<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 Minutes and can you explain it in depth? [/INST] Minutes, also known as minutes of meeting (abbreviation MoM), protocols or, informally, notes, are the instant written record of a meeting or hearing. They typically describe the events of the meeting and may include a list of attendees, a statement of the activities considered by the participants, and related responses or decisions for the activities.

Etymology
The name "minutes" possibly derives from the Latin phrase minuta scriptura (literally "small writing") meaning "rough notes".

Creation
Minutes may be created during the meeting by a typist or court reporter, who may use shorthand notation and then prepare the minutes and issue them to the participants afterwards. Alternatively, the meeting can be audio recorded, video recorded, or a groups appointed or informally assigned secretary may take notes, with minutes prepared later. Many government agencies use minutes recording software to record and prepare all minutes in real-time.

Purpose
Minutes are the official written record of the meetings of an organization or group. They are not transcripts of those proceedings. Using Roberts Rules of Order Newly Revised (RONR), the minutes should contain mainly a record of what was done at the meeting, not what was said by the members. The organization may have its own rules regarding the content of the minutes.
For most organizations or groups, it is important for the minutes to be terse and only include a summary of the decisions. A verbatim report (transcript) is typically not useful. Unless the organizations rules require it, a summary of the discussions in a meeting is neither necessary nor appropriate.The minutes of certain groups, such as a corporate board of directors, must be kept on file and are important legal documents. Minutes from board meetings are kept separately from minutes of general membership meetings within the same organization. Also, minutes of executive sessions may be kept separately. Committees are not required to keep formal minutes although less formal notes may be taken. For committees, their formal records are the reports submitted to their parent body.

Format
The format of the minutes can vary depending on the standards established by an organization, although there are general guidelines. Roberts Rules of Order contains a sample set of minutes.Generally, minutes begin with the name of the body holding the meeting (e.g., a board) and may also include the place, date, list of people present, and the time that the chair called the meeting to order.Since the primary function of minutes is to record the decisions made, all official decisions must be included. If a formal motion is proposed and seconded, then (regardless whether it passes) this is recorded. The voting tally may also be included. The part of the minutes dealing with a routine motion might note merely that a particular motion was "moved by Ann and passed". It is not strictly necessary to include the name of the person who seconds a motion. Where a tally is included, it is sufficient to record the number of people voting for and against a motion, but requests by participants to note their votes by name may be allowed. If a decision is made by roll-call vote, then all of the individual votes are recorded by name. If it is made by general consent without a formal vote, then this fact may be recorded.
The minutes may end with a note of the time that the meeting was adjourned.Minutes are sometimes submitted by the person who is responsible for them (often the secretary) at a subsequent meeting for review. The traditional closing phrase is  "Respectfully submitted" (although this is no longer common), followed by the officers signature, his or her typed (or printed) name, and his or her title.Usually, one of the first items in an order of business or an agenda for a meeting is the reading and approval of the minutes from the previous meeting. If the members of the group agree (usually by unanimous consent) that the written minutes reflect what happened at the previous meeting, then they are approved, and the fact of their approval is recorded in the minutes of the current meeting. If there are significant errors or omissions, then the minutes may be redrafted and submitted again at a later date. Minor changes may be made immediately using the normal amendment procedures, and the amended minutes may be approved "as amended". It is normally appropriate to send a draft copy of the minutes to all the members in advance of the meeting so that the meeting is not delayed by a reading of the draft.

See also
Diary
Gazette

References
Citations
Sources
Further reading
American Institute of Parliamentarians (2014) </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 Macrostomia and can you explain it in depth? [/INST] Macrostomia refers to a mouth that is unusually wide. The term is from the Greek prefix makro- meaning "large" and from Greek στόμα, "mouth".Macrostomia is characterized as a physical abnormality that causes clefts to form on the face of affected individuals. These clefts can form on either or both sides of the face, but they are most commonly seen on the right cheek and have a higher rate of occurrence in males. Macrostomia is very irregular and on average occurs only once in every 150,000 to 300,000 live births. Its unusual for macrostomia to occur on its own and it is included as a symptom for many diseases including craniofacial microsomia. The clefts result from improper development and fusion of the mandibular and maxillary processes. The clefts cause problems with facial muscle development. The origin of macrostomia is not yet fully understood: it could have multiple causes.

Phenotypic variations
There are 4 distinct variations of macrostomia. Classifications are a complete lateral facial cleft, simple macrostomia, macrostomia with diastasis of the facial musculature, and isolated facial musculature diastasis. Each has a different physical appearance with varying levels of severity.The cleft associated with macrostomia is associated with improper or failed fusion of the mandibular and maxillary processes during embryonic development. This can lead to a variety of abnormalities involving skin, subcutaneous tissue, facial muscles, and the mucous membrane. The severity of each abnormality can vary from minor to severe. Environmental contaminants may play a role in causing macrostomia. Many affected individuals were found in Lagos, an industrial area of Nigeria, where water supplies are known to be contaminated by improper disposal of industrial and domestic waste.

Complete lateral facial cleft
The facial cleft runs from the corner of the mouth towards the bottom of the ear. The outside of the ear on the affected side of the face appears as normal and a region of soft tissue connects the cleft to the right lateral posterior hard palate. Internally there is no soft palate.

Simple macrostomia
This version of macrostomia is less severe because it does not affect the facial muscles and is not associated with any soft tissue or bone deformities. A small cleft(s) extends from the mouth and can be repaired surgically.

Diastasis of the facial musculature
Clefts in this variant are slightly more severe than the ones seen in simple macrostomia. It also does not have bone deformities, but it does include minor soft tissue deformities. The defining feature is muscle diastasis which is separation of the masseter </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 Anisakis and can you explain it in depth? [/INST] Anisakis  (a·nuh·saa·keez)
is a genus of parasitic nematodes that have life cycles involving fish and marine mammals. They are infective to humans and cause anisakiasis. People who produce immunoglobulin E in response to this parasite may subsequently have an allergic reaction, including anaphylaxis, after eating fish infected with Anisakis species.

Etymology
The genus Anisakis was defined in 1845 by Félix Dujardin as a subgenus of the genus Ascaris Linnaeus, 1758. Dujardin did not make explicit the etymology, but stated that the subgenus included the species in which the males have unequal spicules ("mâles ayant des spicules inégaux"); thus, the name Anisakis is based on anis- (Greek prefix for different) and akis (Greek for spine or spicule). Two species were included in the new subgenus, Ascaris (Anisakis) distans Rudolphi, 1809 and Ascaris (Anisakis) simplex Rudolphi, 1809.

