<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Generalized tonic–clonic seizure and explain in detail? [/INST] A generalized tonic–clonic seizure, or GTCS, previously known as a Grand mal seizure, is a type of generalized seizure that produces bilateral, convulsive tonic and then clonic muscle contractions. Tonic-clonic seizures are the seizure type most commonly associated with epilepsy and seizures in general and the most common seizure associated with metabolic imbalances. It is a misconception that they are the sole type of seizure, as they are the main seizure type in approximately 10% of those with epilepsy.These seizures typically initiate abruptly with either a focal or generalized onset, the former being known as focal to bilateral tonic-clonic seizure. The seizure itself includes tonic (sustained) and then clonic (repetitive short) contractions. In some seizures, the tonic phase may be preceded by brief, arrhythmic muscle jerks (myoclonus), by a clonic phase or by an absence seizure. After the GTCS, there is an extended postictal state where the person is unresponsive and commonly sleeping with loud snoring. There is usually pronounced confusion upon awakening.

Causes
The vast majority of generalized tonic-clonic seizures have a focal origin they start as a smaller seizure that occurs solely on one side of the brain and is referred to as a focal (or partial) seizure. These unilateral seizure types (formerly known as simple partial seizure or a complex partial seizure and now referred to as focal aware seizure and focal impaired awareness seizure, respectively) can then spread to both hemispheres of the brain and cause a generalized tonic-clonic seizure. This type of seizure has a specific term called "focal to a bilateral tonic-clonic seizure. Other generalized tonic-clonic seizures are idiopathic, start in large networks involving both hemispheres, and have a presumed genetic cause. Precipitating factors include chemical and neurotransmitter imbalances and a genetically or situationally determined seizure threshold, both of which have been implicated. The seizure threshold can be altered by fatigue, malnutrition, lack of sleep or rest, hypertension, stress, diabetes, the presence of strobe-flashes or simple light/dark patterns, raised estrogen levels at ovulation, fluorescent lighting, rapid motion or flight, blood sugar imbalances, anxiety, antihistamines and other factors. Tonic–clonic seizures can also be induced deliberately with electroconvulsive therapy.In the case of symptomatic focal epilepsy, the cause is often determined by MRI or other neuroimaging techniques showing that there is some degree of damage to a large number of neurons. The lesions (i.e., scar tissue) caused by the loss of these neurons can result in groups of neurons forming a seizure "focus" area with episodic abnormal firing that can cause seizures if the focus is not abolished or suppressed via anticonvulsant drugs.

Mechanism
Prodrome
Most generalized tonic–clonic seizures begin without warning and abruptly, but some epileptic patients describe a prodrome. The prodrome of a generalized tonic–clonic seizure is a sort of premonitory feeling hours before a seizure. This type of prodrome is distinct from stereotypic aura of focal seizures that become generalized seizures.
Phases
A tonic–clonic seizure comprises three phases: the tonic phase, clonic phase and postictal phase.

Tonic phaseThe tonic phase is usually the first phase. Consciousness will quickly be lost and the skeletal muscles will suddenly tense, often causing the extremities to be pulled towards the body or rigidly pushed away from it, which will cause the patient to fall if standing or sitting. There may also be upward deviation of the eyes with the mouth open. The tonic phase is usually the shortest part of the seizure, normally lasting only 10–20 seconds. The patient typically expresses brief vocalizations like a loud moan upon entering the tonic stage, due to air being forcefully expelled from the lungs. This vocalization is commonly referred to as an "ictal cry." Starting in the tonic phase, there may also be bluing of the skin from respiration impairment as well as pooling of saliva in the back of the throat. Increased blood pressure, pupillary size and heart rate (sympathetic response) may also be noted with clenching of the jaw possibly resulting in biting the tongue. The initial tonic phase may be preceded by repetitive rhythmic or arrhythmic jerks or by the absence seizure.
Clonic phaseThe clonic phase is an evolution of the tonic phase and is caused by muscle relaxations superimposed on the tonic phase muscle contractions. This phase is longer than the tonic phase with the total ictal period usually lasting no longer than 1 min. Skeletal muscles will start to contract and relax rapidly, causing convulsions. These may range from exaggerated twitches of the limbs to violent shaking or vibrating of the stiffened extremities. The patient may roll and stretch as the seizure spreads. Initially, these contractions are of a high frequency and low amplitude, which will gradually progress to decreased frequency and high amplitude. An eventual decrease in contraction amplitude just before seizure cessation is also typical.Postictal phaseThe postictal phase causes are multifactorial to include alteration of cerebral blood flow and effects on multiple neurotransmitters. These changes after a generalized tonic–clonic seizure cause a period of postictal sleep with stertorous breathing. Confusion and total amnesia upon regaining consciousness are also usually experienced and slowly wear off as the patient becomes gradually aware that a seizure occurred and remembers their identity and location. Most often, patients regain consciousness within 30 minutes. Rarely, impaired consciousness duration can last several hours after a seizure, especially with a compounding central nervous system condition or a prolonged seizure. Occasionally the patient may vomit or burst into tears from the experienced mental trauma. An additional smaller seizure can also occur several minutes after the main seizure, particularly if the patients seizure threshold has been brought unusually low by known factors or combinations of such </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nonunion and explain in detail? [/INST] Nonunion is permanent failure of healing following a broken bone unless intervention (such as surgery) is performed. A fracture with nonunion generally forms a structural resemblance to a fibrous joint, and is therefore often called a "false joint" or pseudoarthrosis (from Greek pseudo-, meaning false, and arthrosis, meaning joint). The diagnosis is generally made when there is no healing between two sets of medical imaging, such as X-ray or CT scan. This is generally after 6–8 months.Nonunion is a serious complication of a fracture and may occur when the fracture moves too much, has a poor blood supply or gets infected. Patients who smoke have a higher incidence of nonunion. The normal process of bone healing is interrupted or stalled.Since the process of bone healing is quite variable, a nonunion may go on to heal without intervention in very few cases. In general, if a nonunion is still evident at 6 months post-injury it will remain unhealed without specific treatment, usually orthopedic surgery. A non-union which does go on to heal is called a delayed union.

Signs and symptoms
A history of a broken bone is usually apparent. The patient complains of persistent pain at the fracture site and may also notice abnormal movement or clicking at the level of the fracture. An x-ray plate of the fractured bone shows a persistent radiolucent line at the fracture. Callus formation may be evident but callus does not bridge across the fracture. If there is doubt about the interpretation of the x-ray, stress x-rays, tomograms or CT scan may be used for confirmation.

Cause
The reasons for non-union are
avascular necrosis (the blood supply was interrupted by the fracture)
the two ends are not apposed (that is, they are not next to each other)
infection (particularly osteomyelitis)
the fracture is not fixed (that is, the two ends are still mobile)
soft-tissue imposition (there is muscle or ligament covering the broken ends and preventing them from touching each other)

Risk factors
Related to the person:
Age: Common in old age
Nutritional status : poor
Habits : Nicotine and alcohol consumption
Metabolic disturbance : Hyperparathyroidism
Can be found in those with NF1
Genetic predisposition
Causes related to fracture:
Related to the fracture site
Soft tissue interposition
Bone loss at the fracture
Infection
Loss of blood supply
Damage of surrounding muscles
Related to treatment
Inadequate reduction
Insufficient immobilization
Improperly applied fixation devices.

Types of Nonunion
There are typically three types of nonunion described.

Hypertrophic nonunion
In a hypertrophic nonunion, the fracture site contains adequate blood supply but the fracture ends fail to heal together.  X-rays show abundant callus formation.  This type of nonunion is thought to occur when the body has adequate biology, such as stem cells and blood supply, but inadequate stability, meaning the bone ends are moving too much.  Typically, the treatment consists of increasing stability of the fracture site with surgical implants.

Atrophic nonunion
In an atrophic nonunion, x-rays show little to no callus formation.  This is usually due to impaired bony healing, for example due to vascular causes (e.g. impaired blood supply to the bone fragments) or metabolic causes (e.g. diabetes or smoking). Failure of initial union, as when bone fragments are separated by soft tissue, may also lead to an atrophic non-union. Atrophic non-unions can be treated by stimulating blood flow and encouraging healing.  This is often done surgically by removing the end layer of bone to provide raw ends for healing and the use of bone grafts.

Oligotrophic nonunion
As the name implies, an oligotrophic nonunion demonstrates some attempt by the body to heal the fracture.  These are thought to arise from adequate biology but displacement at the fracture site.

Diagnosis
A diagnosis of nonunion is made when the clinician feels there will be no further bone healing without intervention.  The FDA defines it as a fracture at least 9 months old that has not shown any signs of radiographic healing within the last 3 months.  CT scans offer a closer look at the fracture and may also be used to evaluate how much of the fracture has healed.  Blood tests can evaluate if the patient has adequate levels of nutrients such as calcium and vitamin D.  Blood tests can also look for markers of infection such as ESR and CRP.

