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Stainless steel – Wikipedia

Steel alloy resistant to corrosion

Stainless steel is an alloy of iron that is resistant to rusting and corrosion. It contains at least 11% chromium and may contain elements such as carbon, other nonmetals and metals to obtain other desired properties. Stainless steel's resistance to corrosion results from the chromium, which forms a passive film that can protect the material and self-heal in the presence of oxygen.[1]:3

The alloy's properties, such as luster and resistance to corrosion, are useful in many applications. Stainless steel can be rolled into sheets, plates, bars, wire, and tubing. These can be used in cookware, cutlery, surgical instruments, major appliances, vehicles, construction material in large buildings, industrial equipment (e.g., in paper mills, chemical plants, water treatment), and storage tanks and tankers for chemicals and food products.

The biological cleanability of stainless steel is superior to both aluminium and copper, having a biological cleanability comparable to glass.[2] Its cleanability, strength, and corrosion resistance have prompted the use of stainless steel in pharmaceutical and food processing plants.[3]

Different types of stainless steel are labeled with an AISI three-digit number,[4] The ISO 15510 standard lists the chemical compositions of stainless steels of the specifications in existing ISO, ASTM, EN, JIS, and GB standards in a useful interchange table.[5]

Like steel, stainless steels are relatively poor conductors of electricity, with significantly lower electrical conductivities than copper. In particular, the electrical contact resistance (ECR) of stainless steel arises as a result of the dense protective oxide layer and limits its functionality in applications as electrical connectors.[6] Copper alloys and nickel-coated connectors tend to exhibit lower ECR values, and are preferred materials for such applications. Nevertheless, stainless steel connectors are employed in situations where ECR poses a lower design criteria and corrosion resistance is required, for example in high temperatures and oxidizing environments.[7]

As with all other alloys, the melting point of stainless steel is expressed in the form of a range of temperatures, and not a singular temperature.[8] This temperature range goes from 1,400 to 1,530C (2,550 to 2,790F)[9] depending on the specific consistency of the alloy in question.

Martensitic, duplex and ferritic stainless steels are magnetic, while austenitic stainless steel is usually non-magnetic.[10] Ferritic steel owes its magnetism to its body-centered cubic crystal structure, in which iron atoms are arranged in cubes (with one iron atom at each corner) and an additional iron atom in the center. This central iron atom is responsible for ferritic steel's magnetic properties. This arrangement also limits the amount of carbon the steel can absorb to around 0.025%.[11] Grades with low coercive field have been developed for electro-valves used in household appliances and for injection systems in internal combustion engines. Some applications require non-magnetic materials, such as magnetic resonance imaging.[citation needed] Austenitic stainless steels, which are usually non-magnetic, can be made slightly magnetic through work hardening. Sometimes, if austenitic steel is bent or cut, magnetism occurs along the edge of the stainless steel because the crystal structure rearranges itself.[12]

The addition of nitrogen also improves resistance to pitting corrosion and increases mechanical strength.[14] Thus, there are numerous grades of stainless steel with varying chromium and molybdenum contents to suit the environment the alloy must endure.[15] Corrosion resistance can be increased further by the following means:

Galling, sometimes called cold welding, is a form of severe adhesive wear, which can occur when two metal surfaces are in relative motion to each other and under heavy pressure. Austenitic stainless steel fasteners are particularly susceptible to thread galling, though other alloys that self-generate a protective oxide surface film, such as aluminium and titanium, are also susceptible. Under high contact-force sliding, this oxide can be deformed, broken, and removed from parts of the component, exposing the bare reactive metal. When the two surfaces are of the same material, these exposed surfaces can easily fuse. Separation of the two surfaces can result in surface tearing and even complete seizure of metal components or fasteners.[16][17] Galling can be mitigated by the use of dissimilar materials (bronze against stainless steel) or using different stainless steels (martensitic against austenitic). Additionally, threaded joints may be lubricated to provide a film between the two parts and prevent galling. Nitronic 60, made by selective alloying with manganese, silicon, and nitrogen, has demonstrated a reduced tendency to gall.[17]

The invention of stainless steel followed a series of scientific developments, starting in 1798 when chromium was first shown to the French Academy by Louis Vauquelin. In the early 1800s, British scientists James Stoddart, Michael Faraday, and Robert Mallet observed the resistance of chromium-iron alloys ("chromium steels") to oxidizing agents. Robert Bunsen discovered chromium's resistance to strong acids. The corrosion resistance of iron-chromium alloys may have been first recognized in 1821 by Pierre Berthier, who noted their resistance against attack by some acids and suggested their use in cutlery.[19]

In the 1840s, both of Britain's Sheffield steelmakers and then Krupp of Germany were producing chromium steel with the latter employing it for cannons in the 1850s.[20] In 1861, Robert Forester Mushet took out a patent on chromium steel in Britain.[21]

These events led to the first American production of chromium-containing steel by J. Baur of the Chrome Steel Works of Brooklyn for the construction of bridges. A US patent for the product was issued in 1869.[22]:2261[23] This was followed with recognition of the corrosion resistance of chromium alloys by Englishmen John T. Woods and John Clark, who noted ranges of chromium from 530%, with added tungsten and "medium carbon". They pursued the commercial value of the innovation via a British patent for "Weather-Resistant Alloys".[22]:261,11[24][full citation needed]

In the late 1890s, German chemist Hans Goldschmidt developed an aluminothermic (thermite) process for producing carbon-free chromium.[25] Between 1904 and 1911, several researchers, particularly Leon Guillet of France, prepared alloys that would be considered stainless steel today.[25][26]

In 1908, the Essen firm Friedrich Krupp Germaniawerft built the 366-ton sailing yacht Germania featuring a chrome-nickel steel hull, in Germany. In 1911, Philip Monnartz reported on the relationship between chromium content and corrosion resistance.[27] On 17 October 1912, Krupp engineers Benno Strauss and Eduard Maurer patented as Nirosta the austenitic stainless steel[28][29][30][27] known today as 18/8 or AISI Type 304.[31]

Similar developments were taking place in the United States, where Christian Dantsizen of General Electric[31] and Frederick Becket (1875-1942) at Union Carbide were industrializing ferritic stainless steel.[32] In 1912, Elwood Haynes applied for a US patent on a martensitic stainless steel alloy, which was not granted until 1919.[33]

While seeking a corrosion-resistant alloy for gun barrels in 1912, Harry Brearley of the Brown-Firth research laboratory in Sheffield, England, discovered and subsequently industrialized a martensitic stainless steel alloy, today known as AISI Type 420.[31] The discovery was announced two years later in a January 1915 newspaper article in The New York Times.[18]

The metal was later marketed under the "Staybrite" brand by Firth Vickers in England and was used for the new entrance canopy for the Savoy Hotel in London in 1929.[34] Brearley applied for a US patent during 1915 only to find that Haynes had already registered one. Brearley and Haynes pooled their funding and, with a group of investors, formed the American Stainless Steel Corporation, with headquarters in Pittsburgh, Pennsylvania.[22]:360

Brearley initially called his new alloy "rustless steel". The alloy was sold in the US under different brand names like "Allegheny metal" and "Nirosta steel". Even within the metallurgy industry, the name remained unsettled; in 1921, one trade journal called it "unstainable steel".[35] Brearley worked with a local cutlery manufacturer, who gave it the name "stainless steel".[36] As late as 1932, Ford Motor Company continued calling the alloy rustless steel in automobile promotional materials.[37]

In 1929, before the Great Depression, over 25,000 tons of stainless steel were manufactured and sold in the US annually.[38]

Major technological advances in the 1950s and 1960s allowed the production of large tonnages at an affordable cost:

There are five main families, which are primarily classified by their crystalline structure: austenitic, ferritic, martensitic, duplex, and precipitation hardening.

