/her family. This is how one author of that study puts it when he explains the very low cost for others: "The reason the number is low is that for private pensions, Social Security, and Medicare — the biggest factors in calculating costs to society — smoking actually saves money. Smokers die at a younger age and dont draw on the funds theyve paid into those systems." Other research demonstrates that premature death caused by smoking may redistribute Social Security income in unexpected ways that affect behavior and reduce the economic well-being of smokers and their dependents. To further support this, whatever the rate of smoking consumption is per day, smokers have a greater lifetime medical cost on average compared to a non-smoker by an estimated $6000 Between the cost for lost productivity and health care expenditures combined, cigarette smoking costs at least 193 billion dollars (Research also shows that smokers earn less money than nonsmokers). As for secondhand smoke, the cost is over 10 billion dollars.By contrast, some non-scientific studies, including one conducted by Philip Morris in the Czech Republic called Public Finance Balance of Smoking in the Czech Republic and another by the Cato Institute, support the opposite position. Philip Morris has explicitly apologised for the former study, saying: "The funding and public release of this study which, among other things, detailed purported cost savings to the Czech Republic due to premature deaths of smokers, exhibited terrible judgment as well as a complete and unacceptable disregard of basic human values. For one of our tobacco companies to commission this study was not just a terrible mistake, it was wrong. All of us at Philip Morris, no matter where we work, are extremely sorry for this. No one benefits from the very real, serious and significant diseases caused by smoking."Between 1970 and 1995, per-capita cigarette consumption in poorer developing countries increased by 67 percent, while it dropped by 10 percent in the richer developed world. Eighty percent of smokers now live in less developed countries. By 2030, the World Health Organization (WHO) forecasts that 10 million people a year will die of smoking-related illness, making it the single biggest cause of death worldwide, with the largest increase to be among women. WHO forecasts the 21st centurys death rate from smoking to be ten times the 20th centurys rate ("Washingtonian" magazine, December 2007).
The tobacco industry is known to be one of the largest global enterprises in the world. The six biggest tobacco companies made a combined profit of $35.1 billion (Jha et al., 2014) in 2010.

Social
Famous smokers of the past used cigarettes or pipes as part of their image, such as Jean-Paul Sartres Gauloises-brand cigarettes; Albert Einsteins, Douglas MacArthurs, Bertrand Russells, and Bing Crosbys pipes; or the news broadcaster Edward R. Murrows cigarette. Writers in particular seem to be known for smoking, for example, Cornell Professor Richard Kleins book Cigarettes are Sublime for the analysis, by this professor of French literature, of the role smoking plays in 19th and 20th century letters. The popular author Kurt Vonnegut addressed his addiction to cigarettes within his novels. British Prime Minister Harold Wilson was well known for smoking a pipe in public as was Winston Churchill for his cigars. Sherlock Holmes, the fictional detective created by Sir Arthur Conan Doyle, smoked a pipe, cigarettes, and cigars. The DC Vertigo comic book character John Constantine, created by Alan Moore, is synonymous with smoking, so much so that the first storyline by Preacher creator Garth Ennis centered around John Constantine contracting lung cancer. Professional wrestler James Fullington, while in character as "The Sandman", is a chronic smoker in order to appear "tough".
The problem of smoking at home is particularly difficult for women in many cultures (especially Arab cultures), where it may not be acceptable for a woman to ask her husband not to smoke at home or in the presence of her children. Studies have shown that pollution levels for smoking areas indoors are higher than levels found on busy roadways, in closed motor garages, and during fire storms. Furthermore, smoke can spread from one room to another, even if doors to the smoking area are closed.The ceremonial smoking of tobacco, and praying with a sacred pipe, is a prominent part of the religious ceremonies of a number of Native American Nations. Sema, the Anishinaabe word for tobacco, is grown for ceremonial use and considered the ultimate sacred plant since its smoke is believed to carry prayers to the spirits. In most major religions, however, tobacco smoking is not specifically prohibited, although it may be discouraged as an immoral habit. Before the health risks of smoking were identified through controlled study, smoking was considered an immoral habit by certain Christian preachers and social reformers. The founder of the Latter Day Saint movement, Joseph Smith, recorded that on 27 February 1833, he received a revelation which discouraged tobacco use. This "Word of Wisdom" was later accepted as a commandment, and faithful Latter-day Saints abstain completely from tobacco. Jehovahs Witnesses base their stand against smoking on the Bibles command to "clean ourselves of every defilement of flesh" (2 Corinthians 7:1). The Jewish Rabbi Yisrael Meir Kagan (1838–1933) was one of the first Jewish authorities to speak out on smoking. In Ahmadiyya Islam, smoking is highly discouraged, although not forbidden. During the month of fasting however, it is forbidden to smoke tobacco. In the Baháʼí Faith, smoking tobacco is discouraged though not forbidden.

Public policy
On 27 February 2005 the WHO Framework Convention on Tobacco Control, took effect. The FCTC is the worlds first public health treaty. Countries that sign on as parties agree to a set of common goals, minimum standards for tobacco control policy, and to cooperate in dealing with cross-border challenges such as cigarette smuggling. Currently the WHO declares that 4 billion people will be covered by the treaty, which includes 168 signatories. Among other steps, signatories are to put together legislation that will eliminate secondhand smoke in indoor workplaces, public transport, indoor public places and, as appropriate, other public places.

Taxation
Many governments have introduced excise taxes on cigarettes in order to reduce the consumption of cigarettes. The World Health Organisation finds that:
The structure of tobacco excise taxes varies considerably across countries, with lower income countries more likely to rely more on ad valorem excises and higher income countries more likely to rely more on specific excise taxes, while many countries at all income levels use a mix of specific and ad valorem excises.
Tobacco excise tax systems are quite complex in several countries, where different tax rates are applied based on prices, product characteristics such as presence/absence of a filter or length, packaging, weight, tobacco content, and/or production or sales volume. These complex systems are difficult to administer, create opportunities for tax avoidance, and are less effective from a public health perspective.

