<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Normal tension glaucoma and can you explain it in depth? [/INST] Normal tension glaucoma (NTG) is an eye disease, a neuropathy of the optic nerve, that shows all the characteristics of primary open angle glaucoma except one: the elevated intraocular pressure (IOP) - the classic hallmark of glaucoma - is missing. Normal tension glaucoma is in many cases closely associated with general issues of blood circulation and of organ perfusion like arterial hypotension, metabolic syndrome, and Flammer syndrome.

Clinical relevance
Over many years, glaucoma has been defined by an intraocular pressure of more than 20 mm Hg. Incompatible with this (now obsolete) definition of glaucoma was the ever larger number of cases that have been reported in medical literature in the 1980s and 1990s who had the typical signs of glaucomatous damage, like optic nerve head excavation and thinning of the retinal nerve fiber layer, while these patients had an IOP that would generally have been regarded as "normal". It is now widely estimated that a larger percentage of patients with primary open-angle glaucoma (POAG) are suffering from normal tension glaucoma. Among Americans of Japanese descent, for instance, the prevalence of NTG is about four times as high as the prevalence of the "classical glaucoma" with an IOP of 22 mm Hg and higher. The pillar of the current understanding of normal tension glaucoma is a reduced IOP tolerance of the retinal ganglion cells and the cells in the optic nerve head - an IOP of, for example, 17 or 19 mm Hg that would not affect a healthy eye leads to damage in the eye of an NTG patient.

Risk factors
In many patients, normal tension glaucoma is common in individuals with a generalized reduced perfusion of organs and certain body tissues. A low blood pressure - whether consistently low or with sudden pressure drops - is associated with NTG as are conditions like Flammer syndrome and obstructive sleep apnea. Flammer syndrome has been attributed to increase the likelihood of ganglion cell damage in normal tension glaucoma patients with disc hemorrhages as a characteristic clinical sign. Besides race (Japanese) and low blood pressure, the female gender is also a risk factor.

Diagnosis
While tonometry, the measuring of IOP and thus a classical instrument in the diagnosis of glaucoma, is not helpful, ophthalmoscopy leads to the diagnosis by showing typical glaucomatous damage, primarily at the optic nerve head, in the absence of elevated IOP. While the excavation of the optic nerve head and the thinning of its rim appear in all kinds of glaucoma (with high tension and with normal tension, in Primary open angle glaucoma (POAG) and in secondary glaucoma), small hemorrhages close to the optic disc have been identified as a characteristic clinical sign of normal tension glaucoma. Visual field is very important to detect NTG. It shows a defect that typically appears deeper, steeper and closer to fixation comparing to patients with POAG.
Since NTG is closely linked to vascular irregularities, a medical check-up by a general practitioner or a specialist in internal medicine is widely recommended in cases of newly diagnosed normal tension glaucoma. An examination that is considered to be of particular importance is a 24-hour monitoring of the blood pressure. NTG patients tend to suffer "dips", sudden and unnoticed drops in blood pressure during sleep.

Treatment
Without treatment, NTG leads to progressive visual field loss and in the last consequence to blindness </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Angiostrongylus cantonensis and can you explain it in depth? [/INST] Angiostrongylus cantonensis is a parasitic nematode (roundworm) that causes angiostrongyliasis, the most common cause of eosinophilic meningitis in Southeast Asia and the Pacific Basin. The nematode commonly resides in the pulmonary arteries of rats, giving it the common name rat lungworm. Snails are the primary intermediate hosts, where larvae develop until they are infectious.
Humans are incidental hosts of this roundworm, and may become infected through ingestion of larvae in raw or undercooked snails or other vectors, or from contaminated water and vegetables. The larvae are then transported via the blood to the central nervous system, where they are the most common cause of eosinophilic meningitis, a serious condition that can lead to death or permanent brain and nerve damage. Angiostrongyliasis is an infection of increasing public health importance, as globalization contributes to the geographic spread of the disease.

History
First described by the renowned Chinese parasitologist Hsin-Tao Chen (1904–1977) in 1935, after examining Cantonese rat specimens, the nematode Angiostrongylus cantonensis was identified in the cerebrospinal fluid of a patient with eosinophilic meningitis by Nomura and Lim in Taiwan in 1944. They noted that raw food eaten by the patient may have been contaminated by rats. In 1955, Mackerass and Sanders identified the lifecycle of the worm in rats, defining snails and slugs as the intermediate hosts, and noting the path of transmission through the blood, brain, and lungs in rats.

Infectious agent
A. cantonensis is a helminth of the phylum Nematoda, order Strongylida, and superfamily Metastrongyloidea. Nematodes are roundworms characterized by a tough outer cuticle, unsegmented bodies, and a fully developed gastrointestinal tract. The order Strongylida includes hookworms and lungworms. Metastrongyloidea are characterized as 2-cm-long, slender, threadlike worms that reside in the lungs of the definitive host. Angiostrongylus costaricensis is a closely related worm that causes intestinal angiostrongyliasis in Central and South America.

Epidemiology and pathogenesis
Following World War II, A. cantonensis spread throughout Southeast Asia and Western Pacific Islands, including Australia, Melanesia, Micronesia, and Polynesia. Cases were soon reported in New Caledonia, the Philippines, Rarotonga, Saipan, Sumatra, Taiwan, and Tahiti. In the 1960s, even more cases were reported from the region from locations such as Cambodia, Guam, Hawaii, Java, Thailand, Sarawak, Vietnam, and Vanuatu.In 1961, an epidemiological study of eosinophilic meningitis in humans was conducted by Rosen, Laigret, and Bories, who hypothesized that the parasite causing these infections was carried by fish. However, Alicata noted that raw fish was consumed by large numbers of people in Hawaii without apparent consequences, and patients presenting with meningitis symptoms had a history of eating raw snails or prawns in the weeks before presenting with symptoms. This observation, along with epidemiology and autopsy of infected brains, confirmed A. cantonensis infection in humans as the cause of the majority of eosinophilic meningitis cases in Southeast Asia and the Pacific Islands.Since then, cases of A. cantonensis infestations have appeared in American Samoa, Australia, Hong Kong, Bombay, Fiji, Hawaii, Honshu, India, Kyushu, New Britain, Okinawa, Ryukyu Islands, Western Samoa, and most recently mainland China. Other sporadic occurrences of the parasite in its rat hosts have been reported in Cuba, Egypt, Louisiana, Madagascar, Nigeria, and Puerto Rico.In 2013, A. cantonensis was confirmed present in Florida, USA, where its range and prevalence are expanding. In 2018, a case was found in a New Yorker who had visited Hawaii.In recent years, the parasite has been shown to be proliferating at an alarming rate due to modern food-consumption trends and global transportation of food products. Scientists are calling for a more thorough study of the epidemiology of A. cantonensis, stricter food-safety policies, and the increase of knowledge on how to properly consume products commonly infested by the parasite, such as snails and slugs that act as intermediate hosts or those that act as paratenic hosts, such as fish, frogs, or freshwater prawns. Ingestion of food items that can be contaminated by the mucus excretions of intermediate or paratenic hosts, such as snails and slugs, or by the feces of rats that act as definitive hosts, can lead to infection of A. cantonensis. The most common route of infection of  A. cantonesis in humans is by ingestion of either intermediate or paratenic hosts of the larvae. Unwashed fruits and vegetables, especially romaine lettuce, can be contaminated with snail and slug mucus or can result in accidental ingestion of these intermediate and paratenic hosts. These items need to be properly washed and handled to prevent accidental ingestion of A. cantonensis larvae or the larvae-containing hosts. The best mechanism of prevention of A. cantonesis outbreak is to institute an aggressive control of snail and slug population, proper cooking of intermediate and paratenic hosts such as fish, freshwater prawn, frogs, molluscs, and snails along with proper food-handling techniques. The common prevention techniques for diarrheal illness are very effective in preventing A. cantonensis infection. Not much is known about why it targets the brain in humans, but a chemically induced chemotaxis has been implicated recently. Acetylcholine has been previously reported to enhance motility of this worm via nicotinic acetylcholine receptors. Experimental assays in animal models are needed to validate a chemically induced chemotaxis  by use of anticholinergic drugs to prevent cerebral infection following infections by A. cantonesis.

Hosts
Intermediate hosts of larvae of for A. cantonensis include:

Land snails: Thelidomus aspera from Jamaica, Pleurodonte sp. from Jamaica, Sagda sp. from Jamaica, Poteria sp. from Jamaica, Achatina fulica, Satsuma mercatoria, Acusta despecta, Bradybaena brevispira, Bradybaena circulus Bradybaena ravida, Bradybaena similaris, Plectotropis appanata and Parmarion martensi from Okinawa and Hawaii, Camaena cicatricosa, Trichochloritis rufopila, Trichochloritis hungerfordianus and Cyclophorus spp.
Freshwater snails: Pila spp., Pomacea canaliculata, Cipangopaludina chinensis, Bellamya aeruginosa and Bellamya quadrata
Slugs: Limax maximus, Limax flavus Deroceras laeve, Deroceras reticulatum, Laevicaulis alte, Sarasinula plebeia, Vaginulus yuxjsjs, Lehmannia valentiana, Phiolomycus bilineatus, Macrochlamys loana, Meghimatium bilineatum and probably other species of slugs.Definitive hosts of A. cantonensis include wild rodents, especially the brown rat (Rattus norvegicus) and the black rat (Rattus rattus).Paratenic hosts of A. cantonensis include the predatory land flatworm Platydemus manokwari and the amphibians, Bufo asiaticus, Rana catesbeiana, Rhacophorus leucomystax and Rana limnocharis.In 2004, a captive yellow-tailed black cockatoo (Calyptorhynchus funereus) and two free-living tawny frogmouths (Podargus strigoides) suffering neurological symptoms were shown to have the parasite. They were the first avian hosts discovered for the organism. In 2018, in Mallorca two North African hedgehogs with signs of acute neurological disease were found to have A. cantonensis in their brains, one of them with a gravid female. It was the first report of hedgehogs as hosts of Angiostrongylus.The Hawaiʻi Dept. of Health states that fresh water opihi can carry the parasite, as well as other aquatic organisms such as prawns, frogs, and water monitor lizards.  House pets may interact with A. cantonensis-carrying animals yet not well studied. Cats are known to carry and spread feline lungworm in rat and snail interactions.

