<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sickle cell trait and can you explain it in depth? [/INST] Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene (is heterozygous), but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele (is homozygous). Those who are heterozygous for the sickle cell allele produce both normal and abnormal hemoglobin (the two alleles are codominant with respect to the actual concentration of hemoglobin in the circulating cells).
Sickle cell disease is a blood disorder wherein there is a single amino acid substitution in the hemoglobin protein of the red blood cells, which causes these cells to assume a sickle shape, especially when under low oxygen tension. Sickling and sickle cell disease also confer some resistance to malaria parasitization of red blood cells, so that individuals with sickle-cell trait (heterozygotes) have a selective advantage in environments where malaria is present.

Symptoms and signs
Sickle cell trait is a hemoglobin genotype AS and is generally regarded as a benign condition. However, individuals with sickle cell trait may have rare complications. For example, in November 2010, Dr. Jeffery K. Taubenberger of the National Institutes of Health discovered the earliest proof of sickle-cell disease while looking for the virus of the 1918 flu during the autopsy of an African-American soldier.  Taubenbergers autopsy results showed that the soldier had had a sickle-cell crisis that contributed to his death even though he had only one copy of the gene. There have been calls to reclassify sickle cell trait as a disease state, based on its malignant clinical presentations. Significance may be greater during exercise.

Association with other medical conditions
Malaria
The sickle cell trait provides a survival advantage against malaria fatality over people with normal hemoglobin in regions where malaria is endemic. The trait is known to cause significantly fewer deaths due to malaria, especially when Plasmodium falciparum is the causative organism. This is a prime example of natural selection, evidenced by the fact that the geographical distribution of the gene for hemoglobin S and the distribution of malaria in Africa virtually overlap. Because of the unique survival advantage, people with the trait become increasingly numerous as the number of malaria-infected people increases. Conversely, people who have normal hemoglobin tend to succumb to the complications of malaria.The way in which sickle cell protects against malaria is attributed to several different things. One of the more common explanations is that the sickle hemoglobin inhibits the plasmodium parasite from infecting the red blood cells which reduces the number of malaria parasites to infect the host. Another factor is the production of heme oxygenase-1 (HO-1) enzyme, which is highly present in the sickle hemoglobin. This enzyme produces carbon monoxide which has been proven to protect against cerebral malaria.

Established associations
Hematuria
Hyposthenuria
Renal medullary carcinoma, a cancer affecting the kidney, is a very rare complication seen in patients with sickle cell trait.
Renal papillary necrosis (only considered "possible" by some sources)
Splenic infarcts at high altitude. Surgery may not always be necessary.
Sudden deaths during physical exertion in African-American US army recruits, and athletes
Urinary tract infection

Suggested
Probable: complicated hyphema, venous thromboembolic events, fetal loss, neonatal deaths, and preeclampsia
Possible: acute chest syndrome, asymptomatic bacteriuria, and anemia in pregnancy
Insufficient evidence: retinopathy, cholelithiasis, priapism, leg ulcers, liver necrosis, avascular necrosis of the femoral head, and stroke. An association with complicated migraines has been suggested.There have been reports of pulmonary venous thromboembolism in pregnant women with sickle cell trait, or men during prolonged airflight, and mild strokes and abnormalities on PET scans in children with the trait.Sickle cell trait appears to worsen the complications seen in diabetes mellitus type 2 (retinopathy, nephropathy and proteinuria) and provoke hyperosmolar diabetic coma nephropathy, especially in male patients.

Genetics
Normally, a person inherits two copies of the gene that produces beta-globin, a protein needed to produce normal hemoglobin (hemoglobin A, genotype AA). A person with sickle cell trait inherits one normal allele and one abnormal allele encoding hemoglobin S (hemoglobin genotype AS).The sickle cell trait can be used to demonstrate the concepts of co-dominance and incomplete dominance. An individual with the sickle cell trait shows incomplete dominance when the shape of the red blood cell is considered. This is because the sickling happens only at low oxygen concentrations. With regards to the actual concentration of hemoglobin in the circulating cells, the alleles demonstrate co-dominance as both normal and mutant forms co-exist in the bloodstream. Thus it is an ambiguous condition showing both incomplete dominance and co-dominance.Unlike the sickle-cell trait, sickle-cell disease is passed on in a recessive manner. Sickle cell anemia affects about 72,000 people in the United States. Most Americans who have sickle cell anemia are of African descent. The disease also affects Americans from the Caribbean, Central America, and parts of South America, Turkey, Greece, Italy, the Middle East and East India.
Sickle-cell disease and the associated trait are most prevalent in Africa and Central America, which is attributed to natural selection:  the sickle-cell trait confers a survival advantage in areas with a high occurrence of malaria, which has a high death rate among individuals without the trait.There also have been studies that show changes in the globin genes. There have been noted changes in the beta-globin sequence, to what is known as the sickle hemoglobin.
The significance of the sickle-cell trait is that it does not show any symptoms, nor does it cause any major difference in blood cell count. The trait confers about 30% protection against malaria and its occurrence appears to have risen tremendously in Africa, India and the Middle East. Some findings also show the reduction of the sickle-cell trait in those who retain much more fetal hemoglobin than usual in adulthood. Fetal hemoglobin likely plays a role in the prevention of sickling. Elevated fetal hemoglobin levels have been observed in populations where sickle-cell disease is prevalent.
Whole genome sequence analysis has identified a single origin of the sickle trait, with one haplotype ancestral to all sickle-cell variants. This haplotype is thought to have originated in the Sahara during the Holocene Wet Phase around 7,300 years ago. Sickle cell variants descended from this ancestral haplotype comprise five haplotypes named after toponyms or ethnolinguistic groups (the Arabian/Indian, Benin, Cameroon, Central African Republic/Bantu, and Senegal variants), and another designation earmarked for atypical sickle-cell haplotypes. Their clinical importance is because some are associated with higher HbF levels (e.g., Senegal and Saudi-Asian variants tend to have milder disease).

In athletes
In some cases, athletes with sickle cell trait do not achieve the same level of performance as elite athletes with normal hemoglobin (AA). Athletes with sickle cell trait and their instructors must be aware of the dangers of the condition during anaerobic exertion especially in hot and dehydrated conditions. In rare cases, exercise-induced dehydration or exhaustion may cause healthy red blood cells to turn sickle-shaped, which can cause death during sporting activities.While more research is necessary on the topic, the correlation found between individuals with sickle cell trait and an increased risk of sudden death appears to be related to microcirculatory disorders, during exercise. In recent years the NCAA has partnered with the ACSM and issued a joint statement, warning athletes about both the prevalence and the potential risk factors of sickle cell trait.  The NCAA has also recently encouraged athletes to become aware of their sickle cell trait status, as the trait itself does not typically result in symptoms under normal conditions but can become dangerous during extreme physical activity similar to the daily training that athletes undergo.Normal hemoglobin (and hemoglobin S in the presence of oxygen) contains a deformability characteristic that allows erythrocytes to essentially squeeze their way into smaller vessels, including those involved in microcirculation to the capillaries within muscle tissue as well as blood supply embedded within organ tissues.  When hemoglobin S is deprived of oxygen, it can polymerize, which is what is proposed to cause the "sickled" cells. The sickled erythrocytes present a decreased deformability when compared to normal erythrocytes, leading to distress in circulation into the smaller vessels involved in microcirculation, particularly, in this case, the capillaries embedded in muscle tissue.The resulting microvasculatory distress in capillaries specific to muscle tissue can cause acute rhabdomyolysis and necrosis within the muscle cells. The inflammation and leakage of intracellular material resulting from muscle cell necrosis releases a particular protein, myoglobin, into the blood stream </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Mydriasis and can you explain it in depth? [/INST] Mydriasis is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of certain types of drugs.
Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.
Fixed, unilateral mydriasis could be a symptom of raised intracranial pressure. The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other.

Causes
There are two types of muscle that control the size of the iris: the iris sphincter, composed of circularly arranged muscle fibers, and the iris dilator, composed of radially arranged muscle fibers. The sphincter is controlled by nerves of the parasympathetic nervous system, and the dilator by the sympathetic nervous system. Sympathetic stimulation of the adrenergic receptors causes the  contraction of the radial muscle and subsequent dilation of the pupil. Conversely, parasympathetic stimulation causes contraction of the circular muscle and constriction of the pupil.
The mechanism of mydriasis depends on the agent being used. It usually involves either a disruption of the parasympathetic nerve supply to the eye (which normally constricts the pupil) or overactivity of the sympathetic nervous system (SNS).