Life cycle
Anisakis species have complex life cycles which pass through a number of hosts through the course of their lives. Eggs hatch in seawater, and larvae are eaten by crustaceans, usually euphausids. The infected crustaceans are subsequently eaten by fish or squid, and the nematodes burrow into the wall of the gut and encyst in a protective coat, usually on the outside of the visceral organs, but occasionally in the muscle or beneath the skin. The life cycle is completed when an infected fish is eaten by a marine mammal, such as a whale, seal, sea lion, dolphin or another animal like a seabird or shark. The nematode excysts in the intestine, feeds, grows, mates, and releases eggs into the seawater in the hosts feces. As the gut of a marine mammal is functionally very similar to that of a human, Anisakis species are able to infect humans who eat raw or undercooked fish.

Reproduction
Sexual reproduction occurs once the larvae have reached a definitive host and completed their final molt, at which point sexual organs are developed. Females are capable of producing 2.6 million eggs, depending on species and size at sexual maturity.The known diversity of the genus has increased greatly since mid-1980s with the advent of modern genetic techniques in species identification. Each final host species was discovered to have its own biochemically and genetically identifiable "sibling species" of Anisakis, which is reproductively isolated. This finding has allowed the proportion of different sibling species in a fish to be used as an indicator of population identity in fish stocks.

Morphology
Anisakis share the common features of all nematodes: the vermiform body plan, round in cross section, and a lack of segmentation. The body cavity is reduced to a narrow pseudocoel. The mouth is located anteriorly and surrounded by projections used in feeding and sensation, with the anus slightly offset from the posterior. The squamous epithelium secretes a layered cuticle to protect the body from digestive acids.
As with all parasites with a complex life cycle involving a number of hosts, details of the morphology vary depending on the host and life cycle stage. In the stage which infects fish, Anisakis species are found in a distinctive "watch-spring coil" shape. They are roughly 2 cm long when uncoiled. When in the final host, anisakids are longer, thicker, and more sturdy, to deal with the hazardous environment of a mammalian gut.

Health implications
Anisakids pose a risk to human health through intestinal infection with worms from the eating of underprocessed fish, and through allergic reactions to chemicals left by the worms in fish flesh.

Anisakiasis
Anisakiasis is a human parasitic infection of the gastrointestinal tract caused by the consumption of raw or undercooked seafood containing larvae of the nematode Anisakis simplex.  The first case of human infection by a member of the family Anisakidae was reported in the Netherlands by Van Thiel, who described the presence of a marine nematode in a patient suffering from acute abdominal pain. It is frequently reported in areas of the world where fish is consumed raw, lightly pickled, or salted.  The areas of highest prevalence are Scandinavia (from cod livers), Japan (after eating sashimi), the Netherlands (by eating infected fermented herrings (maatjes)), Spain (from eating anchovies and other fish marinated in escabeche), and along the Pacific coast of South America (from eating ceviche). The frequency in the United States is unknown, because the disease is not reportable and can go undetected or be mistaken for other illnesses. Anisakiasis was first recognized in the 1960s.
During the 1970s, about 10 cases per year were reported in the literature. The frequency is
probably much higher, due to home preparation of raw or undercooked fish dishes. In Japan,
more than 1,000 cases are reported annually. Development of better diagnostic tools and greater awareness has led to more frequent reporting of anisakiasis.
Within a few hours of ingestion, the parasitic worm tries to burrow though the intestinal wall, but since it cannot penetrate it, it gets stuck and dies. The presence of the parasite triggers an immune response; immune cells surround the worms, forming a ball-like structure that can block the digestive system, causing severe abdominal pain, malnutrition, and vomiting. Occasionally, the larvae are regurgitated.  If the larvae pass into the bowel or large intestine, a severe eosinophilic granulomatous response may also occur one to two weeks following infection, causing symptoms mimicking Crohns disease.Diagnosis can be made by gastroscopic examination, during which the 2-cm larvae are visually observed and removed, or by histopathologic examination of tissue removed at biopsy or during surgery.
Raising consumer and producer awareness about the existence of anisakid worms in fish is a critical and effective prevention strategy. Anisakiasis can be easily prevented by adequate cooking at temperatures greater than 60 °C or freezing. The FDA recommends all shellfish and fish intended for raw consumption be blast frozen to −35 °C or below for 15 hours or be regularly frozen to −20 °C or below for seven days. Salting and marinating will not necessarily kill the parasites, as in Italy where two-thirds of cases were attributed to anchovies marinated in lemon or vinegar. Humans are thought to be more at risk of anisakiasis from eating wild fish rather than farmed fish. Many countries require all types of fish with potential risk intended for raw consumption to be previously frozen to kill parasites. The mandate to freeze herring in the Netherlands has virtually eliminated human anisakiasis in the Netherlands.

Allergic reactions
Even when the fish is thoroughly cooked, Anisakis larvae pose a health risk to humans. Anisakids (and related species such as the sealworm, Pseudoterranova species, and the codworm Hysterothylacium aduncum) release a number of biochemicals into the surrounding tissues when they infect a fish. They are also often consumed whole, accidentally, inside a fillet of fish.

Acute allergic manifestations, such as urticaria and anaphylaxis, may occur with or without accompanying gastrointestinal symptoms. The frequency of allergic symptoms in connection with fish ingestion has led to the concept of gastroallergic anisakiasis, an acute IgE-mediated generalized reaction. Occupational allergy, including asthma, conjunctivitis, and contact dermatitis, has been observed in fish processing workers.
Sensitivization and allergy are determined by skin-prick test and detection of specific antibodies against Anisakis. Hypersensitivity is indicated by a rapid rise in levels of IgE in the first several days following consumption of infected fish. A 2018 review of cases in France has shown that allergic cases were more commonly found, although the number of human Anisakis infections was decreasing.

Treatment
For the worm, humans are a dead-end host. Anisakis and Pseudoterranova larvae cannot survive in humans, and eventually die. In some cases, the infection resolves with only symptomatic treatment. In other cases, however, infection can lead to small bowel obstruction, which may require surgery, although treatment with albendazole alone (avoiding surgery) has been reported to be successful. Intestinal perforation (an emergency) is also possible.

Occurrence
Larval anisakids are common parasites of marine and anadromous fish (e.g. salmon, sardine), and can also be found in squid and cuttlefish </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 Muscle weakness and can you explain it in depth? [/INST] Muscle weakness is a lack of muscle strength. Its causes are many and can be divided into conditions that have either true or perceived muscle weakness.  True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years). The term myasthenia is from my- from Greek μυο meaning "muscle" + -asthenia  ἀσθένεια meaning "weakness".

Types
Neuromuscular fatigue can be classified as either "central" or "peripheral" depending on its cause. Central muscle fatigue manifests as an overall sense of energy deprivation, while peripheral muscle fatigue manifests as a local, muscle-specific inability to do work.

Neuromuscular fatigue
Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.For extremely powerful contractions that are close to the upper limit of a muscles ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscles ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout.  Part of the process of strength training is increasing the nerves ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force.  It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.