Pathogenesis of human angiostrongylosis
The presence of parasitic worms burrowed in the neural tissue of the human central nervous system (CNS) causes complications. All of the following result in damage to the CNS:
Direct mechanical damage to neural tissue from the worms motion
Toxic byproducts such as nitrogenous waste
Antigens released by dead and living parasites

Eosinophilic meningitis
Although the clinical disease caused by Angiostrongylus invasion into the CNS is commonly referred to as "eosinophilic meningitis", the actual pathophysiology is of a meningoencephalitis with invasion not just of the meninges, or superficial lining of the brain, but also deeper brain tissue. Initial invasion through the lining of the brain, the meninges, may cause a typical inflammation of the meninges and a classic meningitis picture of headache, stiff neck, and often fever. The parasites subsequently invade deeper into the brain tissue, causing specific localizing neurological symptoms depending on where in the brain parenchyma they migrate. Neurologic findings and symptoms wax and wane as initial damage is done by the physical in-migration of the worms and secondary damage is done by the inflammatory response to the presence of dead and dying worms. This inflammation can lead in the short term to paralysis, bladder dysfunction, visual disturbance, and coma and in the long term to permanent nerve damage, mental retardation, nerve damage, permanent brain damage, or death.Eosinophilic meningitis is commonly defined by the increased number of eosinophils in the cerebrospinal fluid (CSF). In most cases, eosinophil levels rise to 10 or more eosinophils per μl in the CSF, accounting for at least 10% of the total CSF leukocyte (white blood cell) count. The chemical analysis of the CSF typically resembles the findings in "aseptic meningitis" with slightly elevated protein levels, normal glucose levels, and negative bacterial cultures. Presence of a significantly decreased glucose on CSF analysis is an indicator of severe meningoencephalitis and may indicate a poor medical outcome. Initial CSF analysis early in the disease process may occasionally show no increase of eosinophils, only to have classical increases in eosinophils in subsequent CSF analysis. Caution should be advised in using eosinophilic meningitis as the only criterion for diagnosing angiostrongylus infestation in someone with classic symptoms, as the disease evolves with the migration of the worms into the CNS.Eosinophils are specialized white blood cells of the granulocytic cell line, which contain granules in their cytoplasm. These granules contain proteins that are toxic to parasites. When these granules degranulate, or break down, chemicals are released that combat parasites such as A. cantonensis. Eosinophils, which are located throughout the body, are guided to sites of inflammation by chemokines when the body is infested with parasites such as A. cantonensis. Once at the site of inflammation, type 2 cytokines are released from helper T cells, which communicate with the eosinophils, signaling them to activate. Once activated, eosinophils can begin the process of degranulation, releasing their toxic proteins in the fight against the foreign parasite.

Clinical signs and symptoms
According to a group case study, the most common symptoms in mild eosinophilic meningitis tend to be headache (with 100% of people in the study suffering from this symptom), photophobia or visual disturbance (92%), neck stiffness (83%), fatigue (83%), hyperesthesias (75%), vomiting (67%), and paresthesias (50%). Incubation period is often 3 weeks, but can be 3–36 days and even 80 days.Possible clinical signs and symptoms of mild and severe eosinophilic meningitis are:

Fever is often minor or absent, but the presence of high fever suggests severe disease.
Headaches are progressive and severe, a bitemporal character in the frontal or occipital lobe.
Meningismus - neck stiffness
Photophobia - sensitivity to light
Muscle weakness and fatigue
Nausea with or without vomiting
Paresthesias - tingling, prickling, or numbing of skin, may last for several weeks or months
Hyperesthesia - severe sensitivity to touch; may last for several weeks or months
Radiculitis - pain irradiated along certain areas of skin
Bladder dysfunction with urinary retention
Constipation
Brudzińskis sign
Vertigo
Blindness
Paralysis localized to one area; e.g. paralysis of extraocular muscles and facial palsy
General paralysis (flaccid) often ascending in nature starting with the feet and progressing upwards to involve the entire body
Coma
Death

Treatment
The severity and clinical course of Angiostrongylus disease depends significantly on the ingested load of third-stage larvae, creating great variability from case to case, making clinical trials difficult to design, and effectiveness of treatments difficult to discern. Typical conservative medical management including analgesics and sedatives provide minimal relief for the headaches and hyperesthesias. Removing cerebrospinal fluid at regular 3- to 7-day intervals is the only proven method of significantly reducing intracranial pressure and can be used for symptomatic treatment of headaches. This process may be repeated until improvement is shown. There is growing evidence of moderate quality that suggests corticosteroid therapy using prednisolone or dexamethasone has beneficial effect in treating the CNS symptoms related to A. cantonensis infections. Although early research did not show treatment with antihelminthic agents (parasite-killing drugs) such as thiobendazole or albendazole effective in improving the clinical course of the illness, a number of recent studies from Thailand and China show that the combination of glucocorticoids and antihelminthics is safe and decreases the duration of headaches and the number of patients who had significant headache. Although the addition of antihelminthic agents for management of A. cantonensis infection has a theoretic risk of precipitating a neurologic crisis by releasing an overwhelming load of antigens through simultaneous death of the larvae, no study has shown this to exist in the clinical setting. Additionally, the failure to kill parasites before they attempt to migrate out of the CNS increases the risk of mechanical damage by migrating larvae. Although combination therapy using albendazole and prednisolone has no significant advantage compared to treatment using prednisolone alone in mild cases, the treatment with antihelminthics is demonstrably safe and may have significant benefit for patients with high parasite loads at risk for permanent disability or death.

Diagnosis
The diagnosis of disease caused by A. cantonensis infestation is often difficult and relies heavily on the history of a likely ingestion of a commonly infested host and the presence of typical features of the disease. The presumptive diagnosis is particularly strong when eosinophilic meningoencephalitis can be confirmed. The diagnosis of eosinophilic meningitis can be arrived at through detection of elevated cranial pressure and increased numbers of eosinophils. The diagnosis of the cause of eosinophilic meningitis and the presence of A. cantonensis is remarkably more difficult. A spinal tap, or a sample of CSF, must be taken to search for A. cantonensis worms or larvae. A. cantonensis is undetectable in the CSF of more than half of the infected individuals. Current methods of detecting specific antigens associated with A. cantonensis are also unreliable. Consequently, alternative approaches to detect antigen-antibody reactions are being explored, such as immuno-PCR </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Radial tunnel syndrome and can you explain it in depth? [/INST] Radial tunnel syndrome (RTS) is caused by increased pressure on the radial nerve as it travels from the upper arm (the brachial plexus) to the hand and wrist.

Symptoms and signs
Radial tunnel syndrome causes posterolateral elbow pain that is similar to tennis elbow and may sometimes occur in conjunction with that condition. Patients may typically have weakness of extension at the wrist and third digit. The pain is often reproduced upon resisted supination of the forearm, and pain at the radial tunnel on resisted hyperextension of the wrist.

Cause
The theory is that the radial nerve becomes irritated and/or inflamed from friction caused by compression by muscles in the forearm.Some speculate that radial tunnel syndrome is a type of repetitive strain injury (RSI), but there is no detectable pathophysiology and even the existence of this disorder is questioned.The term "radial tunnel syndrome" is used for compression of the posterior interosseous nerve, a division of the radial nerve, at the lateral intermuscular septum of arm, while "supinator syndrome" is used for compression at the arcade of Frohse.The "radial tunnel" is the region from the humeroradial joint past the proximal origin of the supinator muscle. Some scientists believe the radial tunnel extends as far as the distal border of the supinator. The radial nerve is commonly compressed within a 5 cm region near the elbow, but it can be compressed anywhere along the forearm if the syndrome is caused by injury (e.g. a fracture that puts pressure on the radial nerve). The radial nerve provides sensation to the skin of posterior arm, posterior and lateral forearm and wrist, and the joints of the elbow, wrist and hand. The nerve also provides sensory branches that travel to the periosteum of the lateral epicondyle, the anterior radiohumeral joint, and the annular ligament. It provides motor function through innervation to most extensor muscles of the posterior arm and forearm. Therefore, it is extremely important in upper body extremity movement and can cause significant pain to patients presenting with radial tunnel syndrome. Unlike carpal tunnel syndrome, radial tunnel syndrome does not present tingling or numbness, since the posterior interosseous nerve mainly affects motor function.This problem is often caused by: bone tumors, injury (specifically fractures of the forearm), noncancerous fatty tumors (lipomas), and inflammation of surrounding tissue.

Diagnosis
The diagnosis is based on symptoms and signs alone and objective testing is expected to be normal. This syndrome may be clinically tested by flexing the patients long finger while the patient extends the wrist and fingers. Pain is a positive finding.
The chief complaint of this disease is usually pain in the dorsal aspect of the upper forearm, and any weakness described is secondary to the pain. Tenderness to palpation occurs over the area of the radial neck. Also, the disease can be diagnosed by a positive "middle finger test", where resisted middle finger extension produces pain. Radiographic evaluation of the elbow should be performed to rule out other diagnoses.