Globally, cigarette excise taxes account for less than 45 percent of cigarette prices, on average, while all taxes applied to cigarettes account for just over half of half of price. Higher income countries levy higher taxes on tobacco products and these taxes account for a greater share of price, with both the absolute tax and share of price accounted for by tax falling as country incomes fall.
In 2002, the Centers for Disease Control and Prevention said that each pack of cigarettes sold in the United States costs the nation more than $7 in medical care and lost productivity, around $3400 per year per smoker. Another study by a team of health economists finds the combined price paid by their families and society is about $41 per pack of cigarettes.Substantial scientific evidence shows that higher cigarette prices result in lower overall cigarette consumption. Most studies indicate that a 10% increase in price will reduce overall cigarette consumption by 3% to 5%. Youth, minorities, and low-income smokers are two to three times more likely to quit or smoke less than other smokers in response to price increases. Smoking is often cited as an example of an inelastic good, however, i.e. a large rise in price will only result in a small decrease in consumption.
Many nations have implemented some form of tobacco taxation. As of 1997, Denmark had the highest cigarette tax burden of $4.02 per pack. Taiwan only had a tax burden of $0.62 per pack. The federal government of the United States charges $1.01 per pack.Cigarette taxes vary widely from state to state in the United States. For example, Missouri has a cigarette tax of only 17 cents per pack, the nations lowest, while New York has the highest cigarette tax in the U.S.: $4.35 per pack. In Alabama, Illinois, Missouri, New York City, Tennessee, and Virginia, counties and cities may impose an additional limited tax on the price of cigarettes. Sales taxes are also levied on tobacco products in most jurisdictions.
In the United Kingdom, a packet of 20 cigarettes has a tax added of 16.5% of the retail price plus £4.90. The UK has a significant black market for tobacco, and it has been estimated by the tobacco industry that 27% of cigarette and 68% of handrolling tobacco consumption is non-UK duty paid (NUKDP).In Australia total taxes account for 62.5% of the final price of a packet of cigarettes (2011 figures). These taxes include federal excise or customs duty and Goods and Services Tax.

Restrictions
In June 1967, the US Federal Communications Commission ruled that programmes broadcast on a television station which discussed smoking and health were insufficient to offset the effects of paid advertisements that were broadcast for five to ten minutes each day. In April 1970, the US Congress passed the Public Health Cigarette Smoking Act banning the advertising of cigarettes on television and radio starting on 2 January 1971.The Tobacco Advertising Prohibition Act 1992 expressly prohibited almost all forms of Tobacco advertising in Australia, including the sponsorship of sporting or other cultural events by cigarette brands.
All tobacco advertising and sponsorship on television has been banned within the European Union since 1991 under the Television Without Frontiers Directive (1989). This ban was extended by the Tobacco Advertising Directive, which took effect in July 2005 to cover other forms of media such as the internet, print media, and radio. The directive does not include advertising in cinemas and on billboards or using merchandising – or tobacco sponsorship of cultural and sporting events which are purely local, with participants coming from only one Member State as these fall outside the jurisdiction of the European Commission. However, most member states have transposed the directive with national laws that are wider in scope than the directive and cover local advertising. A 2008 European Commission report concluded that the directive had been successfully transposed into national law in all EU member states, and that these laws were well implemented.Some countries also impose legal requirements on the packaging of tobacco products. For example, in the countries of the European Union, Turkey, Australia and South Africa, cigarette packs must be prominently labeled with the health risks associated with smoking. Canada, Australia, Thailand, Iceland and Brazil have also imposed labels upon cigarette packs warning smokers of the effects, and they include graphic images of the potential health effects of smoking. Cards are also inserted into cigarette packs in Canada. There are sixteen of them, and only one comes in a pack. They explain different methods of quitting smoking. Also, in the United Kingdom, there have been a number of graphic NHS advertisements, one showing a cigarette filled with fatty deposits, as if the cigarette is symbolizing the artery of a smoker.
Some countries have also banned advertisement at point of sale. United Kingdom and Ireland have limited the advertisement of tobacco at retailers. This includes storing of cigarettes behind a covered shelf not visible to the public. They do however allow some limited advertising at retailers. Norway has a complete ban of point of sale advertising. This includes smoking products and accessories. Implementing these policies can be challenging, all of these countries experienced resistance and challenges from the tobacco industry. The World Health Organisation recommends the complete ban of all types of advertisement or product placement, including at vending machines, at airports and on internet shops selling tobacco. The evidence is as yet unclear as to the impact of such bans.
Many countries have a smoking age. In many countries, including the United States, most European Union member states, New Zealand, Canada, South Africa, Israel, India, Brazil, Chile, Costa Rica and Australia, it is illegal to sell tobacco products to minors and in the Netherlands, Austria, Belgium, Denmark and South Africa it is illegal to sell tobacco products to people under the age of 16. On 1 September 2007 the minimum age to buy tobacco products in Germany rose from 16 to 18, as well as in the United Kingdom where on 1 October 2007 it rose from 16 to 18. Underlying such laws is the belief that people should make an informed decision regarding the risks of tobacco use. These laws have a lax enforcement in some nations and states. In China, Turkey, and many other countries usually a child will have little problem buying tobacco products, because they are often told to go to the store to buy tobacco for their parents.
Several countries such as Ireland, Latvia, Estonia, the Netherlands, Finland, Norway, Canada, Australia, Sweden, Portugal, Singapore, Italy, Indonesia, India, Lithuania, Chile, Spain, Iceland, United Kingdom, Slovenia, Turkey and Malta have legislated against smoking in public places, often including bars and restaurants. Restaurateurs have been permitted in some jurisdictions to build designated smoking areas (or to prohibit smoking). In the United States, many states prohibit smoking in restaurants, and some also prohibit smoking in bars. In provinces of Canada, smoking is illegal in indoor workplaces and public places, including bars and restaurants. As of 31 March 2008 Canada has introduced a smoke-free law in all public places, as well as within 10 metres of an entrance to any public place. In Australia, smoke-free laws vary from state to state. Currently, Queensland has completely smoke-free indoor public places (including workplaces, bars, pubs and eateries) as well as patrolled beaches and some outdoor public areas. There are, however, exceptions for designated smoking areas. In Victoria, smoking is restricted in railway stations, bus stops and tram stops as these are public locations where second-hand smoke can affect non-smokers waiting for public transport, and since 1 July 2007 is now extended to all indoor public places. In New Zealand and Brazil, smoking is restricted in enclosed public places including bars, restaurants and pubs. Hong Kong restricted smoking on 1 January 2007 in the workplace, public spaces such as restaurants, karaoke rooms, buildings, and public parks (bars which do not admit minors were exempt until 2009). In Romania smoking is illegal in trains, metro stations, public institutions (except where designated, usually outside) and public transport. In Germany, in addition to smoking bans in public buildings and transport, an anti-smoking ordinance for bars and restaurants was implemented in late 2007. A study by the University of Hamburg (Ahlfeldt and Maennig 2010) demonstrates, that the smoking ban had, if any, only short run impacts on bar and restaurant revenues. In the medium and long run no negative effect was measurable. The results suggest either, that the consumption in bars and restaurants is not affected by smoking bans in the long run, or, that negative revenue impacts by smokers are compensated by increasing revenues through non-smokers.