Central fatigue
Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output.  It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. There has been a great deal of interest in the role of serotonergic pathways for several years because its concentration in the brain increases with motor activity. During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.

Peripheral muscle fatigue
Peripheral muscle fatigue during physical work is an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy.The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation  therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the muscle fiber. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract.

Lactic acid hypothesis
It was once believed that lactic acid build-up was the cause of muscle fatigue.  The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract.  The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles.  This can lower the sensitivity of contractile apparatus to calcium ions (Ca2+) but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell.  This counters inhibiting effects of potassium ions (K+) on muscular action potentials.  Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving K+ as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions.  Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

Pathophysiology
Muscle cells work by detecting a flow of electrical impulses from the brain which signals them to contract through the release of calcium by the sarcoplasmic reticulum.  Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This causes there to be less calcium available for the muscle cell. In addition an enzyme is proposed to be activated by this released calcium which eats away at muscle fibers.Substrates within the muscle generally serve to power muscular contractions.  They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate.  ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model.  Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds </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 Extremities 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 Accident and can you explain it in depth? [/INST] An accident is an unintended, normally unwanted event that was not directly caused by humans.  The term accident implies that nobody should be blamed, but the event may have been caused by unrecognized or unaddressed risks.  Most researchers who study unintentional injury avoid using the term accident and focus on factors that increase risk of severe injury and that reduce injury incidence and severity.  For example, when a tree falls down during a wind storm, its fall may not have been caused by humans, but the trees type, size, health, location, or improper maintenance may have contributed to the result.  Most car wrecks are not true accidents; however English speakers started using that word in the mid-20th century as a result of media manipulation by the US automobile industry.

Types
Physical and non-physical
Physical examples of accidents include unintended motor vehicle collisions, falls, being injured by touching something sharp or hot, or bumping into something while walking.
Non-physical examples are unintentionally revealing a secret or otherwise saying something incorrectly, accidental deletion of data, or forgetting an appointment.

Accidents by activity
Accidents during the execution of work or arising out of it are called work accidents. According to the International Labour Organization (ILO), more than 337 million accidents happen on the job each year, resulting, together with occupational diseases, in more than 2.3 million deaths annually.
In contrast, leisure-related accidents are mainly sports injuries.

Accidents by vehicle
Vehicle collisions are not usually accidents; they are mostly caused by preventable causes such as drunk driving and intentionally driving too fast </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 Pasteurellosis and can you explain it in depth? [/INST] Pasteurellosis is an infection with a species of the bacterial genus Pasteurella, which is found in humans and other animals.
Pasteurella multocida (subspecies P. m. septica and  P. m. multocida) is carried in the mouth and respiratory tract of various animals, including pigs. It is a small, Gram-negative bacillus with bipolar staining by Wayson stain. In animals, it can originate in fulminant septicaemia (chicken cholera), but is also a common commensal.
Until taxonomic revision in 1999,  Mannheimia spp. were classified as Pasteurella spp., and infections by organisms now called Mannheimia spp., as well as by organisms now called Pasteurella spp., were designated as pasteurellosis.  The term "pasteurellosis" is often still applied to mannheimiosis, although such usage has declined.

Types
The several forms of the infection are:

Skin/subcutaneous tissue disease is a septic phlegmon that develops classically in the hand and forearm after a cat bite. Inflammatory signs are very rapid to develop; in 1 or 2 hours, edema, severe pain, and serosanguineous exudate appear. Fever, moderate or very high, can be seen, along with vomiting, headache, and diarrhea. Lymphangitis is common.  Complications are possible, in the form of septic arthritis, osteitis, or evolution to chronicity.
Sepsis is very rare, but can be as fulminant as septicaemic plague, with high fever, rigors, and vomiting, followed by shock and coagulopathy.
Pneumonia disease is also rare and appears in patients with some chronic pulmonary pathology.  It usually presents as bilateral consolidating pneumonia, sometimes very severe.
Zoonosis, pasteurellosis can be transmitted to humans through cats.Other locations are possible, such as septic arthritis, meningitis, and acute endocarditis, but are very rare.

Diagnosis
Diagnosis is made with isolation of Pasteurella multocida in a normally sterile site (blood, pus, or cerebrospinal fluid).

Treatment
As the infection is usually transmitted into humans through animal bites, antibiotics usually treat the infection, but medical attention should be sought if the wound is severely swelling. Pasteurellosis is usually treated with high-dose penicillin if severe. Either tetracycline or chloramphenicol provides an alternative in beta-lactam-intolerant patients </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 Failed back syndrome and can you explain it in depth? [/INST] Failed back syndrome or post-laminectomy syndrome is a condition characterized by chronic pain following back surgeries. Many factors can contribute to the onset or development of FBS, including residual or recurrent spinal disc herniation, persistent post-operative pressure on a spinal nerve, altered joint mobility, joint hypermobility with instability, scar tissue (fibrosis), depression, anxiety, sleeplessness, spinal muscular deconditioning and even Cutibacterium acnes infection.  An individual may be predisposed to the development of FBS due to systemic disorders such as diabetes, autoimmune disease and peripheral blood vessels (vascular) disease.
Common symptoms associated with FBS include diffuse, dull and aching pain involving the back or legs. Abnormal sensibility may include sharp, pricking, and stabbing pain in the extremities. The term "post-laminectomy syndrome" is used by some doctors to indicate the same condition as failed back syndrome.
The treatments of post-laminectomy syndrome include physical therapy, microcurrent electrical neuromuscular stimulator, minor nerve blocks, transcutaneous electrical nerve stimulation (TENS), behavioral medicine, non-steroidal anti-inflammatory (NSAID) medications, membrane stabilizers, antidepressants, spinal cord stimulation, and intrathecal morphine pump. Use of epidural steroid injections may be minimally helpful in some cases.  The targeted anatomic use of a potent anti-inflammatory anti-TNF therapeutics is being investigated.
The number of spinal surgeries varies around the world.  The United States and the Netherlands report the highest number of spinal surgeries, while the United Kingdom and Sweden report the fewest.  Recently, there have been calls for more aggressive surgical treatment in Europe.  Success rates of spinal surgery vary for many reasons.