Treatment
Non-surgical treatment of radial tunnel syndrome includes rest, NSAID, therapy with modalities, work modification, ergonomic modification, injection if associated with lateral epicondylitis.Patients whose conditions are more adapted to surgical intervention are those who do not respond to prolonged conservative treatment. The patient must have pain with resisted supination, positive middle finger test, positive electrodiagnostic findings, and pain relief after anesthetic injection into the radial tunnel. Based on 2002 data, surgical decompression leads to 60–70% good or excellent results.

See also
Golfers elbow
Repetitive strain injury
Tennis elbow

References
Further reading
Books
Rind, Libi; Pobre, Thomas; Weiss, Frederick; Magyar, Yasha; Ruotolo, Charles; Aldad, Tamir; Mahboubian, Shahab; Knijnikov, Alexander; Asheld, Wilbur J. (2010). "Radial tunnel syndrome and supinator syndrome".  In Weiss, Lyn D.; Weiss, Jay M.; Pobre, Thomas (eds.). Oxford American Handbook of Physical Medicine & Rehabilitation. Oxford University Press. pp. 96–7. ISBN 978-0-19-536777-5.
Wertsch, Jacqueline J.; Hoch, Anne Zeni (2009). "Radial Tunnel Syndrome".  In Akuthota, Venu; Herring, Stanley A. (eds.). Nerve and Vascular Injuries in Sports Medicine. Berlin: Springer. pp. 79–80. ISBN 978-0-387-76599-0.
Russell, Stephen M. (2006). "Radial Tunnel Syndrome". Examination of peripheral nerve injuries: an anatomical approach. Stuttgart: Thieme. p. 62. ISBN 978-3-13-143071-7.
Saladin, Kenneth S. (2012). Anatomy & Physiology: The Unity of Form and Function. McGraw Hill. p. 496. ISBN 978-0-07-337825-1.

Journals
Dickerman, Rob D.; Stevens, Qualls E. J.; Cohen, Anders J.; Jaikumar, S. (2002). "Radial tunnel syndrome in an elite power athlete: a case of direct compressive neuropathy". Journal of the Peripheral Nervous System. 7 (4): 229–32. doi:10.1046/j.1529-8027.2002.02030.x. PMID 12477169.
Huisstede, Bionka; Miedema, Harald S.; van Opstal, Twan; de Ronde, Manon T.; Verhaar, Jan A.; Koes, Bart W. (2008). "Interventions for Treating the Radial Tunnel Syndrome: A Systematic Review of Observational Studies". The Journal of Hand Surgery. 33 (1): 72–8. doi:10.1016/j.jhsa.2007.10.001. PMID 18261668.
Henry, Mark; Stutz, Christopher (2006). "A Unified Approach to Radial Tunnel Syndrome and Lateral Tendinosis". Techniques in Hand and Upper Extremity Surgery. 10 (4): 200–5. doi:10.1097/01.bth.0000231580.32406.71. PMID 17159475. S2CID 9709553.
Cleary, C (2006). "Management of Radial Tunnel Syndrome: A Therapists Clinical Perspective". Journal of Hand Therapy. 19 (2): 186–91. doi:10.1197/j.jht.2006.02.020. PMID 16713866.
Sarris, Ioannis K.; Papadimitriou, Nikolaos G.; Sotereanos, Dean G. (2002). "Radial Tunnel Syndrome". Techniques in Hand and Upper Extremity Surgery. 6 (4): 209–12. doi:10.1097/00130911-200212000-00010. PMID 16520604.
Smola, C. (2004). "Zur Problematik des algetischen Supinatorsyndroms oder Wo hört der Tennisarm auf und wo fängt das Supinatorsyndrom an?" [About the problem of radial tunnel syndrome or where does the tennis elbow end and where does the radial tunnel syndrome begin?]. Handchirurgie, Mikrochirurgie, Plastische Chirurgie (in German). 36 (4): 241–5. doi:10.1055/s-2004-817947. PMID 15368151.
Loh, YC; Lam, WL; Stanley, JK; Soames, RW (2004). "A new clinical test for radial tunnel syndrome—the Rule-of-Nine test: A cadaveric study" (PDF). Journal of Orthopaedic Surgery. 12 (1): 83–6. doi:10.1177/230949900401200115. PMID 15237127. S2CID 14049155.
Rosenbaum, Richard (1999). "Disputed radial tunnel syndrome". Muscle & Nerve. 22 (7): 960–7. doi:10.1002/(SICI)1097-4598(199907)22:7<960::AID-MUS26>3.0.CO;2-C. PMID 10398221.
Portilla Molina, A. E.; Bour, C.; Oberlin, C.; Nzeusseu, A.; Vanwijck, R. (1998). "The posterior interosseous nerve and the radial tunnel syndrome: an anatomical study". International Orthopaedics. 22 (2): 102–6. doi:10.1007/s002640050218. PMC 3619716. PMID 9651775.
Jebson, Peter J. L.; Engber, William D. (1997). "Radial tunnel syndrome: Long-term results of surgical decompression" </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Selenium and can you explain it in depth? [/INST] Selenium is a chemical element with the symbol Se and atomic number 34. It is a nonmetal (more rarely considered a metalloid) with properties that are intermediate between the elements above and below in the periodic table, sulfur and tellurium, and also has similarities to arsenic. It seldom occurs in its elemental state or as pure ore compounds in the Earths crust. Selenium – from Greek selḗnē (σελήνη Moon) – was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium (named for the Earth).
Selenium is found in metal sulfide ores, where it partially replaces the sulfur. Commercially, selenium is produced as a byproduct in the refining of these ores, most often during production. Minerals that are pure selenide or selenate compounds are known but rare. The chief commercial uses for selenium today are glassmaking and pigments. Selenium is a semiconductor and is used in photocells. Applications in electronics, once important, have been mostly replaced with silicon semiconductor devices. Selenium is still used in a few types of DC power surge protectors and one type of fluorescent quantum dot.
Although trace amounts of selenium are necessary for cellular function in many animals, including humans, both elemental selenium and (especially) selenium salts are toxic in even small doses, causing selenosis. Selenium is listed as an ingredient in many multivitamins and other dietary supplements, as well as in infant formula, and is a component of the antioxidant enzymes glutathione peroxidase and thioredoxin reductase (which indirectly reduce certain oxidized molecules in animals and some plants) as well as in 3 deiodinase enzymes. Selenium requirements in plants differ by species, with some plants requiring relatively large amounts and others apparently not requiring any.

Characteristics
Physical properties
Selenium forms several allotropes that interconvert with temperature changes, depending somewhat on the rate of temperature change. When prepared in chemical reactions, selenium is usually an amorphous, brick-red powder. When rapidly melted, it forms the black, vitreous form, usually sold commercially as beads. The structure of black selenium is irregular and complex and consists of polymeric rings with up to 1000 atoms per ring. Black Se is a brittle, lustrous solid that is slightly soluble in CS2. Upon heating, it softens at 50 °C and converts to gray selenium at 180 °C; the transformation temperature is reduced by presence of halogens and amines.The red α, β, and γ forms are produced from solutions of black selenium by varying the evaporation rate of the solvent (usually CS2). They all have a relatively low, monoclinic crystal symmetry (space group 14) and contain nearly identical puckered Se8 rings with different arrangements, as in sulfur. The eight atoms of a ring are not equivalent (i.e. they are not mapped one onto another by any symmetry operation), and in fact in the γ-monoclinic form, half the rings are in one configuration (and its mirror image) and half in another. The packing is most dense in the α form. In the Se8 rings, the Se-Se distance varies depending on where the pair of atoms is in the ring, but the average is 233.5 pm, and the Se-Se-Se angle is on average 105.7° . Other selenium allotropes may contain Se6 or Se7 rings.The most stable and dense form of selenium is gray and has a chiral hexagonal crystal lattice (space group 152 or 154 depending on the chirality) consisting of helical polymeric chains, where the Se-Se distance is 237.3 pm and Se-Se-Se angle is 103.1° . The minimum distance between chains is 343.6 pm. Gray Se is formed by mild heating of other allotropes, by slow cooling of molten Se, or by condensing Se vapor just below the melting point. Whereas other Se forms are insulators, gray Se is a semiconductor showing appreciable photoconductivity. Unlike the other allotropes, it is insoluble in CS2. It resists oxidation by air and is not attacked by nonoxidizing acids. With strong reducing agents, it forms polyselenides. Selenium does not exhibit the changes in viscosity that sulfur undergoes when gradually heated.

Optical properties
Owing to its use as a photoconductor in flat-panel x-ray detectors (see below), the optical properties of amorphous selenium (α-Se) thin films have been the subject of intense research.

Isotopes
Selenium has seven naturally occurring isotopes. Five of these, 74Se, 76Se, 77Se, 78Se, 80Se, are stable, with 80Se being the most abundant (49.6% natural abundance). Also naturally occurring is the long-lived primordial radionuclide 82Se, with a half-life of 9.2×1019 years. The non-primordial radioisotope 79Se also occurs in minute quantities in uranium ores as a product of nuclear fission. Selenium also has numerous unstable synthetic isotopes ranging from 64Se to 95Se; the most stable are 75Se with a half-life of 119.78 days and 72Se with a half-life of 8.4 days. Isotopes lighter than the stable isotopes primarily undergo beta plus decay to isotopes of arsenic, and isotopes heavier than the stable isotopes undergo beta minus decay to isotopes of bromine, with some minor neutron emission branches in the heaviest known isotopes.