Ignition safety
An indirect public health problem posed by cigarettes is that of accidental fires, usually linked with consumption of alcohol. Enhanced combustion using nitrates was traditionally used but cigarette manufacturers have been silent on this subject claiming at first that a safe cigarette was technically impossible, then that it could only be achieved by modifying the paper. Roll your own cigarettes contain no additives and are fire safe. Numerous fire safe cigarette designs have been proposed, some by tobacco companies themselves, which would extinguish a cigarette left unattended for more than a minute or two, thereby reducing the risk of fire. Among American tobacco companies, some have resisted this idea, while others have embraced it. RJ Reynolds was a leader in making prototypes of these cigarettes in 1983 and will make all of their U.S. market cigarettes to be fire-safe by 2010 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Retrograde amnesia and explain in detail? [/INST] In neurology, retrograde amnesia (RA) is a loss of memory-access to events that occurred or information that was learned in the past. It is caused by an injury or the onset of a disease. It tends to negatively affect episodic, autobiographical, and declarative memory, while keeping procedural memory intact without increasing difficulty for learning new information. RA can be temporally graded, or more permanent based on the severity of its cause. It is usually consistent with Ribots law. The law states that subjects are more likely to lose memories closer to the traumatic incident than more memories that happened further from the incident. The type of information that is forgotten can range from a specific memory, such as a single event, or a more general memory. This would resemble generic amnesia. Anterograde amnesia is a similar condition that deals with the inability to form new memories following the onset of an injury or disease.

Cause
RA commonly results from damage to regions of the brain that are associated with episodic and declarative memory, including autobiographical information. In extreme cases, individuals may completely forget who they are. Generally, this is a more severe type of amnesia known as global, or generalized amnesia. However, memory loss can also be selective or categorical, manifested by a persons inability to remember events related to a specific incident or topic. Patients also differ in durations of RA (how long they cant recall information) and durations of what is forgotten (past time frame for which information is unavailable).

Temporally graded retrograde amnesia
In temporally graded retrograde amnesia, patients eventually recover most memories following the onset of RA. This suggests that the hippocampal formation/ consolidation, the process of coding new information, is only used in systematic consolidation for temporary storage, and short periods of time. Systemic consolidation then moves the information and long-term consolidation takes place in other brain structures. The fact that damage to the hippocampal formation can eventually overcome RA suggests that other brain structures are able to take over the jobs of the malfunctioning regions. RA can also progress and further deteriorate memory recollection, as in the case of Korsakoff syndrome and Alzheimers disease, due to the ongoing nature of the damage caused by the illnesses. The degree to which different patients recover from RA differs in time (some take a few days while others a few decades) and content (some will only remember certain specific instances while others more).

Focal, isolated, and pure retrograde amnesia
Focal isolated, and pure retrograde amnesia are terms used to describe a pure form of RA, with an absence of anterograde amnesia (AA). In addition, Focal RA in particular, has also been used to describe a RA situation in which there is a lack of observable physical deficit as well. This could be described as a psychogenic form of amnesia with mild anterograde and retrograde loss. A case study of DH revealed that the patient was unable to provide personal or public information, however there was no parahippocampal or entorhinal damage found. Individuals with focal brain damage have minimal RA.Isolated RA is associated with a visible thalamic lesion. Consistent with other forms of RA, the isolated form is marked by the inability to recall past information.Pure retrograde amnesia (PRA) refers to the behavioral syndrome that is characterized by the inability to retrieve remote information in the face of a normal ability to learn new information, with no other ecological or psychometric evidence of cognitive impairment. It should not be confused with brief periods of peritraumatic amnesia that are common in mild concussive head traumas. The findings of pure retrograde amnesia have helped form the dissociation between mechanisms for RA and AA. Several studies have found numerous causes for PRA like vascular diseases, head traumas ranging from mild to severe, encephalitis, as well as purely psychological conditions and totally unidentifiable etiologies. Most people who have PRA can function normally and learn new informationA pure form of RA is rare as most cases of RA co-occur with AA. A famous example is that of patient ML. The patients MRI revealed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a band of fibers previously thought to mediate retrieval of specific events from ones personal past.During consolidation, the hippocampus acts as an intermediate tool that quickly stores new information until it is transferred to the neocortex for the long-term. The temporal lobe, which holds the hippocampus, entorhinal, perirhinal and parahippocampal cortices, has a reciprocal connection with the neocortex. The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe.Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of RA. Damage can be limited to the CA1 field of the hippocampus, causing very limited RA for about one to two years. More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years. Another study suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive RA, covering 40 to 50 years. These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.
The common studied causes of RA do not always lead to the onset of RA. It may even be that in some cases both conscious feigning and unconscious processes are at play.

Traumatic brain injury (TBI) or post-traumatic amnesia
Traumatic brain injury (TBI), also known as post-traumatic amnesia, occurs from an external force that causes structural damage to the brain, such as a sharp blow to the head, a diffuse axonal injury, or childhood brain damage (e.g., shaken baby syndrome). In cases of sudden rapid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions.TBI varies according to impact of external forces, location of structural damage, and severity of damage ranging from mild to severe. Retrograde amnesia can be one of the many consequences of brain injury but it is important to note that it is not always the outcome of TBI. An example of a subgroup of people who are often exposed to TBI are individuals who are involved in high-contact sports. Research on football players takes a closer look at some of the implications to their high-contact activities. Enduring consistent head injuries can have an effect on the neural consolidation of memory.Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA. In this specific case there was an onset of isolated RA following a severe head injury. The brain damage did not affect the persons ability to form new memories. Therefore, the idea that specific sections of retrograde memory are independent of anterograde is supported. Normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists.