Cause
Patients who have undergone one or more operations on the lumbar spine and continue to experience pain afterward can be divided into two groups. The first group comprise those in whom surgery was not actually indicated or the surgery performed was not likely to achieve the desired result, and those in whom surgery was indicated but which technically did not achieve the intended result. Patients whose pain complaints are of a radicular nature have a better chance for a good outcome than those whose pain complaints are limited to pain in the back.
The second group includes patients who had incomplete or inadequate operations.  Lumbar spinal stenosis may be overlooked, especially when it is associated with disc protrusion or herniation.  Removal of a disc, while not addressing the underlying presence of stenosis, can lead to disappointing results. Occasionally operating on the wrong level occurs, as does failure to recognize an extruded or sequestered disc fragment.  Inadequate or inappropriate surgical exposure can lead to other problems in not getting to the underlying pathology.  Hakelius reported a 3% incidence of serious nerve root damage.In 1992, Turner et al. published a survey of 74 journal articles which reported the results after decompression for spinal stenosis.  Good to excellent results were on average reported by 64% of the patients.  There was, however, a wide variation in outcomes reported.  There was a better result in patients who had a degenerative spondylolisthesis. A similarly designed study by Mardjekto et al. found that a concomitant spinal arthrodesis (fusion) had a greater success rate.  Herron and Trippi  evaluated 24 patients, all with degenerative spondylolisthesis treated with laminectomy alone.  At follow-up varying between 18 and 71 months after surgery, 20 out of the 24 patients reported a good result.  Epstein  reported on 290 patients treated over a 25-year period.  Excellent results were obtained in 69% and good results in 13%.  These optimistic reports do not correlate with "return to competitive employment" rates, which for the most part are dismal in most spinal surgery series.In the past two decades there has been a dramatic increase in fusion surgery in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006. In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year.
For patients with continued pain after surgery which is not due to the above complications or conditions, interventional pain physicians speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patients pain. To be effective, the surgeon must operate on the correct anatomic structure, but is often not possible to determine the source of the pain. The reason for this is that many patients with chronic pain often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain. In addition, spinal fusion itself, particularly if more than one spinal level is operated on, may result in "adjacent segment degeneration".  This is thought to occur because the fused segments may result in increased torsional and stress forces being transmitted to the intervertebral discs located above and below the fused vertebrae. This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery.  But fusion surgeons argue that spinal fusion is more time-tested, and artificial discs contain metal hardware that is unlikely to last as long as biological material without shattering and leaving metal fragments in the spinal canal. These represent different schools of thought. (See discussion on disc replacement infra.)
Another highly relevant consideration is the increasing recognition of the importance of "chemical radiculitis" in the generation of back pain.  A primary focus of surgery is to remove "pressure" or reduce mechanical compression on a neural element: either the spinal cord, or a nerve root. But it is increasingly recognized that back pain, rather than being solely due to compression, may instead entirely be due to chemical inflammation of the nerve root.  It has been known for several decades that disc herniations result in a massive inflammation of the associated nerve root. In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain.  This inflammatory molecule, called tumor necrosis factor-alpha (TNF), is released not only by the herniated or protruding disc, but also in cases of disc tear (annular tear), by facet joints, and in spinal stenosis. In addition to causing pain and inflammation, TNF may also contribute to disc degeneration.    If the cause of the pain is not compression, but rather is inflammation mediated by TNF, then this may well explain why surgery might not relieve the pain, and might even exacerbate it, resulting in FBSS.

Role of sacroiliac joint (SIJ) in lower back pain (LBP)
A 2005 review by Cohen concluded,The SI joint is a real yet underappreciated pain generator in an estimated 15% to 25% of patients with axial LBP. Studies by Ha, et al., show that the incidence of SI joint degeneration in post-lumbar fusion surgery is 75% at 5 years post-surgery, based on imaging. Studies by DePalma and Liliang, et al., demonstrate that 40–61% of post-lumbar fusion patients were symptomatic for SI joint dysfunction based on diagnostic blocks.

Smoking
Recent studies have shown that cigarette smokers will routinely fail all spinal surgery, if the goal of that surgery is the decrease of pain and impairment.  Many surgeons consider smoking to be an absolute contraindication to spinal surgery.  Nicotine appears to interfere with bone metabolism through induced calcitonin resistance and decreased osteoblastic function.  It may also restrict small blood vessel diameter leading to increased scar formation.There is an association between cigarette smoking, back pain and chronic pain syndromes of all types.In a report of 426 spinal surgery patients in Denmark, smoking was shown to have a negative effect on fusion and overall patient satisfaction, but no measurable influence on the functional outcome.There is a validation of the hypothetical assumption that postoperative smoking cessation helps to reverse the impact of cigarette smoking on outcome after spinal fusion.  If patients cease cigarette smoking in the immediate post operative period, there is a positive impact on success.Regular smoking in adolescence was associated with low back pain in young adults. Pack-years of smoking showed an exposure-response relationship among girls.A recent study suggested  that cigarette smoking adversely affects serum hydrocodone levels. Prescribing physicians should be aware that in some cigarette smokers, serum hydrocodone levels might not be detectable.In a study from Denmark reviewing many reports in the literature, it was concluded that  smoking should be considered a weak risk indicator and not a cause of low back pain. In a multitude of epidemiologic studies, an association between smoking and low back pain has been reported, but variations in approach and study results make this literature difficult to reconcile.
In a massive study of 3482 patients undergoing lumbar spine surgery from the National Spine Network, comorbidities of (1) smoking, (2) compensation, (3) self reported poor overall health and (4) pre-existing psychological factors were predictive in a high risk of failure.  Followup was carried out at 3 months and one year after surgery.  Pre-operative depressive disorders tended not to do well.Smoking has been shown to increase the incidence of post operative infection as well as decrease fusion rates.  One study showed 90% of post operative infections occurred in smokers, as well as myonecrosis (muscle destruction) around the wound.

Pathology
Before the advent of CT scanning, the pathology in failed back syndrome was difficult to understand. Computerized tomography in conjunction with metrizamide myelography in the late 1960s and 1970s allowed direct observation of the mechanisms involved in post operative failures.  Six distinct pathologic conditions were identified:

Recurrent or persistent disc herniation
Spinal stenosis
Post operative infection
Epidural post-operative fibrosis
Adhesive arachnoiditis
Nerve Injury

Recurrent or persistent disc herniation
Removal of a disc at one level can lead to disc herniation at a different level at a later time.  Even the most complete surgical excision of the disc still leaves 30–40% of the disc, which cannot be safely removed.  This retained disc can re-herniate sometime after surgery. Virtually every major structure in the abdomen and the posterior retroperitoneal space has been injured, at some point, by removing discs using posterior laminectomy/discectomy surgical procedures.  The most prominent of these is a laceration of the left internal iliac vein, which lies in close proximity to the anterior portion of the disc. In some studies, recurrent pain in the same radicular pattern or a different pattern can be as high as 50% after disc surgery.   Many observers have noted that the most common cause of a failed back syndrome is caused from recurrent disc herniation at the same level originally operated.  A rapid removal in a second surgery can be curative.  The clinical picture of a recurrent disc herniation usually involves a significant pain-free interval.  However, physical findings may be lacking, and a good history is necessary. The time period for the emergence of new symptoms can be short or long.  Diagnostic signs such as the straight leg raise test may be negative even if real pathology is present. The presence of a positive myelogram may represent a new disc herniation, but can also be indicative of a post operative scarring situation simply mimicking a new disc.  Newer MRI imaging techniques have clarified this dilemma somewhat.   Conversely, a recurrent disc can be difficult to detect in the presence of post op scarring.  Myelography is inadequate to completely evaluate the patient for recurrent disc disease, and CT or MRI scanning is necessary.  Measurement of tissue density can be helpful.Even though the complications of laminectomy for disc herniation can be significant, a recent series of studies involving thousands of patients published under auspices of Dartmouth Medical School concluded at four-year follow-up that those who underwent surgery for a lumbar disc herniation achieved greater improvement than nonoperatively treated patients in all primary and secondary outcomes except work status.