Chemical compounds
Selenium compounds commonly exist in the oxidation states −2, +2, +4, and +6.

Chalcogen compounds
Selenium forms two oxides: selenium dioxide (SeO2) and selenium trioxide (SeO3). Selenium dioxide is formed by the reaction of elemental selenium with oxygen:

            Se

              8

          +
          8

            O

              2

          ⟶
          8

            SeO

              2

    {\displaystyle {\ce {Se8 + 8 O2 -> 8 SeO2}}}
  It is a polymeric solid that forms monomeric SeO2 molecules in the gas phase. It dissolves in water to form selenous acid, H2SeO3. Selenous acid can also be made directly by oxidizing elemental selenium with nitric acid:

          3

          Se
          +
          4

            HNO

              3

          +

            H

              2

          O
          ⟶
          3

            H

              2

            SeO

              3

          +
          4

          NO

    {\displaystyle {\ce {3 Se + 4 HNO3 + H2O -> 3 H2SeO3 + 4 NO}}}
  Unlike sulfur, which forms a stable trioxide, selenium trioxide is thermodynamically unstable and decomposes to the dioxide above 185 °C:

          2

            SeO

              3

          ⟶
          2

            SeO

              2

          +

            O

              2

    {\displaystyle {\ce {2 SeO3 -> 2 SeO2 + O2}}}
   (ΔH = −54 kJ/mol)Selenium trioxide is produced in the laboratory by the reaction of anhydrous potassium selenate (K2SeO4) and sulfur trioxide (SO3).Salts of selenous acid are called selenites. These include silver selenite (Ag2SeO3) and sodium selenite (Na2SeO3).
Hydrogen sulfide reacts with aqueous selenous acid to produce selenium disulfide:

            H

              2

            SeO

              3

          +
          2

            H

              2

          S
          ⟶

            SeS

              2

          +
          3

            H

              2

          O

    {\displaystyle {\ce {H2SeO3 + 2 H2S -> SeS2 + 3 H2O}}}
  Selenium disulfide consists of 8-membered rings. It has an approximate composition of SeS2, with individual rings varying in composition, such as Se4S4 and Se2S6. Selenium disulfide has been used in shampoo as an antidandruff agent, an inhibitor in polymer chemistry, a glass dye, and a reducing agent in fireworks.Selenium trioxide may be synthesized by dehydrating selenic acid, H2SeO4, which is itself produced by the oxidation of selenium dioxide with hydrogen peroxide:

            SeO

              2

          +

            H

              2

            O

              2

          ⟶

            H

              2

            SeO

              4

    {\displaystyle {\ce {SeO2 + H2O2 -> H2SeO4}}}
  Hot, concentrated selenic acid can react with gold to form gold(III) selenate.

Halogen compounds
Iodides of selenium are not well known. The only stable chloride is selenium monochloride (Se2Cl2), which might be better known as selenium(I) chloride; the corresponding bromide is also known. These species are structurally analogous to the corresponding disulfur dichloride. Selenium dichloride is an important reagent in the preparation of selenium compounds (e.g. the preparation of Se7). It is prepared by treating selenium with sulfuryl chloride (SO2Cl2). Selenium reacts with fluorine to form selenium hexafluoride:

            Se

              8

          +
          24

            F

              2

          ⟶
          8

            SeF

              6

    {\displaystyle {\ce {Se8 + 24 F2 -> 8 SeF6}}}
  In comparison with its sulfur counterpart (sulfur hexafluoride), selenium hexafluoride (SeF6) is more reactive and is a toxic pulmonary irritant.
Some of the selenium oxyhalides, such as selenium oxyfluoride (SeOF2) and selenium oxychloride (SeOCl2) have been used as specialty solvents.

Selenides
Analogous to the behavior of other chalcogens, selenium forms hydrogen selenide, H2Se. It is a strongly odiferous, toxic, and colorless gas. It is more acidic than H2S. In solution it ionizes to HSe−. The selenide dianion Se2− forms a variety of compounds, including the minerals from which selenium is obtained commercially. Illustrative selenides include mercury selenide (HgSe), lead selenide (PbSe), zinc selenide (ZnSe), and copper indium gallium diselenide (Cu(Ga,In)Se2). These materials are semiconductors. With highly electropositive metals, such as aluminium, these selenides are prone to hydrolysis:

            Al

              2

            Se

              3

          +
          3

            H

              2

          O
          ⟶

            Al

              2

            O

              3

          +
          3

            H

              2

          Se

    {\displaystyle {\ce {Al2Se3 + 3 H2O -> Al2O3 + 3 H2Se}}}
  Alkali metal selenides react with selenium to form polyselenides, Se2−n, which exist as chains.

Other compounds
Tetraselenium tetranitride, Se4N4, is an explosive orange compound analogous to tetrasulfur tetranitride (S4N4). It can be synthesized by the reaction of selenium tetrachloride (SeCl4) with [((CH3)3Si)2N]2Se.Selenium reacts with cyanides to yield selenocyanates:

          8

          KCN
          +

            Se

              8

          ⟶
          8

          KSeCN

    {\displaystyle {\ce {8 KCN + Se8 -> 8 KSeCN}}}

Organoselenium compounds
Selenium, especially in the II oxidation state, forms stable bonds to carbon, which are structurally analogous to the corresponding organosulfur compounds. Especially common are selenides (R2Se, analogues of thioethers), diselenides (R2Se2, analogues of disulfides), and selenols (RSeH, analogues of thiols). Representatives of selenides, diselenides, and selenols include respectively selenomethionine, diphenyldiselenide, and benzeneselenol. The sulfoxide in sulfur chemistry is represented in selenium chemistry by the selenoxides (formula RSe(O)R), which are intermediates in organic synthesis, as illustrated by the selenoxide elimination reaction. Consistent with trends indicated by the double bond rule, selenoketones, R(C=Se)R, and selenaldehydes, R(C=Se)H, are rarely observed.

History
Selenium (Greek σελήνη selene meaning "Moon") was discovered in 1817 by Jöns Jacob Berzelius and Johan Gottlieb Gahn. Both chemists owned a chemistry plant near Gripsholm, Sweden, producing sulfuric acid by the lead chamber process. The pyrite from the Falun Mine created a red precipitate in the lead chambers which was presumed to be an arsenic compound, so the pyrites use to make acid was discontinued. Berzelius and Gahn wanted to use the pyrite and they also observed that the red precipitate gave off a smell like horseradish when burned. This smell was not typical of arsenic, but a similar odor was known from tellurium compounds. Hence, Berzeliuss first letter to Alexander Marcet stated that this was a tellurium compound. However, the lack of tellurium compounds in the Falun Mine minerals eventually led Berzelius to reanalyze the red precipitate, and in 1818 he wrote a second letter to Marcet describing a newly found element similar to sulfur and tellurium. Because of its similarity to tellurium, named for the Earth, Berzelius named the new element after the Moon.In 1873, Willoughby Smith found that the electrical resistance of grey selenium was dependent on the ambient light. This led to its use as a cell for sensing light. The first commercial products using selenium were developed by Werner Siemens in the mid-1870s. The selenium cell was used in the photophone developed by Alexander Graham Bell in 1879. Selenium transmits an electric current proportional to the amount of light falling on its surface. This phenomenon was used in the design of light meters and similar devices. Seleniums semiconductor properties found numerous other applications in electronics. The development of selenium rectifiers began during the early 1930s, and these replaced copper oxide rectifiers because they were more efficient. These lasted in commercial applications until the 1970s, following which they were replaced with less expensive and even more efficient silicon rectifiers.
Selenium came to medical notice later because of its toxicity to industrial workers. Selenium was also recognized as an important veterinary toxin, which is seen in animals that have eaten high-selenium plants. In 1954, the first hints of specific biological functions of selenium were discovered in microorganisms by biochemist, Jane Pinsent. It was discovered to be essential for mammalian life in 1957. In the 1970s, it was shown to be present in two independent sets of enzymes. This was followed by the discovery of selenocysteine in proteins. During the 1980s, selenocysteine was shown to be encoded by the codon UGA. The recoding mechanism was worked out first in bacteria and then in mammals (see SECIS element).

Occurrence
Native (i.e., elemental) selenium is a rare mineral, which does not usually form good crystals, but, when it does, they are steep rhombohedra or tiny acicular (hair-like) crystals. Isolation of selenium is often complicated by the presence of other compounds and elements.
Selenium occurs naturally in a number of inorganic forms, including selenide, selenate, and selenite, but these minerals are rare. The common mineral selenite is not a selenium mineral, and contains no selenite ion, but is rather a type of gypsum (calcium sulfate hydrate) named like selenium for the moon well before the discovery of selenium. Selenium is most commonly found as an impurity, replacing a small part of the sulfur in sulfide ores of many metals.In living systems, selenium is found in the amino acids selenomethionine, selenocysteine, and methylselenocysteine. In these compounds, selenium plays a role analogous to that of sulfur. Another naturally occurring organoselenium compound is dimethyl selenide.Certain soils are selenium-rich, and selenium can be bioconcentrated by some plants. In soils, selenium most often occurs in soluble forms such as selenate (analogous to sulfate), which are leached into rivers very easily by runoff. Ocean water contains significant amounts of selenium.Typical background concentrations of selenium do not exceed 1 ng/m3 in the atmosphere; 1 mg/kg in soil and vegetation and 0.5 μg/L in freshwater and seawater.Anthropogenic sources of selenium include coal burning, and the mining and smelting of sulfide ores.