Pupil diameter also increases in reaction to cognitive tasks requiring memory and attention, and this phenomenon is used as an indicator of mental activation (‘arousal’) in psychophysiological experiments.

Drugs
A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horners syndrome.
Mydriasis can be induced via modulation of adrenergic or cholinergic signalling.
Drugs that can cause mydriasis include:

Stimulants (typically monoaminergics) such as amphetamines, cocaine, MDMA, and mephedrone.
Anticholinergics such as diphenhydramine, atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hurler–Scheie syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Rabies and can you explain it in depth? [/INST] Rabies is a viral disease that causes encephalitis in humans and other mammals. Early symptoms can include fever and tingling at the site of exposure. These symptoms are followed by one or more of the following symptoms: nausea, vomiting, violent movements, uncontrolled excitement, fear of water, an inability to move parts of the body, confusion, and loss of consciousness. Once symptoms appear, the result is virtually always death, regardless of treatment. The time period between contracting the disease and the start of symptoms is usually one to three months but can vary from less than one week to more than one year. The time depends on the distance the virus must travel along peripheral nerves to reach the central nervous system.Rabies is caused by lyssaviruses, including the rabies virus and Australian bat lyssavirus. It is spread when an infected animal bites or scratches a human or other animals. Saliva from an infected animal can also transmit rabies if the saliva comes into contact with the eyes, mouth, or nose. Globally, dogs are the most common animal involved.  In countries where dogs commonly have the disease, more than 99% of rabies cases are the direct result of dog bites. In the Americas, bat bites are the most common source of rabies infections in humans, and less than 5% of cases are from dogs. Rodents are very rarely infected with rabies. The disease can be diagnosed only after the start of symptoms.Animal control and vaccination programs have decreased the risk of rabies from dogs in a number of regions of the world. Immunizing people before they are exposed is recommended for those at high risk, including those who work with bats or who spend prolonged periods in areas of the world where rabies is common. In people who have been exposed to rabies, the rabies vaccine and sometimes rabies immunoglobulin are effective in preventing the disease if the person receives the treatment before the start of rabies symptoms. Washing bites and scratches for 15 minutes with soap and water, povidone-iodine, or detergent may reduce the number of viral particles and may be somewhat effective at preventing transmission. As of 2016, only fourteen people were documented to have survived a rabies infection after showing symptoms. However, research conducted in 2010 among a population of people in Perú with a self-reported history of one or more bites from vampire bats (commonly infected with rabies), found that out of 73 individuals reporting previous bat bites, 7 people had rabies virus-neutralizing antibodies (rVNA). Since only one member of this group reported prior vaccination for rabies, the findings of the research suggest previously undocumented cases of infection and viral replication followed by an abortive infection. This could indicate that in rare cases people may have an exposure to the virus without treatment and develop natural antibodies as a result.
Rabies causes about 59,000 deaths worldwide per year, about 40% of which are in children under the age of 15.  More than 95% of human deaths from rabies occur in Africa and Asia.Rabies is present in more than 150 countries and on all continents but Antarctica. More than 3 billion people live in regions of the world where rabies occurs. A number of countries, including Australia and Japan, as well as much of Western Europe, do not have rabies among dogs. Many Pacific islands do not have rabies at all. It is classified as a neglected tropical disease.

Etymology
The name rabies is derived from the Latin rabies, "madness". This, in turn, may be related to the Sanskrit rabhas, "to rage". The Greeks derived the word lyssa, from lud or "violent"; this root is used in the genus name of the rabies virus, Lyssavirus.

Signs and symptoms
The period between infection and the first symptoms (incubation period) is typically 1–3 months in humans. This period may be as short as four days or longer than six years, depending on the location and severity of the wound and the amount of virus introduced. Initial symptoms of rabies are often nonspecific such as fever and headache. As rabies progresses and causes inflammation of the brain and meninges, symptoms can include slight or partial paralysis, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, terror, and hallucinations. The person may also have fear of water.The symptoms eventually progress to delirium, and coma. Death usually occurs 2 to 10 days after first symptoms. Survival is almost unknown once symptoms have presented, even with intensive care.Rabies has also occasionally been referred to as hydrophobia ("fear of water") throughout its history. It refers to a set of symptoms in the later stages of an infection in which the person has difficulty swallowing, shows panic when presented with liquids to drink, and cannot quench their thirst. Any mammal infected with the virus may demonstrate hydrophobia. Saliva production is greatly increased, and attempts to drink, or even the intention or suggestion of drinking, may cause excruciatingly painful spasms of the muscles in the throat and larynx. Since the infected individual cannot swallow saliva and water, the virus has a much higher chance of being transmitted, because it multiplies and accumulates in the salivary glands and is transmitted through biting. Hydrophobia is commonly associated with furious rabies, which affects 80% of rabies-infected people. The remaining 20% may experience a paralytic form of rabies that is marked by muscle weakness, loss of sensation, and paralysis; this form of rabies does not usually cause fear of water.

Cause
Rabies is caused by a number of lyssaviruses including the rabies virus and Australian bat lyssavirus. Duvenhage lyssavirus may cause a rabies-like infection.The rabies virus is the type species of the Lyssavirus genus, in the family Rhabdoviridae, order Mononegavirales. Lyssavirions have helical symmetry, with a length of about 180 nm and a cross-section of about 75 nm. These virions are enveloped and have a single-stranded RNA genome with negative sense. The genetic information is packed as a ribonucleoprotein complex in which RNA is tightly bound by the viral nucleoprotein. The RNA genome of the virus encodes five genes whose order is highly conserved: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and the viral RNA polymerase (L).To enter cells, trimeric spikes on the exterior of the membrane of the virus interact with a specific cell receptor, the most likely one being the acetylcholine receptor. The cellular membrane pinches in a procession known as pinocytosis and allows entry of the virus into the cell by way of an endosome. The virus then uses the acidic environment, which is necessary, of that endosome and binds to its membrane simultaneously, releasing its five proteins and single-strand RNA into the cytoplasm.Once within a muscle or nerve cell, the virus undergoes replication. The L protein then transcribes five mRNA strands and a positive strand of RNA all from the original negative strand RNA using free nucleotides in the cytoplasm. These five mRNA strands are then translated into their corresponding proteins (P, L, N, G and M proteins) at free ribosomes in the cytoplasm. Some proteins require post-translative modifications. For example, the G protein travels through the rough endoplasmic reticulum, where it undergoes further folding, and is then transported to the Golgi apparatus, where a sugar group is added to it (glycosylation).When there are enough viral proteins, the viral polymerase will begin to synthesize new negative strands of RNA from the template of the positive-strand RNA. These negative strands will then form complexes with the N, P, L and M proteins and then travel to the inner membrane of the cell, where a G protein has embedded itself in the membrane. The G protein then coils around the N-P-L-M complex of proteins taking some of the host cell membrane with it, which will form the new outer envelope of the virus particle. The virus then buds from the cell.From the point of entry, the virus is neurotropic, traveling along the neural pathways into the central nervous system. The virus usually first infects muscle cells close to the site of infection, where they are able to replicate without being noticed by the hosts immune system. Once enough virus has been replicated, they begin to bind to acetylcholine receptors at the neuromuscular junction. The virus then travels through the nerve cell axon via retrograde transport, as its P protein interacts with dynein, a protein present in the cytoplasm of nerve cells. Once the virus reaches the cell body it travels rapidly to the central nervous system (CNS), replicating in motor neurons and eventually reaching the brain. After the brain is infected, the virus travels centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the salivary glands, where it is ready to be transmitted to the next host.: 317