Traumatic events
RA can occur without any anatomical damage to the brain, lacking an observable neurobiological basis. Primarily referred to as psychogenic amnesia or psychogenic fugue, it often occurs due to a traumatic situation that individuals wish to consciously or unconsciously avoid through intrapsychic conflicts or unconscious repressions. The onset of psychogenic amnesia can be either global (i.e., individual forgets all history) or situation specific (i.e., individual is unable to retrieve memories of specific situations).Patients experiencing psychogenic amnesia have impaired episodic memory, instances of wandering and traveling, and acceptance of a new identity as a result of inaccessible memories pertaining to their previous identity.Recent research has begun to investigate the effects of stress and fear-inducing situations with the onset of RA. Long-term potentiation (LTP) is the process by which there is a signal transmission between neurons after the activation of a neuron, which has been known to play a strong role in the hippocampus in learning and memory. Common changes in the hippocampus have been found to be related to stress and induced LTP. The commonalities support the idea that variations of stress can play a role in producing new memories as well as the onset of RA for other memories. The amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking RA.Studies of specific cases, such as AMN, support evidence  of traumatic experiences as a plausible cause of RA. AMN escaped a small fire in his house, did not inhale any smoke, and had no brain damage. Nevertheless, he was unable to recall autobiographical knowledge the next day. This case shows that RA can occur in the absence of structural brain damage.After a traumatic head injury, emotional disturbances can occur at three different levels: neurological, reactionary, and long-term disturbances. Neurological disturbances can change emotional and motivational responses. Reactionary disturbances effect emotional and motivational responses as well, but reflect the failure to cope with environmental demands. Someone with this might withdraw from the environment that they are placed in because they no longer know how to handle the cognitive resources.

Nutritional deficiency
RA has been found among alcohol-dependent patients who have Korsakoffs syndrome. Korsakoffs syndrome patients develop retrograde amnesia due to a thiamine deficiency (lack of vitamin B1). Also, chronic alcohol use disorders are associated with a decrease in the volume of the left and right hippocampus.These patients regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for typical development and maintenance. Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately develop RA. However, some of the drawbacks of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.

Infections
Infections that pass the blood–brain barrier can cause brain damage (encephalitis), sometimes resulting in the onset of RA. In the case of patient SS, the infection led to focal or isolated retrograde amnesia where there was an absence of or limited AA. Brain scans show abnormalities in the bilateral medial temporal lobes, including two thirds of the hippocampal formation and the posterior part of the amygdala.

Surgery
Henry Molaison had epilepsy that progressed and worsened by his late twenties. The severity of his condition caused him to undergo surgery in an effort to prevent his seizures. Unfortunately, due to a lack of overall known neurological knowledge, Molaisons surgeons removed his bilateral medial temporal lobe, causing profound AA and RA. The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system. HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory.
Patients who have RA due to surgery are "P.B." and "F.C." who had unilateral removal of the medial areas in the left temporal lobe.

Controlled induction
Clinically induced RA has been achieved using different forms of electrical induction.

Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory. Tests show that information from days and weeks before the ECT can be permanently lost. The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation).
Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects. Researchers induce RA in rats, for example, by giving daily ECS treatments. This is done to further understand RA.

Brain structures
The most commonly affected areas are associated with episodic and declarative memory such as the hippocampus, the diencephalon, and the temporal lobes.
The hippocampus deals largely with memory consolidation, where information from the working memory and short-term memory is encoded into long-term storage for future retrieval. Amnesic patients with damage to the hippocampus are able to demonstrate some degree of unimpaired semantic memory, despite a loss of episodic memory, due to spared parahippocampal cortex. In other words, retrograde amnesics "know" about information or skill, but cannot "remember" how they do.
The diencephalon and the surrounding areas role in memory is not well understood. However, this structure appears to be involved in episodic memory recall.
The temporal lobes are essential for semantic and factual memory processing. Aside from helping to consolidate memory with the hippocampus, the temporal lobes are extremely important for semantic memory. Damage to this region of the brain can result in the impaired organization and categorization of verbal material, disturbance of language comprehension, and impaired long-term memory. The right frontal lobe is critical for the retrieval of episodic information, while the left frontal region is more active for the retrieval of semantic information. [56] Lesions in the right hemisphere and right frontal lobes result in the impaired recall of non-verbal material, such as music and drawings. Difficulties in studying this region of the brain extends to its duties in comprehension, naming objects, verbal memory, and other language functions.Brain plasticity has helped explain the recovery process of brain damage induced retrograde amnesia, where neuro-structures use different neural pathways to avoid the damaged areas while still performing their tasks. Thus, the brain can learn to be independent of the impaired hippocampus, but only to a certain extent.
For example, older memories are consolidated over time and in various structures of the brain, including Wernickes area and the neocortex, making retrieval through alternate pathways possible.

Diagnosis
Testing for retrograde amnesia
As previously mentioned, RA can affect peoples memories in different degrees, but testing is required to help determine if someone is experiencing RA. Several tests exist, for example, testing for factual knowledge such as known public events. A problem with this form of testing is that people generally differ in their knowledge of such subjects. The tests also have to be changed regularly to adapt to the period of time patients have been alive, and include questions about autobiographical events that range in amount of detail. Due to the nature of the information being tested, it is often difficult to verify the accuracy of the memories being recalled, especially if they are from a distant past. One way to confirm information is by consulting close family members or caregivers. Another problem that arises is that this type of testing can result in a significant amount of data that needs to be processed and confirmed. Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI). A test that comprises names of relatives, personal information, and job history. The AMI was created by Kopelman, Wilson, and Baddeley (1990).  This information could help  determine if someone is experiencing RA and the degree of memory affected. Some researchers have found that the time interval after the head injury occurred did not seem to matter. The effect of the memory loss was the same no matter how long it had been after from the injury.Brain abnormalities can be measured using magnetic resonance imaging (MRI),  computed tomography scan (CT) and electroencephalography (EEG), which can provide detailed information about specific brain structures. In many cases, an autopsy helps identify the exact brain region affected and the extent of the damage that caused RA once the patient has died.
There are some aspects essential to the patient that remain unaffected by RA. In many patients, their personality remains the same. Also, semantic memory, that is general knowledge about the world, is usually unaffected. However, episodic memory, which refers to ones life experiences, is impaired.Another real life problem with RA is malingering, which is conceived as the rational output of a neurologically normal brain aiming at the surreptitious achievement of a well identified gain. Since it is common for people who have committed a crime to report having RA for that specific event in order to avoid their punishment, the legal system has pushed for the creation of a standardized test of amnesia. However, since most cases differ in onset, duration, and content forgotten, this task has shown to be a rather complex one.