Treatment
Surgery
Currently, there are different strategies to augment the bone-regeneration process, however, there is no standardised clinical treatment guideline yet. Surgical treatment options include:
Debridement: radical surgical removal of necrotic or infected soft tissue and bone tissue is deemed essential for the healing process.
Immobilization of the fracture with internal or external fixation. Metal plates, pins, screws, and rods, that are screwed or driven into a bone, are used to stabilize the broken bone fragments.
Bone grafting. Filling of the bone defect resulting from debridement must be performed.  Autologous bone graft is the "gold standard" treatment and possesses osteogenic, osteoinductive, and osteoconductive properties, although only a limited sample can be taken and there is a high risk of side effects.
Bone graft substitutes. Inorganic bone substitutes may be used to complement or replace autologous bone grafting. The advantage is that there is no morbidity on sampling and their availability is not restricted. S53P4 bioactive glass has shown good results as a promising bone graft substitute in treatment of nonunions, due to its osteostimulative, osteoconductive and antimicrobial properties.In simple cases, healing may be evident within 3 months. Gavriil Ilizarov revolutionized the treatment of recalcitrant nonunions demonstrating that the affected area of the bone could be removed, the fresh ends "docked" and the remaining bone lengthened using an external fixator device </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bismuth and explain in detail? [/INST] Bismuth is a chemical element with the symbol Bi and atomic number 83. It is a weakly radioactive post-transition metal and one of the pnictogens, with chemical properties resembling its lighter group 15 siblings arsenic and antimony. Elemental bismuth may occur naturally, and its sulfide and oxide forms are important commercial ores. The free element is 86% as dense as lead. It is a brittle metal with a silvery-white color when freshly produced. Surface oxidation generally gives samples of the metal a somewhat rosy cast. Further oxidation under heat can give bismuth a vividly iridescent appearance due to thin-film interference. Bismuth is both the most diamagnetic element and one of the least thermally conductive metals known.
Bismuth was long considered the element with the highest atomic mass whose nuclei do not spontaneously decay. However, in 2003 it was discovered to be extremely weakly radioactive. The metals only primordial isotope, bismuth-209, experiences alpha decay at such a minute rate that its half-life is more than a billion times the estimated age of the observable universe. For all but the most exotic of uses bismuth may be considered stable because of its tremendously long half-life.Bismuth metal has been known since ancient times. Before modern analytical methods bismuths metallurgical similarities to lead and tin often led it to be confused for those metals. The etymology of "bismuth" is uncertain. The name may come from mid-sixteenth century New Latin translations of the German words weiße Masse or Wismuth, meaning white mass, which were rendered as bisemutum or bisemutium.

Main uses
Bismuth compounds account for about half the global production of bismuth. They are used in cosmetics; pigments; and a few pharmaceuticals, notably bismuth subsalicylate, used to treat diarrhea. Bismuths unusual propensity to expand as it solidifies is responsible for some of its uses, as in the casting of printing type. Bismuth has unusually low toxicity for a heavy metal. As the toxicity of lead and the cost of its environmental remediation became more apparent during the 20th century, suitable bismuth alloys have gained popularity as replacements for lead. Presently, around a third of global bismuth production is dedicated to needs formerly met by lead.

History and etymology
Bismuth metal has been known since ancient times and it was one of the first 10 metals to have been discovered. The name bismuth dates to around 1665 and is of uncertain etymology. The name possibly comes from obsolete German Bismuth, Wismut, Wissmuth (early 16th century), perhaps related to Old High German hwiz ("white"). The New Latin bisemutium (coined by Georgius Agricola, who Latinized many German mining and technical words) is from the German Wismuth, itself perhaps from weiße Masse, meaning "white mass".The element was confused in early times with tin and lead because of its resemblance to those elements. Because bismuth has been known since ancient times, no one person is credited with its discovery. Agricola (1546) states that bismuth is a distinct metal in a family of metals including tin and lead. This was based on observation of the metals and their physical properties.Miners in the age of alchemy also gave bismuth the name tectum argenti, or "silver being made" in the sense of silver still in the process of being formed within the Earth.Bismuth was also known to the Incas and used (along with the usual copper and tin) in a special bronze alloy for knives.

Beginning with Johann Heinrich Pott in 1738, Carl Wilhelm Scheele, and Torbern Olof Bergman, the distinctness of lead and bismuth became clear, and Claude François Geoffroy demonstrated in 1753 that this metal is distinct from lead and tin.

Characteristics
Physical characteristics
Bismuth is a brittle metal with a dark, silver-pink hue, often with an iridescent oxide tarnish showing many colors from yellow to blue. The spiral, stair-stepped structure of bismuth crystals is the result of a higher growth rate around the outside edges than on the inside edges. The variations in the thickness of the oxide layer that forms on the surface of the crystal cause different wavelengths of light to interfere upon reflection, thus displaying a rainbow of colors. When burned in oxygen, bismuth burns with a blue flame and its oxide forms yellow fumes. Its toxicity is much lower than that of its neighbors in the periodic table, such as lead, antimony, and polonium.
No other metal is verified to be more naturally diamagnetic than bismuth. (Superdiamagnetism is a different physical phenomenon.) Of any metal, it has one of the lowest values of thermal conductivity (after manganese, and maybe neptunium and plutonium) and the highest Hall coefficient. It has a high electrical resistivity. When deposited in sufficiently thin layers on a substrate, bismuth is a semiconductor, despite being a post-transition metal. Elemental bismuth is denser in the liquid phase than the solid, a characteristic it shares with germanium, silicon, gallium, and water. Bismuth expands 3.32% on solidification; therefore, it was long a component of low-melting typesetting alloys, where it compensated for the contraction of the other alloying components to form almost isostatic bismuth-lead eutectic alloys.
Though virtually unseen in nature, high-purity bismuth can form distinctive, colorful hopper crystals. It is relatively nontoxic and has a low melting point just above 271 °C, so crystals may be grown using a household stove, although the resulting crystals will tend to be of lower quality than lab-grown crystals.At ambient conditions, bismuth shares the same layered structure as the metallic forms of arsenic and antimony, crystallizing in the rhombohedral lattice (Pearson symbol hR6, space group R3m No. 166) of the trigonal crystal system. When compressed at room temperature, this Bi-I structure changes first to the monoclinic Bi-II at 2.55 GPa, then to the tetragonal Bi-III at 2.7 GPa, and finally to the body-centered cubic Bi-V at 7.7 GPa. The corresponding transitions can be monitored via changes in electrical conductivity; they are rather reproducible and abrupt and are therefore used for calibration of high-pressure equipment.

Chemical characteristics
Bismuth is stable to both dry and moist air at ordinary temperatures. When red-hot, it reacts with water to make bismuth(III) oxide.
2 Bi + 3 H2O → Bi2O3 + 3 H2It reacts with fluorine to make bismuth(V) fluoride at 500 °C or bismuth(III) fluoride at lower temperatures (typically from Bi melts); with other halogens it yields only bismuth(III) halides. The trihalides are corrosive and easily react with moisture, forming oxyhalides with the formula BiOX.
4 Bi + 6 X2 → 4 BiX3 (X = F, Cl, Br, I)
4 BiX3 + 2 O2 → 4 BiOX + 4 X2Bismuth dissolves in concentrated sulfuric acid to make bismuth(III) sulfate and sulfur dioxide.
6 H2SO4 + 2 Bi → 6 H2O + Bi2(SO4)3 + 3 SO2It reacts with nitric acid to make bismuth(III) nitrate (which decomposes into nitrogen dioxide when heated).
Bi + 6 HNO3 → 3 H2O + 3 NO2 + Bi(NO3)3It also dissolves in hydrochloric acid, but only with oxygen present.
4 Bi + 3 O2 + 12 HCl → 4 BiCl3 + 6 H2OIt is used as a transmetalating agent in the synthesis of alkaline-earth metal complexes:

3 Ba + 2 BiPh3 → 3 BaPh2 + 2 Bi

Isotopes
The only primordial isotope of bismuth, bismuth-209, was traditionally regarded as the heaviest stable isotope, but it had long been suspected to be unstable on theoretical grounds. This was finally demonstrated in 2003, when researchers at the Institut dAstrophysique Spatiale in Orsay, France, measured the alpha emission half-life of 209Bi to be 2.01×1019 years (3 Bq/Mg), over a billion times longer than the current estimated age of the universe. Owing to its extraordinarily long half-life, for all presently known medical and industrial applications, bismuth can be treated as if it is stable and nonradioactive. The radioactivity is of academic interest because bismuth is one of a few elements whose radioactivity was suspected and theoretically predicted before being detected in the laboratory. Bismuth has the longest known alpha decay half-life, although tellurium-128 has a double beta decay half-life of over 2.2×1024 years. Bismuths extremely long half-life means that less than approximately one-billionth of the bismuth present at the formation of the planet Earth would have decayed into thallium since then.
Several isotopes of bismuth with short half-lives occur within the radioactive disintegration chains of actinium, radium, and thorium, and more have been synthesized experimentally. Bismuth-213 is also found on the decay chain of neptunium-237 and uranium-233.Commercially, the radioactive isotope bismuth-213 can be produced by bombarding radium with bremsstrahlung photons from a linear particle accelerator. In 1997, an antibody conjugate with bismuth-213, which has a 45-minute half-life and decays with the emission of an alpha particle, was used to treat patients with leukemia. This isotope has also been tried in cancer treatment, for example, in the targeted alpha therapy (TAT) program.