Transmission
All warm-blooded species, including humans, may become infected with the rabies virus and develop symptoms. Birds were first artificially infected with rabies in 1884; however, infected birds are largely, if not wholly, asymptomatic, and recover. Other bird species have been known to develop rabies antibodies, a sign of infection, after feeding on rabies-infected mammals.The virus has also adapted to grow in cells of cold-blooded vertebrates. Most animals can be infected by the virus and can transmit the disease to humans. Worldwide, about 99% of human rabies cases come from domestic dogs. Other sources of rabies in humans include bats, monkeys, raccoons, foxes, skunks, cattle, wolves, coyotes, cats, and mongooses (normally either the small Asian mongoose or the yellow mongoose).Rabies may also spread through exposure to infected bears, domestic farm animals, groundhogs, weasels, and other wild carnivorans. However, lagomorphs, such as hares and rabbits, and small rodents, such as chipmunks, gerbils, guinea pigs, hamsters, mice, rats, and squirrels, are almost never found to be infected with rabies and are not known to transmit rabies to humans. Bites from mice, rats, or squirrels rarely require rabies prevention because these rodents are typically killed by any encounter with a larger, rabid animal, and would, therefore, not be carriers. The Virginia opossum (a marsupial, unlike the other mammals named in this paragraph, which are all eutherians/placental), has a lower internal body temperature than the rabies virus prefers and therefore is resistant but not immune to rabies.  Marsupials, along with monotremes (platypuses and echidnas), typically have lower body temperatures than similarly sized eutherians.The virus is usually present in the nerves and saliva of a symptomatic rabid animal. The route of infection is usually, but not always, by a bite. In many cases, the infected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise uncharacteristic behavior. This is an example of a viral pathogen modifying the behavior of its host to facilitate its transmission to other hosts. After a typical human infection by bite, the virus enters the peripheral nervous system. It then travels retrograde along the efferent nerves toward the central nervous system. During this phase, the virus cannot be easily detected within the host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. When the virus reaches the brain, it rapidly causes encephalitis, the prodromal phase, which is the beginning of the symptoms. Once the patient becomes symptomatic, treatment is almost never effective and mortality is over 99%. Rabies may also inflame the spinal cord, producing transverse myelitis.Although it is theoretically possible for rabies-infected humans to transmit it to others by biting or otherwise, no such cases have ever been documented, because infected humans are usually hospitalized and necessary precautions taken. Casual contact, such as touching a person with rabies or contact with non-infectious fluid or tissue (urine, blood, feces), does not constitute an exposure and does not require post-exposure prophylaxis. But as the virus is present in sperm and vaginal secretions, it might be possible for rabies to spread through sex. There are only a handful of recorded cases of human-to-human transmission of rabies, and all occurred through organ transplants from infected donors.

Diagnosis
Rabies can be difficult to diagnose because, in the early stages, it is easily confused with other diseases or even with a simple aggressive temperament. The  reference method for diagnosing rabies is the fluorescent antibody test (FAT),  an immunohistochemistry procedure, which is recommended by the World Health Organization (WHO). The FAT relies on the ability of a detector molecule (usually fluorescein isothiocyanate) coupled with a rabies-specific antibody, forming a conjugate, to bind to and allow the visualisation of rabies antigen using fluorescent microscopy techniques. Microscopic analysis of samples is the only direct method that allows for the identification of rabies virus-specific antigen in a short time and at a reduced cost, irrespective of geographical origin and status of the host. It has to be regarded as the first step in diagnostic procedures for all laboratories. Autolysed samples can, however, reduce the sensitivity and specificity of the FAT. The RT PCR assays proved to be a sensitive and specific tool for routine diagnostic purposes, particularly in decomposed samples or archival specimens. The diagnosis can be reliably made from brain samples taken after death. The diagnosis can also be made from saliva, urine, and cerebrospinal fluid samples, but this is not as sensitive or reliable as brain samples. Cerebral inclusion bodies called Negri bodies are 100% diagnostic for rabies infection but are found in only about 80% of cases. If possible, the animal from which the bite was received should also be examined for rabies.Some light microscopy techniques may also be used to diagnose rabies at a tenth of the cost of traditional fluorescence microscopy techniques, allowing identification of the disease in less-developed countries. A test for rabies, known as LN34, is easier to run on a dead animals brain and might help determine who does and does not need post-exposure prevention. The test was developed by the CDC in 2018.The differential diagnosis in a case of suspected human rabies may initially include any cause of encephalitis, in particular infection with viruses such as herpesviruses, enteroviruses, and arboviruses such as West Nile virus. The most important viruses to rule out are herpes simplex virus type one, varicella zoster virus, and (less commonly) enteroviruses, including coxsackieviruses, echoviruses, polioviruses, and human enteroviruses 68 to 71.New causes of viral encephalitis are also possible, as was evidenced by the 1999 outbreak in Malaysia of 300 cases of encephalitis with a mortality rate of 40% caused by Nipah virus, a newly recognized paramyxovirus. Likewise, well-known viruses may be introduced into new locales, as is illustrated by the outbreak of encephalitis due to West Nile virus in the eastern United States.

Prevention
Almost all human exposure to rabies was fatal until a vaccine was developed in 1885 by Louis Pasteur and Émile Roux. Their original vaccine was harvested from infected rabbits, from which the virus in the nerve tissue was weakened by allowing it to dry for five to ten days. Similar nerve tissue-derived vaccines are still used in some countries, as they are much cheaper than modern cell culture vaccines.
The human diploid cell rabies vaccine was started in 1967. Less expensive purified chicken embryo cell vaccine and purified vero cell rabies vaccine are now available. A recombinant vaccine called V-RG has been used in Belgium, France, Germany, and the United States to prevent outbreaks of rabies in undomesticated animals. Immunization before exposure has been used in both human and nonhuman populations, where, as in many jurisdictions, domesticated animals are required to be vaccinated. The Missouri Department of Health and Senior Services Communicable Disease Surveillance 2007 Annual Report states the following can help reduce the risk of contracting rabies:Vaccinating dogs, cats, and ferrets against rabies
Keeping pets under supervision
Not handling wild animals or strays
Contacting an animal control officer upon observing a wild animal or a stray, especially if the animal is acting strangely
If bitten by an animal, washing the wound with soap and water for 10 to 15 minutes and contacting a healthcare provider to determine if post-exposure prophylaxis is required28 September is World Rabies Day, which promotes the information, prevention, and elimination of the disease.In Asia and in parts of the Americas and Africa, dogs remain the principal host. Mandatory vaccination of animals is less effective in rural areas. Especially in developing countries, pets may not be privately kept and their destruction may be unacceptable. Oral vaccines can be safely distributed in baits, a practice that has successfully reduced rabies in rural areas of Canada, France, and the United States. In Montreal, Quebec, Canada, baits are successfully used on raccoons in the Mount-Royal Park area. Vaccination campaigns may be expensive, but cost-benefit analysis suggests baits may be a cost-effective method of control. In Ontario, a dramatic drop in rabies was recorded when an aerial bait-vaccination campaign was launched.The number of recorded human deaths from rabies in the United States has dropped from 100 or more annually in the early 20th century to one or two per year due to widespread vaccination of domestic dogs and cats and the development of human vaccines and immunoglobulin treatments. Most deaths now result from bat bites, which may go unnoticed by the victim and hence untreated.

Treatment
After exposure
Treatment after exposure can prevent the disease if given within 10 days. The rabies vaccine is 100% effective if given early, and still has a chance of success if delivery is delayed. Every year, more than 15 million people get vaccinated after potential exposure. While this works well, the cost is significant. In the US it is recommended people receive one dose of human rabies immunoglobulin (HRIG) and four doses of rabies vaccine over a 14-day period. HRIG is expensive and makes up most of the cost of post-exposure treatment, ranging as high as several thousand dollars. In the UK, one dose of HRIG costs the National Health Service £1,000, although this is not flagged as a "high-cost medication". A full course of vaccine costs £120–180. As much as possible of HRIG should be injected around the bites, with the remainder being given by deep intramuscular injection at a site distant from the vaccination site.People who have previously been vaccinated against rabies do not need to receive the immunoglobulin—only the postexposure vaccinations on days 0 and 3. The side effects of modern cell-based vaccines are similar to the side effects of flu shots. The old nerve-tissue-based vaccination required multiple injections into the abdomen with a large needle but is inexpensive. It is being phased out and replaced by affordable World Health Organization intradermal-vaccination regimens. In children less than a year old, the lateral thigh is recommended. Thoroughly washing the wound as soon as possible with soap and water for approximately five minutes is effective in reducing the number of viral particles. Povidone-iodine or alcohol is then recommended to reduce the virus further.Awakening to find a bat in the room, or finding a bat in the room of a previously unattended child or mentally disabled or intoxicated person, is an indication for post-exposure prophylaxis (PEP). The recommendation for the precautionary use of PEP in bat encounters where no contact is recognized has been questioned in the medical literature, based on a cost–benefit analysis. However, a 2002 study has supported the protocol of precautionary administration of PEP where a child or mentally compromised individual has been alone with a bat, especially in sleep areas, where a bite or exposure may occur with the victim being unaware.

After onset
At least two treatment schemes have been proposed for treating rabies after the onset of symptoms, the Milwaukee Protocol and the Recife Protocol. The Milwaukee Protocol was first used in 2004 on Jeanna Giese, who became the first person known to have survived rabies without preventive treatments before symptom onset. The protocol puts a person into a chemically induced coma and uses antiviral medications to prevent fatal dysautonomia. The overall protocol is complex; the sixth version of the protocol last updated in 2018 consists of 17 pages with 22 steps of treatment, detailed monitoring, and a timeline of expected complications. The Recife Protocol follows the same principle but differs in details like termination of sedation and supplementary medication.