Spinal stenosis
Spinal stenosis can be a late complication after laminectomy for disc herniation or when surgery was performed for the primary pathologic condition of spinal stenosis.
In the Maine Study, among patients with lumbar spinal stenosis completing 8- to 10-year follow-up, low back pain relief, predominant symptom improvement, and satisfaction with the current state were similar in patients initially treated surgically or nonsurgically. However, leg pain relief and greater back-related functional status continued to favor those initially receiving surgical treatment.A large study of spinal stenosis from Finland found the prognostic factors for ability to work after surgery were ability to work before surgery, age under 50 years, and no prior back surgery. The very long-term outcome (mean follow-up time of 12.4 years) was excellent-to-good in 68% of patients (59% women and 73% men). Furthermore, in the longitudinal follow-up, the result improved between 1985  and 1991. No special complications were manifested during this very long-term follow-up time. The patients with total or subtotal block in preoperative myelography achieved the best result.  Furthermore, patients with block stenosis improved their result significantly in the longitudinal follow-up. The postoperative stenosis seen in computed tomography (CT) scans was observed in 65% of 90 patients, and it was severe in 23 patients (25%). However, this successful or unsuccessful surgical decompression did not correlate with patients subjective disability, walking capacity or severity of pain. Previous back surgery had a strong worsening effect on surgical results. This effect was very clear in patients with total block in the preoperative myelography. The surgical result of a patient with previous back surgery was similar to that of a patient without previous back surgery when the time interval between the last two operations was more than 18 months.Post-operative MRI findings of stenosis are probably of limited value compared to symptoms experienced by patients.   Patients perception of improvement had a much stronger correlation with long-term surgical outcome than structural findings seen on postoperation magnetic resonance imaging. Degenerative findings had a greater effect on patients walking capacity than stenotic findings.Postoperative radiologic stenosis was very common in patients operated on for lumbar spinal stenosis, but this did not correlate with clinical outcome. The clinician must be cautious when reconciling clinical symptoms and signs with postoperative computed tomography findings in patients operated on for lumbar spinal stenosis.A study from Georgetown University reported on one-hundred patients who had undergone decompressive surgery for lumbar stenosis between 1980 and 1985.  Four patients with postfusion stenosis were included. A 5-year follow-up period was achieved in 88 patients. The mean age was 67 years, and 80% were over 60 years of age. There was a high incidence of coexisting medical diseases, but the principal disability was lumbar stenosis with neurological involvement.  Initially there was a high incidence of success, but recurrence of neurological involvement and persistence of low-back pain led to an increasing number of failures. By 5 years this number had reached 27% of the available population pool, suggesting that the failure rate could reach 50% within the projected life expectancies of most patients. Of the 26 failures, 16 were secondary to renewed neurological involvement, which occurred at new levels of stenosis in eight and recurrence of stenosis at operative levels in eight. Reoperation was successful in 12 of these 16 patients, but two required a third operation. The incidence of spondylolisthesis at 5 years was higher in the surgical failures (12 of 26 patients) than in the surgical successes (16 of 64). Spondylolisthetic stenosis tended to recur within a few years following decompression.  Because of age and associated illnesses, fusion may be difficult to achieve in this group.

Post operative infection
A small minority of lumbar surgical patients will develop a post operative infection. In most cases, this is a bad complication and does not bode well for eventual improvement or future employability.  Reports from the surgical literature indicate an infection rate anywhere from 0% to almost 12%. The incidence of infection tends to increase as the complexity of the procedure and operating time increase.  Usage of metal implants (instrumentation) tends to increase the risk of infection.  Factors associated with an increased infection include diabetes mellitus, obesity, malnutrition, smoking, previous infection, rheumatoid arthritis, and immunodeficiency.
Previous wound infection should be considered as a contraindication to any further spinal surgery, since the likelihood of improving such patients with more surgery is small.
Antimicrobial prophylaxis (giving antibiotics during or after surgery before an infection begins) reduces the rate of surgical site infection in lumbar spine surgery, but a great deal of variation exists regarding its use.  In a Japanese study, utilizing the Centers for Disease Control recommendations for antibiotic prophylaxis, an overall rate of 0.7% infection was noted, with a single dose antibiotic group having 0.4% infection rate and multiple dosage antibiotic infection rate of 0.8%.  The authors had previously used prophylactic antibiotics for 5 to 7 postoperative days. Based on the Centers for Disease Control and Prevention  guideline, their antibiotic prophylaxis was changed to the day of surgery only. It was concluded there was no statistical difference in the rate of infection between the two different antibiotic protocols. Based on the CDC guideline, a single dose of prophylactic antibiotic was proven to be efficacious for the prevention of infection in lumbar spine surgeries.

Epidural post-operative fibrosis
Epidural scarring following a laminectomy for disc excision is a common feature when re-operating for recurrent sciatica or radiculopathy. When the scarring is associated with a disc herniation and/or recurrent spinal stenosis, it is relatively common, occurring in more than 60% of cases.  For a time, it was theorized that placing a fat graft over the dural could prevent post operative scarring.  However, initial enthusiasm has waned in recent years. In an extensive laminectomy involving 2 or more vertebra, post operative scarring is the norm.  It is most often seen around the L5 and S1 nerve roots.