Chemical compounds
Bismuth forms trivalent and pentavalent compounds, the trivalent ones being more common. Many of its chemical properties are similar to those of arsenic and antimony, although they are less toxic than derivatives of those lighter elements.

Oxides and sulfides
At elevated temperatures, the vapors of the metal combine rapidly with oxygen, forming the yellow trioxide, Bi2O3. When molten, at temperatures above 710 °C, this oxide corrodes any metal oxide and even platinum. On reaction with a base, it forms two series of oxyanions: BiO−2, which is polymeric and forms linear chains, and BiO3−3. The anion in Li3BiO3 is a cubic octameric anion, Bi8O24−24, whereas the anion in Na3BiO3 is tetrameric.The dark red bismuth(V) oxide, Bi2O5, is unstable, liberating O2 gas upon heating. The compound NaBiO3 is a strong oxidising agent.Bismuth sulfide, Bi2S3, occurs naturally in bismuth ores. It is also produced by the combination of molten bismuth and sulfur.

Bismuth oxychloride (BiOCl, see figure at right) and bismuth oxynitrate (BiONO3) stoichiometrically appear as simple anionic salts of the bismuthyl(III) cation (BiO+) which commonly occurs in aqueous bismuth compounds. However, in the case of BiOCl, the salt crystal forms in a structure of alternating plates of Bi, O, and Cl atoms, with each oxygen coordinating with four bismuth atoms in the adjacent plane. This mineral compound is used as a pigment and cosmetic (see below).

Bismuthine and bismuthides
Unlike the lighter pnictogens nitrogen, phosphorus, and arsenic, but similar to antimony, bismuth does not form a stable hydride. Bismuth hydride, bismuthine (BiH3), is an endothermic compound that spontaneously decomposes at room temperature. It is stable only below −60 °C. Bismuthides are intermetallic compounds between bismuth and other metals.In 2014 researchers discovered that sodium bismuthide can exist as a form of matter called a “three-dimensional topological Dirac semi-metal” (3DTDS) that possess 3D Dirac fermions in bulk. It is a natural, three-dimensional counterpart to graphene with similar electron mobility and velocity. Graphene and topological insulators (such as those in 3DTDS) are both crystalline materials that are electrically insulating inside but conducting on the surface, allowing them to function as transistors and other electronic devices. While sodium bismuthide (Na3Bi) is too unstable to be used in devices without packaging, it can demonstrate potential applications of 3DTDS systems, which offer distinct efficiency and fabrication advantages over planar graphene in semiconductor and spintronics applications.

Halides
The halides of bismuth in low oxidation states have been shown to adopt unusual structures. What was originally thought to be bismuth(I) chloride, BiCl, turns out to be a complex compound consisting of Bi5+9 cations and BiCl2−5 and Bi2Cl2−8 anions. The Bi5+9 cation has a distorted tricapped trigonal prismatic molecular geometry and is also found in Bi10Hf3Cl18, which is prepared by reducing a mixture of hafnium(IV) chloride and bismuth chloride with elemental bismuth, having the structure [Bi+] [Bi5+9] [HfCl2−6]3.: 50  Other polyatomic bismuth cations are also known, such as Bi2+8, found in Bi8(AlCl4)2. Bismuth also forms a low-valence bromide with the same structure as "BiCl". There is a true monoiodide, BiI, which contains chains of Bi4I4 units. BiI decomposes upon heating to the triiodide, BiI3, and elemental bismuth. A monobromide of the same structure also exists.
In oxidation state +3, bismuth forms trihalides with all of the halogens: BiF3, BiCl3, BiBr3, and BiI3. All of these except BiF3 are hydrolyzed by water.Bismuth(III) chloride reacts with hydrogen chloride in ether solution to produce the acid HBiCl4.The oxidation state +5 is less frequently encountered. One such compound is BiF5, a powerful oxidizing and fluorinating agent. It is also a strong fluoride acceptor, reacting with xenon tetrafluoride to form the XeF+3 cation:
BiF5 + XeF4 → XeF+3BiF−6

Aqueous species
In aqueous solution, the Bi3+ ion is solvated to form the aqua ion Bi(H2O)3+8 in strongly acidic conditions. At pH > 0 polynuclear species exist, the most important of which is believed to be the octahedral complex [Bi6O4(OH)4]6+.

Occurrence and production
In the Earths crust, bismuth is about twice as abundant as gold. The most important ores of bismuth are bismuthinite and bismite. Native bismuth is known from Australia, Bolivia, and China.
The difference between mining and refining production reflects bismuths status as a byproduct of extraction of other metals such as lead, copper, tin, molybdenum and tungsten. World bismuth production from refineries is a more complete and reliable statistic.Bismuth travels in crude lead bullion (which can contain up to 10% bismuth) through several stages of refining, until it is removed by the Kroll-Betterton process which separates the impurities as slag, or the electrolytic Betts process. Bismuth will behave similarly with another of its major metals, copper. The raw bismuth metal from both processes contains still considerable amounts of other metals, foremost lead. By reacting the molten mixture with chlorine gas the metals are converted to their chlorides while bismuth remains unchanged. Impurities can also be removed by various other methods for example with fluxes and treatments yielding high-purity bismuth metal (over 99% Bi).

Price
The price for pure bismuth metal has been relatively stable through most of the 20th century, except for a spike in the 1970s. Bismuth has always been produced mainly as a byproduct of lead refining, and thus the price usually reflected the cost of recovery and the balance between production and demand.Prior to World War II, demand for bismuth was small and mainly pharmaceutical — bismuth compounds were used to treat such conditions as digestive disorders, sexually transmitted diseases and burns. Minor amounts of bismuth metal were consumed in fusible alloys for fire sprinkler systems and fuse wire. During World War II bismuth was considered a strategic material, used for solders, fusible alloys, medications and atomic research. To stabilize the market, the producers set the price at $1.25 per pound ($2.75 /kg) during the war and at $2.25 per pound ($4.96 /kg) from 1950 until 1964.In the early 1970s, the price rose rapidly as a result of increasing demand for bismuth as a metallurgical additive to aluminium, iron and steel. This was followed by a decline owing to increased world production, stabilized consumption, and the recessions of 1980 and 1981–1982. In 1984, the price began to climb as consumption increased worldwide, especially in the United States and Japan. In the early 1990s, research began on the evaluation of bismuth as a nontoxic replacement for lead in ceramic glazes, fishing sinkers, food-processing equipment, free-machining brasses for plumbing applications, lubricating greases, and shot for waterfowl hunting. Growth in these areas remained slow during the middle 1990s, in spite of the backing of lead replacement by the United States federal government, but intensified around 2005. This resulted in a rapid and continuing increase in price.

Recycling
Most bismuth is produced as a byproduct of other metal-extraction processes including the smelting of lead, and also of tungsten and copper. Its sustainability is dependent on increased recycling, which is problematic.It was once believed that bismuth could be practically recycled from the soldered joints in electronic equipment. Recent efficiencies in solder application in electronics mean there is substantially less solder deposited, and thus less to recycle. While recovering the silver from silver-bearing solder may remain economic, recovering bismuth is substantially less so.Next in recycling feasibility would be sizeable catalysts with a fair bismuth content, such as bismuth phosphomolybdate. Bismuth used in galvanizing, and as a free-machining metallurgical additive.Bismuth in uses where it is dispersed most widely include certain stomach medicines (bismuth subsalicylate), paints (bismuth vanadate), pearlescent cosmetics (bismuth oxychloride), and bismuth-containing bullets. Recycling bismuth from these uses is impractical.

Applications
Bismuth has few commercial applications, and those applications that use it generally require small quantities relative to other raw materials. In the United States, for example, 733 tonnes of bismuth were consumed in 2016, of which 70% went into chemicals (including pharmaceuticals, pigments, and cosmetics) and 11% into bismuth alloys.Some manufacturers use bismuth as a substitute in equipment for potable water systems such as valves to meet "lead-free" mandates in the U.S. (began in 2014). This is a fairly large application since it covers all residential and commercial building construction.In the early 1990s, researchers began to evaluate bismuth as a nontoxic replacement for lead in various applications.