Production
Selenium is most commonly produced from selenide in many sulfide ores, such as those of copper, nickel, or lead. Electrolytic metal refining is particularly productive of selenium as a byproduct, obtained from the anode mud of copper refineries. Another source was the mud from the lead chambers of sulfuric acid plants, a process that is no longer used. Selenium can be refined from these muds by a number of methods. However, most elemental selenium comes as a byproduct of refining copper or producing sulfuric acid. Since its invention, solvent extraction and electrowinning (SX/EW) production of copper produces an increasing share of the worldwide copper supply. This changes the availability of selenium because only a comparably small part of the selenium in the ore is leached with the copper.Industrial production of selenium usually involves the extraction of selenium dioxide from residues obtained during the purification of copper. Common production from the residue then begins by oxidation with sodium carbonate to produce selenium dioxide, which is mixed with water and acidified to form selenous acid (oxidation step). Selenous acid is bubbled with sulfur dioxide (reduction step) to give elemental selenium.About 2,000 tonnes of selenium were produced in 2011 worldwide, mostly in Germany (650 t), Japan (630 t), Belgium (200 t), and Russia (140 t), and the total reserves were estimated at 93,000 tonnes. These data exclude two major producers: the United States and China. A previous sharp increase was observed in 2004 from $4–$5 to $27/lb. The price was relatively stable during 2004–2010 at about US$30 per pound (in 100 pound lots) but increased to $65/lb in 2011. The consumption in 2010 was divided as follows: metallurgy – 30%, glass manufacturing – 30%, agriculture – 10%, chemicals and pigments – 10%, and electronics – 10%. China is the dominant consumer of selenium at 1,500–2,000 tonnes/year.

Applications
Fertilizers
Researchers found that application of selenium fertilizer to lettuce crops decreased the accumulation of lead and cadmium. Peaches and pears given a foliar selenium spray contained higher levels of selenium and also stayed firm and ripe longer when in storage. In low doses, selenium has shown a beneficial effect on plant resistance to various environmental stress factors including drought, UV-B, soil salinity, and cold or hot temperatures. However, it can damage plants at higher doses.

Manganese electrolysis
During the electrowinning of manganese, the addition of selenium dioxide decreases the power necessary to operate the electrolysis cells. China is the largest consumer of selenium dioxide for this purpose. For every tonne of manganese, an average 2 kg selenium oxide is used.

Glass production
The largest commercial use of Se, accounting for about 50% of consumption, is for the production of glass. Se compounds confer a red color to glass. This color cancels out the green or yellow tints that arise from iron impurities typical for most glass. For this purpose, various selenite and selenate salts are added. For other applications, a red color may be desired, produced by mixtures of CdSe and CdS.

Alloys
Selenium is used with bismuth in brasses to replace more toxic lead. The regulation of lead in drinking water applications such as in the US with the Safe Drinking Water Act of 1974, made a reduction of lead in brass necessary. The new brass is marketed under the name EnviroBrass. Like lead and sulfur, selenium improves the machinability of steel at concentrations around 0.15%. Selenium produces the same machinability improvement in copper alloys.

Lithium–selenium batteries
The lithium–selenium (Li–Se) battery is one of the most promising systems for energy storage in the family of lithium batteries. The Li–Se battery is an alternative to the lithium–sulfur battery, with an advantage of high electrical conductivity.

Solar cells
Selenium was the basis of the very first solar cells, with the first example of rooftop solar being a selenium cell from 1884. Such cells were later used in battery-free light meters for photography. Copper indium gallium selenide is a material used in solar cells.

Photoconductors
Amorphous selenium (α-Se) thin films have found application as photoconductors in flat panel x-ray detectors. These detectors use amorphous selenium to capture and convert incident x-ray photons directly into electric charge.

Rectifiers
Selenium rectifiers were first used in 1933. Their use continued into the 1990s.

Other uses
Small amounts of organoselenium compounds have been used to modify the catalysts used for the vulcanization for the production of rubber.The demand for selenium by the electronics industry is declining. Its photovoltaic and photoconductive properties are still useful in photocopying, photocells, light meters and solar cells. Its use as a photoconductor in plain-paper copiers once was a leading application, but in the 1980s, the photoconductor application declined (although it was still a large end-use) as more and more copiers switched to organic photoconductors. Though once widely used, selenium rectifiers have mostly been replaced (or are being replaced) by silicon-based devices. The most notable exception is in power DC surge protection, where the superior energy capabilities of selenium suppressors make them more desirable than metal-oxide varistors.
Zinc selenide was the first material for blue LEDs, but gallium nitride dominates that market. Cadmium selenide was an important component in quantum dots. Sheets of amorphous selenium convert X-ray images to patterns of charge in xeroradiography and in solid-state, flat-panel X-ray cameras. Ionized selenium (Se+24) is one of the active mediums used in X-ray lasers.Selenium is a catalyst in some chemical reactions, but it is not widely used because of issues with toxicity. In X-ray crystallography, incorporation of one or more selenium atoms in place of sulfur helps with multiple-wavelength anomalous dispersion and single wavelength anomalous dispersion phasing.Selenium is used in the toning of photographic prints, and it is sold as a toner by numerous photographic manufacturers. Selenium intensifies and extends the tonal range of black-and-white photographic images and improves the permanence of prints.75Se is used as a gamma source in industrial radiography.

Pollution
In high concentrations, selenium acts as an environmental contaminant.  Sources of pollution include waste materials from certain mining, agricultural, petrochemical, and industrial manufacturing operations.  In Belews Lake North Carolina, 19 species of fish were eliminated from the lake due to 150–200 μg Se/L wastewater discharged from 1974 to 1986 from a Duke Energy coal-fired power plant.  At the Kesterson National Wildlife Refuge in California, thousands of fish and waterbirds were poisoned by selenium in agricultural irrigation drainage.
Substantial physiological changes may occur in fish with high tissue concentrations of selenium. Fish affected by selenium may experience swelling of the gill lamellae, which impedes oxygen diffusion across the gills and blood flow within the gills. Respiratory capacity is further reduced due to selenium binding to hemoglobin. Other problems include degeneration of liver tissue, swelling around the heart, damaged egg follicles in ovaries, cataracts, and accumulation of fluid in the body cavity and head. Selenium often causes a malformed fish fetus which may have problems feeding or respiring; distortion of the fins or spine is also common. Adult fish may appear healthy despite their inability to produce viable offspring.
Selenium is bioaccumulated in aquatic habitats, which results in higher concentrations in organisms than the surrounding water. Organoselenium compounds can be concentrated over 200,000 times by zooplankton when water concentrations are in the 0.5 to 0.8 μg Se/L range. Inorganic selenium bioaccumulates more readily in phytoplankton than zooplankton. Phytoplankton can concentrate inorganic selenium by a factor of 3000.  Further concentration through bioaccumulation occurs along the food chain, as predators consume selenium rich prey. It is recommended that a water concentration of 2 μg Se/L be considered highly hazardous to sensitive fish and aquatic birds. Selenium poisoning can be passed from parents to offspring through the egg, and selenium poisoning may persist for many generations. Reproduction of mallard ducks is impaired at dietary concentrations of 7 μg Se/L. Many benthic invertebrates can tolerate selenium concentrations up to 300 μg/L of Se in their diet.Selenium pollution might impact some aquatic systems and may be caused by anthropogenic factors such as farming runoff and industrial processes. Fish are a major source of protein for humans, people who eat more fish are generally healthier than those who eat less, indicating selenium pollution does not appear to be a problem, although it might be useful to be aware that selenium has a potential effect on humans.Bioaccumulation of selenium in aquatic environments causes fish kills depending on the species in the affected area. There are, however, a few species that have been seen to survive these events and tolerate the increased selenium. It has also been suggested that season could have an impact on the harmful effects of selenium on fish.Selenium poisoning of water systems may result whenever new agricultural run-off courses through dry lands. This process leaches natural soluble selenium compounds (such as selenates) into the water, which may then be concentrated in wetlands as the water evaporates. Selenium pollution of waterways also occurs when selenium is leached from coal flue ash, mining and metal smelting, crude oil processing, and landfill. High selenium levels in waterways were found to cause congenital disorders in oviparous species, including wetland birds and fish. Elevated dietary methylmercury levels can amplify the harm of selenium toxicity in oviparous species.

Biological role
Although it is toxic in large doses, selenium is an essential micronutrient for animals. In plants, it occurs as a bystander mineral, sometimes in toxic proportions in forage (some plants may accumulate selenium as a defense against being eaten by animals, but other plants, such as locoweed, require selenium, and their growth indicates the presence of selenium in soil).Selenium is a component of the unusual amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for reduction of antioxidant enzymes, such as glutathione peroxidases and certain forms of thioredoxin reductase found in animals and some plants (this enzyme occurs in all living organisms, but not all forms of it in plants require selenium).
The glutathione peroxidase family of enzymes (GSH-Px) catalyze certain reactions that remove reactive oxygen species such as hydrogen peroxide and organic hydroperoxides:

2 GSH + H2O2----GSH-Px → GSSG + 2 H2OThe thyroid gland and every cell that uses thyroid hormone use selenium, which is a cofactor for the three of the four known types of thyroid hormone deiodinases, which activate and then deactivate various thyroid hormones and their metabolites; the iodothyronine deiodinases are the subfamily of deiodinase enzymes that use selenium as the otherwise rare amino acid selenocysteine. (Only the deiodinase iodotyrosine deiodinase, which works on the last breakdown products of thyroid hormone, does not use selenium.)Selenium may inhibit Hashimotos disease, in which the bodys own thyroid cells are attacked as foreign. A reduction of 21% on TPO antibodies is reported with the dietary intake of 0.2 mg of selenium.Increased dietary selenium reduces the effects of mercury toxicity, although it is effective only at low to modest doses of mercury. Evidence suggests that the molecular mechanisms of mercury toxicity includes the irreversible inhibition of selenoenzymes that are required to prevent and reverse oxidative damage in brain and endocrine tissues. An antioxidant, selenoneine, which is derived from selenium and has been found to be present in the blood of bluefin tuna, is the subject of scientific research regarding its possible roles in inflammatory and chronic diseases, methylmercury detoxification, and oxidative damages. It seems as though when mercury levels in a marine fish rise, so do the selenium levels. To the knowledge of researchers, there are no reports of mercury levels exceeding that of selenium levels in ocean fish.