Adhesive arachnoiditis
Fibrous scarring can also be a complication within the subarachnoid space.  It is notoriously difficult to detect and evaluate.  Prior to the development of magnetic resonance imaging, the only way to ascertain the presence of arachnoiditis was by opening the dura.   In the days of CT scanning and Pantopaque and later, Metrizamide myelography, the presence of arachnoiditis could be speculated based on radiographic findings.  Often, myelography prior to the introduction of Metrizamide was the cause of arachnoiditis.   It can also be caused by the long term pressure brought about with either a severe disc herniation or spinal stenosis.  The presence of both epidural scarring and arachnoiditis in the same patient are probably quite common.
Arachnoiditis is a broad term denoting inflammation of the meninges and subarachnoid space. A variety of causes exist, including infectious, inflammatory, and neoplastic processes.
Infectious causes include bacterial, viral, fungal, and parasitic agents. Noninfectious inflammatory processes include surgery, intrathecal hemorrhage, and the administration of intrathecal (inside the dural canal) agents such as myelographic contrast media, anesthetics (e.g. chloroprocaine), and steroids (e.g. Depo-Medrol, Kenalog). Lately iatrogenic arachnoiditis has been attributed to misplaced Epidural Steroid Injection therapy when accidentally administered intrathecally. The preservatives and suspension agents found in all steroid injectates, which arent indicated for epidural administration by the U.S. Food & Drug Administration due to reports of severe adverse events including arachnoiditis, paralysis and death, have now been directly linked to the onset of the disease following the initial stage of chemical meningitis.
Neoplasia includes the hematogenous spread of systemic tumors, such as breast and lung carcinoma, melanoma, and non-Hodgkin lymphoma. Neoplasia also includes direct seeding of the cerebrospinal fluid (CSF) from primary central nervous system (CNS) tumors such as glioblastoma multiforme, medulloblastoma, ependymoma, and choroid plexus carcinoma.    Strictly speaking, the most common cause of arachnoiditis in failed back syndrome is not infectious or from cancer.  It is due to non-specific scarring secondary to the surgery or the underlying pathology.

Nerve injury
Laceration of a nerve root, or damage from cautery or traction can lead to chronic pain, however this can be difficult to determine. Chronic compression of the nerve root by a persistent agent such as disc, bone (osteophyte) or scarring can also permanently damage the nerve root.  Epidural scarring caused by the initial pathology or occurring after the surgery can also contribute to nerve damage.  In one study of failed back patients, the presence of pathology was noted to be at the same site as the level of  surgery performed in 57% of cases.  The remaining cases developed pathology at a different level, or on the opposite side, but at the same level as the surgery was performed.   In theory, all failed back patients have some sort of nerve injury or damage which leads to a persistence of symptoms after a reasonable healing time.

Diagnosis
Avoiding post-laminectomy/laminotomy syndrome
Smaller procedures that do not remove bone (such as Endoscopic Transforaminal Lumbar Discectomy and Reconfiguration) do not cause post laminectomy/laminotomy syndrome.

Management
Failed back syndrome (FBS) is a well-recognized complication of surgery of the lumbar spine. It can result in chronic pain and disability, often with disastrous emotional and financial consequences to the patient. Many patients have traditionally been classified as "spinal cripples" and are consigned to a life of long-term narcotic treatment with little chance of recovery.  Despite extensive work in recent years, FBS remains a challenging and costly disorder.

Opioids
A study of chronic pain patients from the University of Wisconsin found that methadone is most widely known for its use in the treatment of opioid dependence, but methadone also provides effective analgesia.  Patients who experience inadequate pain relief or intolerable side effects with other opioids or who suffer from neuropathic pain may benefit from a transition to methadone as their analgesic agent. Adverse effects, particularly respiratory depression and death, make a fundamental knowledge of methadones pharmacological properties essential to the provider considering methadone as analgesic therapy for a patient with chronic pain.

Patient selection
Patients who have sciatic pain (pain in the back, radiating down the buttock to the leg) and clear clinical findings of an identifiable radicular nerve loss caused by a herniated disc will have a better post operative course than those who simply have low back pain.  If a specific disc herniation causing pressure on a nerve root cannot be identified, the results of surgery are likely to be disappointing.  Patients involved in workers compensation, tort litigation or other compensation systems tend to fare more poorly after surgery.  Surgery for spinal stenosis usually has a good outcome, if the surgery is done in an extensive manner, and done within the first year or so of the appearance of symptoms.Oaklander and North define the Failed Back Syndrome as a chronic pain patient after one or more surgical procedure to the spine.  They delineated these characteristics of the relation between the patient and the surgeon:

The patient makes increasing demands on the surgeon for pain relief.  The surgeon may feel a strong responsibility to provide a remedy when the surgery has not achieved the desired goals.
The patient grows increasingly angry at the failure and may become litigious.
There is an escalation of narcotic pain medication which can be habituating or addictive.
In the face of expensive conservative treatments which are likely to fail, the surgeon is persuaded to attempt further surgery, even though this is likely to fail as well.
The probability of returning to gainful employment decreases with increasing length of disability.
The financial incentives to remain disabled may be perceived as outweighing the incentive to recover.In the absence of a financial source for disability or workers compensation, other psychological features may limit the ability of the patient to recover from surgery.  Some patients are simply unfortunate, and fall into the category of "chronic pain" despite their desire to recover and the best efforts of the physicians involved in their care. Even less invasive forms of surgery are not uniformly successful; approximately 30,000–40,000 laminectomy patients obtain either no relief of symptomatology or a recurrence of symptoms. Another less invasive form of spinal surgery, percutaneous disc surgery, has reported revision rates as high as 65%. It is no surprise, therefore, that FBSS is a significant medical concern which merits further research and attention by the medical and surgical communities.

Total disc replacement
Lumbar total disc replacement was originally designed to be an alternative to lumbar arthrodesis (fusion).   The procedure was met with great excitement and heightened expectations both in the United States and Europe.  In late 2004, the first lumbar total disc replacement received approval from the U.S. Food and Drug Administration (FDA). More experience existed in Europe.  Since then, the initial excitement has given way to skepticism and concern.   Various failure rates and strategies for revision of total disc replacement have been reported.The role of artificial or total disc replacement in the treatment of spinal disorders remains ill-defined and unclear. Evaluation of any new technique is difficult or impossible because physician experience may be minimal or lacking.  Patient expectations may be distorted. It has been difficult to establish clear cut indications for artificial disc replacement.  It may not be a replacement procedure or alternative to fusion, since recent studies have shown that 100% of fusion patients had one or more contraindications to disc replacement.   The role of disc replacement must come from new indications not defined in todays literature or a relaxation of current contraindications.A study by Regan     found the result of replacement was the same at L4-5 and L5-S1 with the CHARITE disc.  However, the ProDisc II had more favorable results at L4-5 compared with L5-S1.A younger age was predictive of a better outcome in several studies. In others it has been found to be a negative predictor or of no predictive value.  Older patients may have more complications.Prior spinal surgery has mixed effects on disc replacement.  It has been reported to be negative in several studies.  It has been reported to have  no effect in other studies. Many studies are simply inconclusive. Existing evidence does not allow drawing definite conclusions about the status of disc replacement at present.

Electrical stimulation
Many failed back patients are significantly impaired by chronic pain in the back and legs.   Many of these will be treated with some form of electrical stimulation.  This can be either a transcutaneous electrical nerve stimulation device placed on the skin over the back or a nerve stimulator implanted into the back  with electrical probes which directly touch the spinal cord.   Also, some chronic pain patients utilize fentanyl or narcotic patches.  These patients are generally severely impaired and it is unrealistic to conclude that application of neurostimulation will reduce that impairment.  For example, it is doubtful that neurostimulation will improve the patient enough to return to competitive employment.  Neurostimulation is palliative.   TENS units work by blocking neurotransmission as described by the pain theory of Melzack and Wall. Success rates for implanted neurostimulation has been reported to be 25% to 55%.  Success is defined as a relative decrease in pain.