Medicines
Bismuth is an ingredient in some pharmaceuticals, although the use of some of these substances is declining.
Bismuth subsalicylate is used as an antidiarrheal; it is the active ingredient in such "pink bismuth" preparations as Pepto-Bismol, as well as the 2004 reformulation of Kaopectate. It is also used to treat some other gastro-intestinal diseases like shigellosis and cadmium poisoning. The mechanism of action of this substance is still not well documented, although an oligodynamic effect (toxic effect of small doses of heavy metal ions on microbes) may be involved in at least some cases. Salicylic acid from hydrolysis of the compound is antimicrobial for toxogenic E. coli, an important pathogen in travelers diarrhea.
A combination of bismuth subsalicylate and bismuth subcitrate is used to treat the bacteria causing peptic ulcers.
Bibrocathol is an organic bismuth-containing compound used to treat eye infections.
Bismuth subgallate, the active ingredient in Devrom, is used as an internal deodorant to treat malodor from flatulence and feces.
Bismuth compounds (including sodium bismuth tartrate) were formerly used to treat syphilis. Arsenic combined with either bismuth or mercury was a mainstay of syphilis treatment from the 1920s until the advent of penicillin in 1943.
"Milk of bismuth" (an aqueous suspension of bismuth hydroxide and bismuth subcarbonate) was marketed as an alimentary cure-all in the early 20th century, and has been used to treat gastrointestinal disorders.
Bismuth subnitrate (Bi5O(OH)9(NO3)4) and bismuth subcarbonate (Bi2O2(CO3)) are also used in medicine.

Cosmetics and pigments
Bismuth oxychloride (BiOCl) is sometimes used in cosmetics, as a pigment in paint for eye shadows, hair sprays and nail polishes. This compound is found as the mineral bismoclite and in crystal form contains layers of atoms (see figure above) that refract light chromatically, resulting in an iridescent appearance similar to nacre of pearl. It was used as a cosmetic in ancient Egypt and in many places since. Bismuth white (also "Spanish white") can refer to either bismuth oxychloride or bismuth oxynitrate (BiONO3), when used as a white pigment. Bismuth vanadate is used as a light-stable non-reactive paint pigment (particularly for artists paints), often as a replacement for the more toxic cadmium sulfide yellow and orange-yellow pigments. The most common variety in artists paints is a lemon yellow, visually indistinguishable from its cadmium-containing alternative.

Metal and alloys
Bismuth is used in metal alloys with other metals such as iron. These alloys are used in automatic sprinkler systems for fires. It forms the largest part (50%) of Roses metal, a fusible alloy, which also contains 25–28% lead and 22–25% tin. It was also used to make bismuth bronze which was used in the Bronze Age, having been found in Inca knives at Machu Picchu.

Lead replacement
The density difference between lead (11.32 g/cm3) and bismuth (9.78 g/cm3) is small enough that for many ballistics and weighting applications, bismuth can substitute for lead. For example, it can replace lead as a dense material in fishing sinkers. It has been used as a replacement for lead in shot, bullets and less-lethal riot gun ammunition. The Netherlands, Denmark, England, Wales, the United States, and many other countries now prohibit the use of lead shot for the hunting of wetland birds, as many birds are prone to lead poisoning owing to mistaken ingestion of lead (instead of small stones and grit) to aid digestion, or even prohibit the use of lead for all hunting, such as in the Netherlands. Bismuth-tin alloy shot is one alternative that provides similar ballistic performance to lead. (Another less expensive but also more poorly performing alternative is "steel" shot, which is actually soft iron.) Bismuths lack of malleability does, however, make it unsuitable for use in expanding hunting bullets.Bismuth, as a dense element of high atomic weight, is used in bismuth-impregnated latex shields to shield from X-ray in medical examinations, such as CTs, mostly as it is considered non-toxic.The European Unions Restriction of Hazardous Substances Directive (RoHS) for reduction of lead has broadened bismuths use in electronics as a component of low-melting point solders, as a replacement for traditional tin-lead solders. Its low toxicity will be especially important for solders to be used in food processing equipment and copper water pipes, although it can also be used in other applications including those in the automobile industry, in the European Union, for example.Bismuth has been evaluated as a replacement for lead in free-machining brasses for plumbing applications, although it does not equal the performance of leaded steels.

Other metal uses and specialty alloys
Many bismuth alloys have low melting points and are found in specialty applications such as solders. Many automatic sprinklers, electric fuses, and safety devices in fire detection and suppression systems contain the eutectic In19.1-Cd5.3-Pb22.6-Sn8.3-Bi44.7 alloy that melts at 47 °C (117 °F) This is a convenient temperature since it is unlikely to be exceeded in normal living conditions. Low-melting alloys, such as Bi-Cd-Pb-Sn alloy which melts at 70 °C, are also used in automotive and aviation industries. Before deforming a thin-walled metal part, it is filled with a melt or covered with a thin layer of the alloy to reduce the chance of breaking. Then the alloy is removed by submerging the part in boiling water.Bismuth is used to make free-machining steels and free-machining aluminium alloys for precision machining properties. It has similar effect to lead and improves the chip breaking during machining. The shrinking on solidification in lead and the expansion of bismuth compensate each other and therefore lead and bismuth are often used in similar quantities. Similarly, alloys containing comparable parts of bismuth and lead exhibit a very small change (on the order 0.01%) upon melting, solidification or aging. Such alloys are used in high-precision casting, e.g. in dentistry, to create models and molds. Bismuth is also used as an alloying agent in production of malleable irons and as a thermocouple material.Bismuth is also used in aluminium-silicon cast alloys in order to refine silicon morphology. However, it indicated a poisoning effect on modification of strontium. Some bismuth alloys, such as Bi35-Pb37-Sn25, are combined with non-sticking materials such as mica, glass and enamels because they easily wet them allowing to make joints to other parts. Addition of bismuth to caesium enhances the quantum yield of caesium cathodes. Sintering of bismuth and manganese powders at 300 °C produces a permanent magnet and magnetostrictive material, which is used in ultrasonic generators and receivers working in the 10–100 kHz range and in magnetic and holographic memory devices.

Other uses as compounds
Bismuth is included in BSCCO (bismuth strontium calcium copper oxide) which is a group of similar superconducting compounds discovered in 1988 that exhibit the highest superconducting transition temperatures.
Bismuth subnitrate is a component of glazes that produces an iridescence and is used as a pigment in paint.
Bismuth telluride is a semiconductor and an excellent thermoelectric material. Bi2Te3 diodes are used in mobile refrigerators, CPU coolers, and as detectors in infrared spectrophotometers.
Bismuth oxide, in its delta form, is a solid electrolyte for oxygen. This form normally breaks down below a high-temperature threshold, but can be electrodeposited well below this temperature in a highly alkaline solution.
Bismuth germanate is a scintillator, widely used in X-ray and gamma ray detectors.
Bismuth vanadate is an opaque yellow pigment used by some artists oil, acrylic, and watercolor paint companies, primarily as a replacement for the more toxic cadmium sulfide yellows in the greenish-yellow (lemon) to orange-toned yellow range. It performs practically identically to the cadmium pigments, such as in terms of resistance to degradation from UV exposure, opacity, tinting strength, and lack of reactivity when mixed with other pigments. The most commonly-used variety by artists paint makers is lemon in color. In addition to being a replacement for several cadmium yellows, it also serves as a non-toxic visual replacement for the older chromate pigments made with zinc, lead, and strontium. If a green pigment and barium sulfate (for increased transparency) are added it can also serve as a replacement for barium chromate, which possesses a more greenish cast than the others. In comparison with lead chromates, it does not blacken due to hydrogen sulfide in the air (a process accelerated by UV exposure) and possesses a particularly brighter color than them, especially the lemon, which is the most translucent, dull, and fastest to blacken due to the higher percentage of lead sulfate required to produce that shade. It is also used, on a limited basis due to its cost, as a vehicle paint pigment.
A catalyst for making acrylic fibers.
As an electrocatalyst in the conversion of CO2 to CO.
Ingredient in lubricating greases.
In crackling microstars (dragons eggs) in pyrotechnics, as the oxide, subcarbonate or subnitrate.
As catalyst for the fluorination of arylboronic pinacol esters through a Bi(III)/Bi(V) catalytic cycle, mimicking transition metals in electrophilic fluorination.

Toxicology and ecotoxicology
See also bismuthia, a rare dermatological condition that results from the prolonged use of bismuth.Scientific literature indicates that some of the compounds of bismuth are less toxic to humans via ingestion than other heavy metals (lead, arsenic, antimony, etc.) presumably due to the comparatively low solubility of bismuth salts. Its biological half-life for whole-body retention is reported to be 5 days but it can remain in the kidney for years in people treated with bismuth compounds.Bismuth poisoning can occur and has according to some reports been common in relatively recent times. As with lead, bismuth poisoning can result in the formation of a black deposit on the gingiva, known as a bismuth line. Poisoning may be treated with dimercaprol; however, evidence for benefit is unclear.Bismuths environmental impacts are not well known; it may be less likely to bioaccumulate than some other heavy metals, and this is an area of active research.

Bioremediation
The fungus Marasmius oreades can be used for the biological remediation of bismuth in polluted soils.