Prognosis
Vaccination after exposure, PEP, is highly successful in preventing rabies. In unvaccinated humans, rabies is virtually always fatal after neurological symptoms have developed.

Epidemiology
In 2010, an estimated 26,000 people died from rabies, down from 54,000 in 1990. The majority of the deaths occurred in Asia and Africa. As of 2015, India, followed by China (approximately 6,000) and the Democratic Republic of the Congo (5,600), had the most cases. A 2015 collaboration between the World Health Organization, World Organization of Animal Health (OIE), Food and Agriculture Organization of the United Nation (FAO), and Global Alliance for Rabies Control has a goal of eliminating deaths from rabies by 2030.

India
India has the highest rate of human rabies in the world, primarily because of stray dogs, whose number has greatly increased since a 2001 law forbade the killing of dogs. Effective control and treatment of rabies in India is hindered by a form of mass hysteria known as puppy pregnancy syndrome (PPS). Dog bite victims with PPS, male as well as female, become convinced that puppies are growing inside them, and often seek help from faith healers rather than medical services. An estimated 20,000 people die every year from rabies in India, more than a third of the global total.

Australia
Australia has an official rabies-free status, although Australian bat lyssavirus  (ABLV), discovered in 1996, is a strain of rabies prevalent in Australian native bat populations.

United States
Canine-specific rabies has been eradicated in the United States. But rabies is common among wild animals in the United States, and an average of 100 dogs become infected from other wildlife each year.Due to high public awareness of the virus, efforts at vaccination of domestic animals and curtailment of feral populations, and availability of postexposure prophylaxis, incidence of rabies in humans is very rare in the United States. From 1960 to 2018, a total of 125 human rabies cases were reported in the United States; 36 (28%) were attributed to dog bites during international travel. Among the 89 infections acquired in the United States, 62 (70%) were attributed to bats. The most recent rabies death in the United States was an Illinois man who refused treatment after waking up in the night with a bat on his neck; the man died a month later. Occurring in 2021, it was the first case of human rabies in the United States in nearly three years.

Europe
Either no or very few cases of rabies are reported each year in Europe; cases are contracted both during travel and in Europe.In Switzerland the disease was virtually eliminated after scientists placed chicken heads laced with live attenuated vaccine in the Swiss Alps. The foxes of Switzerland, proven to be the main source of rabies in the country, ate the chicken heads and immunized themselves.Italy, after being declared rabies-free from 1997 to 2008, has witnessed a reemergence of the disease in wild animals in the Triveneto regions (Trentino-Alto Adige/Südtirol, Veneto and Friuli-Venezia Giulia), due to the spreading of an epidemic in the Balkans that also affected Austria. An extensive wild animal vaccination campaign eliminated the virus from Italy again, and it regained the rabies-free country status in 2013, the last reported case of rabies being reported in a red fox in early 2011.The United Kingdom has been free of rabies since the early 20th century except for a rabies-like virus (EBLV-2) in a few Daubentons bats. There has been one fatal case of EBLV-2 transmission to a human. There have been four deaths from rabies, transmitted abroad by dog bites, since 2000.  The last infection in the UK occurred in 1922, and the last death from indigenous rabies was in 1902.Sweden and mainland Norway have been free of rabies since 1886. Bat rabies antibodies (but not the virus) have been found in bats. On Svalbard, animals can cross the arctic ice from Greenland or Russia.

Mexico
Mexico was certified by the World Health Organization as being free of dog-transmitted rabies in 2019 because no case of dog-human transmission had been recorded in two years.

History
Rabies has been known since around 2000 BC. The first written record of rabies is in the Mesopotamian Codex of Eshnunna (c. 1930 BC), which dictates that the owner of a dog showing symptoms of rabies should take preventive measures against bites. If another person were bitten by a rabid dog and later died, the owner was heavily fined.In Ancient Greece, rabies was supposed to be caused by Lyssa, the spirit of mad rage.Ineffective folk remedies abounded in the medical literature of the ancient world. The physician Scribonius Largus prescribed a poultice of cloth and hyena skin; Antaeus recommended a preparation made from the skull of a hanged man.Rabies appears to have originated in the Old World, the first epizootic in the New World occurring in Boston in 1768.Rabies was considered a scourge for its prevalence in the 19th century. In France and Belgium, where Saint Hubert was venerated, the "St Huberts Key" was heated and applied to cauterize the wound. By an application of magical thinking, dogs were branded with the key in hopes of protecting them from rabies.
It was not uncommon for a person bitten by a dog merely suspected of being rabid to commit suicide or to be killed by others.In ancient times the attachment of the tongue (the lingual frenulum, a mucous membrane) was cut and removed as this was where rabies was thought to originate. This practice ceased with the discovery of the actual cause of rabies. Louis Pasteurs 1885 nerve tissue vaccine was successful, and was progressively improved to reduce often severe side-effects.In modern times, the fear of rabies has not diminished, and the disease and its symptoms, particularly agitation, have served as an inspiration for several works of zombie or similarly themed fiction, often portraying rabies as having mutated into a stronger virus which fills humans with murderous rage or incurable illness, bringing about a devastating, widespread pandemic.

Other animals
Rabies is infectious to mammals; three stages of central nervous system infection are recognized. The first stage is a one- to three-day period characterized by behavioral changes and is known as the prodromal stage. The second is the excitative stage, which lasts three to four days. This stage is often known as "furious rabies" for the tendency of the affected animal to be hyper-reactive to external stimuli and bite at anything near. The third is the paralytic stage and is caused by damage to motor neurons </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Anterograde amnesia and can you explain it in depth? [/INST] In neurology, anterograde amnesia is the inability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

Signs and symptoms
People with anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia.
In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch. One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below).

Causes
This disorder is usually acquired in one of four ways: One cause is benzodiazepine drugs such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, triazolam, clonazepam, alprazolam, diazepam, and nimetazepam; all of these are known to have powerful amnesic effects. This has also been recorded in non-benzodiazepine sedatives or "z-drugs" which act on the same set of receptors; such as zolpidem (also known as Ambien), eszopiclone (also known as Lunesta), and zopiclone (also known by brand names Imovane and Zimovane). A second cause is a traumatic brain injury in which damage is usually done to the hippocampus or surrounding cortices. It may also be caused by a PTSD, a shocking event, or an emotional disorder.Illness, though much rarer, can also cause anterograde amnesia if it causes encephalitis, which is the inflammation of brain tissue. There are several types of encephalitis: one such is herpes simplex encephalitis (HSV), which, if left untreated, can lead to neurological deterioration. How HSV gains access to the brain is unknown; the virus shows a distinct predilection for certain parts of the brain. Initially, it is present in the limbic cortices; it may then spread to the adjacent frontal and temporal lobes. Damage to specific areas can result in reduced or eliminated ability to encode new explicit memories, giving rise to anterograde amnesia. Patients with anterograde amnesia may have episodic, semantic, or both types of explicit memory impaired for events after the trauma that caused the amnesia. This suggests that memory consolidation for different types of memory takes place in different regions of the brain. Despite this, current knowledge on human memory is still insufficient to "map out" the wiring of a human brain to discover which parts of which lobe are responsible for the various episodic and semantic knowledge within a persons memory.
Amnesia is seen in patients who, for the reason of preventing another more serious disorder, have parts of their brains known to be involved in memory circuits removed, the most notable of which is known as the medial temporal lobe (MTL) memory system, described below. Patients with seizures originating in the MTL may have either side or both structures removed (there is one structure per hemisphere). In addition, patients with tumors who undergo surgery will often sustain damage to these structures, as is described in a case below. Damage to any part of this system, including the hippocampus and surrounding cortices, results in amnesic syndromes. This is why after a stroke people have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus.
Finally, anterograde amnesia can be the first clinical sign that Alzheimers disease develops in within the brain. Although later the complications can be much more widespread and strongly impair cognitive processes, at the initial stage of Alzheimers the changes observed can be restricted to anterograde amnesia and a mild deficit in retaining newly learnt sequences. This is explained by the fact that the disease is initiated within the medial temporal lobe and first affacts the entorhinal cortex that directly sends and receives information from the hippocampal formation.

Alcohol intoxication
Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brains ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy peoples long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for infrequent drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.Chronic alcoholism often leads to a thiamine (vitamin B1) deficiency in the brain, causing Korsakoffs syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernickes encephalopathy (WE).
The memory impairment that is pathognomonic to Korsakoffs syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory.