Austenitic stainless steel[43][44] is the largest family of stainless steels, making up about two-thirds of all stainless steel production.[45] They possess an austenitic microstructure, which is a face-centered cubic crystal structure.[46] This microstructure is achieved by alloying steel with sufficient nickel and/or manganese and nitrogen to maintain an austenitic microstructure at all temperatures, ranging from the cryogenic region to the melting point.[46] Thus, austenitic stainless steels are not hardenable by heat treatment since they possess the same microstructure at all temperatures.[46]

Austenitic stainless steels sub-groups, 200 series and 300 series:

Ferritic stainless steels possess a ferrite microstructure like carbon steel, which is a body-centered cubic crystal structure, and contain between 10.5% and 27% chromium with very little or no nickel. This microstructure is present at all temperatures due to the chromium addition, so they are not hardenable by heat treatment. They cannot be strengthened by cold work to the same degree as austenitic stainless steels. They are magnetic. Additions of niobium (Nb), titanium (Ti), and zirconium (Zr) to Type 430 allow good weldability. Due to the near-absence of nickel, they are less expensive than austenitic steels and are present in many products, which include:

Martensitic stainless steels have a body-centered cubic crystal structure, and offer a wide range of properties and are used as stainless engineering steels, stainless tool steels, and creep-resistant steels. They are magnetic, and not as corrosion-resistant as ferritic and austenitic stainless steels due to their low chromium content. They fall into four categories (with some overlap):[53]

Martensitic stainless steels can be heat treated to provide better mechanical properties. The heat treatment typically involves three steps:[55]

Replacing some carbon in martensitic stainless steels by nitrogen is a recent development.[when?] The limited solubility of nitrogen is increased by the pressure electroslag refining (PESR) process, in which melting is carried out under high nitrogen pressure. Steel containing up to 0.4% nitrogen has been achieved, leading to higher hardness and strength and higher corrosion resistance. As PESR is expensive, lower but significant nitrogen contents have been achieved using the standard AOD process.[56][57][58][59][60]

Duplex stainless steels have a mixed microstructure of austenite and ferrite, the ideal ratio being a 50:50 mix, though commercial alloys may have ratios of 40:60. They are characterized by higher chromium (1932%) and molybdenum (up to 5%) and lower nickel contents than austenitic stainless steels. Duplex stainless steels have roughly twice the yield strength of austenitic stainless steel. Their mixed microstructure provides improved resistance to chloride stress corrosion cracking in comparison to austenitic stainless steel Types 304 and 316. Duplex grades are usually divided into three sub-groups based on their corrosion resistance: lean duplex, standard duplex, and super duplex. The properties of duplex stainless steels are achieved with an overall lower alloy content than similar-performing super-austenitic grades, making their use cost-effective for many applications. The pulp and paper industry was one of the first to extensively use duplex stainless steel. Today, the oil and gas industry is the largest user and has pushed for more corrosion resistant grades, leading to the development of super duplex and hyper duplex grades. More recently, the less expensive (and slightly less corrosion-resistant) lean duplex has been developed, chiefly for structural applications in building and construction (concrete reinforcing bars, plates for bridges, coastal works) and in the water industry.

Precipitation hardening stainless steels have corrosion resistance comparable to austenitic varieties, but can be precipitation hardened to even higher strengths than other martensitic grades. There are three types of precipitation hardening stainless steels:[61]

Solution treatment at about 1,040C (1,900F)followed by quenching results in a relatively ductile martensitic structure. Subsequent aging treatment at 475C (887F) precipitates Nb and Cu-rich phases that increase the strength up to above 1000 MPa yield strength. This outstanding strength level is used in high-tech applications such as aerospace (usually after remelting to eliminate non-metallic inclusions, which increases fatigue life). Another major advantage of this steel is that aging, unlike tempering treatments, is carried out at a temperature that can be applied to (nearly) finished parts without distortion and discoloration.

Typical heat treatment involves solution treatment and quenching. At this point, the structure remains austenitic. Martensitic transformation is then obtained either by a cryogenic treatment at 75C (103F) or by severe cold work (over 70% deformation, usually by cold rolling or wire drawing). Aging at 510C (950F) which precipitates the Ni3Al intermetallic phaseis carried out as above on nearly finished parts. Yield stress levels above 1400MPa are then reached.

The structure remains austenitic at all temperatures.

Typical heat treatment involves solution treatment and quenching, followed by aging at 715C (1,319F). Aging forms Ni3Ti precipitates and increases the yield strength to about 650MPa (94ksi) at room temperature. Unlike the above grades, the mechanical properties and creep resistance of this steel remain very good at temperatures up to 700C (1,300F). As a result, A286 is classified as an Fe-based superalloy, used in jet engines, gas turbines, and turbo parts.

There are over 150 grades of stainless steel, of which 15 are most commonly used. There are several systems for grading stainless and other steels, including US SAE steel grades. The Unified Numbering System for Metals and Alloys (UNS) was developed by the ASTM in 1970. The Europeans have developed EN 10088 for the same purpose.[31]

In its early history, stainless steel was sometimes called rustless steel. Both adjectives, stainless and rustless, are duly recognized and accepted as exaggerations: stainless steel is not literally incapable of rusting, but its established name is "stainless steel" nonetheless.

In technical datasets, stainless steel may sometimes be designated as inox (inoxidizable), CRES (corrosion-resistant), or SS or SST (stainless steel). It may also be designated by subclass or grade without further specification, as for example 188, 17-4 PH, 316, 303, or 304.