See also
Lead-bismuth eutectic
List of countries by bismuth production
Bismuth minerals
Patterns in nature

References
Bibliography
This article incorporates text from this source, which is in the public domain:  Brown, R. D., Jr. "Annual Average Bismuth Price", USGS (1998)

Greenwood, N. N. & Earnshaw, A. (1997). Chemistry of the Elements (2nd ed.). Oxford: Butterworth-Heinemann. ISBN 978-0-7506-3365-9.
Krüger, Joachim; Winkler, Peter; Lüderitz, Eberhard; Lück, Manfred; Wolf, Hans Uwe (2003). "Bismuth, Bismuth Alloys, and Bismuth Compounds". Ullmanns Encyclopedia of Industrial Chemistry. Wiley-VCH, Weinheim. pp. 171–189. doi:10.1002/14356007.a04_171 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Developmental language disorder and explain in detail? [/INST] Developmental language disorder (DLD) is identified when a child has problems with language development that continue into school age and beyond. The language problems have a significant impact on everyday social interactions or educational progress, and occur in the absence of autism spectrum disorder, intellectual disability or a known biomedical condition. The most obvious problems are difficulties in using words and sentences to express meanings, but for many children, understanding of language (receptive language) is also a challenge. This may not be evident unless the child is given a formal assessment.

Classification
Terminology
The term developmental language disorder (DLD) was endorsed in a consensus study involving a panel of experts (CATALISE Consortium) in 2017. The study was conducted in response to concerns that a wide range of terminology was used in this area, with the consequence that there was poor communication, lack of public recognition, and in some cases children were denied access to services. Developmental language disorder is a subset of language disorder, which is itself a subset of the broader category of speech, language and communication needs (SLCN).
The terminology for childrens language disorders has been extremely wide-ranging and confusing, with many labels that have overlapping but not necessarily identical meanings. In part this confusion reflected uncertainty about the boundaries of DLD, and the existence of different subtypes. Historically, the terms "developmental dysphasia" or "developmental aphasia" were used to describe children with the clinical picture of DLD. These terms have, however, largely been abandoned, as they suggest parallels with adult-acquired aphasia. This is misleading, as DLD is not caused by brain damage.Although the term DLD has been used for many years, it has been less common than the term specific language impairment (SLI), which has been widely adopted, especially in North America. The definition of SLI overlaps with DLD, but was rejected by the CATALISE panel because it was seen as overly restrictive in implying that the child had relatively pure problems with language in the absence of any other impairments. Children with such selective problems are relatively rare, and there is no evidence that they respond differently to intervention, or have different causal factors, from other children with language problems.In the UK education system, the term speech, language and communication needs (SLCN) is widely used, but this is far broader than DLD, and includes children with speech, language and social communication difficulties arising from a wide range of causes.The question of whether to refer to childrens language problems as a disorder was a topic of debate among the CATALISE consortium, but the conclusion was that disorder conveyed the serious nature and potential consequences of persistent language deficits. It is also parallel with other neurodevelopmental conditions and consistent with diagnostic frameworks such as the DSM-5 and ICD-11. Where there are milder or more transient difficulties, language difficulties may be a more appropriate term.

Areas of language difficulty
DLD can affect a range of areas of language and the degree of impairment in different areas of language can vary from child to child. However, although there have been attempts to define different subtypes, these have not generally resulted in robust categories. The recommendation of the CATALISE panel was that the specific areas of impairment should be assessed and documented for individual children, while recognizing that different children might have different combinations of problems. The areas which can be affected are:

Grammar – This involves the ability to combine words into grammatically correct sentences (syntax) and to combine parts of words together (morphology) such as adding grammatical endings to verbs like -ing or -ed or to add prefixes and suffixes like dis- or -ation. For instance, a child may say me jump here, instead of I jumped here. Comprehension of sentences can also be affected. For instance, there may be difficulty understanding meaning expressed by word order, and so confusion about what is blue in a sentence like the pencil on the shoe is blue, and a tendency to use general knowledge rather than linguistic cues to meaning, or problems in interpreting grammatical markers of number or tense.
Semantics – This refers to childrens ability to understand the meaning of words and how meanings are expressed by combining words together. Children with DLD often have limited vocabulary and may make heavy use of a small set of words with rather general meanings. As children with developmental language disorder get older, they may have a hard time understanding that some words have multiple meanings, for example the word "cold", which can mean a low temperature, a sickness, or being unfriendly.
Word finding – Children with word finding difficulties may know a word, but have difficulty accessing it for production – similar to the tip of the tongue phenomenon.
Pragmatics – Pragmatics refers to the ability to select the appropriate message, or interpret what others say, in relation to context. Pragmatic difficulties can give an impression of oddity, with the content of language not fitting the environmental or social context; comprehension may be over-literal; the child may chatter incessantly, be poor at turn-taking in conversation and maintaining a topic
Discourse – Discourse refers to a level of organization of language beyond the sentence. Child with limitations in this domain may have limited ability to tell a story or describe a set of events in a logical sequence
Verbal memory and learning – Problems with remembering words or sentences can affect both the learning of new vocabulary, and the understanding of long or complex sentences. Young children with DLD may say their first words later than other children. It may also take children with DLD longer to learn and remember novel words.
Phonology – Phonology is the branch of linguistics concerned with the way sounds are combined in words. Children with difficulties with phonology may fail to distinguish between certain speech sounds, such as t and k, so that cake is produced as tate. Such difficulties are not unusual as part of typical development in toddlers, but they would usually resolve by the time children are 4–5 years old. Difficulties with producing some speech sounds accurately may reduce intelligibility of speech. In addition, more subtle difficulties in recognising specific sounds in words (phonological awareness) can lead to literacy difficulties.

Relationship with speech disorders
Speech is the act of articulating sounds, and this can be impaired for all kinds of reasons – a structural problem such as cleft lip and cleft palate, a neurological problem affecting motor control of the speech apparatus dysarthria, or inability to perceive distinctions between sounds because of hearing loss. Some distortions of speech sounds, such as a lisp, are commonly seen in young children. These misarticulations should not be confused with language problems, which involve the ability to select and combine linguistic elements to express meanings, and the ability to comprehend meanings.Although speech disorders can be distinguished from language disorders, they can also co-occur. When a child fails to produce distinctions between speech sounds for no obvious reason, this is typically regarded as a language problem affecting the learning of phonological contrasts. The classification of and terminology for disorders of speech sound production is a subject of considerable debate. In practice, even for those with specialist skills, it is not always easy to distinguish between phonological disorders and other types of speech production problem.
Speech sound disorder (SSD) is any problem with speech production arising from any cause.Speech sound disorders of unknown cause that are not accompanied by other language problems are a relatively common reason for young children to be referred to speech-language therapy (speech-language pathology). These often resolve by around 4–5 years of age with specialist intervention, and so would not meet criteria for DLD. Where such problems continue beyond five years of age, they are usually accompanied by problems in broader language domains and have a poorer prognosis, so a diagnosis of DLD with SSD is then appropriate.

Relationship with other neurodevelopmental disorders
DLD often co-occurs with milder neurodevelopmental disorders of unknown origin, such as attention-deficit hyperactivity disorder, developmental dyslexia or developmental coordination disorder. These do not preclude a diagnosis of DLD, but should be noted as co-occurring conditions.

Risk factors
It is generally accepted that DLD is strongly influenced by genetic factors. The best evidence comes from the twin study method. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, much more common in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability. There can be some variation in the severity and persistence of DLD in identical twins, indicating that non-genetic factors affect the course of disorder, but it is unusual to find a child with DLD who has an identical twin with typical language.There was considerable excitement when a large, multigenerational family with a high rate of DLD were found to have a mutation of the FOXP2 gene just in the affected family members. However, subsequent studies have found that, though DLD runs in families, it is not usually caused by a mutation in FOXP2 or another specific gene. Current evidence suggests that there are many different genes that can influence language learning, and DLD results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. Nevertheless, study of the mode of action of the FOXP2 gene has helped identify other common genetic variants involved in the same neural pathways that may play a part in causing DLD.Language disorders are associated with aspects of home environment, and it is often assumed that this is a causal link, with poor language stimulation leading to weak language skills. Twin studies, however, show that two children in the same home environment can have very different language outcomes, suggesting we should consider other explanations for the link. Children with DLD often grow up into adults who have relatively low educational attainments, and their children may share a genetic risk for language disorder.One non-genetic factor that is known to have a specific impact on language development is being a younger sibling in a large family.

Associated factors
It has long been noted that males are more affected by DLD than females, with a sex ratio of affected males-to-females around 3 or 4:1. However, the sex difference is much less striking in epidemiological samples, suggesting that similar problems may exist in females but are less likely to be detected. The reason for the sex difference is not well understood.Poor motor skills are commonly found in children with DLD. Standardized measures of motor ability confirm that children with DLD exhibit deficits in fine and gross motor skill, both simple and complex. These difficulties also extend to speech-motor ability, particularly with the control of their articulatory movements. Children with DLD have difficulty with motor sequence learning and may show deficits in other procedural motor processes as well.Brain scans do not usually reveal any obvious abnormalities in children with DLD, although quantitative comparisons have found differences in brain size or relative proportions of white or grey matter in specific regions. In some cases, unusual brain gyri are found. To date, no consistent neural signature for DLD has been found, although some studies have noted evidence for involvement of subcortical systems. Differences in the brains of children with DLD versus typically developing children are subtle and may overlap with atypical patterns seen in other neurodevelopmental disorders.