Chiropractic
Limited case series have shown improvement for patients with failed back surgery who were managed with chiropractic care.

Prognosis
Under rules promulgated by Titles II and XVI of the United States Social Security Act, chronic radiculopathy, arachnoiditis and spinal stenosis are recognized as disabling conditions under Listing 1.04 A (radiculopathy), 1.04 B (arachnoiditis) and 1.04 C (spinal stenosis).

Return to work
In a groundbreaking Canadian study, Waddell et al. reported on the value of repeat surgery and the return to work in workers compensation cases.  They concluded that workers who undergo spinal surgery take longer to return to their jobs.  Once two spinal surgeries are performed, few if any ever return to gainful employment of any kind.  After two spinal surgeries, most people in the workers comp system will not be made better by more surgery.  Most will be worse after a third surgery.
Episodes of back pain associated with on the job injuries in the workers compensation setting are usually of short duration.  About 10% of such episodes will not be simple, and will degenerate into chronic and disabling back pain conditions, even if surgery is not performed.It has been hypothesized that job dissatisfaction and individual perception of physical demands are associated with an increased time of recovery or an increased risk of no recovery at all. Individual psychological and social work factors, as well as worker-employer relations are also likely to be associated with time and rates of recovery.A Finnish study of return to work in patients with spinal stenosis treated by surgery found that: (1) none of the patients who had retired before the operation returned to work afterward. (2) The variables that predicted postoperative ability to work for women were: being fit to work at the time of operation, age < 50 years at the time of operation, and duration of lumbar spinal stenosis symptoms < 2 years. (3) For men, these variables were: being fit to work at the time of operation, age < 50 years at the time of operation, no prior surgery, and the extent of the surgical procedure equal to or less than one laminectomy. Womens and mens working capacity do not differ after lumbar spinal stenosis operation. If the aim is to maximize working capacity, then, when a lumbar spinal stenosis operation is indicated, it should be performed without delay. In lumbar spinal stenosis patients who are > 50 years old and on sick leave, it is unrealistic to expect that they will return to work. Therefore, after such an extensive surgical procedure, re-education of patients for lighter jobs could improve the chances of these patients returning to work.In a related Finnish study, a total of 439 patients operated on for lumbar spinal stenosis during the period 1974–1987 was re-examined and evaluated for working and functional capacity approximately 4 years after the decompressive surgery.   The ability to work before or after the operation and a history of no prior back surgery were variables predictive of a good outcome. Before the operation 86 patients were working, 223 patients were on sick leave, and 130 patients were retired. After the operation 52 of the employed patients and 70 of the unemployed patients returned to work. None of the retired patients returned to work. Ability to work preoperatively, age under 50 years at the time of operation and the absence of prior back surgery predicted a postoperative ability to work.A report from Belgium noted that patients reportedly return to work an average of 12 to 16 weeks after surgery for lumbar disc herniation. However, there are studies that lend credence to the value of an earlier stimulation for return to work and performance of normal activities after a limited discectomy. At follow-up assessment, it was found that no patient had changed employment because of back or leg pain.
The sooner the recommendation is made to return to work and perform normal activities, the more likely the patient is to comply. Patients with ongoing disabling back conditions have a low priority for return to work. The probability of return to work decreases as time off work increases.   This is especially true in Belgium, where 20% of individuals did not resume work activities after surgery for a disc herniation of the lumbar spine.
In Belgium, the medical advisers of sickness funds have an important role legally in the assessment of working capacity and medical rehabilitation measures for employees whose fitness for work is jeopardized or diminished for health reasons. The measures are laid down in the sickness and invalidity legislation. They are in accordance with the principle of preventing long-term disability. It is apparent from the authors experience that these measures are not adapted consistently in medical practice. Most of the medical advisers are focusing purely on evaluation of corporal damage, leaving little or no time for rehabilitation efforts. In many other countries, the evaluation of work capacity is done by social security doctors with a comparable task.In a comprehensive set of studies carried out by the University of Washington School of Medicine, it was determined that the outcome of lumbar fusion performed on injured workers was worse than reported in most published case series.  They found 68% of lumbar fusion patients still unable to return to work two years after surgery.  This was in stark contrast to reports of 68% post-op satisfaction in many series. In a follow-up study it was found that the use of intervertebral fusion devices rose rapidly after their introduction in 1996.  This increase in metal usage was associated with a greater risk of complication  without improving disability or re-operation rates.

Research
The identification of tumor necrosis factor-alpha (TNF) as a central cause of inflammatory spinal pain now suggests the possibility of an entirely new approach to selected patients with FBSS.  Specific and potent inhibitors of TNF became available in the U.S. in 1998, and were demonstrated to be potentially effective for treating sciatica in experimental models beginning in 2001. Targeted anatomic administration of one of these anti-TNF agents, etanercept, a patented treatment method, has been suggested in published pilot studies to be effective for treating selected patients with chronic disc-related pain and FBSS. The scientific basis for pain relief in these patients is supported by the many current review articles. In the future new imaging methods may allow non-invasive identification of sites of neuronal inflammation, thereby enabling more accurate localization of the "pain generators" responsible for symptom production.  These treatments are still experimental.
If chronic pain in FBSS has a chemical component producing inflammatory pain, then prior to additional surgery it may make sense to use an anti-inflammatory approach.  Often this is first attempted with non-steroidal anti-inflammatory medications, but the long-term use of Non-steroidal anti-inflammatory drugs (NSAIDS) for patients with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity; and NSAIDs have limited value to intervene in TNF-mediated processes.  An alternative often employed is the injection of cortisone into the spine adjacent to the suspected pain generator, a technique known as "epidural steroid injection".   Although this technique began more than a decade ago for FBSS, the efficacy of epidural steroid injections is now generally thought to be limited to short term pain relief in selected patients only. In addition, epidural steroid injections, in certain settings, may result in serious complications. Fortunately there are now emerging new methods that directly target TNF.  These TNF-targeted methods represent a highly promising new approach for patients with chronic severe spinal pain, such as those with FBSS. Ancillary approaches, such as rehabilitation, physical therapy, anti-depressants, and, in particular, graduated exercise programs, may all be useful adjuncts to anti-inflammatory approaches. In addition, more invasive modalities, such as spinal cord stimulation, may offer relief for certain patients with FBSS, but these modalities, although often referred to as "minimally invasive", require additional surgery, and have complications of their own.