Unlike carbon steel, stainless steels do not suffer uniform corrosion when exposed to wet environments. Unprotected carbon steel rusts readily when exposed to a combination of air and moisture. The resulting iron oxide surface layer is porous and fragile. In addition, as iron oxide occupies a larger volume than the original steel, this layer expands and tends to flake and fall away, exposing the underlying steel to further attack. In comparison, stainless steels contain sufficient chromium to undergo passivation, spontaneously forming a microscopically thin inert surface film of chromium oxide by reaction with the oxygen in the air and even the small amount of dissolved oxygen in the water. This passive film prevents further corrosion by blocking oxygen diffusion to the steel surface and thus prevents corrosion from spreading into the bulk of the metal.[3] This film is self-repairing, even when scratched or temporarily disturbed by an upset condition in the environment that exceeds the inherent corrosion resistance of that grade.[63][64]

The resistance of this film to corrosion depends upon the chemical composition of the stainless steel, chiefly the chromium content. It is customary to distinguish between four forms of corrosion: uniform, localized (pitting), galvanic, and SCC (stress corrosion cracking). Any of these forms of corrosion can occur when the grade of stainless steel is not suited for the working environment.

The designation "CRES" refers to corrosion-resistant steel.[65]

Uniform corrosion takes place in very aggressive environments, typically where chemicals are produced or heavily used, such as in the pulp and paper industries. The entire surface of the steel is attacked, and the corrosion is expressed as corrosion rate in mm/year (usually less than 0.1mm/year is acceptable for such cases). Corrosion tables provide guidelines.[66]

This is typically the case when stainless steels are exposed to acidic or basic solutions. Whether stainless steel corrodes depends on the kind and concentration of acid or base and the solution temperature. Uniform corrosion is typically easy to avoid because of extensive published corrosion data or easily performed laboratory corrosion testing.

Acidic solutions can be put into two general categories: reducing acids, such as hydrochloric acid and dilute sulfuric acid, and oxidizing acids, such as nitric acid and concentrated sulfuric acid. Increasing chromium and molybdenum content provides increased resistance to reducing acids while increasing chromium and silicon content provides increased resistance to oxidizing acids. Sulfuric acid is one of the most-produced industrial chemicals. At room temperature, Type 304 stainless steel is only resistant to 3% acid, while Type 316 is resistant to 3% acid up to 50C (120F) and 20% acid at room temperature. Thus Type 304 SS is rarely used in contact with sulfuric acid. Type 904L and Alloy 20 are resistant to sulfuric acid at even higher concentrations above room temperature.[67][68] Concentrated sulfuric acid possesses oxidizing characteristics like nitric acid, and thus silicon-bearing stainless steels are also useful.[citation needed] Hydrochloric acid damages any kind of stainless steel and should be avoided.[1]:118[69] All types of stainless steel resist attack from phosphoric acid and nitric acid at room temperature. At high concentrations and elevated temperatures, attack will occur, and higher-alloy stainless steels are required.[70][71] In general, organic acids are less corrosive than mineral acids such as hydrochloric and sulfuric acid. As the molecular weight of organic acids increases, their corrosivity decreases. Formic acid has the lowest molecular weight and is a weak acid. Type 304 can be used with formic acid, though it tends to discolor the solution. Type 316 is commonly used for storing and handling acetic acid, a commercially important organic acid.[72]

Type 304 and Type 316 stainless steels are unaffected by weak bases such as ammonium hydroxide, even in high concentrations and at high temperatures. The same grades exposed to stronger bases such as sodium hydroxide at high concentrations and high temperatures will likely experience some etching and cracking.[73] Increasing chromium and nickel contents provide increased resistance.

All grades resist damage from aldehydes and amines, though in the latter case Type 316 is preferable to Type 304; cellulose acetate damages Type 304 unless the temperature is kept low. Fats and fatty acids only affect Type 304 at temperatures above 150C (300F) and Type 316 SS above 260C (500F), while Type 317 SS is unaffected at all temperatures. Type 316L is required for the processing of urea.[1][pageneeded]

Localized corrosion can occur in several ways, e.g. pitting corrosion and crevice corrosion. These localized attacks are most common in the presence of chloride ions. Higher chloride levels require more highly alloyed stainless steels.

Localized corrosion can be difficult to predict because it is dependent on many factors, including:

Pitting corrosion is considered the most common form of localized corrosion. The corrosion resistance of stainless steels to pitting corrosion is often expressed by the PREN, obtained through the formula:

where the terms correspond to the proportion of the contents by mass of chromium, molybdenum, and nitrogen in the steel. For example, if the steel consisted of 15% chromium %Cr would be equal to 15.

The higher the PREN, the higher the pitting corrosion resistance. Thus, increasing chromium, molybdenum, and nitrogen contents provide better resistance to pitting corrosion.

Though the PREN of certain steel may be theoretically sufficient to resist pitting corrosion, crevice corrosion can still occur when the poor design has created confined areas (overlapping plates, washer-plate interfaces, etc.) or when deposits form on the material. In these select areas, the PREN may not be high enough for the service conditions. Good design, fabrication techniques, alloy selection, proper operating conditions based on the concentration of active compounds present in the solution causing corrosion, pH, etc. can prevent such corrosion.[74]

Stress corrosion cracking (SCC) is a sudden cracking and failure of a component without deformation. It may occur when three conditions are met:

The SCC mechanism results from the following sequence of events:

Whereas pitting usually leads to unsightly surfaces and, at worst, to perforation of the stainless sheet, failure by SCC can have severe consequences. It is therefore considered as a special form of corrosion.

As SCC requires several conditions to be met, it can be counteracted with relatively easy measures, including:

Galvanic corrosion[75] (also called "dissimilar-metal corrosion") refers to corrosion damage induced when two dissimilar materials are coupled in a corrosive electrolyte. The most common electrolyte is water, ranging from freshwater to seawater. When a galvanic couple forms, one of the metals in the couple becomes the anode and corrodes faster than it would alone, while the other becomes the cathode and corrodes slower than it would alone. Stainless steel, due to having a more positive electrode potential than for example carbon steel and aluminium, becomes the cathode, accelerating the corrosion of the anodic metal. An example is the corrosion of aluminium rivets fastening stainless steel sheets in contact with water.[76] The relative surface areas of the anode and the cathode are important in determining the rate of corrosion. In the above example, the surface area of the rivets is small compared to that of the stainless steel sheet, resulting in rapid corrosion.[76] However, if stainless steel fasteners are used to assemble aluminium sheets, galvanic corrosion will be much slower because the galvanic current density on the aluminium surface will be many orders of magnitude smaller.[76] A frequent mistake is to assemble stainless steel plates with carbon steel fasteners; whereas using stainless steel to fasten carbon-steel plates is usually acceptable, the reverse is not. Providing electrical insulation between the dissimilar metals, where possible, is effective at preventing this type of corrosion.[76]