Diagnosis
DLD is defined purely in behavioural terms: there is no biological test. There are three points that need to be met for a diagnosis of DLD:
The child has language difficulties that create obstacles to communication or learning in everyday life,
The childs language problems are unlikely to resolve by five years of age, and
The problems are not associated with a known biomedical condition such as brain injury, neurodegenerative conditions, genetic conditions or chromosome disorders such as Down syndrome, sensorineural hearing loss, autism spectrum disorder, or intellectual disability.For research and epidemiological purposes, specific cutoffs on language assessments have been used to document the first criterion. Tomblin et al. proposed the EpiSLI criterion, based on five composite scores representing performance in three domains of language (vocabulary, grammar, and narration) and two modalities (comprehension and production). Children scoring in the lowest 10% on two or more composite scores are identified as having language disorder.
The second criterion, persistence of language problems, can be difficult to judge in a young child, but longitudinal studies have shown that difficulties are less likely to resolve for children who have poor language comprehension, rather than difficulties confined to expressive language. In addition, children with isolated difficulties in just one of the areas noted under subtypes tend to make better progress than those whose language is impaired in several areas.The third criterion specifies that DLD is used for children whose language disorder is not part of another biomedical condition, such as a genetic syndrome, a sensorineural hearing loss, neurological disease, autism spectrum disorder or intellectual disability – these were termed differentiating conditions by the CATALISE panel. Language disorders occurring with these conditions need to be assessed and children offered appropriate intervention, but a terminological distinction is made so that these cases would be diagnosed as language disorder associated with the main diagnosis being specified: e.g. "language disorder associated with autism spectrum disorder." The reasoning behind these diagnostic distinctions is discussed further by Bishop (2017).

Benchmarks for children with developmental language disorder
Common red flags at one year of age:

No reaction to sound
No babbling
Difficulty feeding
No imitation
Limited use of gesturesAt two years of age:

Makes minimal attempts to communicate with gestures or words
Has not spoken their first words
Difficulty following simple directions
Inconsistent response to "no"At three years of age:

Limited use of speech
Incomprehensible speech
Limited understanding of simple questions
Difficulty naming objects
Frustration related to communicationAt four years of age:

Uses only 3-word phrases
Speech is not understandable to parents
Takes a long time to understand others
Difficulty asking questions and finding words to express thoughtsAt five years of age:

Speaks only in simple sentences
Speech is not understandable to teachers
Difficulty answering questions
Difficulty with complex directions
Difficulty telling stories
Difficulty with peer interactions

Assessment
Assessment will usually include an interview with the childs caregiver, observation of the child in an unstructured setting, a hearing test, and standardized tests of language. There is a wide range of language assessments in English. Some are restricted for use by experts in speech-language pathology: speech and language therapists (SaLTs/SLTs) in the UK, speech-language pathologists (SLPs) in the US and Australia. A commonly used test battery for diagnosis of DLD is the Clinical Evaluation of Language Fundamentals (CELF).
Assessments that can be completed by a parent or teacher can be useful to identify children who may require more in-depth evaluation. The Children’s Communication Checklist (CCC–2) is a parent questionnaire suitable for assessing everyday use of language in children aged four years and above who can speak in sentences.
Informal assessments, such as language samples, are often used by speech-language therapists/pathologists to complement formal testing and give an indication of the childs language in a more naturalistic context. A language sample may be of a conversation or narrative retell. In a narrative language sample, an adult may tell the child a story using a wordless picture book (e.g. Frog Where Are You?, Mayer, 1969), then ask the child to use the pictures and tell the story back. Language samples can be transcribed using computer software such as the Systematic Analysis of Language Software, and then analyzed for a range of features: e.g., the grammatical complexity of the childs utterances,  whether the child introduces characters to their story or jumps right in, whether the events follow a logical order, and whether the narrative includes a main idea or theme and supporting details.

Treatment
Treatment is usually carried out by speech and language therapists/pathologists, who use a wide range of techniques to stimulate language learning. In the past, there was a vogue for drilling children in grammatical exercises, using imitation and elicitation, but such methods fell into disuse when it became apparent that there was little generalisation to everyday situations. Contemporary approaches to enhancing development of language structure, for younger children at least, are more likely to adopt milieu methods, in which the intervention is interwoven into natural episodes of communication, and the therapist builds on the childs utterances, rather than dictating what will be talked about. Interventions for older children, may be more explicit, telling the children what areas are being targeted and giving explanations regarding the rules and structures they are learning, often with visual supports.In addition, there has been a move away from a focus solely on grammar and phonology toward interventions that develop childrens social use of language, often working in small groups that may include typically developing as well as language-impaired peers.Another way in contemporary remediation differ from the past is that parents are more likely to be directly involved, but this approach is largely used with preschool children, rather than those whose problems persist into school age.For school-aged children, teachers are increasingly involved in intervention, either in collaboration with speech and language therapists/pathologists, or as the main agents of delivery of the intervention. Evidence for the benefits of a collaborative approach is emerging, but the benefits of asking education staff to be the main deliverers of SLT intervention (the "consultative" approach) are unclear. When SLT intervention is delivered indirectly by trained SLT assistants, however, there are indications that this can be effective.In this field, randomized controlled trial methodology has not been widely used, and this makes it difficult to assess clinical efficacy with confidence. Childrens language will tend to improve over time, and without controlled studies, it can be hard to know how much of observed change is down to a specific treatment. There is, however, increasing evidence that direct 1:1 intervention with an SLT/P can be effective for improving vocabulary and expressive language. There have been few studies of interventions that target receptive language, though some positive outcomes have been reported.

How to help a child with developmental language disorder
Talk to the child often to help them learn new words
Read to them every day. Point out words you see
Point to signs in the grocery store, at school, and outside
Speak to the child in the language you know best
Listen and answer when the child talks
Get the child to ask you questions
Give the child time to answer questions
Keep them in school: children who are school-refusers have poorer language skills overall, and a higher incidence of language impairments

Outcome
Longitudinal studies indicate that problems are largely resolved by five years of age in around 40% of four-year-olds with early language delays who have no other presenting risk factors. However, for children who still have significant language difficulties at school entry, reading problems are common, even for children who receive specialist help, and educational attainments are typically poor. Poor outcomes are most common in cases where comprehension as well as expressive language is affected. There is also evidence that scores on tests of nonverbal ability of children with DLD decrease over the course of development.DLD is associated with an elevated risk of social, emotional and mental health concerns. For instance, in a UK survey, 64% of a sample of 11-year-olds with DLD scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. In the longer-term, studies of adult outcomes of children with DLD have found elevated rates of unemployment, social isolation and psychiatric disorder among those with early comprehension difficulties. However, better outcomes are found for children who have milder difficulties and do not require special educational provision.

Prevalence
Epidemiological surveys in the US and the UK converge in estimating the prevalence of DLD in five-year-olds at around 7%. Therefore, the prevalence is about one in every 15 children.  By these statistics, in a classroom of 30 students, 2 would have DLD. In research by Tomblin et al., prevalence of DLD in racial/ethnic groups was highest in Native Americans, with African Americans being the next highest, followed by Hispanic people, and then White people. No students of Asian descent presented with DLD; however, other research does indicate that DLD is present in children of Asian descent.

Research
Much research has focused on trying to identify what makes language learning difficult for some children. A major divide is between theories that attribute the difficulties to a low-level problem with auditory temporal processing, and those that propose there is a deficit in a specialised language-learning system. Other accounts emphasise deficits in specific aspects of learning and memory. It can be difficult to choose between theories because they do not always make distinctive predictions, and there is considerable heterogeneity among children with DLD. It has also been suggested that DLD may only arise when more than one underlying deficit is present.

Developmental learning disorder in adults
Relatively little research has been conducted to test the outcomes of DLD in adults. In a study comparing 17 men with DLD to siblings without DLD, researchers found that the DLD men had normal intelligence with higher performance IQ than verbal IQ. The participants still exhibited a severe and persisting language disorder, severe literacy impairments, and significant deficits in theory of mind and phonological processing. Within the DLD cohort, higher childhood intelligence and language were associated with superior cognitive and language ability at final adult outcome. In their mid-thirties, the DLD cohort had significantly worse social adaptation (with prolonged unemployment and a paucity of close friendships and love relationships) compared with both their siblings and National Child Development Study (NCDS) control cohorts, matched on childhood IQ and social class. Self-reports showed a higher rate of schizotypal features but not schizoaffective disorder </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Anophthalmia and explain in detail? [/INST] Anophthalmia, (Greek: ἀνόφθαλμος, "without eye"), is the medical term for the absence of one or both eyes. Both the globe (human eye) and the ocular tissue are missing from the orbit. The absence of the eye will cause a small bony orbit, a constricted mucosal socket, short eyelids, reduced palpebral fissure and malar prominence. Genetic mutations, chromosomal abnormalities, and prenatal environment can all cause anophthalmia. Anophthalmia is an extremely rare disease and is mostly rooted in genetic abnormalities. It can also be associated with other syndromes.