Pathophysiology
The pathophysiology of anterograde amnesic syndromes varies with the extent of damage and the regions of the brain that were damaged. The most well-described regions indicated in this disorder are the medial temporal lobe (MTL), basal forebrain, and fornix. Beyond the details described below, the precise process of how we remember – on a micro scale – remains a mystery. Neuropsychologists and scientists are still not in total agreement over whether forgetting is due to faulty encoding, accelerated forgetting, or faulty retrieval, although a great deal of data seem to point to the encoding hypothesis. In addition, neuroscientists are also in disagreement about the length of time involved in memory consolidation. Though most researchers, including Hasselmo et al., have found the consolidation process is spread out over several hours before transitioning from a fragile to a more permanent state, others, including Brown et al., posit that memory consolidation can take months or even years in a drawn-out process of consolidation and reinforcement. Further research into the length of time of memory consolidation will shed more light on why anterograde amnesia sometimes affects some memories gained after the event(s) that caused the amnesia, but does not affect other such memories.

Medial temporal lobe
The MTL memory system includes the hippocampal formation (CA fields, dentate gyrus, subicular complex), perirhinal, entorhinal, and parahippocampal cortices. It is known to be important for the storage and processing of declarative memory, which allows for factual recall. It is also known to communicate with the neocortex in the establishment and maintenance of long-term memories, although its known functions are independent of long-term memory. Nondeclarative memory, on the other hand, which allows for the performance of different skills and habits, is not part of the MTL memory system. Most data point to a "division of labor" among the parts of this system, although this is still being debated and is described in detail below.In animal models, researchers have shown monkeys with damage to both the hippocampus and its adjacent cortical regions were more severely impaired in terms of anterograde amnesia than monkeys with damage localized to hippocampal structures. However, conflicting data in another primate study point to the observation that the amount of tissue damaged does not necessarily correlate with the severity of the memory loss. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic memory and semantic memory (described below).An important finding in amnesic patients with MTL damage is the impairment of memory in all sensory modalities – sound, touch, smell, taste, and sight. This reflects the fact that the MTL is a processor for all of the sensory modalities, and helps store these kind of thoughts into memory. In addition, subjects can often remember how to perform relatively simple tasks immediately (on the order of 10 seconds), but when the task becomes more difficult, even on the same time scale, subjects tend to forget. This demonstrates the difficulty of separating procedural memory tasks from declarative memory; some elements of declarative memory may be used in learning procedural tasks.MTL amnesic patients with localized damage to the hippocampus retain other perceptual abilities, such as the ability to intelligently function in society, to make conversation, to make ones bed, etc. Additionally, anterograde amnesics without combined retrograde disorders (localized damage to the MTL system) have memories prior to the traumatic event. For this reason, the MTL is not the storage place of all memories; other regions in the brain also store memories. The key is the MTL is responsible for the learning of new materials.

Other memory systems
A limited number of cases have been described in which patients with damage to other parts of the brain acquired anterograde amnesia. Easton and Parker observed damage to either the hippocampus or the surrounding cortices does not seem to result in severe amnesia in primate models. They suggested damage to the hippocampus and surrounding structures alone does not explain the amnesia they saw in patients, or increasing damage does not correlate with the degree of impairment. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic and semantic memory. To demonstrate their hypothesis, they used a primate model with damage to the basal forebrain. They proposed that the disruption of neurons that project from the basal forebrain to the MTL are responsible for some of the impairment in anterograde amnesia. Easton and Parker also reported MRI scans of patients with severe anterograde amnesia showed damage beyond to cortical areas around the hippocampus and amygdala (a region of brain involved in emotions) and to surrounding white matter (white matter in the brain consists of axons, long projections of neuronal cell bodies).
Another case described the onset of anterograde amnesia as a result of cell death in the fornix, another structure that carries information from the hippocampus to the structures of the limbic system and the diencephalon. The patient in this case did not show any disconnection syndrome, which is unexpected since the structures involved divide the brain hemispheres (both sides of her brain were able to communicate). Instead, she showed signs of amnesia. The final diagnosis was made by MRI. This particular amnesic syndrome is difficult to diagnose and often is misdiagnosed by physicians as an acute psychiatric disorder.

Reorganization of memory
When there is damage to just one side of the MTL, there is opportunity for normal functioning or near-normal function for memories. Neuroplasticity describes the ability of the cortex to remap when necessary. Remapping can occur in cases like the one above and with time the patient can recover and become more skilled at memory retention. A case report describing a patient who had two lobectomies – in the first, doctors removed part of her right MTL first because of seizures originating from the region, and later her left because she developed a tumor – demonstrates this. This case is unique because it is the only one in which both sides of the MTL were removed at different times. The authors observed that the patient was able to recover some ability to learn when she had only one MTL, but observed the deterioration of function when both sides of the MTL were affected. The reorganization of brain function for epileptic patients has had limited investigation, but imaging results show that it may occur.

Rehabilitation
Approaches used to treat those with anterograde amnesia often use interventions which focus on compensatory techniques, such as beepers, written notes, diaries or through intensive training programs involving the active participation of the individual concerned, along with their supporting network of family and friends.
In this perspective, environmental adaptation techniques are used, such as the compensatory technique education to training (exercise), organizational strategies, visual imagery and verbal labeling. In addition, other techniques are also used in rehabilitation, such as implicit tasks, speech and mnemotechnic methods.
So far, it has been proven that education techniques of compensatory strategies for memory disorders are effective in individuals with minor traumatic brain injuries. In moderately or severely injured individuals, effective interventions are those appealing to external aids, such as reminders in order to facilitate particular knowledge or skill acquisition. Reality orientation techniques are also considered; their purpose is to enhance orientation using stimulation and repetition of the basic orientation information. These techniques are regularly applied in populations of patients primarily presenting with dementia and head injuries.

Controversies
Episodic versus semantic memory
As described above, patients with anterograde amnesia have a wide range of forgetfulness. Declarative memory can be further subdivided into episodic and semantic memory. Episodic memory is the recollection of autobiographical information with a temporal and/or spatial context, whereas semantic memory involves recall of factual information with no such association (language, history, geography, etc.). In a case study of a girl who developed anterograde amnesia during childhood, it was determined that the patient ("C.L.") retained semantic memory while having an extreme impairment of episodic memory.One patient, known by the codename "Gene", was involved in a motorcycle accident that damaged significant portions of his frontal and temporal lobes, including his left hippocampus. As a result, he cannot remember any specific episode in his life, such as a train derailment near his house. However, his semantic memory is intact; he remembers that he owns a car and two motorcycles, and he can even remember the names of his classmates in a school photograph.
In stark contrast, a woman whose temporal lobes were damaged in the front due to encephalitis lost her semantic memory; she lost her memory of many simple words, historical events, and other trivial information categorized under semantic memory. However, her episodic memory was left intact; she can recall episodes such as her wedding and her fathers death with great detail.
Vicari et al. describe that it remains unclear whether neural circuits involved in semantic and episodic memory overlap partially or completely, and this case seems to suggest that the two systems are independent. Both of the patients hippocampal and diencephalic structures on the right and left sides were disconnected. When C.L. came to Vicari et al.s office, her chief complaint was forgetfulness involving both semantic and episodic memory. After administering a battery of neuropsychological tests, Vicari determined that C.L. performed well in tests of visual naming and sentence comprehension, visual-spatial ability, and "general semantic knowledge about the world". They also noted an improved vocabulary and general knowledge base after 18 months. C.L.s episodic memory, on the other hand, was far below expectations: She could not retain daily events, where she had gone on vacation, the names of places she had been, and other such information. However, this study and others like it are susceptible to subjectivity, since it is not always possible to clearly distinguish between episodic and semantic memory. For this reason, the topic remains controversial and debated.

Familiarity and the fractionation of memory
The right hippocampus is clearly necessary for familiarity in spatial tasks, whereas the left hippocampus is necessary for familiarity-based recollection in verbal tasks. Some researchers claim the hippocampus is important for the retrieval of memories, whereas adjacent cortical regions can support familiarity-based memories. These memory decisions are made based on matching already-existing memories (before the onset of pathology) to the current situation. According to Gilboa et al., patients with localized hippocampal damage can score well on a test if it is based on familiarity.Poreh et al. describe a case study of patient A.D., whose damage to the fornix rendered the hippocampus useless, but spared adjacent cortical areas – a fairly rare injury. When the patient was given a test with something with which he had some familiarity, the patient was able to score well. In general, however, A.D. had severely impaired episodic memory, but had some ability to learn semantic knowledge. Other studies show animals with similar injuries can recognize objects with which they are familiar, but, when the objects are presented in an unexpected context, they do not score well on recognition tests.