Spontaneous recovery
When someone has RA, their memory cannot be recovered by simply being informed about their personal experiences and their identity. This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information, which cannot reverse RA. Thus, reminding the patient about details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity.

Case studies
Since researchers are interested in examining the effects of disrupted brain areas and conducting experiments for further understanding of an unaffected, normal brain, many individuals with brain damage have volunteered to undergo countless tests to advance our scientific knowledge of the human brain. For example, Henry Molaison (HM) was someone with significant brain damage and participated in a lot of neurological research. Furthermore, he was also the most tested person in neuropsychology. All living people who participate are referred to in literature using only their initials to protect privacy.
Each case of RA has led to different symptoms and durations, where some patients have exhibited an inability to describe future plans, whether in the near future (e.g., this afternoon) or in the distant future (e.g., next summer) because of their inability to consolidate memories. Furthermore, researchers have also found that some patients can identify themselves and loved ones in photographs, but cannot determine the time or place the photo was taken. It has also been found that patients with RA greatly differ from the general population in remembering past events.A few case examples are:

After a head injury, AB had to relearn personal information. Many of ABs habits had also changed.
Patient CD reported disorientation of place and time following his injuries as well as relearning previously learned information and activities (e.g., using a razor).
EF was examined and found to be very confused about social norms (e.g., appropriate attire outside his home). EF exhibited memory loss of his personal experiences (e.g., childhood), and the impaired ability to recognize his wife and parents.
JG is the first recorded patient with isolated RA.
GH, a mother and a wife, had surgery in August 2002. When GH woke up after the surgery, she believed it was May 1989. Due to her amnesia, GH experienced great difficulty in her social environment, being overwhelmed by relationships to others.
DH, a learning disabilities instructor and husband, sustained a closed head injury. He did not show any normal signs of memory loss but he could not recall anything prior to the accident.
CDA is a 20-year-old man who fell and experienced head trauma after being unconscious for a little less than an hour. He had a self-identity loss and a retrograde deficit limited to the autobiographical events 5 years before the trauma. He often showed signs of spontaneous speech that was iterative and sometimes incoherent. When he saw his family and friends, he was shocked at how old they looked because he remembered them from 5 years earlier. This case also included amnesia for procedural skills like the fear of shaving or driving, which ultimately was overcome. There were no psychological, neuropsychological, or brain damage problems. His recovery of memory was progressive and spontaneous, where after several months the amnesia was limited to the two years preceding the trauma. This was a classic case of PRA. [57]
GC was a 38 year old accountant that was found in a town square unable to remember anything about himself and unaware of where he was and how he got there. He was eventually able to recall basic information about himself and his family, but could not recall emotionally charged autobiographical events pertaining to the last 7 years of his life. Within 3–4 days, it was determined that his autobiographical amnesia was clearly and strictly selective for professional events, as he could remember everything that was not related to his job. It was ultimately learned that the job had created severe emotional stress and anxiety due to the extreme hours that triggered a sudden fugue state. He was eventually able to recover most of his memories minus a single work event where he had stolen money from the company. This was a classic case of psychogenic amnesia. [57]
AF is a 15-year-old boy who hit his head and lost consciousness. He could not remember anything but was able to play songs on the piano, showing that his procedural memory was still intact. He gradually recovered some memories within the first 2–3 days but had autobiographical amnesia as well as significant memory loss for famous public facts and events for the 2 years prior to the injury. [57]Although it may seem that people living with brain damage have great difficulty continuing the usual day-to-day aspects, they still can accomplish many feats. People with RA are able to lead a normal life </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Leg and explain in detail? [/INST] A leg is a weight-bearing and locomotive anatomical structure, usually having a columnar shape. During locomotion, legs function as "extensible struts".  The combination of movements at all joints can be modeled as a single, linear element capable of changing length and rotating about an omnidirectional "hip" joint.
As an anatomical animal structure it is used for locomotion. The distal end is often modified to distribute force (such as a foot). Most animals have an even number of legs.
As a component of furniture, it is used for the economy of materials needed to provide the support for the useful surface such as the table top or chair seat.

Terminology
Uniped: 1 leg, such as clams
Biped: 2 legs, such as humans and birds
Triped: 3 legs, which typically does not occur naturally in healthy animals
Quadruped: 4 legs, such as dogs and horsesMany taxa are characterized by the number of legs:

Tetrapods have four legs. Squamates of genus Bipes have only two </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Burkitt lymphoma and explain in detail? [/INST] Burkitt lymphoma is a cancer of the lymphatic system, particularly B lymphocytes found in the germinal center.  It is named after Denis Parsons Burkitt, the Irish surgeon who first described the disease in 1958 while working in equatorial Africa. The overall cure rate for Burkitt lymphoma in developed countries is about 90%, and it is worse in low-income countries. Burkitt lymphoma is uncommon in adults, in whom it has a worse prognosis.