At elevated temperatures, all metals react with hot gases. The most common high-temperature gaseous mixture is air, of which oxygen is the most reactive component. To avoid corrosion in air, carbon steel is limited to approximately 480C (900F). Oxidation resistance in stainless steels increases with additions of chromium, silicon, and aluminium. Small additions of cerium and yttrium increase the adhesion of the oxide layer on the surface.[77] The addition of chromium remains the most common method to increase high-temperature corrosion resistance in stainless steels; chromium reacts with oxygen to form a chromium oxide scale, which reduces oxygen diffusion into the material. The minimum 10.5% chromium in stainless steels provides resistance to approximately 700C (1,300F), while 16% chromium provides resistance up to approximately 1,200C (2,200F). Type 304, the most common grade of stainless steel with 18% chromium, is resistant to approximately 870C (1,600F). Other gases, such as sulfur dioxide, hydrogen sulfide, carbon monoxide, chlorine, also attack stainless steel. Resistance to other gases is dependent on the type of gas, the temperature, and the alloying content of the stainless steel.[78][79] With the addition of up to 5% aluminium, ferritic grades Fr-Cr-Al are designed for electrical resistance and oxidation resistance at elevated temperatures. Such alloys include Kanthal, produced in the form of wire or ribbons.[80]

Standard mill finishes can be applied to flat rolled stainless steel directly by the rollers and by mechanical abrasives. Steel is first rolled to size and thickness and then annealed to change the properties of the final material. Any oxidation that forms on the surface (mill scale) is removed by pickling, and a passivation layer is created on the surface. A final finish can then be applied to achieve the desired aesthetic appearance.[81][82]

The following designations are used in the U.S. to describe stainless steel finishes by ASTM A480/A480M-18 (DIN):[83]

A wide range of joining processes are available for stainless steels, though welding is by far the most common.[84][49]

The ease of welding largely depends on the type of stainless steel used. Austenitic stainless steels are the easiest to weld by electric arc, with weld properties similar to those of the base metal (not cold-worked). Martensitic stainless steels can also be welded by electric-arc but, as the heat-affected zone (HAZ) and the fusion zone (FZ) form martensite upon cooling, precautions must be taken to avoid cracking of the weld. Improper welding practices can additionally cause sugaring (oxide scaling) and/or heat tint on the backside of the weld. This can be prevented with the use of back-purging gases, backing plates, and fluxes.[85] Post-weld heat treatment is almost always required while preheating before welding is also necessary in some cases.[49] Electric arc welding of Type 430 ferritic stainless steel results in grain growth in the HAZ, which leads to brittleness. This has largely been overcome with stabilized ferritic grades, where niobium, titanium, and zirconium form precipitates that prevent grain growth.[86][87] Duplex stainless steel welding by electric arc is a common practice but requires careful control of the process parameters. Otherwise, the precipitation of unwanted intermetallic phases occurs, which reduces the toughness of the welds.[88]

Electric arc welding processes include:[84]

MIG, MAG and TIG welding are the most common methods.

Other welding processes include:

Stainless steel may be bonded with adhesives such as silicone, silyl modified polymers, and epoxies. Acrylic and polyurethane adhesives are also used in some situations.[89]

Most of the world's stainless steel production is produced by the following processes:

World stainless steel production figures are published yearly by the International Stainless Steel Forum. Of the EU production figures, Italy, Belgium and Spain were notable, while Canada and Mexico produced none. China, Japan, South Korea, Taiwan, India the US and Indonesia were large producers while Russia reported little production.[45]

European Union

Americas

China

Asia excluding China

Other countries

Breakdown of production by stainless steels families in 2017:

Stainless steel is used in a multitude of fields including architecture, art, chemical engineering, food and beverage manufacture, vehicles, medicine, energy and firearms.

Life cycle cost (LCC) calculations are used to select the design and the materials that will lead to the lowest cost over the whole life of a project, such as a building or a bridge.[90][91]

The formula, in a simple form, is the following:[92][citation needed][93]

where LCC is the overall life cycle cost, AC is the acquisition cost, IC the installation cost, OC the operating and maintenance costs, LP the cost of lost production due to downtime, and RC the replacement materials cost.

In addition, N is the planned life of the project, i the interest rate, and n the year in which a particular OC or LP or RC is taking place. The interest rate (i) is used to convert expenses from different years to their present value (a method widely used by banks and insurance companies) so they can be added and compared fairly. The usage of the sum formula ( {textstyle sum } ) captures the fact that expenses over the lifetime of a project must be cumulated[clarification needed] after they are corrected for interest rate.[citation needed]

Application of LCC in materials selection

Stainless steel used in projects often results in lower LCC values compared to other materials. The higher acquisition cost (AC) of stainless steel components are often offset by improvements in operating and maintenance costs, reduced loss of production (LP) costs, and the higher resale value of stainless steel components.[citation needed]

LCC calculations are usually limited to the project itself. However, there may be other costs that a project stakeholder may wish to consider:[citation needed]

The average carbon footprint of stainless steel (all grades, all countries) is estimated to be 2.90kg of CO2 per kg of stainless steel produced,[94] of which 1.92kg are emissions from raw materials (Cr, Ni, Mo); 0.54kg from electricity and steam, and 0.44kg are direct emissions (i.e., by the stainless steel plant). Note that stainless steel produced in countries that use cleaner sources of electricity (such as France, which uses nuclear energy) will have a lower carbon footprint. Ferritics without Ni will have a lower CO2 footprint than austenitics with 8% Ni or more. Carbon footprint must not be the only sustainability-related factor for deciding the choice of materials:

Stainless steel is 100% recyclable.[95][96][97] An average stainless steel object is composed of about 60% recycled material of which approximately 40% originates from end-of-life products, while the remaining 60% comes from manufacturing processes.[98] What prevents a higher recycling content is the availability of stainless steel scrap, in spite of a very high recycling rate. According to the International Resource Panel's Metal Stocks in Society report, the per capita stock of stainless steel in use in society is 80 to 180kg (180 to 400lb) in more developed countries and 15kg (33lb) in less-developed countries. There is a secondary market that recycles usable scrap for many stainless steel markets. The product is mostly coil, sheet, and blanks. This material is purchased at a less-than-prime price and sold to commercial quality stampers and sheet metal houses. The material may have scratches, pits, and dents but is made to the current specifications.[citation needed]

The stainless steel cycle starts with carbon steel scrap, primary metals, and slag. The next step is the production of hot-rolled and cold-finished steel products in steel mills. Some scrap is produced, which is directly reused in the melting shop. The manufacturing of components is the third step. Some scrap is produced and enters the recycling loop. Assembly of final goods and their use does not generate any material loss. The fourth step is the collection of stainless steel for recycling at the end of life of the goods (such as kitchenware, pulp and paper plants, or automotive parts). This is where it is most difficult to get stainless steel to enter the recycling loop, as shown in the table below:

Stainless steel nanoparticles have been produced in the laboratory.[100][101] These may have applications as additives for high-performance applications. For example, sulfurization, phosphorization, and nitridation treatments to produce nanoscale stainless steel based catalysts could enhance the electrocatalytic performance of stainless steel for water splitting.[102]

There is extensive research indicating some probable increased risk of cancer (particularly lung cancer) from inhaling fumes while welding stainless steel.[103][104][105][106][107][108] Stainless steel welding is suspected of producing carcinogenic fumes from cadmium oxides, nickel, and chromium.[109] According to Cancer Council Australia, "In 2017, all types of welding fumes were classified as a Group 1 carcinogen."[109]