Islands of memory
Patients with anterograde amnesia have trouble recalling new information and new autobiographical events, but the data are less consistent in regard to the latter. Medveds and Hirst recorded the presence of islands of memory – detailed accounts – that were described by such patients. The island memories were a combination of semantic and episodic memories. The researchers recorded patients giving long narratives with a fair amount of detail that resembled memories that the patients had prior to the trauma. The appearance of islands of memory could have something to do with the functioning of adjacent cortical areas and the neocortex. In addition, the researchers suspect that the amygdala played a role in the narratives.

Notable cases
The most famous case reported is that of patient Henry Molaison, known as H.M., in March 1953. Molaisons chief complaint was the persistence of severe seizures and therefore had a bilateral lobectomy (both of his medial temporal lobes were removed). As a result, Molaison had bilateral damage to both the hippocampal formation and the perirhinal cortex. Molaison had average intelligence and perceptual ability and a decent vocabulary. However, he could not learn new words or remember things that had happened more than a few minutes earlier. He could remember anything from his childhood. If the memory was created from before his lobectomy, he still had the ability to retrieve it and remember. However, he was able to learn some new skills. He was the first well-documented case of severe anterograde amnesia, and was studied until his death in 2008.A similar case involved Clive Wearing, an accomplished musicologist who contracted a cold sore virus that attacked his brain, causing herpes simplex encephalitis. As a result, Wearing developed both anterograde and retrograde amnesia, so he has little memory of what happened before the virus struck him in 1985, and cannot learn new declarative knowledge after the virus struck him either. As a result of anterograde amnesia, Wearing repeatedly "wakes up" every day usually in 30-second intervals. He has a history of repeatedly recording these moments of waking up in his journal (e.g., On Sept 2, 2013, I woke up, etc. etc.) and crossing out prior entries, as if the other moments of waking up were not real. His episodic memory is nonfunctional (so he does not consciously recall having woken up 30 seconds prior). Clive is often elated to see his wife, as if he has not seen her for a while. Despite this, however, Wearing maintained his ability to play the piano and conduct choirs. This case is significant because it demonstrates declarative and procedural memory are separate. Therefore, despite anterograde amnesia preventing Wearing from learning new bits of information that can be explained in words (declarative memory), and also preventing him from storing new memories of events or episodes (also part of declarative memory), he has little trouble in retaining his musical abilities (procedural memory), though he has no conscious memory of having learned music.Another case in the literature is Eugene Pauly, known as E.P., a severely amnesic patient (owing to viral encephalitis) who was able to learn three-word sentences. He performed better on consecutive tests over a 12-week period (24 study sessions). However, when asked how confident he was about the answers, his confidence did not appear to increase. Bayley and Squire proposed his learning was similar to the process required by procedural memory tasks; E.P. could not get the answers right when one word in the three-word sentence was changed or the order of words was changed, and his ability to answer correctly, thus, became more of a "habit". Bayley and Squire claim the learning may have happened in the neocortex, and it happened without the conscious knowledge of E.P. They hypothesized the information may be acquired directly by the neocortex (to which the hippocampus projects) when there is repetition. This case illustrates the difficulty in separating procedural from declarative tasks; this adds another dimension to the complexity of anterograde amnesia.

In fiction
Notable examples include Lucy Whitmore in 50 First Dates, Jonathan Archer in the Star Trek: Enterprise episode "Twilight", Joseph Gordon-Levitt in The Lookout, Kaori Fujimiya in One Week Friends, Chihiro Shindou in Ef: A Fairy Tale of the Two, Christine Lucas in Before I Go to Sleep, Gus in Remember Sunday.
Christopher Nolans psychological crime film Memento (2000) contains a distinguished depiction of anterograde amnesia, in that the memory-impaired protagonist Leonard Shelby is trying to identify and kill the man who raped and murdered his wife, and does so through a system of writing crucial details related to the search on his body and on the blank spaces of Polaroid photographs. Mental health experts have described Memento as one of the most accurate depictions of amnesia in film history, an accuracy that was enhanced by the films fragmented, non-linear structure that mimics the protagonists memory problems.Dory, the happy-go-lucky Regal Blue Tang from Finding Nemo (2003) and Finding Dory (2016), suffers from anterograde amnesia. While Dory forgets conversations within minutes of having them, she never quite forgets who she is, or the fact that she has short-term memory loss, and can therefore explain her bizarre behavior to those around her.Ghajini (2008), a Hindi language film of India based on Memento, in which the main protagonist Sanjay Singhania played by Amir Khan has short-term memory loss, this variant of amnesia. In the film he is behind Ghajini, the killer of his fiancée Kalpana.
In the TV series Perception, an episode revolved around a crime victim with this condition. The main character Latro in Gene Wolfes novels Soldier of the Mist, and the anime characters Vash the Stampede from Trigun and Index and Tōma from A Certain Magical Index had both retrograde and anterograde amnesia. The disorder has also been portrayed in music by English the Caretaker in Theoretically Pure Anterograde Amnesia (2005).In the 1965 film 36 Hours, Rod Taylor plays Nazi Major Walter Gerber, a psychiatrist who has developed an effective method for treating German soldiers with what is now known as PTSD – and for painlessly extracting information from Allied prisoners. The technique involves convincing patients that years have passed, the war is over, and that they have anterograde amnesia, which supposedly can be cured with talk therapy. A few days before D-Day, U.S. Army Major Jeff Pike (James Garner) is drugged, kidnapped and taken to what appears to be a hospital run by American Occupation Forces, where his appearance is altered overnight. Pike knows that the invasion is aimed at Normandy, not Pas de Calais, as the Nazi high command expects. He buys Gerbers explanation of anterograde amnesia – using the double doors of a wardrobe as illustration – and speaks casually of Normandy. Salt in a papercut alerts him to the horrible truth, and the drama proceeds from there.
In the 2011 light novel Danganronpa Zero, the protagonist and "Ultimate Analyst" Ryoko Otonashi has anterograde amnesia as a result of "The Tragedy", keeping note of her memories by writing into a journal at all times and using her speedreading to keep herself up to date </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Typhus and can you explain it in depth? [/INST] Typhus, also known as typhus fever, is a group of infectious diseases that include epidemic typhus, scrub typhus, and murine typhus. Common symptoms include fever, headache, and a rash. Typically these begin one to two weeks after exposure.The diseases are caused by specific types of bacterial infection. Epidemic typhus is due to Rickettsia prowazekii spread by body lice, scrub typhus is due to Orientia tsutsugamushi spread by chiggers, and murine typhus is due to Rickettsia typhi spread by fleas.Vaccines have been developed, but none are commercially available. Prevention is achieved by reducing exposure to the organisms that spread the disease. Treatment is with the antibiotic doxycycline. Epidemic typhus generally occurs in outbreaks when poor sanitary conditions and crowding are present. While once common, it is now rare. Scrub typhus occurs in Southeast Asia, Japan, and northern Australia. Murine typhus occurs in tropical and subtropical areas of the world.Typhus has been described since at least 1528. The name comes from the Greek tûphos (τῦφος) meaning fever or delusion, describing the state of mind of those infected. While "typhoid" means "typhus-like", typhus and typhoid fever are distinct diseases caused by different types of bacteria. Note, however, that in some languages such as German, typhus does mean "typhoid fever".

Signs and symptoms
These signs and symptoms refer to epidemic typhus, as it is the most important of the typhus group of diseases.Signs and symptoms begin with sudden onset of fever and other flu-like symptoms about one to two weeks after being infected. Five to nine days after the symptoms have started, a rash typically begins on the trunk and spreads to the extremities. This rash eventually spreads over most of the body, sparing the face, palms, and soles. Signs of meningoencephalitis begin with the rash and continue into the second or third weeks. Other signs of meningoencephalitis include sensitivity to light (photophobia), altered mental status (delirium), or coma. Untreated cases are often fatal.

Causes
Multiple diseases include the word "typhus" in their descriptions. Types include:

Prevention
As of 2020, no vaccine is commercially available. A vaccine has been in development for scrub typhus known as the scrub typhus vaccine.

Treatment
The American Public Health Association recommends treatment based upon clinical findings and before culturing confirms the diagnosis. Without treatment, death may occur in 10% to 60% of people with epidemic typhus, with people over age 60 having the highest risk of death.  In the antibiotic era, death is uncommon if doxycycline is given. In one study of 60 people hospitalized with epidemic typhus, no one died when given doxycycline or chloramphenicol.