Classification
Burkitt lymphoma can be divided into three main clinical variants: the endemic, the sporadic, and the immunodeficiency-associated variants. By morphology (i.e., microscopic appearance), immunophenotype, and genetics, the variants of Burkitt lymphoma are alike.
The endemic variant (also called "African variant") most commonly occurs in children living in malaria-endemic regions of the world (e.g., equatorial Africa, Brazil, and Papua New Guinea). Epstein–Barr virus (EBV) infection is found in nearly all patients. Chronic malaria is believed to reduce resistance to EBV, allowing it to take hold. The disease characteristically involves the jaw or other facial bone, distal ileum, cecum, ovaries, kidney, or breast.
The sporadic type of Burkitt lymphoma (also known as "non-African") is the most common variant found in places where malaria is not prevalent such as North America and parts of Europe. The tumor cells have a similar appearance to the cancer cells of classical endemic Burkitt lymphoma. Sporadic lymphomas are rarely associated with the EBV. The jaw is less commonly involved in this variant. The abdominal region is the common site of involvement.
Immunodeficiency-associated Burkitt lymphoma is usually associated with HIV infection, but can also occur in the setting of post-transplant patients.Burkitt lymphoma is commonly associated with the infection of B cell lymphocytes with the EBV and in these cases is considered to be one form of the Epstein–Barr virus-associated lymphoproliferative diseases. The endemic variant of Burkitt lymphoma is in almost all cases associated with EBV infection. The fact that some Burkitt lymphoma cases do not involve EBV allows that many cases of the disease are not caused and/or promoted by EBV, i.e. the virus may be an innocent passenger virus in these cases. However, the almost ubiquitous presence of the virus in the endemic variant of Burkitt lymphoma suggests that it contributes to the development and/or progression of this variant. The mutational landscape in Burkitt lymphoma has recently been found to differ between tumors with and without EBV infection, further strengthening the role of the virus in disease origin.

Pathophysiology
Genetics
All types of Burkitt lymphoma are characterized by dysregulation of the c-myc gene by one of three chromosomal translocations. This gene is found at 8q24.

The most common variant is t(8;14)(q24;q32), which accounts for about 85% of cases. This involves c-myc and IGH@. A variant of this, a three-way translocation, t(8;14;18), has also been identified.
A rare variant is at t(2;8)(p12;q24). This involves IGK@ and c-myc.
Another rare variant is t(8;22)(q24;q11). This involves IGL@ and c-myc.Combined, the two less-common translocations, t(2;8)(p12;q24) and t(8;22)(q24;q11), account for the remaining 15% of cases not due to the t(8;14)(q24;q32) translocation.The c-myc gene found on chromosome 8 is part of the Myc family of genes that serve as regulators of cellular transcription and is associated with Burkitt lymphoma. Expression of the c-myc gene results in the synthesis of transcriptional factors that increase the expression of other genes involved in aerobic glycolysis. Ultimately, an increase in aerobic glycolysis plays a role in providing the necessary energy for cellular growth to occur. The translocation of the c-myc gene to the IGH, IGK, or IGL region moves the gene to a location in the genome near immunoglobulin enhancers which increases the expression of the c-myc gene. Overall, this translocation leads to increased cellular proliferation that is found in Burkitt lymphoma. Point mutations can also be present in the translocated c-myc gene resulting in the expressed c-myc protein being overactive. Other mutations found include the TCF transcription factor mutation, which increases cellular proliferation via the increased expression of other genes. Along with mutations that support cell proliferation, Burkitt lymphoma has been found to also harbor mutations in the TP53 gene that is a tumor suppressor and would normally function to limit cellular growth.

Virology
The complete role of EBV in the pathogenesis of endemic Burkitt lymphoma is not completely elucidated, but it has been shown to cause DNA damage, dysfunction of telomeres, and genome instability. B cell infection with EBV is latent, and the virus does not undergo replication. These latently infected B cells can then go on to produce proteins that function to promote cellular growth through modification of normal signaling pathways. EBV promotes the development of malignant B cells via proteins that limit apoptosis in cells that had the c-myc translocation. Apoptosis is limited by EBV through various means such as the EBNA-1 protein, BHF1 protein, EBER transcripts, vIL-10 gene, BZLF1, and LMP1. Malaria has been found to cause genomic instability in endemic Burkitt lymphoma. Malaria can lead to the reactivation of latent EBV and also MYC translocations via activation of the toll-like receptor 9. Malaria also promotes B-cell proliferation by altering the regular immune response. The immune system targets antigens (e.g., EBNA2 and LMP-1) and eliminates most B cells infected with EBV. Downregulation of antigens targeted by the immune system leads to the development of persistent B cells. These B cells can then undergo further mutations (e.g., c-myc translocation) that promote cancer development.

Immunology
Burkitt Lymphoma cells express HLA class I molecules normally, as well as some HLA class II complexes; however, CD4+ T cells are not properly activated. Burkitt lymphoma cells only express EBNA 1, a poorly antigenic EBV-associated antigen, that is able to escape HLA class I presentation, thus evades an immune response. EBNA 1 can be presented via HLA class II molecules, however HLA Class II pathway is unable to activate the CD4+ T cells.

Diagnosis
Malignant B cell characteristics
Normal B cells of a germinal center possess rearranged immunoglobulin heavy and light chain genes, and each isolated B cell possesses a unique IgH gene rearrangement. Since Burkitt lymphoma and other B-cell lymphomas are a clonal proliferative process, all tumor cells from one patient are supposed to possess identical IgH genes. When the DNA of tumor cells is analyzed using electrophoresis, a clonal band can be demonstrated, since identical IgH genes will move to the same position.  On the contrary, when a normal or reactive lymph node is analyzed using the same technique, a smear rather than a distinct band will be seen. This technique is useful since sometimes benign reactive processes (e.g. infectious mononucleosis) and malignant lymphoma can be difficult to distinguish.

Microscopy
The tumor consists of sheets of a monotonous (i.e., similar in size and morphology) population of medium-sized lymphoid cells with high proliferative and apoptotic activity.  The "starry sky" appearance seen under low power is due to scattered tingible body-laden macrophages (macrophages containing dead apoptotic tumor cells). The old descriptive term of "small non-cleaved cell" is misleading. The tumor cells are mostly medium in size (i.e., tumor nuclei size similar to that of histiocytes or endothelial cells). "Small non-cleaved cells" are compared to "large non-cleaved cells" of normal germinal center lymphocytes. Tumor cells possess small amounts of basophilic cytoplasm with three to four small nucleoli. The cellular outline usually appears squared off.