Evolution in biology
From about three billion years ago, prokaryotic selenoprotein families drive the evolution of selenocysteine, an amino acid. Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea, and eukaryotes as selenocysteine, where selenoprotein peroxiredoxins protect bacterial and eukaryotic cells against oxidative damage. Selenoprotein families of GSH-Px and the deiodinases of eukaryotic cells seem to have a bacterial phylogenetic origin. The selenocysteine-containing form occurs in species as diverse as green algae, diatoms, sea urchins, fish, and chickens. Selenium enzymes are involved in the small reducing molecules glutathione and thioredoxin. One family of selenium-bearing molecules (the glutathione peroxidases) destroys peroxide and repairs damaged peroxidized cell membranes, using glutathione. Another selenium-bearing enzyme in some plants and in animals (thioredoxin reductase) generates reduced thioredoxin, a dithiol that serves as an electron source for peroxidases and also the important reducing enzyme ribonucleotide reductase that makes DNA precursors from RNA precursors.Trace elements involved in GSH-Px and superoxide dismutase enzymes activities, i.e. selenium, vanadium, magnesium, copper, and zinc, may have been lacking in some terrestrial mineral-deficient areas. Marine organisms retained and sometimes expanded their selenoproteomes, whereas the selenoproteomes of some terrestrial organisms were reduced or completely lost. These findings suggest that, with the exception of vertebrates, aquatic life supports selenium use, whereas terrestrial habitats lead to reduced use of this trace element. Marine fishes and vertebrate thyroid glands have the highest concentration of selenium and iodine. From about 500 million years ago, freshwater and terrestrial plants slowly optimized the production of "new" endogenous antioxidants such as ascorbic acid (vitamin C), polyphenols (including flavonoids), tocopherols, etc. A few of these appeared more recently, in the last 50–200 million years, in fruits and flowers of angiosperm plants. In fact, the angiosperms (the dominant type of plant today) and most of their antioxidant pigments evolved during the late Jurassic period.The deiodinase isoenzymes constitute another family of eukaryotic selenoproteins with identified enzyme function. Deiodinases are able to extract electrons from iodides, and iodides from iodothyronines. They are, thus, involved in thyroid-hormone regulation, participating in the protection of thyrocytes from damage by H2O2 produced for thyroid-hormone biosynthesis. About 200 million years ago, new selenoproteins were developed as mammalian GSH-Px enzymes.

Nutritional sources of selenium
Dietary selenium comes from meat, nuts, cereals and mushrooms. Brazil nuts are the richest dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs).The US Recommended Dietary Allowance (RDA) of selenium for teenagers and adults is 55 µg/day. Selenium as a dietary supplement is available in many forms, including multi-vitamins/mineral supplements, which typically contain 55 or 70 µg/serving. Selenium-specific supplements typically contain either 100 or 200 µg/serving.
In June 2015, the US Food and Drug Administration (FDA) published its final rule establishing the requirement of minimum and maximum levels of selenium in infant formula.The selenium content in the human body is believed to be in the 13–20 mg range.

Indicator plant species
Certain species of plants are considered indicators of high selenium content of the soil because they require high levels of selenium to thrive. The main selenium indicator plants are Astragalus species (including some locoweeds), princes plume (Stanleya sp.), woody asters (Xylorhiza sp.), and false goldenweed (Oonopsis sp.)

Detection in biological fluids
Selenium may be measured in blood, plasma, serum, or urine to monitor excessive environmental or occupational exposure, to confirm a diagnosis of poisoning in hospitalized victims, or investigate a suspected case of fatal overdose. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Both organic and inorganic forms of selenium are largely converted to monosaccharide conjugates (selenosugars) in the body prior to elimination in the urine. Cancer patients receiving daily oral doses of selenothionine may achieve very high plasma and urine selenium concentrations.

Toxicity
Although selenium is an essential trace element, it is toxic if taken in excess. Exceeding the Tolerable Upper Intake Level of 400 micrograms per day can lead to selenosis. This 400 µg Tolerable Upper Intake Level is based primarily on a 1986 study of five Chinese patients who exhibited overt signs of selenosis and a follow up study on the same five people in 1992. The 1992 study actually found the maximum safe dietary Se intake to be approximately 800 micrograms per day (15 micrograms per kilogram body weight), but suggested 400 micrograms per day to avoid creating an imbalance of nutrients in the diet and to accord with data from other countries. In China, people who ingested corn grown in extremely selenium-rich stony coal (carbonaceous shale) have suffered from selenium toxicity. This coal was shown to have selenium content as high as 9.1%, the highest concentration in coal ever recorded.Signs and symptoms of selenosis include a garlic odor on the breath, gastrointestinal disorders, hair loss, sloughing of nails, fatigue, irritability, and neurological damage. Extreme cases of selenosis can exhibit cirrhosis of the liver, pulmonary edema, or death. Elemental selenium and most metallic selenides have relatively low toxicities because of low bioavailability. By contrast, selenates and selenites have an oxidant mode of action similar to that of arsenic trioxide and are very toxic. The chronic toxic dose of selenite for humans is about 2400 to 3000 micrograms of selenium per day. Hydrogen selenide is an extremely toxic, corrosive gas. Selenium also occurs in organic compounds, such as dimethyl selenide, selenomethionine, selenocysteine and methylselenocysteine, all of which have high bioavailability and are toxic in large doses.
On 19 April 2009, 21 polo ponies died shortly before a match in the United States Polo Open. Three days later, a pharmacy released a statement explaining that the horses had received an incorrect dose of one of the ingredients used in a vitamin/mineral supplement compound that had been incorrectly prepared by a compounding pharmacy. Analysis of blood levels of inorganic compounds in the supplement indicated the selenium concentrations were 10 to 15 times higher than normal in the blood samples, and 15 to 20 times higher than normal in the liver samples. Selenium was later confirmed to be the toxic factor.

In fish and other wildlife, selenium is necessary for life, but toxic in high doses. For salmon, the optimal concentration of selenium is about 1 microgram selenium per gram of whole body weight. Much below that level, young salmon die from deficiency; much above, they die from toxic excess.The Occupational Safety and Health Administration (OSHA) has set the legal limit (permissible exposure limit) for selenium in the workplace at 0.2 mg/m3 over an 8-hour workday. The National Institute for Occupational Safety and Health (NIOSH) has set a Recommended exposure limit (REL) of 0.2 mg/m3 over an 8-hour workday. At levels of 1 mg/m3, selenium is immediately dangerous to life and health.

Deficiency
Selenium deficiency can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, and in those of advanced age (over 90). Also, people dependent on food grown from selenium-deficient soil are at risk. Although New Zealand soil has low levels of selenium, adverse health effects have not been detected in the residents.Selenium deficiency, defined by low (<60% of normal) selenoenzyme activity levels in brain and endocrine tissues, occurs only when a low selenium level is linked with an additional stress, such as high exposures to mercury or increased oxidant stress from vitamin E deficiency.Selenium interacts with other nutrients, such as iodine and vitamin E. The effect of selenium deficiency on health remains uncertain, particularly in relation to Kashin-Beck disease. Also, selenium interacts with other minerals, such as zinc and copper. High doses of Se supplements in pregnant animals might disturb the Zn:Cu ratio and lead to Zn reduction; in such treatment cases, Zn levels should be monitored. Further studies are needed to confirm these interactions.In the regions (e.g </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Parry–Romberg syndrome and can you explain it in depth? [/INST] Parry–Romberg syndrome (PRS)  is a rare disease characterized by progressive shrinkage and degeneration of the tissues beneath the skin, usually on only one side of the face (hemifacial atrophy) but occasionally extending to other parts of the body. An autoimmune mechanism is suspected, and the syndrome may be a variant of localized scleroderma, but the precise cause and pathogenesis of this acquired disorder remains unknown. It has been reported in the literature as a possible consequence of sympathectomy. The syndrome has a higher prevalence in females and typically appears between 5 and 15 years of age.
In addition to the connective tissue disease, the condition is sometimes accompanied by neurological, ocular and oral symptoms. The range and severity of associated symptoms and findings are highly variable.