Stainless steel is generally considered to be biologically inert. However, during cooking, small amounts of nickel and chromium leach out of new stainless steel cookware into highly acidic food.[110] Nickel can contribute to cancer risksparticularly lung cancer and nasal cancer.[111][112] However, no connection between stainless steel cookware and cancer has been established.[113]

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Stainless steel - Wikipedia

Corticobasal syndrome: a practical guide | Practical Neurology

Case vignette 1 (with video)

A 68-year-old woman had a 2-year history of motor symptoms. Her first symptom had been her left hand not doing what it was told to do when drying the dishes. She also developed difficulties getting her words out. On examination, she had pseudobulbar speech and made dysphasic errors, and there was apraxia and hypometria of saccades, particularly leftward (video 1). She showed ideomotor apraxia and features of alien-limb syndrome in the left arm, and intermittent dystonic posturing of the left arm and leg but minimal limb rigidity. Her cognition was preserved.

Schematic of typical saccade abnormalities in CBS, compared with PD and PSP. In this schematic of eye movement recordings, patients were asked to make a leftward saccade of 20 towards a target as quickly as possible. Y axis is displacement amplitude, the X axis is time. Mild undershoot followed by a small secondary saccade is normal. Patients with PD commonly show mild hypometria (undershooting) requiring two or more corrective saccades to reach target. In CBS the degree of saccadic hypometria is often greater than in PD with the key feature being delayed launching of saccades (saccadic apraxia). In PSP the hallmark is early saccadic slowing (especially vertically) with considerable hypometria developing over time. CBS, corticobasal syndrome; PD, Parkinsons disease; PSP, progressive supranuclear palsy. Figure by Bronstein & Anderson (2021), distributed at https://doi.org/10.6084/m9.figshare.14390951 under an open CC-BY 4.0 license.

We diagnosed corticobasal syndrome referred her to physiotherapy and occupational therapy. An MR scan of brain showed only mild involutional changes consistent with age but no perirolandic atrophy.

Her condition progressed over the next 4years. She lost vertical eye movements and her alien limb became very pronounced. Her speech deteriorated to yes and no, although she could still comprehend. She became more rigid with worsening dystonia particularly of neck extension, and her postural reflexes became impaired. We gave an unsuccessful trial of levodopa and sought speech and language involvement; botulinum injections into the neck extensors gave some benefit. She continued to deteriorate and died 6years from symptom onset.

A 79-year-old woman reported decreased coordination, slowed movement and subtle right arm weakness that appeared to follow a fall. Over the next 9 months, her right arm became increasing difficult to use, causing difficulty with tasks such as doing up a bra and cutting food. Her walking felt more uncertain and she had one significant fall. On examination, there was marked right arm rigidity with a grasp reflex, significant bradykinesia and ideomotor apraxia. Eye movements were normal and there were no pyramidal nor cerebellar signs. Our impression was likely corticobasal syndrome. We arranged physiotherapy and occupational therapy, requested brain imaging and gave an empirical trial of levodopa.

Her right arm deficits progressed despite levodopa, which we later stopped. Her right arm became of little use to her, and she held it in a dystonic posture, without pain, though she still felt some agency over it. Her balance deteriorated further with frequent falls. She developed difficulty with speech, stumbling over longer words but her cognition remained unaffected. MR scan of brain showed left perirolandic atrophy consistent with corticobasal syndrome (figure 4). She remained at home with increasing support from physiotherapy and occupational therapy.

In 1968, Rebeiz et al published three cases detailing the clinical and post mortem pathological findings of a hitherto unrecognised disorder of the central nervous system.1 All three had an asymmetric movement disorder characterised by slowed and awkward voluntary movements with additional involuntary movements. Pathological assessment identified frontoparietal atrophy driven by neuronal loss, gliosis and swelling of cell bodies, resulting in resistance to histological staining methods. While the cortex was primarily involved, the substantia nigra was abnormal in all three, and the dentatorubrothalamic system was abnormal in two. They coined the term corticodentatonigral degeneration with neuronal achromasia. Three decades later Gibb et al reported three further patients with similar clinical and histopathological findings. They adopted the shorter name corticobasal degeneration,2 and the next decade saw many further descriptions of this newly named disorder. The clinical phenotype expanded from primarily a movement disorder to include various cognitive and neurobehavioural deficits35 while the underlying pathology of clinically diagnosed cases also expanded to include Alzheimers disease, progressive supranuclear palsy (PSP), Picks disease and Creutzfeldt-Jakob disease.69 Thus, the etymology has slowly transitioned to corticobasal syndrome as a clinical rather than a pathological diagnosis.10 Table 1 shows the current consensus diagnostic criteria for both the clinically defined corticobasal degeneration11 and the pathologically defined corticobasal syndrome.12 13 Figure 1 shows the common clinical phenotypes of corticobasal degeneration and the common pathologies underlying corticobasal syndrome.

Proposed criteria for corticobasal syndrome (the Cambridge criteria, modified Bak and Hodges)12

Unpicking corticobasal syndrome and corticobasal degeneration. From phenotype to underlying pathophysiology. This is a simplified view and includes only the common phenotypes of corticobasal degeneration and common pathological substrates underlying corticobasal syndrome. CBS, corticobasal syndrome; CBD, corticobasal disease; AD, Alzheimers disease; FTLD-TDP43, frontotemporal lobe degeneration TDP43; PSP, progressive supranuclear palsy; FTD Tau, frontotemporal dementia; FBSS, frontal behavioural-spatial syndrome; PPA, primary progressive aphasia.

Corticobasal degeneration is a pathologically established four-repeat tauopathy.14 Its pathological features are cortical and striatal tau-positive neuronal and glial lesions of both white and grey matter, coupled with focal cortical and substantia nigra neuronal loss.14 Importantly, there is not a 1:1 mapping between corticobasal degeneration and corticobasal syndrome, and corticobasal degeneration pathology is associated with various clinical phenotypes (figure 1). There are four suggested broad clinical phenotypes:

Corticobasal syndrome.

Frontal behavioural-spatial syndrome.

Non-fluent/agrammatic variant of primary progressive aphasia.