Immunohistochemistry
The tumor cells in Burkitt lymphoma generally strongly express markers of B cell differentiation (CD20, CD22, CD19), as well as CD10 and BCL6.  The tumor cells are generally negative for BCL2 and TdT.  The high mitotic activity of Burkitt lymphoma is confirmed by nearly 100% of the cells staining positive for Ki67.

Treatment
In general, the first line of treatment for Burkitt lymphoma is chemotherapy. A few of these regimens are: the GMALL-B-ALL/NHL2002 protocol, the modified Magrath regimen (R-CODOX-M/IVAC). COPADM, hyper-CVAD, and the Cancer and Leukemia Group B (CALGB) 8811 regimen; these can be associated with rituximab. In older patients, treatment may be dose-adjusted EPOCH with rituximab.The effects of the chemotherapy, as with all cancers, depend on the time of diagnosis. With faster-growing cancers, such as Burkitt, the cancer actually responds faster than with slower-growing cancers. This rapid response to chemotherapy can be hazardous to the patient, as a phenomenon called "tumor lysis syndrome" could occur. Close monitoring of the patient and adequate hydration is essential during the process. Since Burkitt lymphoma has high propensity to spread to the central nervous system (lymphomatous meningitis), intrathecal chemotherapy with methotrexate and/or ARA-C and/or prednisolone is given along with systemic chemotherapy.Chemotherapy

cyclophosphamide
doxorubicin
vincristine
methotrexate
cytarabine
ifosfamide
etoposide
rituximabOther treatments for Burkitt lymphoma include immunotherapy, bone marrow transplants, stem cell transplant, surgery to remove the tumor, and radiotherapy.

Prognosis
The prognosis for Burkitt lymphoma is superior in children and increased age is a negative prognostic indicator.
The overall cure rate for sporadic Burkitt lymphoma in developed countries is about 90%. In adults, Burkitt lymphoma is uncommon and has poor outcomes. Unsatisfactory initial response to the treatment of Burkitt lymphoma with cyclophosphamide, vincristine, and prednisolone indicates a negative prognosis. Furthermore, failed initial treatment and return of Burkitt lymphoma after a six-month stint of time serve as a poor prognostic indicator. The adequate utilization of therapeutic drugs during initial treatment limits additional treatment options following the return of the disease. Notably, in areas of the world where the initial treatment of Burkitt lymphoma is inadequate further treatment options may remain for cases when the disease returns. Laboratory studies such as lactate dehydrogenase (LDH), CD4 count, and other cytogenetic studies are also prognostic indicators. Unsatisfactory outcomes have been associated with an LDH that is found to be two times above the upper limit of normal. Specifically, there is a poor prognosis associated with a CD4 count that is decreased in the immunodeficiency-associated variant of Burkitt lymphoma. Genetic mutations extending beyond the previously described MYC translocation may also serve as negative prognostic indicators. Some notable genetic findings that may be associated with poor outcomes include: 13q deletion, 7q gain, ID3 and CCND3 double-hit mutations, and 18q21 CN-LOH mutations. The prognosis for Burkitt lymphoma can be better determined following staging utilizing imaging modalities such as positron emission tomography and computed tomography scans where tumor burden and invasion of the central nervous system have been found to indicate a poor prognosis.

Epidemiology
As a non-Hodgkin lymphoma (NHL), Burkitt lymphoma makes up 1-5% of cases, and it is more common in males than females with a 3–4 to 1 ratio. The endemic variant mainly impacts areas with an increased prevalence of malaria and EBV in Africa and Papua New Guinea. For children less than 18 years of age from equatorial Africa, the annual incidence of Burkitt lymphoma is 4–5/100,000. Additionally, in equatorial Africa, 50% of tumors that are diagnosed during childhood as well as 90% of lymphoma cases can be attributed to Burkitt lymphoma. The peak incidence for endemic Burkitt lymphoma is from ages 4 to 7 with an average age of 6 years </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Interstitial nephritis and explain in detail? [/INST] Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of the kidney known as the renal interstitium, which consists of a collection of cells, extracellular matrix, and fluid surrounding the renal tubules. In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney.There are a variety of known factors that can provoke the inflammatory process within the renal interstitium, including pharmacologic, environmental, infectious and systemic disease contributors. The spectrum of disease presentation can range from an acute process to a chronic condition with progressive tubular cell damage and renal dysfunction.

Signs and symptoms
Interstitial nephritis may present with a variety of signs and symptoms, many of these nonspecific. Fever is the most common, occurring in 30-50% of patients, particularly those with drug-induced interstitial nephritis. Other general symptoms that occur with variable frequency include nausea, vomiting, fatigue, lack of appetite, and weight loss. More specific symptoms, such as flank pain, pain with urination, and visible blood in the urine, as well as signs like hypertension can be helpful in increasing suspicion for the diagnosis. The "classic" triad of symptoms reported in early documented cases consisted of rash, joint pain, and increased eosinophils in the blood; however, more recent epidemiology suggests that this grouping of symptoms only occurs in a small minority (5-10%) of patients.  With modern drugs causing between 70 and 90% of current cases, the possibility of a change in presentation exists.

Causes
Common causes include infection, or reaction to medication such as an analgesic, anti-inflammatory, or antibiotics such as methicillin (meticillin). Reaction to medications causes 71% to 92% of cases.

Drugs
This disease is also caused by other diseases and toxins that damage the kidney. Both acute and chronic tubulointerstitial nephritis can be caused by a bacterial infection in the kidneys known as pyelonephritis, but the most common cause is by an adverse reaction to a medication. The medications that are known to cause this sort of reaction are β-lactam antibiotics such as penicillin
and cephalexin, and nonsteroidal anti-inflammatory drugs (aspirin less frequently than others), as well as proton-pump inhibitors, rifampicin, sulfa medications, fluoroquinolones, diuretics, allopurinol, mesalamine, and phenytoin.  The time between exposure to the drug and the development of acute tubulointerstitial nephritis can be anywhere from 5 days to 5 months (fenoprofen-induced).

Diagnosis
The condition can appear without symptoms. When present they may appear widely varied and can occur rapidly or gradually.When caused by an allergic reaction, the symptoms of acute tubulointerstitial nephritis are fever (27% of patients), rash (15% of patients), and enlarged kidneys.  Some people experience dysuria, and lower back pain.
In chronic tubulointerstitial nephritis the patient can experience symptoms such as nausea, vomiting, fatigue, and weight loss.  Other conditions that may develop include a high concentration of potassium in the blood, metabolic acidosis, and kidney failure.