Epidemiology
According to the World Health Organization, the current death rate from typhus is about one  of every 5,000,000 people per year.Only a few areas of epidemic typhus exist today.  Since the late 20th century, cases have been reported in Burundi, Rwanda, Ethiopia, Algeria, and a few areas in South and Central America.Except for two cases, all instances of epidemic typhus in the United States have occurred east of the Mississippi River. An examination of a cluster of cases in Pennsylvania concluded the source of the infection was flying squirrels. Sylvatic cycle (diseases transmitted from wild animals) epidemic typhus remains uncommon in the US.  The Centers for Disease Control and Prevention have documented only 47 cases from 1976 to 2010. An outbreak of flea-borne murine typhus was identified in downtown Los Angeles, California, in October 2018.

History
Middle Ages
The first reliable description of typhus appears in 1489 AD during the Spanish siege of Baza against the Moors during the War of Granada (1482–1492). These accounts include descriptions of fever; red spots over arms, back, and chest; attention deficit, progressing to delirium; and gangrenous sores and the associated smell of rotting flesh. During the siege, the Spaniards lost 3,000 men to enemy action, but an additional 17,000 died of typhus.In historical times, "jail fever" or "gaol fever" was common in English prisons, and is believed by modern authorities to have been typhus. It often occurred when prisoners were crowded together into dark, filthy rooms where lice spread easily. Thus, "imprisonment until the next term of court" was often equivalent to a death sentence. Prisoners brought before the court sometimes infected members of the court. The Black Assize of Exeter 1586 was another notable outbreak. During the Lent assizes court held at Taunton in 1730, gaol fever caused the death of the Lord Chief Baron, as well as the High Sheriff, the sergeant, and hundreds of others. During a time when persons were executed for capital offenses, more prisoners died from gaol fever than were put to death by all the public executioners in the British realm. In 1759, an English authority estimated that each year, a quarter of the prisoners had died from gaol fever. In London, gaol fever frequently broke out among the ill-kept prisoners of Newgate Prison and then moved into the general city population. In May 1750, the Lord Mayor of London, Sir Samuel Pennant, and many court personnel were fatally infected in the courtroom of the Old Bailey, which adjoined Newgate Prison.

Early modern epidemics
Epidemics occurred routinely throughout Europe from the 16th to the 19th centuries, including during the English Civil War, the Thirty Years War, and the Napoleonic Wars. Pestilence of several kinds raged among combatants and civilians in Germany and surrounding lands from 1618 to 1648. According to Joseph Patrick Byrne, "By wars end, typhus may have killed more than 10 percent of the total German population, and disease in general accounted for 90 percent of Europes casualties."

19th century
During Napoleons retreat from Moscow in 1812, more French soldiers died of typhus than were killed by the Russians.A major epidemic occurred in Ireland between 1816 and 1819, during the famine caused by a worldwide reduction in temperature known as the Year Without a Summer. An estimated 100,000 people perished. Typhus appeared again in the late 1830s, and yet another major typhus epidemic occurred during the Great Irish Famine between 1846 and 1849. The Irish typhus spread to England, where it was sometimes called "Irish fever" and was noted for its virulence. It killed people of all social classes, as lice were endemic and inescapable, but it hit particularly hard in the lower or "unwashed" social strata.In the United States, a typhus epidemic broke out in Philadelphia in 1837 and killed the son of Franklin Pierce (14th President of the United States) in Concord, New Hampshire, in 1843. Several epidemics occurred in Baltimore, Memphis, and Washington, DC, between 1865 and 1873. Typhus was also a significant killer during the US Civil War, although typhoid fever was the more prevalent cause of US Civil War "camp fever". Typhoid fever is caused by the bacterium Salmonella enterica Serovar Typhi.In Canada alone, the typhus epidemic of 1847 killed more than 20,000 people from 1847 to 1848, mainly Irish immigrants in fever sheds and other forms of quarantine, who had contracted the disease aboard the crowded coffin ships in fleeing the Great Irish Famine. Officials neither knew how to provide sufficient sanitation under conditions of the time nor understood how the disease spread.

20th century
Typhus was endemic in Poland and several neighboring countries prior to World War I (1914–1918), but became epidemic during the war </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Arteritis and can you explain it in depth? [/INST] Arteritis is the inflammation of the walls of arteries, usually as a result of infection or autoimmune response. Arteritis, a complex disorder, is still not entirely understood. Arteritis may be distinguished by its different types, based on the organ systems affected by the disease. A complication of arteritis is thrombosis, which can be fatal. Arteritis and phlebitis are forms of vasculitis.

Signs and Symptoms
Symptoms of general arteritis may include:
Inflammation
Fever
Increased production of red blood cells (erythrocytes)
Limping
Reduced pulse

Diagnosis
Diagnosis of arteritis is based on unusual medical symptoms.  Similar symptoms may be caused by a number of other conditions, such as Ehlers-Danlos syndrome and Marfan syndrome (both heritable disorders of connective tissue), tuberculosis, syphilis, spondyloarthropathies, Cogans syndrome, Buergers, Behcets, and Kawasaki disease.  Various imaging techniques may be used to diagnose and monitor disease progression. Imaging modalities may include direct angiography, magnetic resonance angiography, and ultrasonography.Angiography is commonly used in the diagnosis of Takayasu arteritis,  especially in the advanced stages of the disease, when arterial stenosis, occlusion, and aneurysms may be observed.  However, angiography is a relatively invasive investigation, exposing patients to large doses of radiation, so is not recommended for routine, long-term monitoring of disease progression in patients with Takayasu arteritis.Computed tomography angiography can determine the size of the aorta and its surrounding branches, and can identify vessel wall lesions in middle to late stages of arteritis.  CTA can also show the blood flow within the blood vessels.  Like angiography, CTA exposes patients to high dosages of radiation.Magnetic resonance angiography is used to diagnose Takayasu arteritis in the early stages, showing changes such as the thickening of the vessel wall. Even small changes may be measured, making MRA a useful tool for monitoring disease progression without exposing patients to the radiation of direct angiography or CTA. MRA is an expensive investigation, and shows calcification of the aorta and distal branches less clearly than other imaging methods.Ultrasonography is an ideal method of diagnosing patients in early stages of arteritis when inflammation in the vessel walls occurs.  It can also show the blood flow within the blood vessels. Ultrasonography is a popular first-line investigation for diagnosis because it is relatively quick, cheap, noninvasive, and does not expose patients to radiation.  It is also used for long-term monitoring of disease progression in Takayasu arteritis. Not all vascular lesions are visible on ultrasound, and the accuracy of the scan depends, to some extent, on the person reading the scan, as the results are observed in real time.

Types
Arteritis may be primary or secondary to some other disease process. The primary types are:

An example of a secondary arteritis is arteritis caused by infection with the fungal pathogen Candida albicans.

Giant cell arteritis
Giant cell arteritis contains two different types of arteritides that are almost indistinguishable from one another.  It includes two types, temporal arteritis and Takayasu arteritis. Both types contain an occupancy of medium- and larger-sized arteries which are categorized based on the infiltration of the giant cells.

Takayasu arteritis
This type of arteritis is most common in females, with a median age of 25 years. Takayasu arteritis is more common in women of Asian descent who are in their reproductive years. However, over the past decades, its incidence  in Africa, Europe, and North America has been increasing. Takayasu arteritis is an inflammatory disease that mainly affects the larger vessels such as the aorta and its surrounding branches. Research focused on Takayasu arteritis in the western parts of the world remains limited. An estimation suggests that, each year, the number of cases per million people is 2.6.

Temporal arteritis
Temporal arteritis, the second type of giant cell arteritis, is also a chronic, inflammatory disease involving mid- to large-sized arteries. Temporal arteritis has a higher incidence in people of Scandinavian descent.  However, the incidence rate differs based on population, region and races. Temporal arteritis is not uncommon in North America. The incidence rate is around 0.017% for individuals over 50 years of age.Symptoms of temporal arteritis are classified as specific and nonspecific.Nonspecific symptoms:
Headache
Low grade fever
Sweating
Anorexia (loss of appetite)
Weight loss
General malaiseSpecific symptoms:
Claudication of the jaw
Engorged, tender vesselsSpecific symptoms usually develop in the advanced stages of temporal arteritis.Polyarteritis nodosa of  unknown mechanism can cause testicular pain. It is often associated with aneurysms and Hepatitis B.