PSP syndrome.11

Probable corticobasal degeneration criteria require an insidious onset and gradual progression for at least 1year, age at onset >50 years, no similar family history or known tau mutations, and one of the clinical phenotypes outlined above. Features suggesting Parkinsons disease (characteristic tremor, hallucinations, response to levodopa), or multiple system atrophy (prominent autonomic or cerebellar signs) are exclusions. However, the criteria still lack antemortem specificity to separate pathologically proven corticobasal degeneration from its mimics.15

It is difficult to ascertain the true prevalence and incidence of corticobasal syndrome, given the varied use of the term and its interchangeability in early reviews with corticobasal degeneration. Estimates are therefore at best a guide and even then, remain crude. The estimated prevalence of corticobasal degeneration is 4.97.3 cases per 100000 population.16 The annual incidence calculated from the prevalence and life expectancy would be between 0.5 and 1 per 100000 per year, though this is higher than the rate observed in a population based study.17 The typical age of presentation is 50s70s and average lifespan from diagnosis to death is 7 years. There does not appear to be any sex bias.18

A single pathogenic mutation is unlikely to contribute greatly to the pathogenesis of corticobasal syndrome. However, familial clustering can occur with up to 31% have a family history of parkinsonism or dementia19 The most common monogenic mutations associated with familial corticobasal syndrome are in microtubule-associated protein tau (MAPT) resulting in frontotemporal lobar degeneration (FTLD)-tau pathology strongly resembling corticobasal degeneration,20 although genome-wide association studies have identified other single nucleotide polymorphisms.21 More recently corticobasal syndrome has been associated with FTLD with ubiquitin-immunoreactive inclusions (FTLD)22 or TAR DNA-binding protein 43 (TDP-43) leading to frontal temporal lobe degeneration (FTLD-TDP)23 both of which are most often caused by progranulin mutations24 but not always.25 Pathogenic GGGCC expansion with mutations in C9orf72 (chromosome 9 open reading frame 72) and mutations in LRRK2 (previously limited to Parkinsons disease)26 are also associated with corticobasal syndrome.27 Outside of familial monogenic mutations, a casecontrol study suggests single-nucleotide polymorphisms in the H1 haplotype of the MAPT gene may predispose to sporadic corticobasal syndrome.28

Corticobasal syndrome has an insidious onset and is slowly progressive.12 29 Patients with dramatic presentations and/or rapidly progressive disease courses should be considered mimics (see below).

Extrapyramidal motor features are common with no dramatic or sustained response to levodopa therapy.12 29 Rigidity is the most frequent extrapyramidal motor sign, present in 73%100% of cases, mostly presenting as an asymmetric akineticrigid syndrome.13 29 30 Dystonia is much less common than rigidity and tends to affect a single limb, often the upper and usually early in the disease course.12 13 Other extrapyramidal features such as bradykinesia and postural instability may also occur.12 A tremor can develop but is an action or postural jerky movement that subsides with rest, and is quite unlike a resting Parkinsons disease tremor.12 13 29 It can overlap with another common motor featuremyoclonuswhich occurs in roughly 40% of cases.12 13 29 Electrophysiology studies suggest the myoclonus is cortical or subcortical in origin.3133

The alien limb syndrome comprises involuntary limb movements combined with an altered sense of limb belonging or ownership. It usually involves the hand but may uncommonly occur only in the leg, or both arm and leg, and rarely is bilateral.34 35 A detailed account of the underlying neurobiological processes causing alien limb is beyond this review but proposed mechanisms have been suggested.36 The alien limb is easily confused with other neurological signs (table 2). There are three recognised variants: frontal, callosal (together termed anterior) and posterior (figure 2).

Alien limb differential diagnosis

Classification algorithm of the alien limb syndrome. Modified from Hassan and Josephs. 72 CBS, corticobasal syndrome; CJD, Creutzfeldt-Jakob disease.

The posterior variant is the most often encountered type in corticobasal syndrome and usually affects the non-dominant upper limb, with lesions involving the non-dominant parietal lobe.35 It is characterised by a sense that the affected limb does not belong to the person. There are usually other parietal cortical deficits including sensory hemineglect, and astereognosis. The typical motor features are not as intrusive as in the frontal variant but may take the form of levitation and other non-purposeful actions, abnormal posturing and ataxia.

Corticobasal syndrome is easily the most common cause of an alien limb (two-thirds of cases).35 By the same token the alien limb syndrome develops in about a half of people with corticobasal syndrome.35 37 While the asymmetry of corticobasal syndrome involves the left and right hemispheres equally, alien limb in this condition usually develops in the non-dominant limb, for unclear reasons.36 In patients presenting with alien limb, the timing of onset during the disease may help to suggest the cause; for example, it can be the presenting symptom of Creutzfeldt-Jakob disease but occurs a median of 1year after disease onset in corticobasal syndrome.35 The associated neurology can also help in the differential diagnosis. Thus, mirror movements develop in 40% of corticobasal syndrome patients with the alien limb but are uncommon in other causes, while intermanual conflict is very uncommon in corticobasal syndrome.36 Myoclonus is usual in patients with Creutzfeldt-Jakob disease but common in corticobasal syndrome, and uncommon in other causes of alien limb.35

There are no proven treatments for alien limb syndrome and management approaches are based on anecdotal experience and the type of alien limb. The frontal variant may respond to sensory tricks (eg, wearing a glove), distracting tasks (eg, holding a ball in the hand), verbal cues that enhance voluntary action and cognitivebehavioural therapy for anxiety reduction. For the posterior variant (common in corticobasal syndrome), treatments used have included clonazepam, botulinum toxin injections into the most active proximal muscles, visualisation strategies (eg, putting the affected hand into a mirror box) and spatial recognition tasks, but these approaches are not always well tolerated or maintained and there is scant information on their long-term benefits.38

Limb apraxia is among the most commonly identified signs that suggests cortical dysfunction in the corticobasal syndrome, occurring in 70%80%.3941 Apraxia is defined as a disorder of higher level motor control, manifesting as impaired skilled and learnt motor acts, despite intact primary sensory and motor pathways39 Apraxia generally affects both sides of the body. Because corticobasal syndrome is usually asymmetrical, finding apraxia on the less affected side (as is common) adds weight to the conclusion that abnormality of movements are not simply due to extrapyramidal features such as rigidity and bradykinesia.40

When screening patients for the presence of apraxia, it can help to test different types of complex movementsthought to correspond to different underlying neurobiological processes that can be disrupted by brain pathology.39 These include:

Performing a gesture, miming the use of tools and copying meaningless gestures. Deficits in these movements, usually referred to as ideomotor apraxia, are common in corticobasal syndrome and can be readily assessed in the clinic.

Performing complex, multistep tasks. Deficits in these processes are often referred to as conceptual, or ideational apraxias, capturing the idea that it is loss of knowledge about objects and their associated actions that underlies the patients difficulties. This is harder to screen for in a routine clinic appointment but may be inferred from the history, or from a formal occupational therapy assessment. Ideational apraxia can be extremely disabling for a persons day-to-day functioning.

Performing repetitive distal limb movements such as tapping the thumb with each finger in turn. Deficits such as clumsy or inaccurate movements, are referred to as limb-kinetic apraxiaa somewhat controversial classification that can be difficult to distinguish from the effects of weakness or bradykinesia.