Blood tests
About 23% of patients have a high level of eosinophils in the blood.

Urinary findings
Urinary findings include:

Eosinophiluria: Original studies with Methicillin-induced AIN showed sensitivity of 67% and specificity of 83%. The sensitivity is higher in patients with interstitial nephritis induced by methicillin or when the Hansels stain is used. However, a 2013 study showed that the sensitivity and specificity of urine eosinophil testing are 35.6% and 68% respectively.
Isosthenuria
Blood in the urine and occasional RBC casts
Sterile pyuria: white blood cells and no bacteria. About 50% of patients with AIN have pyuria.
Nephrotic-range amount of protein in the urine may be seen with NSAID-associated AIN. Low grade proteinuria may be seen in a majority of other causes of AIN.
White blood cell (WBC) casts: Fewer than one in five patients with AIN have WBC casts in urine.

Pathology
While non-invasive patient evaluation (physical examination, blood and urine testing, imaging studies) can be suggestive, the only way to definitively diagnosis interstitial nephritis is with a tissue diagnosis obtained by kidney biopsy. Pathologic examination will reveal the presence of interstitial edema and inflammatory infiltration with various white blood cells, including neutrophils, eosinophils, and lymphocytes. Generally, blood vessels and glomeruli are not affected. Electron microscopy shows mitochondrial damage in the tubular epithelial cells, vacuoles in the cytoplasm, and enlarged endoplasmic reticulum.

Gallium scan
The sensitivity of an abnormal gallium scan has been reported to range from 60% to 100%. A study of Gallium scan in 76 patients [23 with AIN, 8 with biopsy-proven AIN] showed an AUC of 0.75.

Novel biomarkers
Given the challenges with clinical diagnosis of AIN due to lack of clinical features and lack of accuracy of existing tests, there has been significant interest in identifying non-invasive biomarkers for this disease. One study showed that monocyte chemotactic protein-1 (chemokine CCL-2) and neutrophil gelatinase associated lipocalin (NGAL) were higher in patients with AIN than in controls (in this case healthy participants). A more recent study, showed that urine cytokines interleukin-9 and tumor necrosis factor-α were higher in patients with AIN than in controls without AIN who underwent a biopsy for evaluation of acute kidney injury and showed an AUC of 0.79 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Abnormal posturing and explain in detail? [/INST] Abnormal posturing is an involuntary flexion or extension of the arms and legs, indicating severe brain injury. It occurs when one set of muscles becomes incapacitated while the opposing set is not, and an external stimulus such as pain causes the working set of muscles to contract. The posturing may also occur without a stimulus. Since posturing is an important indicator of the amount of damage that has occurred to the brain, it is used by medical professionals to measure the severity of a coma with the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants).
The presence of abnormal posturing indicates a severe medical emergency requiring immediate medical attention. Decerebrate and decorticate posturing are strongly associated with poor outcome in a variety of conditions. For example, near-drowning patients that display decerebrate or decorticate posturing have worse outcomes than those that do not. Changes in the condition of the patient may cause alternation between different types of posturing.

Types
Three types of abnormal posturing are decorticate posturing, with the arms flexed over the chest; decerebrate posturing, with the arms extended at the sides; and opisthotonus, in which the head and back are arched backward.

Decorticate
Decorticate posturing is also called decorticate response, decorticate rigidity, flexor posturing, or, colloquially, "mummy baby". Patients with decorticate posturing present with the arms flexed, or bent inward on the chest, the hands are clenched into fists, and the legs extended and feet turned inward. A person displaying decorticate posturing in response to pain gets a score of three in the motor section of the Glasgow Coma Scale, caused by the flexion of muscles due to the neuro-muscular response to the trauma.There are two parts to decorticate posturing.

The first is the disinhibition of the red nucleus with facilitation of the rubrospinal tract. The rubrospinal tract facilitates motor neurons in the cervical spinal cord supplying the flexor muscles of the upper extremities. The rubrospinal tract and medullary reticulospinal tract biased flexion outweighs the medial and lateral vestibulospinal and pontine reticulospinal tract biased extension in the upper extremities.
The second component of decorticate posturing is the disruption of the lateral corticospinal tract which facilitates motor neurons in the lower spinal cord supplying flexor muscles of the lower extremities. Since the corticospinal tract is interrupted, the pontine reticulospinal and the medial and lateral vestibulospinal biased extension tracts greatly overwhelm the medullary reticulospinal biased flexion tract.The effects on these two tracts (corticospinal and rubrospinal) by lesions above the red nucleus is what leads to the characteristic flexion posturing of the upper extremities and extensor posturing of the lower extremities.Decorticate posturing indicates that there may be damage to areas including the cerebral hemispheres, the internal capsule, and the thalamus. It may also indicate damage to the midbrain. While decorticate posturing is still an ominous sign of severe brain damage, decerebrate posturing is usually indicative of more severe damage at the rubrospinal tract, and hence, the red nucleus is also involved, indicating a lesion lower in the brainstem.

Decerebrate
Decerebrate posturing is also called decerebrate response, decerebrate rigidity, or extensor posturing. It describes the involuntary extension of the upper extremities in response to external stimuli. In decerebrate posturing, the head is arched back, the arms are extended by the sides, and the legs are extended. A hallmark of decerebrate posturing is extended elbows. The arms and legs are extended and rotated internally. The patient is rigid, with the teeth clenched. The signs can be present on only one side of the body or on both sides, and they may be present just in the arms, and they may be intermittent.A person displaying decerebrate posturing in response to pain receives a score of two in the motor section of the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants), due to the muscles extending because of the neuro-muscular response to the trauma.Decerebrate posturing indicates brain stem damage, specifically damage below the level of the red nucleus (e.g. mid-collicular lesion). It is exhibited by people with lesions or compression in the midbrain and lesions in the cerebellum. Decerebrate posturing is commonly seen in pontine strokes. A patient with decorticate posturing may begin to show decerebrate posturing, or may go from one form of posturing to the other </s>