Causes
SOX2
The most common genetic cause for anophthalmia is mutated SOX2 gene. Sox2 anophthalmia syndrome is caused by a mutation in the Sox2 gene that does not allow it to produce the Sox2 protein that regulates the activity of other genes by binding to certain regions of DNA. Without this Sox2 protein, the activity of genes that is important for the development of the eye is disrupted. Sox2 anophthalmia syndrome is an autosomal dominant inheritance, but the majority of patients who suffer from Sox2 anophthalmia are the first in their family history to have this mutation. In certain cases, one parent will possess the mutated gene only in their egg or sperm cell and the offspring will inherit it through that. This is called germline mosaicism. There are at least 33 mutations in the Sox2 gene that have been known to cause anophthalmia. Some of these gene mutations will cause the Sox2 protein not to be formed, while other mutations will yield a non-functional version of this protein.

RBP4
RBP4 has recently been linked to autosomal dominant form of anophthalmia. This form of anophthalmia has variable penetrance and a unique maternal inheritance effect that is rooted in pregnancy. Specifically, the disease only occurs when a mother and fetus both carry a RBP4 mutation which predisposes the fetus to vitamin A deficiency (a known environmental risk factor for anophthalmia) during pregnancy. If Vitamin A deficiency occurs during the first several months when the eye is developing, it may lead to anophthalmia. This form of anophthalmia is the first that may be intervened upon with vitamin A supplementation of retinyl esters during the first several months of pregnancy. This strategy exploits an RBP-independent pathway. Clinical research is underway. See RBP4 for more information.

Other influential genes
SOX2 and RBP4 are not the only genes that can cause anophthalmia.  Other important genes include OTX2, CHX10 and RAX. Each of these genes are an important in retinal expression. Mutations in these genes can cause a failure of retinal differentiation. OTX2 is dominantly inherited. Mutation effects vary in severity, and can include microphthalmia. BMP4 is also linked to anophthalmia, as well as causing myopia and microphthalmia. It is dominantly inherited. BMP4 interacts with the Sonic hedgehog (SHH) pathway and can cause anophthalmia.

Environmental influence
Many environmental conditions have also been known to cause anophthalmia. The strongest support for environmental causes has been studies where children have had gestational-acquired infections. These infections are typically viral. A few known pathogens that can cause anophthalmia are Toxoplasma, rubella, and certain strains of the influenza virus. Other known environmental conditions that have led to anophthalmia are maternal vitamin A deficiency, exposure to X-rays during gestation, solvent abuse, and exposure to thalidomide.

Chromosome 14
An interstitial deletion of chromosome 14 has been known to occasionally be the source of anophthalmia. The deletion of this region of chromosome has also been associated with patients having a small tongue, and high arched palate, developmental and growth retardation, undescended testes with a micropenis, and hypothyroidism. The region that has been deleted is region q22.1-q22.3. This confirms that region 22 on chromosome 14 influences the development of the eye.

Classifications
There are three classifications for this condition:

Primary anophthalmia is a complete absence of eye tissue due to a failure of the part of the brain that forms the eye.
Secondary anophthalmia the eye starts to develop and for some reason stops, leaving the infant with only residual eye tissue or extremely small eyes which can only be seen under close examination.
Degenerative anophthalmia the eye started to form and, for some reason, degenerated. One reason for this occurring could be a lack of blood supply to the eye.

Prenatal diagnosis
Ultrasounds
Ultrasounds can be used to diagnose anophthalmia during gestation. Due to the resolution of the ultrasound, it is difficult to diagnose it until the second trimester. The earliest time to detect anophthalmia this way is approximately 20 weeks.

Amniocentesis
It is possible to diagnose prenatally with amniocentesis, but it may not show a correct negative result. Amniocentesis can only diagnose anophthalmia when there is a chromosomal abnormality. Chromosomal abnormalities are only a minority of cases of anophthalmia.

Postnatal diagnosis
MRI/CT
MRIs and CTs can be used to scan the brain and orbits. Radiologists use this to assess the internal structures of the globe, the optic nerve and extraocular muscles, and brain anatomy.

Examination
Physicians, specifically ophthalmologists, can examine the child and give a correct diagnosis. Some will do molecular genetics tests to see if the cause is linked with gene mutations.
Genetic testing can include chromosomal microarray analysis, single-gene testing, or multigene-panel testing. Genomic testing including exome sequencing, genome sequencing, and mitochondrial sequencing may be considered if single-gene testing or use of a multigene panel fails to confirm a molecular diagnosis.

Associations
There are a few conditions that are associated with Anophthalmia. These include:
Trisomy 13
Lenz Syndrome
Goldenhar-Gorlin Syndrome
Waardenburg syndromeAside from these associative conditions, anophthalmia in only one eye tends to be associated with complications in the other eye. These risks include a higher chance of having glaucoma or a detached retina.

Treatments
Prosthetic eye
Currently, there is not a treatment option for regaining vision by developing a new eye. There are, however, cosmetic options so the absence of the eye is not as noticeable. Typically, the child will need to go to a prosthetic specialist to have conformers fitted into the eye. Conformers are made of clear plastic and are fitted into the socket to promote socket growth and expansion. As the childs face grows and develops, the conformer will need to be changed. An expander may also be needed in anophthalmia to expand the socket that is present. The conformer is changed every few weeks the first two years of life. After that, a painted prosthetic eye can be fitted for the childs socket. The prosthetic eye can be cleaned with mild baby soap and water. Rubbing alcohol should be avoided because it may damage the prosthetic eye. Children need to be checked regularly to ensure the fit and size is appropriate.A Cochrane Review published in 2016 asked the question would the type of material used to make the prosthetic eye affect the success of the operation?  Prosthetic eyes can be made from two types of material; porous or non-porous material. "If the material is porous then the artificial eye can become integrated into the body because new blood vessels can grow into the material. If the material is non‐porous, then the artificial eye remains separate from the rest of the bodys tissue." After assessing three studies, the review concluded that there wasnt enough evidence to conclude which material was better.

Cosmetic surgery
If the proper actions are not taken to expand the orbit, many physical deformities can appear. It is important that if these deformities do appear, that surgery is not done until at least the first two years of life. Many people get eye surgery, such as upper eyelid ptosis surgery and lower eyelid tightening. These surgeries can restore the function of the surrounding structures like the eyelid in order to create the best appearance possible. This is more common with people who have degenerative anophthalmia.

Epidemiology
Anophthalmia has been reported to be present in 3 out of every 100,000 births </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cinchonism and explain in detail? [/INST] Cinchonism is a pathological condition caused by an overdose of quinine or its natural source, cinchona bark.  Quinine and its derivatives are used medically to treat malaria and lupus erythematosus. In much smaller amounts, quinine is an ingredient of tonic drinks, acting as a bittering agent. Cinchonism can occur from therapeutic doses of quinine, either from one or several large doses. Quinidine (a Class 1A anti-arrhythmic) can also cause cinchonism symptoms to develop with as little as a single dose.

Signs and symptoms
Signs and symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity), vertigo, dizziness, nausea, vomiting and diarrhea.
Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Collagenous colitis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Tarsal tunnel syndrome and explain in detail? [/INST] Tarsal tunnel syndrome (TTS) is a compression neuropathy and painful foot condition in which the tibial nerve is compressed as it travels through the tarsal tunnel. This tunnel is found along the inner leg behind the medial malleolus (bump on the inside of the ankle). The posterior tibial artery, tibial nerve, and tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus muscles travel in a bundle through the tarsal tunnel. Inside the tunnel, the nerve splits into three segments. One nerve (calcaneal) continues to the heel, the other two (medial and lateral plantar nerves) continue on to the bottom of the foot. The tarsal tunnel is delineated by bone on the inside and the flexor retinaculum on the outside.
Patients with TTS typically complain of numbness in the foot radiating to the big toe and the first three toes, pain, burning, electrical sensations, and tingling over the base of the foot and the heel. Depending on the area of entrapment, other areas can be affected.  If the entrapment is high, the entire foot can be affected as varying branches of the tibial nerve can become involved. Ankle pain is also present in patients who have high level entrapments. Inflammation or swelling can occur within this tunnel for a number of reasons. The flexor retinaculum has a limited ability to stretch, so increased pressure will eventually cause compression on the nerve within the tunnel. As pressure increases on the nerves, the blood flow decreases. Nerves respond with altered sensations like tingling and numbness. Fluid collects in the foot when standing and walking and this makes the condition worse. As small muscles lose their nerve supply they can create a cramping feeling.

Symptoms
Some of the symptoms are:

Pain and tingling in and around ankles and sometimes the toes
Swelling of the feet and ankle area.
Painful burning, tingling, or numb sensations in the lower legs. Pain worsens and spreads after standing for long periods; pain is worse with activity and is relieved by rest.
Electric shock sensations
Pain radiating up into the leg, behind the shin, and down into the arch, heel, and toes
Hot and cold sensations in the feet
A feeling as though the feet do not have enough padding
Pain while operating automobiles
Pain along the posterior tibial nerve path
Burning sensation on the bottom of foot that radiates upward reaching the knee
"Pins and needles"-type feeling and increased sensation on the feet
A positive Tinels signTinels sign is a tingling electric shock sensation that occurs when you tap over an affected nerve. The sensation usually travels into the foot but can also travel up the inner leg as well.