Signs and symptoms
Skin and connective tissues
Initial facial changes usually involve the area of the face covered by the temporal or buccinator muscles. The disease progressively spreads from the initial location, resulting in atrophy of the skin and its adnexa, as well as underlying subcutaneous structures such as connective tissue, (fat, fascia, cartilage, bones) and/or muscles of one side of the face. The mouth and nose are typically deviated towards the affected side of the face.The process may eventually extend to involve tissues between the nose and the upper corner of the lip, the upper jaw, the angle of the mouth, the area around the eye and brow, the ear, and/or the neck. The syndrome often begins with a circumscribed patch of scleroderma in the frontal region of the scalp which is associated with a loss of hair and the appearance of a depressed linear scar extending down through the midface on the affected side. This scar is referred to as a "coup de sabre" lesion because it resembles the scar of a wound made by a sabre, and is indistinguishable from the scar observed in frontal linear scleroderma.In 20% of cases, the hair and skin overlying affected areas may become hyperpigmented or hypopigmented with patches of unpigmented skin. In up to 20% of cases the disease may involve the ipsilateral (on the same side) or contralateral (on the opposite side) neck, trunk, arm, or leg. The cartilage of the nose, ear and larynx can be involved. The disease has been reported to affect both sides of the face in 5 to 10% of cases.Symptoms and physical findings usually become apparent during the first or early during the second decade of life. The average age of onset is nine years of age, and the majority of individuals experience symptoms before 20 years of age. The disease may progress for several years before eventually going into remission (abruptly ceasing).

Neurological
Neurological abnormalities are common. Roughly 45% of people with Parry–Romberg syndrome also have trigeminal neuralgia (severe pain in the tissues supplied by the ipsilateral trigeminal nerve, including the forehead, eye, cheek, nose, mouth and jaw) and/or migraine (severe headaches that may be accompanied by visual abnormalities, nausea and vomiting).10% of affected individuals develop a seizure disorder as part of the disease. The seizures are typically Jacksonian in nature (characterized by rapid spasms of a muscle group that subsequently spread to adjacent muscles) and occur on the side contralateral to the affected side of the face. Half of these cases are associated with abnormalities in both the gray and white matter of the brain—usually ipsilateral but sometimes contralateral—that are detectable on magnetic resonance imaging (MRI) scan.

Ocular
Enophthalmos (recession of the eyeball within the orbit) is the most common eye abnormality observed in Parry–Romberg syndrome. It is caused by a loss of subcutaneous tissue around the orbit. Other common findings include drooping of the eyelid (ptosis), constriction of the pupil (miosis), redness of the conjunctiva, and decreased sweating (anhidrosis) of the affected side of the face. Collectively, these signs are referred to as Horners syndrome. Other ocular abnormalities include ophthalmoplegia (paralysis of one or more of the extraocular muscles) and other types of strabismus, uveitis, and heterochromia of the iris.

Oral
The tissues of the mouth, including the tongue, gingiva, teeth and soft palate are commonly involved in Parry–Romberg syndrome. 50% of affected individuals develop dental abnormalities such as delayed eruption, dental root exposure, or resorption of the dental roots on the affected side. 35% have difficulty or inability to normally open the mouth or other jaw symptoms, including temporomandibular joint disorder and spasm of the muscles of mastication on the affected side. 25% experience atrophy of one side of the upper lip and tongue.

Causes
The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Further, the National Organization for Rare Disorders has stated there is currently no evidence that Parry–Romberg syndrome is genetic or that it can be passed on to children. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.

Diagnosis
Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset. Oligoclonal bands and an elevated IgG index may be found in 50% of the patients.

Management
Medical
Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Surgical
Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Epidemiology
Parry–Romberg syndrome appears to occur randomly and for unknown reasons. Prevalence is higher in females than males, with a ratio of roughly 3:2. The condition is observed on the left side of the face about as often as on the right side.

History
The disease was first described in 1825 by Caleb Hillier Parry (1755–1822), in a collection of his medical writings which were published posthumously by his son Charles Henry Parry (1779–1860). It was described a second time in 1846 by Moritz Heinrich Romberg (1795–1873) and Eduard Heinrich Henoch (1820–1910). German neurologist Albert Eulenburg (1840–1917) was the first to use the descriptive title "progressive hemifacial atrophy" in 1871.

See also
Hemifacial microsomia
List of cutaneous conditions
Trigeminal trophic lesion

References
Further reading
Karim A, Laghmari M, Ibrahimy W, Essakali HN, Mohcine Z (October 2005). "[Neuroretinitis, Parry-Romberg syndrome, and scleroderma]". Journal Français dOphtalmologie (in French). 28 (8): 866–70. doi:10.1016/S0181-5512(05)81008-3. PMID 16249769.
Lakhani PK, David TJ (February 1984). "Progressive hemifacial atrophy with scleroderma and ipsilateral limb wasting (Parry-Romberg syndrome)". Journal of the Royal Society of Medicine. 77 (2): 138–9. doi:10.1177/014107688407700215. PMC 1439690. PMID 6737396.
Larner AJ, Bennison DP (September 1993). "Some observations on the aetiology of progressive hemifacial atrophy ("Parry-Romberg syndrome")". Journal of Neurology, Neurosurgery, and Psychiatry. 56 (9): 1035–6. doi:10.1136/jnnp.56.9.1035-a. PMC 489747. PMID 8410030.
Miller MT, Spencer MA (1995). "Progressive hemifacial atrophy. A natural history study". Transactions of the American Ophthalmological Society. 93: 203–15, discussion 215–7. PMC 1312058. PMID 8719679.
Pinheiro TP, Silva CC, Silveira CS, Botelho PC, Pinheiro MD, Pinheiro JJ (March 2006) </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hernia and can you explain it in depth? [/INST] A hernia is the abnormal exit of tissue or an organ, such as the bowel, through the wall of the cavity in which it normally resides. Various types of hernias can occur, most commonly involving the abdomen, and specifically the groin. Groin hernias are most commonly of the inguinal type but may also be femoral. Other types of hernias include hiatus, incisional, and umbilical hernias. Symptoms are present in about 66% of people with groin hernias. This may include pain or discomfort in the lower abdomen, especially with coughing, exercise, or urinating or defecating. Often, it gets worse throughout the day and improves when lying down. A bulge may appear at the site of hernia, that becomes larger when bending down. Groin hernias occur more often on the right than left side. The main concern is bowel strangulation, where the blood supply to part of the bowel is blocked. This usually produces severe pain and tenderness in the area. Hiatus, or hiatal hernias often result in heartburn but may also cause chest pain or pain while eating.Risk factors for the development of a hernia include smoking, chronic obstructive pulmonary disease, obesity, pregnancy, peritoneal dialysis, collagen vascular disease and previous open appendectomy, among others. Predisposition to hernias is genetic and occur more often in certain families. Deleterious mutations causing predisposition to hernias seem to have dominant inheritance (especially for men). It is unclear if groin hernias are associated with heavy lifting. Hernias can often be diagnosed based on signs and symptoms. Occasionally, medical imaging is used to confirm the diagnosis or rule out other possible causes. The diagnosis of hiatus hernias is often by endoscopy.Groin hernias that do not cause symptoms in males do not need to be repaired. Repair, however, is generally recommended in women due to the higher rate of femoral hernias, which have more complications. If strangulation occurs, immediate surgery is required. Repair may be done by open surgery or laparoscopic surgery. Open surgery has the benefit of possibly being done under local anesthesia rather than general anesthesia. Laparoscopic surgery generally has less pain following the procedure. A hiatus hernia may be treated with lifestyle changes such as raising the head of the bed, weight loss and adjusting eating habits. The medications H2 blockers or proton pump inhibitors may help. If the symptoms do not improve with medications, a surgery known as laparoscopic Nissen fundoplication may be an option.About 27% of males and 3% of females develop a groin hernia at some point in their lives. Inguinal, femoral and abdominal hernias were present in 18.5 million people and resulted in 59,800 deaths in 2015. Groin hernias occur most often before the age of 1 and after the age of 50. It is not known how commonly hiatus hernias occur, with estimates in North America varying from 10% to 80%. The first known description of a hernia dates back to at least 1550 BC, in the Ebers Papyrus from Egypt.

Signs and symptoms
By far the most common hernias develop in the  abdomen when a weakness in the abdominal wall evolves into a localized hole, or "defect", through which adipose tissue, or abdominal organs covered with peritoneum, may protrude. Another common hernia involves the spinal discs and causes sciatica. A hiatus hernia occurs when the stomach protrudes into the mediastinum through the esophageal opening in the diaphragm.
Hernias may or may not present with either pain at the site, a visible or palpable lump, or in some cases more vague symptoms resulting from pressure on an organ that has become "stuck" in the hernia, sometimes leading to organ dysfunction. Fatty tissue usually enters a hernia first, but it may be followed or accompanied by an organ.
Hernias are caused by a disruption or opening in the fascia, or fibrous tissue, which forms the abdominal wall. It is possible for the bulge associated with a hernia to come and go, but the defect in the tissue will persist.
Symptoms and signs vary depending on the type of hernia. Symptoms may or may not be present in some inguinal hernias. In the case of reducible hernias, a bulge in the groin or in another abdominal area can often be seen and felt. When standing, such a bulge becomes more obvious. Besides the bulge, other symptoms include pain in the groin that may also include a heavy or dragging sensation, and in men, there is sometimes pain and swelling in the scrotum around the testicular area.Irreducible abdominal hernias or incarcerated hernias may be painful, but their most relevant symptom is that they cannot return to the abdominal cavity when pushed in. They may be chronic, although painless, and can lead to strangulation (loss of blood supply), obstruction (kinking of intestine), or both. Strangulated hernias are always painful and pain is followed by tenderness. Nausea, vomiting, or fever may occur in these cases due to bowel obstruction. Also, the hernia bulge, in this case, may turn red, purple or dark and pink.
In the diagnosis of abdominal hernias, imaging is the principal means of detecting internal diaphragmatic and other nonpalpable or unsuspected hernias. Multidetector CT (MDCT) can show with precision the anatomic site of the hernia sac, the contents of the sac, and any complications. MDCT also offers clear detail of the abdominal wall allowing wall hernias to be identified accurately.