Other sorts of higher order cortical dysfunction are often termed apraxiasfor example, gait apraxia, constructional apraxia, dressing apraxia, orobuccal apraxia and apraxia of speech (to name a few). When present, these point towards cortical dysfunction signs that can provide evidence for the presence of a corticobasal syndrome.

The traditional oculomotor hallmark of clinically diagnosed corticobasal syndrome is saccade apraxia,42 43 which manifests clinically as difficulty and delay in initiating saccades towards a target, usually with the use of an assisting simultaneous or preceding head movement, and in the laboratory as a substantial increase in saccade latency.44 45 Typically, the saccadic apraxia is greatest towards the side with the greatest limb apraxia.42 43 In contrast to PSP, saccade velocities in patients with corticobasal syndrome are normal46 47 (figure 3). Smooth pursuit can also be moderately impaired but not as severely as in patients with PSP. The neuropathological substrate of saccadic apraxia in corticobasal syndrome awaits further clarification but it remains a distinctly useful clinical diagnostic feature.

The typical language disturbance in corticobasal syndrome is non-fluent variant primary progressive aphasia, with slowed, effortful and/or groping (apraxia of speech) speech and grammatical errors being common.48 However, patients can also develop a logopenic aphasia, characterised by prominent difficulty in word retrieval and sentence repetition.48 The latter is commonly associated with underlying Alzheimers disease pathology, while non-fluent variant primary progressive aphasia, including apraxia of speech, may suggest tau pathology. Therefore, aside from providing evidence of cortical involvement, the pattern of aphasia may help to identify the pathology underlying corticobasal syndrome, but further research is required.

Corticobasal syndrome has a range of neuropsychiatric comorbidities. However, the lack of large scale studies means that while we commonly see features such as depression, apathy, anxiety and agitation (among others) in the clinic, we do not have accurate estimates of their prevalence at different stages of corticobasal syndromeor know whether these features associate with particular underlying pathologies.49 A study of 15 patients with what we would now refer to as corticobasal syndrome found particularly high rates of depression and apathy and also an absence of hallucinations.50 This latter point suggests that the presence of visual hallucinations in a patient with parkinsonism and cognitive deficits should raise concerns they may in fact have an alpha-synucleinopathy such as dementia with Lewy bodies.

We advocate for screening all patients presenting with corticobasal syndrome for neuropsychiatric symptoms, particularly as these features have a major impact on quality of life for patients and their families. Screening can be performed formally (eg, using the neuropsychiatric inventory,51 or by questioning both the patient and an informant for presence of mood disturbance (dysphoria, anhedonia, anxiety), behavioural change (apathy, obsessive or compulsive behaviours, agitation, irritability, impulsivity, loss of empathy) and psychotic features (hallucinations, delusions). Education of caregivers about the possibility of emergence of these complications can be helpful.

Brain imaging has three roles in the assessment of patients with corticobasal syndromeruling out mimics/structural causes (see below), providing support for the clinical diagnosis of a corticobasal syndrome, and providing clues to the underlying pathology.33

Corticobasal syndrome is associated with asymmetrical cortical changes in markers of neuronal loss or dysfunction (grey matter atrophy, hypometabolism or hypoperfusion). This particularly affects frontal-parietal regions encompassing premotor, motor and sensory association cortex, and typically develop contralateral to the more affected side of the body33 52 53 (figure 4). Notably, such perirolandic patterns of change do not appear specific to any underlying pathology but instead associate directly with the clinical features of corticobasal syndrome, consistent with the importance of these regions for processing higher order sensory information and translating this into motor actions. Therefore, finding asymmetrical perirolandic atrophy or hypometabolism on clinical imaging supports a clinical diagnosis of corticobasal syndrome, though its absence does not exclude it. This can be particularly helpful early in the disease course, when the differential may include Parkinsons disease or other parkinsonian syndromes.

Example of an MR scan of a brain in a patient with corticobasal syndrome A. Small arrows show moderate focal asymmetric left perirolandic atrophy on T2-weighted imaging.

Striatal dopamine transporter (DAT) density can be imaged and measured using single-photon emission CT or positron-emission tomography (PET). Most, but not all, patients with corticobasal syndrome have a positive DAT scan.54 One follow-up study suggests that in time all such patients will have a positive result.55 For the clinician, the DAT scans limitation is that it does not differentiate corticobasal syndrome from other parkinsonian disorders.

There has been a recent emphasis on developing measures to identify reliably the underlying pathology in corticobasal syndrome.53 Such measures will be increasingly relevant as protein-specific treatments hopefully emerge over the coming years.33 Ultimately their utility will depend on their ability to distinguish between pathologies at individual rather than at group level.

These strategies can be split into techniques that identify the presence of abnormal protein (such as imaging to detect increased concentrations of brain amyloid protein), and techniques that identify patternseither in neuronal loss/metabolism or brain connectivityclosely associated with the underlying pathology. The use of amyloid PET imaging to identify corticobasal syndrome caused by Alzheimers pathology is the clearest example of the former approach. In turn, researchers are now examining clinical and standard imaging correlates of amyloid positive and negative groups to further refine understanding of how corticobasal syndrome may differ between pathologies.56 Given that there is often an associated underlying tauopathy, emerging tau-based PET techniqueswhich are still troubled by some technical issues such as off-target bindingare also generating strong interest for their potential to identify underlying corticobasal degeneration or progressive supranuclear pathology.33 57

Finally, the distribution of neuronal loss or brain hypometabolism in patients with corticobasal syndrome predicts the underlying pathology, at least at a group level. In particular, corticobasal syndrome caused by Alzheimers pathology often has a posterior pattern of hypometabolism, while corticobasal degeneration may show more subcortical hypometabolism, and PSP pathology shows more frontal hypometabolism.52 58 More complicated techniques assessing brain structural (white matter) or functional connectivity are also showing promise for distinguishing between pathologies but are not yet clinically useful.59

In summary, a corticobasal syndrome diagnosis can be supportedbut not refutedby imaging features, while emerging techniques may direct the neurologist to the underlying pathological cause of a patients syndromeinformation that over time will have practical relevance.

There are currently no proven treatments for corticobasal syndrome. Recent advances in the treatment of tauopathies with immunotherapies and gene expression show promise,60 61 but for the moment we emphasise the importance of making a diagnosis that can explain a puzzling array of problems for a patient and their family. It provides a valid explanation for their symptoms and allows a reframing of priorities from obtaining a diagnosis to coping with the problem. Ideally, treatment should be provided within a multidisciplinary setting with expertise provided by a neurologist, physiotherapist, occupational therapist, speech language therapist, psychiatrist and, ultimately, palliative care services.