Treatment
Medications
The first-line treatment for arteritis is oral glucocorticoid (steroid) medication, such as prednisone, taken daily for a period of three months. After this initial phase, the medication may be reduced in dose or frequency, e.g </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ancylostomiasis and can you explain it in depth? [/INST] Ancylostomiasis  is a hookworm disease caused by infection with Ancylostoma hookworms. The name is derived from Greek ancylos αγκύλος  "crooked, bent" and stoma στόμα "mouth".
Ancylostomiasis is also known as miners anaemia, tunnel disease, brickmakers anaemia and Egyptian chlorosis. Helminthiasis may also refer to ancylostomiasis, but this term also refers to all other parasitic worm diseases as well. In the United Kingdom, if acquired in the context of working in a mine, the condition is eligible for Industrial Injuries Disability Benefit. It is a prescribed disease (B4) under the relevant legislation.§Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency anemia by sucking blood from the hosts intestinal walls.

Signs and symptoms
Depending on the organism, the signs and symptoms vary. Ancylostoma duodenale and Necator americanus can enter the blood stream while Ancylostoma braziliensis cannot. Signs and symptoms of Ancylostoma duodenale and Necator americanus are given in corresponding page.In Ancylostoma braziliensis as the larvae are in an abnormal host, they do not mature to adults but instead migrate through the skin until killed by the hosts inflammatory response. This migration causes local intense itching and a red serpiginous lesion. Treatment with a single dose of oral ivermectin results in cure rates of 94–100%.

Causes
The infection is usually contracted by people walking barefoot over
contaminated soil. In penetrating the skin, the larvae may cause an allergic
reaction. It is due to the itchy patch at the site of entry that the early
infection gets its nickname "ground itch". Once larvae have broken through the skin,
they enter the bloodstream and are carried to the lungs (however, unlike ascarids, hookworms do not usually cause pneumonia). The larvae migrate from
the lungs up the windpipe to be swallowed and carried back down to the
intestine. If humans come into contact with larvae of the dog hookworm or the
cat hookworm, or of certain other hookworms that do not infect humans, the
larvae may penetrate the skin. Sometimes, the larvae are unable to complete their
migratory cycle in humans. Instead, the larvae migrate just below the skin
producing snake-like markings. This is referred to as a creeping eruption or
cutaneous larva migrans.

Diagnosis
They commonly infect the skin, eyes, and viscera in humans.
Ancylostoma brasiliensis causes cutaneous larva migrans.
Toxocara causes visceral larva migrans.

Prevention
Control of this parasite should be directed against reducing the level of
environmental contamination. Treatment of heavily infected individuals is one
way to reduce the source of contamination (one study has estimated that 60% of
the total worm burden resides in less than 10% of the population). Other
obvious methods are to improve access to sanitation, e.g. toilets, but also
convincing people to maintaining them in a clean, functional state, thereby making
them conducive to use.

Treatment
The drug of choice for the treatment of hookworm disease is mebendazole which is effective against both species, and in addition, will remove the intestinal worm Ascaris also, if present. The drug is very efficient, requiring only a single dose and is inexpensive. However, treatment requires
more than giving the anthelmintic, the patient should also receive dietary supplements to improve their general level of health, in particular iron supplementation is very important. Iron is an important constituent of a multitude of enzyme systems involved in energy metabolism, DNA synthesis and
drug detoxification.An infection of N. americanus parasites can be treated by using benzimidazoles, albendazole, and mebendazole. A blood transfusion may be necessary in severe cases of anemia. Light infections are usually left untreated in areas where reinfection is common. Iron supplements and a diet high in protein will speed the recovery process.  In a case study involving 56–60 men with Trichuris trichiura and/or N. americanus infections, both albendazole and mebendazole were 90% effective in curing T. trichiura.  However, albendazole had a 95% cure rate for N </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Spasm and can you explain it in depth? [/INST] A spasm is a sudden involuntary contraction of a muscle, a group of muscles, or a hollow organ such as the bladder.
A spasmodic muscle contraction may be caused by many medical conditions, including dystonia. Most commonly, it is a muscle cramp which is accompanied by a sudden burst of pain. A muscle cramp is usually harmless and ceases after a few minutes </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gerstmann–Sträussler–Scheinker syndrome and can you explain it in depth? [/INST] Gerstmann–Sträussler–Scheinker syndrome (GSS) is an extremely rare, usually familial, fatal neurodegenerative disease that affects patients from 20 to 60 years in age. It is exclusively heritable, and is found in only a few families all over the world. It is, however, classified with the transmissible spongiform encephalopathies (TSE) due to the causative role played by PRNP, the human prion protein. GSS was first reported by the Austrian physicians Josef Gerstmann, Ernst Sträussler and Ilya Scheinker in 1936.Familial cases are associated with autosomal-dominant inheritance.Certain symptoms are common to GSS, such as progressive ataxia, pyramidal signs, and dementia; they worsen as the disease progresses.

Symptoms and signs
Symptoms start with slowly developing dysarthria (difficulty speaking) and cerebellar truncal ataxia (unsteadiness) and then the progressive dementia becomes more evident.  Loss of memory can be the first symptom of GSS. Extrapyramidal and pyramidal symptoms and signs may occur and the disease may mimic spinocerebellar ataxias in the beginning stages. Myoclonus (spasmodic muscle contraction) is less frequently seen than in Creutzfeldt–Jakob disease. Many patients also exhibit nystagmus (involuntary movement of the eyes), visual disturbances, and even blindness or deafness. The neuropathological findings of GSS include widespread deposition of amyloid plaques composed of abnormally folded prion protein.Four clinical phenotypes are recognized: typical GSS, GSS with areflexia and paresthesia, pure dementia GSS and Creutzfeldt-Jakob disease-like GSS.

Causes
GSS is part of a group of diseases called transmissible spongiform encephalopathies. These diseases are caused by prions, which are a class of pathogenic proteins that are resistant to proteases. These prions then form clusters in the brain, which are responsible for the neurodegenerative effects seen in patients.The P102L mutation, which causes a substitution of proline to a leucine in codon 102, has been found in the prion protein gene (PRNP, on chromosome 20) of most affected individuals. Therefore, it appears this genetic change is usually required for the development of the disease.

Diagnosis
GSS can be identified through genetic testing. Testing for GSS involves a blood and DNA examination in order to attempt to detect the mutated gene at certain codons. If the genetic mutation is present, the patient will eventually develop GSS.

Treatment
There is no cure for GSS, nor is there any known treatment to slow the progression of the disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fear of flying and can you explain it in depth? [/INST] Fear of flying is a fear of being on an airplane, or other flying vehicle, such as a helicopter, while in flight. It is also referred to as flying anxiety, flying phobia, flight phobia, aviophobia, aerophobia, or pteromechanophobia (although aerophobia also means a fear of drafts or of fresh air).Acute anxiety caused by flying can be treated with anti-anxiety medication.  The condition can be treated with exposure therapy, which works better when combined with cognitive behavioral therapy.

Signs and symptoms
People with fear of flying experience intense, persistent fear or anxiety when they consider flying, as well as during flying.  They will avoid flying if they can, and the fear, anxiety, and avoidance cause significant distress and impair their ability to function.  Take-off, bad weather, and turbulence appear to be the most anxiety provoking aspects of flying.The most extreme manifestations can include panic attacks or vomiting at the mere sight or mention of an aircraft or air travel.Around 60% of people with fear of flying report having some other anxiety disorder.

Cause
The causes of flight phobia and the mechanisms by which it is maintained were not well understood as of 2016.  It is not clear if it is really one condition; it appears to be heterogenous. It appears that some people get aerophobia from being or having claustrophobia to the small spaces inside the fuselage of the plane or helicopter.

Diagnosis
The diagnosis is clinical.  It is often difficult to determine if the specific phobia of fear of flight should be the primary diagnosis, or if fear of flying is a symptom of a generalized anxiety disorder or another anxiety disorder such as agoraphobia or claustrophobia.

Classification
Fear of flying is a specific phobia classified as such in the DSM-5.

Management
Acute anxiety caused by flying can be treated with anti-anxiety medication.  The condition can be treated with exposure therapy, including use of virtual reality equipment, which works better when combined with cognitive behavioral therapy.  Relaxation techniques and education about aviation safety can also be helpful in combination with other approaches.A new and advanced treatment for aviophobia is virtual reality exposure therapy. This type of treatment uses computer technology where the patient enters a virtual reality of flying.

Virtual reality exposure therapy
Effective treatment for phobias such as fear of flying would be one that activates and modifies the fear structure. Activation of the fear structure can be achieved by exposing the patient to the feared stimuli, flying in this case, to elicit the fearful response. Modification of the fear structure can be achieved by the processes of habituation and extinction after eliciting the fearful response several times </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Less and can you explain it in depth? [/INST]  </s>