Complications
Complications may arise post-operation, including rejection of the mesh that is used to repair the hernia. In the event of a mesh rejection, the mesh will very likely need to be removed. Mesh rejection can be detected by obvious, sometimes localized swelling and pain around the mesh area. Continuous discharge from the scar is likely for a while after the mesh has been removed.
A surgically treated hernia can lead to complications such as inguinodynia, while an untreated hernia may be complicated by:

Inflammation
Obstruction of any lumen, such as bowel obstruction in intestinal hernias
Strangulation
Hydrocele of the hernial sac
Hemorrhage
Autoimmune problems
Irreducibility or incarceration, in which it cannot be reduced, or pushed back into place, at least not without very much external effort. In intestinal hernias, this also substantially increases the risk of bowel obstruction and strangulation.

Causes
Causes of hiatus hernia vary depending on each individual. Among the multiple causes, however, are the mechanical causes which include: improper heavy weight lifting, hard coughing bouts, sharp blows to the abdomen, and incorrect posture.Furthermore, conditions that increase the pressure of the abdominal cavity may also cause hernias or worsen the existing ones. Some examples would be: obesity, straining during a bowel movement or urination (constipation, enlarged prostate), chronic lung disease, and also, fluid in the abdominal cavity (ascites).Also, if muscles are weakened due to poor nutrition, smoking, and overexertion, hernias are more likely to occur.
The physiological school of thought contends that in the case of inguinal hernia, the above-mentioned are only an anatomical symptom of the underlying physiological cause. They contend that the risk of hernia is due to a physiological difference between patients who have hernia and those who do not, namely the presence of aponeurotic extensions from the transversus abdominis aponeurotic arch.Abdominal wall hernia may occur due to trauma. If this type of hernia is due to blunt trauma it is an emergency condition and could be associated with various solid organs and hollow viscus injuries.

Diagnosis
Inguinal
By far the most common hernias (up to 75% of all abdominal hernias) are inguinal hernias, which are further divided into the more common indirect inguinal hernia (2/3, depicted here), in which the inguinal canal is entered via a congenital weakness at its entrance (the internal inguinal ring), and the direct inguinal hernia type (1/3), where the hernia contents push through a weak spot in the back wall of the inguinal canal. Inguinal hernias are the most common type of hernia in both men and women. In some selected cases, they may require surgery.
There are special cases where a direct and indirect hernia appear together. A pantaloon hernia (or saddlebag hernia) is a combined direct and indirect hernia when the hernial sac protrudes on either side of the inferior epigastric vessels.
Additionally, though very rare, two or more indirect hernias may appear together such as in a double indirect hernia.

Femoral
Femoral hernias occur just below the inguinal ligament, when abdominal contents pass into the weak area at the posterior wall of the femoral canal. They can be hard to distinguish from the inguinal type (especially when ascending cephalad): however, they generally appear more rounded, and, in contrast to inguinal hernias, there is a strong female preponderance in femoral hernias. The incidence of strangulation in femoral hernias is high. Repair techniques are similar for femoral and inguinal hernia.
A Coopers hernia is a femoral hernia with two sacs, the first being in the femoral canal, and the second passing through a defect in the superficial fascia and appearing almost immediately beneath the skin.

Umbilical
They involve protrusion of intra-abdominal contents through a weakness at the site of passage of the umbilical cord through the abdominal wall.
Umbilical hernias in adults are largely acquired, and are more frequent in obese or pregnant women. Abnormal decussation of fibers at the linea alba may be a contributing factor.

Incisional
An incisional hernia occurs when the defect is the result of an incompletely healed surgical wound. When these occur in median laparotomy incisions in the linea alba, they are termed ventral hernias. These can be the most frustrating and difficult to treat, as the repair utilizes already attenuated tissue. These occur in about 13% of people at 2 years following surgery.

Diaphragmatic
Higher in the abdomen, an (internal) "diaphragmatic hernia" results when part of the stomach or intestine protrudes into the chest cavity through a defect in the diaphragm.
A hiatus hernia is a particular variant of this type, in which the normal passageway through which the esophagus meets the stomach (esophageal hiatus) serves as a functional "defect", allowing part of the stomach to (periodically) "herniate" into the chest. Hiatus hernias may be either "sliding", in which the gastroesophageal junction itself slides through the defect into the chest, or non-sliding (also known as para-esophageal), in which case the junction remains fixed while another portion of the stomach moves up through the defect. Non-sliding or para-esophageal hernias can be dangerous as they may allow the stomach to rotate and obstruct. Repair is usually advised.
A congenital diaphragmatic hernia is a distinct problem, occurring in up to 1 in 2000 births, and requiring pediatric surgery. Intestinal organs may herniate through several parts of the diaphragm, posterolateral (in Bochdaleks triangle (lumbocostal triangle), resulting in a Bochdalek hernia), or anteromedial-retrosternal (in the cleft of foramina of Morgagni (sternocostal triangle), resulting in a Morgagnis hernia).

Other hernias
Since many organs or parts of organs can herniate through many orifices, it is very difficult to give an exhaustive list of hernias, with all synonyms and eponyms. The above article deals mostly with "visceral hernias", where the herniating tissue arises within the abdominal cavity. Other hernia types and unusual types of visceral hernias are listed below, in alphabetical order:

Abdominal wall hernias:
Umbilical hernia
Epigastric hernia: a hernia through the linea alba above the umbilicus.
Spigelian hernia, also known as spontaneous lateral ventral hernia
Amyands hernia: containing the appendix vermiformis within the hernia sac
Brain herniation, sometimes referred to as brain hernia, is a potentially deadly side effect of very high intracranial pressure that occurs when a part of the brain is squeezed across structures within the skull.
Broad ligament hernia, of the uterus.
Double indirect hernia: an indirect inguinal hernia with two hernia sacs, without a concomitant direct hernia component (as seen in a pantaloon hernia).
Hiatus hernia: a hernia due to "short oesophagus" — insufficient elongation — stomach is displaced into the thorax
Littres hernia: a hernia involving a Meckels diverticulum. It is named after the French anatomist Alexis Littré (1658–1726).
Lumbar hernia: a hernia in the lumbar region (not to be confused with a lumbar disc hernia), contains the following entities:
Petits hernia: a hernia through Petits triangle (inferior lumbar triangle). It is named after French surgeon  Jean Louis Petit (1674–1750).
Grynfeltts hernia: a hernia through Grynfeltt-Lesshaft triangle (superior lumbar triangle). It is named after physician Joseph Grynfeltt (1840–1913).
Maydls hernia: two adjacent loops of small intestine are within a hernial sac with a tight neck. The intervening portion of bowel within the abdomen is deprived of its blood supply and eventually becomes necrotic.
Obturator hernia: hernia through obturator canal
Parastomal hernias, which is when tissue protrudes adjacent to a stoma tract.
Paraumbilical hernia: a type of umbilical hernia occurring in adults
Perineal hernia: a perineal hernia protrudes through the muscles and fascia of the perineal floor. It may be primary but usually is acquired following perineal prostatectomy, abdominoperineal resection of the rectum, or pelvic exenteration.
Properitoneal hernia: rare hernia located directly above the peritoneum, for example, when part of inguinal hernia projects from the deep inguinal ring to the preperitoneal space.
Richters hernia: a hernia involving only one sidewall of the bowel, which can result in bowel strangulation leading to perforation through ischaemia without causing bowel obstruction or any of its warning signs. It is named after German surgeon August Gottlieb Richter (1742–1812).
Sliding hernia: occurs when an organ drags along part of the peritoneum, or, in other words, the organ is part of the hernia sac. The colon and the urinary bladder are often involved. The term also frequently refers to sliding hernias of the stomach.
Sciatic hernia: this hernia in the greater sciatic foramen most commonly presents as an uncomfortable mass in the gluteal area. Bowel obstruction may also occur. This type of hernia is only a rare cause of sciatic neuralgia.
Sports hernia: a hernia characterized by chronic groin pain in athletes and a dilated superficial inguinal ring.
Tibialis anterior hernia: can present as a bulge in the shins. Pain on rest, walking, or during exercise may occur. The bulge can typically not be present unless pressure or flexing of the leg occurs.
Velpeau hernia: a hernia in the groin in front of the femoral blood vessels

Treatment
Truss
The benefits of the use of an external device to maintain reduction of the hernia without repairing the underlying defect (such as hernia trusses, trunks, belts, etc.) are unclear.

Surgery
Surgery is recommended for some types of hernias to prevent complications such as obstruction of the bowel or strangulation of the tissue, although umbilical hernias and hiatus hernias may be watched, or are treated with medication. Most abdominal hernias can be surgically repaired, but surgery has complications. Time needed for recovery after treatment is reduced if hernias are operated on laparoscopically. However, open surgery can be done sometimes without general anesthesia. Robot-assisted hernia surgery has also recently gained popularity as safe alternatives to open surgery.
Uncomplicated hernias are principally repaired by pushing back, or "reducing", the herniated tissue, and then mending the weakness in muscle tissue (an operation called herniorrhaphy). If complications have occurred, the surgeon will check the viability of the herniated organ and remove part of it if necessary.
Muscle reinforcement techniques often involve synthetic materials (a mesh prosthesis). The mesh is placed either over the defect (anterior repair) or under the defect (posterior repair). At times staples are used to keep the mesh in place. These mesh repair methods are often called "tension free" repairs because, unlike some suture methods (e.g., Shouldice), muscle is not pulled together under tension </s>


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