Although parkinsonism in corticobasal syndrome does not generally respond well to levodopa, most patients will try it as part of their initial assessments (often when the diagnosis is less clear), and it is reasonable to push the dose up towards at least 1000mg/day before classifying a patient as a non-responder.62 In our experience, other dopaminergic therapies (dopamine agonists, monoamine oxidase inhibitors) also have very limited efficacy in treating motor symptoms of corticobasal syndrome, but a dopamine agonist may be worth considering in those with prominent apathy. Options for treating troublesome myoclonus include levetiracetam and clonazepam. Dystonia can be functionally disabling and at times painful. Anticholinergics, benzodiazepines and amantadine provide modest help at best, and adverse effectsespecially cognitive impairment, hallucinations and confusionoften outweigh any benefit, particularly in older patients, while amantadine can also cause insomnia and leg oedema.63 Botulinum toxin injections can help, depending on the dystonic pattern. Particularly when treating upper limb dystonia, the disabling effects of symptoms must be weighed against the potential limb weakness resulting from injectionsbut as with other interventions a pragmatic trial is certainly reasonable.37 Physiotherapy input is also important in optimising mobility following botulinum toxin injections.

Specific options to consider for the alien limb syndrome are summarised above. Management to mitigate the effects of apraxia is best coordinated by an occupational therapist with knowledge of the condition. Speech therapists can teach patients techniques to overcome some of their language deficits and it is worth seeking their input when speech difficulties are a prominent featurethey can also provide patients with practical advice if swallowing difficulties develop. We often refer patients for physiotherapy aimed at strength and balance training as well as gait assessmentthe addition of gait aids can allow some people to maintain relative physical independence. Although there are no proven treatments for cognitive deficits such as memory and attentional impairment in corticobasal syndrome, many clinicians consider trialling cholinesterase inhibitors if there is a strong suggestion from the history (memory impairment), examination (predominate cortical signs) and cognitive assessment (visuospatial or memory deficits) to suggest an underlying Alzheimers disease pathology.

There are several available pharmacological options for neuropsychiatric manifestations.62 Many mild behavioural issues may be better managed non-pharmacologically (caregiver education, environment changes, etc) but undoubtedly medications can help with more severe disruptions. Seeking psychiatric guidance is useful and building a strong relationship with an interested psychiatrist can help patient management and improve job satisfaction. Selective serotonin reuptake inhibitors are useful for treating common problems such as anxiety, depression and obsessive-compulsive disorder. Apathy, or reduced motivated behaviour, is common, debilitating and difficult to treat. Informing caregivers that it is part of the disease process can help. Agents targeting dopaminergic, cholinergic and serotonergic neuromodulatory networks may help apathy in other degenerative disorders, but there is no good evidence to guide use of these treatments in corticobasal syndrome. Finally, some patients will develop marked behavioural disturbances, including irritability/aggression and psychosis. Management can be difficult but can include atypical antipsychotics, for example, quetiapine or clozapine with appropriate blood count monitoring.

Other practical issues to address include driving safety and checking whether driving licensing agencies need to be informed, the importance of updating a persons will, and establishing an enduring power of attorney early in the disease course, as these can be problematic later if significant cognitive impairment develops. Lastly, putting patients in touch with local charities can greatly help patients and families. If specific charities are not available (eg, the PSP association in the UK and curePSP in the USA) exploring Parkinsons and dementia charities is a reasonable first step.

Conditions that may initially be diagnosed as corticobasal syndrome but turn out to be something else tend to be those with subacute or chronic onset, and those that have some, but not all, symptoms and signs resembling true neurodegenerative corticobasal syndrome. Most of these mimics feature alien limb syndrome with or without myoclonus, and/or one of the rapidly progressive dementias, often with aphasia. Thus, many of the non-neurodegenerative causes of the alien limb syndrome may mimic corticobasal syndrome, including stiff-person syndrome,64 Hashimotos encephalitis,65 66 thalamic cavernoma,67 as well as Creutzfeldt-Jakob disease68 and other rapidly progressive dementias.69 Mimics can usually be distinguished from true corticobasal syndrome by the careful neurological examination to identify peripheral (such as areflexia, proprioceptive loss) or central (eg, pyramidal) nervous system signs, combined with appropriate investigations such as MR scan of brain, electroencephalogram, serum antineuronal and other autoantibody assays, which together may indicate an alternative diagnosis. It is critical to identify these mimics as early as possible as many are treatable or have a better prognosis than true corticobasal syndrome. A careful family history is also important, and clinicians should have a low threshold for genetic testing especially in younger patients with atypical features.

The prognosis for a patient diagnosed with corticobasal syndrome depends mainly on the underlying neuropathology (i.e. cause), the difficulty being that that cause is not easily determined during life. Consequently, there is little available information to assist counselling of the patient and family. In a study of 10 Japanese patients with corticobasal syndrome coming to post mortem (three each with corticobasal degeneration, PSP and Alzheimers disease pathology, and one with atypical tauopathy) median survival was 7 years with a range of 415 years. Survival was similar across pathologies.70 An earlier study of 14 patients with pathologically confirmed corticobasal degeneration reported a median survival time after onset of symptoms of 7.9 years with a considerable range of 2.512.5 years. Survival was shorter in those with early and widespread parkinsonism or frontal lobe syndrome.71 In summary, on present knowledge, average survival in corticobasal syndrome is 78 years but with a considerable range of some 315 years.

Corticobasal syndrome is a disorder of movement, cognition and behaviour, caused by several underlying pathologies including corticobasal degeneration. Clinicians should consider the diagnosis in patients presenting with any combination of extrapyramidal features, apraxia or other parietal signs, aphasia and alien limb phenomena. Neuroimaging showing asymmetrical perirolandic cortical changes supports the diagnosis and advanced neuroimaging may give insight into the underlying pathology. We suggest neuropsychological screening in all patients presenting with corticobasal syndrome. Identifying corticobasal syndrome carries some prognostic significance, management implications and in the future if protein-based treatments arisemay direct further investigations as to underlying pathology.

Corticobasal syndrome is a clinical entity with many different underlying pathologies, including corticobasal degeneration.

Corticobasal degeneration is a pathological diagnosis associated with several clinical syndromes, one of which is corticobasal syndrome.

Corticobasal syndrome has a varied presentation: distinguishing clinical features include asymmetric parkinsonism, myoclonus, alien limb, cortical sensory loss, eye and limb apraxia, and imaging may show asymmetric perirolandic atrophy.

Corticobasal syndrome has several important mimics (eg, Creutzfeldt-Jakob disease, Hashimotos encephalitis), some of which are treatable.

Armstrong MJ, Litvan I, Lang AE, et al. Criteria for the diagnosis of corticobasal degeneration. Neurology 2013;80(5):496503. doi: 10.1212/WNL.0b013e31827f0fd1

Mathew R, Bak TH, Hodges JR. Diagnostic criteria for corticobasal syndrome: a comparative study. J Neurol Neurosurg Psych 2012;83(4):40510. doi: 10.1136/jnnp-2011-300875

Pardini M, Huey ED, Spina S, et al. FDG-PET patterns associated with underlying pathology in corticobasal syndrome. Neurology 2019;92(10):e112135. doi: 10.1212/WNL.0000000000007038

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