Causes
It is difficult to determine the exact cause of tarsal tunnel syndrome. It is important to attempt to determine the source of the problem. Treatment and the potential outcome of the treatment may depend on the cause. Anything that creates pressure in the tarsal tunnel can cause TTS. This would include benign tumors or cysts, bone spurs, inflammation of the tendon sheath, nerve ganglions, or swelling from a broken or sprained ankle. Varicose veins (that may or may not be visible) can also cause compression of the nerve. TTS is more common in athletes and other active people. These people put more stress on the tarsal tunnel area. Flat feet may cause an increase in pressure in the tunnel region and this can cause nerve compression. Those with lower back problems may have symptoms. Back problems with the L4, L5 and S1 regions are suspect and might suggest a "Double Crush" issue: one "crush" (nerve pinch or entrapment) in the lower back, and the second in the tunnel area. In some cases, TTS can simply be idiopathic.

Rheumatoid Arthritis has also been associated with TTS.Neurofibromatosis can also cause TTS. This is a disease that results in the formation of pigmented, cutaneous neurofibromas. These masses, in a specific case, were shown to have the ability to invade the tarsal tunnel causing pressure, therefore resulting in TTS.Diabetes makes the peripheral nerve susceptible to nerve compression, as part of the double crush hypothesis. In contrast to carpal tunnel syndrome due to one tunnel at the wrist for the median nerve, there are four tunnels in the medial ankle for tarsal tunnels syndrome. If there is a positive Tinel sign when you tap over the inside of the ankle, such that tingling is felt into the foot, then there is an 80% chance that decompressing the tarsal tunnel will relieve the symptoms of pain and numbness in a diabetic with tarsal tunnel syndrome.

Risk factors
Anything compromising the tunnel of the posterior tibial nerve proves significant in the risk of causing TTS. Neuropathy can occur in the lower limb through many modalities, some of which include obesity and inflammation around the joints. By association, this includes risk factors such as RA, compressed shoes, pregnancy, diabetes and thyroid diseases

Diagnosis
Diagnosis is based upon physical examination findings. Patients pain history and a positive Tinels sign are the first steps in evaluating the possibility of tarsal tunnel syndrome. X-ray can rule out fracture. MRI can assess for space occupying lesions or other causes of nerve compression. Ultrasound can assess for synovitis or ganglia. Nerve conduction studies alone are not, but they may be used to confirm the suspected clinical diagnosis. Common causes include trauma, varicose veins, neuropathy and space-occupying anomalies within the tarsal tunnel. Tarsal tunnel syndrome is also known to affect both athletes and individuals that stand a lot.A neurologist or a physiatrist usually administers nerve conduction tests or supervises a trained technologist. During this test, electrodes are placed at various spots along the nerves in the legs and feet. Both sensory and motor nerves are tested at different locations. Electrical impulses are sent through the nerve and the speed and intensity at which they travel is measured. If there is compression in the tunnel, this can be confirmed and pinpointed with this test. Some doctors do not feel that this test is necessarily a reliable way to rule out TTS. Some research indicates that nerve conduction tests will be normal in at least 50% of the cases.
Given the unclear role of electrodiagnostics in the diagnosis of tarsal tunnel syndrome, efforts have been made in the medical literature to determine which nerve conduction studies are most sensitive and specific for tibial mononeuropathy at the level of the tarsal tunnel. An evidence-based practice topic put forth by the professional organization, the American Association of Neuromuscular & Electrodiagnostic Medicine has determined that Level C, Class III evidence exists for the use of tibial motor nerve conduction studies, medial and lateral plantar mixed nerve conduction studies, and medial and lateral plantar sensory nerve conduction studies. The role of needle electromyography remains less defined.Tarsal tunnel syndrome (TTS) is most closely related to carpal tunnel syndrome (CTS). However, the commonality to its counterpart is much less or even rare in prevalence Studies have found that patients with rheumatoid arthritis (RA) show signs of distal limb neuropathy. The posterior tibial nerve serves victim to peripheral neuropathy and often show signs of TTS amongst RA patients. Therefore, TTS is a common discovery found in the autoimmune disorder of rheumatoid arthritis

Prevention
The exact cause of tarsal tunnel syndrome (TTS) can vary from patient to patient. However the same result is true for all patients, the compression of the posterior tibial nerve and it branches as it travels around the medial malleolus causes pain and irritation for the patient. There are many possible causes for compression of the tibial nerve therefore there are a variety of prevention strategies.  One being immobilization, by placing the foot in a neutral position with a brace, pressure is relieved from the tibial nerve thus reducing patients pain. Eversion, inversion, and plantarflexion all can cause compression of the tibial nerve therefore in the neutral position the tibial nerve is less agitated. Typically this is recommended for the patient to do while sleeping. Another common problem is improper footwear, having shoes deforming the foot due to being too tight can lead to increased pressure on the tibial nerve. Having footwear that tightens the foot for extended periods of time even will lead to TTS. Therefore, by simply having properly fitted shoes TTS can be prevented.

Treatment
Treatments typically include rest, manipulation, strengthening of tibialis anterior, tibialis posterior, peroneus and short toe flexors, casting with a walker boot, corticosteroid and anesthetic injections, hot wax baths, wrapping, compression hose, and orthotics.  Medications may include various anti-inflammatories such as Anaprox, or other medications such as Ultracet, Neurontin and Lyrica.  Lidocaine patches are also a treatment that helps some patients.

Conservative treatment (nonsurgical)
There are multiple ways that tarsal tunnel can be treated and the pain can be reduced. The initial treatment, whether it be conservative or surgical, depends on the severity of the tarsal tunnel and how much pain the patient is in. There was a study done that treated patients diagnosed with tarsal tunnel syndrome with a conservative approach. Meaning that the program these patients were participated in consisted of physiotherapy exercises and orthopedic shoe inserts in addition to that program. There were fourteen patients that had supplementary tibial nerve mobilization exercises. They were instructed to sit on the edge of a table in a slumped position, have their ankle taken into dorsiflexion and ankle eversion then the knee was extended and flexed to obtain the optimal tibial nerve mobilization. Patients in both groups showed positive progress from both programs. The medial calcaneal, medial plantar and lateral plantar nerve areas all had a reduction in pain after successful nonoperative or conservative treatment. There is also the option of localized steroid or cortisone injection that may reduce the inflammation in the area, therefore relieving pain. Or just a simple reduction in the patients weight to reduce the pressure in the area.

Surgical treatment
If non-invasive treatment measures fail, tarsal tunnel release surgery may be recommended to decompress the area. The incision is made behind the ankle bone and then down towards but not as far as the bottom of foot. The posterior tibial nerve is identified above the ankle. It is separated from the accompanying artery and vein and then followed into the tunnel. The nerves are released. Cysts or other space-occupying problems may be corrected at this time. If there is scarring within the nerve or branches, this is relieved by internal neurolysis. Neurolysis is when the outer layer of nerve wrapping is opened and the scar tissue is removed from within nerve. Following surgery, a large bulky cotton wrapping immobilizes the ankle joint without plaster. The dressing may be removed at the one-week point and sutures at about three weeks.
Complications may include bleeding, infection, and unpredictable healing. The incision may open from swelling. There may be considerable pain and cramping. Regenerating nerve fibers may create shooting pains. Patients may have hot or cold sensations and may feel worse than before surgery. Crutches are usually recommended for the first two weeks, as well as elevation to minimize swelling. The nerve will grow at about one inch per month. One can expect to continue the healing process over the course of about one year.
Many patients report good results.  Some, however, experience no improvement or a worsening of symptoms.  In the Pfeiffer article (Los Angeles, 1996), fewer than 50% of the patients reported improvement, and there was a 13% complication rate.
Tarsal tunnel can greatly impact patients quality of life.  Depending on the severity, the ability to walk distances people normally take for granted (such as grocery shopping) may become compromised.  Proper pain management and counseling is often required.
Results of surgery can be maximized if all four of the medial ankle tunnels are released and you walk with a walker the day after surgery. Success can be improved to 80%.

Incidence
Though TTS is rare, its cause can be determined in 70% of reported cases. In the workplace TTS is considered a musculoskeletal disorder and accounts for 1.8 million cases a year, which accumulates to about $15–$20 billion a year New studies indicate an occurrence of TTS in sports placing high loads on the ankle joint (3). This can be seen in figure 1. TTS occurs more dominantly in active adults, with a higher pervasiveness among women. Active adults that experience more jumping and landing on the ankle joint are more susceptible (see figure 2). Though athletics and sport are correlations, cases are individualistically assessed because of the oddity.

Athletic activities
The athletic population tends to put themselves at greater risk of TTS due to the participation in sports that involve the lower extremities. Strenuous activities involved in athletic activities put extra strain on the ankle and therefore can lead to the compression of the tibial nerve </s>