Worldwide perspective
A report from Spain noted that the investigation and development of new techniques for instrumented surgery of the spine is not free from conflicts of interest. The influence of financial forces in the development of new technologies and its immediate application to spine surgery, shows the relationship between the published results and the industry support. Authors who have developed and defended fusion techniques have also published new articles praising new spinal technologies. The author calls spinal surgery the  "American Stock and Exchange" and "the bubble of spine surgery". The scientific literature doesnt show clear evidence in the cost-benefit studies of most instrumented surgical interventions of the spine compared with the conservative treatments. It has not been yet demonstrated that fusion surgery and disc replacement are better options than the conservative treatment. Its necessary to point out that at present "there are relationships between the industry and back pain, and there is also an industry of the back pain". Nonetheless, the "market of the spine surgery" is growing  because patients are demanding solutions for their back problems. The tide of scientific evidence seems to go against the spinal fusions in the degenerative disc disease, discogenic pain and in specific back pain. After decades of advances in this field, the results of spinal fusions are mediocre. New epidemiological studies show that "spinal fusion must be accepted as a non proved or experimental method for the treatment of back pain". The surgical literature on spinal fusion published in the last 20 years establishes that instrumentation seems to slightly increase the fusion rate and that instrumentation doesnt improve the clinical results in general. We still are in need of randomized studies to compare the surgical results with the natural history of the disease, the placebo effect, or conservative treatment. The European Guidelines for lumbar chronic pain management show  "strong evidence" indicating that complex and demanding spine surgery where different instrumentation is used, is not more effective than a simple, safer and cheaper posterolateral fusion without instrumentation. Recently, the literature published in this field is sending a message to use "minimally invasive techniques"; – the abandonment of  transpedicular fusions.   Surgery in general, and usage of metal fixation should be discarded in most cases.In Sweden, the national registry of lumbar spine surgery reported in the year 2000 that 15% of patients with spinal stenosis surgery underwent a concomitant fusion.    Despite the traditionally conservative approach to spinal surgery in Sweden, there have been calls from that country for a more aggressive approach to lumbar procedures in recent years.
Cherkin et al., evaluated worldwide surgical attitudes.  There were twice the number of surgeons per capita in the United States compared to the United Kingdom.  Numbers were similar to Sweden </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 Necatoriasis and can you explain it in depth? [/INST] Necatoriasis is the condition of infection by Necator hookworms, such as Necator americanus. This hookworm infection is a type of helminthiasis (infection) which is a type of neglected tropical disease.

Signs and symptoms
When adult worms attach to the villi of the small intestine, they suck on the hosts blood, which may cause abdominal pain, diarrhea, cramps, and weight loss that can lead to anorexia. Heavy infections can lead to the development of iron deficiency and hypochromic microcytic anemia. This form of anemia in children can give rise to physical and mental retardation. Infection caused by cutaneous larvae migrans, a skin disease in humans, is characterized by skin ruptures and severe itching.

Cause
Necatoriasis is caused by N. americanus. N. americanus can be divided into two areas – larvae and adult stage. The third stage larvae are guided to human skin by following thermal gradients. Typically, the larvae enter through the hands and feet following contact with contaminated soil. A papular, pruritic, itchy rash will develop around the site of entry into the human host. This is also known as "ground itch". Generally, migration through the lungs is asymptomatic but a mild cough and pharyngeal irritation may occur during larval migration in the airways. Once larvae break through the alveoli and are swallowed, they enter the gastrointestinal tract and attach to the intestinal mucosa where they mature into adult worms. The hookworms attach to the mucosal lining using their cutting plates which allows them to penetrate blood vessels and feed on the hosts blood supply. Each worm consumes 30 μl of blood per day. The major issue results from this intestinal blood loss which can lead to iron-deficiency anemia in moderate to heavy infections. Other common symptoms include epigastric pain and tenderness, nausea, exertional dyspnea, pain in lower extremities and in joints, sternal pain, headache, fatigue, and impotence. Death is rare in humans.

Diagnosis
The standard method for diagnosing necatoriasis is through identification of N. americanus eggs in a fecal sample using a microscope. Eggs can be difficult to visualize in a lightly infected sample so a concentration method is generally used such as flotation or sedimentation. However, the eggs of A. duodenale and N. americanus cannot be distinguished; thus, the larvae must be examined to identify these hookworms.  Larvae cannot be found in stool specimens unless the specimen was left at ambient temperature for a day or more.The most common technique used to diagnose a hookworm infection is to take a stool sample, fix it in 10% formalin, concentrate it using the formalin-ethyl acetate sedimentation technique, and then create a wet mount of the sediment for viewing under a microscope.

Prevention
Education, improved sanitation, and controlled disposal of human feces are critical for prevention.  Nonetheless, wearing shoes in endemic areas helps reduce the prevalence of infection.

Treatment
An infection of N. americanus parasites can be treated by using benzimidazoles: albendazole or mebendazole. A blood transfusion may be necessary in severe cases of anemia. Light infections are usually left untreated in areas where reinfection is common. Iron supplements and a diet high in protein will speed the recovery process.  In a case study involving 56-60 men with Trichuris trichiura and/or N. americanus infections, both albendazole and mebendazole were 90% effective in curing T. trichiura.  However, albendazole had a 95% cure rate for N. americanus, while mebendazole only had a 21% cure rate.  This suggests albendazole is most effective for treating both T. trichiura and N. americanus.Cryotherapy by application of liquid nitrogen to the skin has been used to kill cutaneous larvae migrans, but the procedure has a low cure rate and a high incidence of pain and severe skin damage, so it now is passed over in favor of suitable pharmaceuticals </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 Tick-borne encephalitis and can you explain it in depth? [/INST] Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis or meningoencephalitis. Myelitis and spinal paralysis also occurs. In about one third of cases sequelae, predominantly cognitive dysfunction, persists for a year or more.The number of reported cases has been increasing in most countries. TBE is posing a concerning health challenge to Europe, as the number of reported human cases of TBE in all endemic regions of Europe have increased by almost 400% within the last three decades.The tick-borne encephalitis virus is known to infect a range of hosts including ruminants, birds, rodents, carnivores, horses, and humans. The disease can also be spread from animals to humans, with ruminants and dogs providing the principal source of infection for humans.

Signs and symptoms
The disease is most often biphasic. After an incubation period of approximately one week (range: 4–28 days) from exposure (tick bite) non-speciﬁc symptoms occurs. These symptoms are fever, malaise, headache, nausea, vomiting and myalgias that persist for about 5 days. Then, after approximately one week without symptoms, some of the infected develop neurological symptoms, i.e. meningitis, encephalitis or meningoencephalitis. Myelitis also occurs with or without encephalitis.Sequelae persists for a year or more in approximately one third of people who develop neurological disease. Most common long-term symptoms are headache, concentration difficulties, memory impairment and other symptoms of cognitive dysfunction.Mortality depends on the subtype of the virus. For the European subtype mortality rates are 0.5% to 2% for people who develop neurological disease.In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death.In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.

Cause
TBE is caused by tick-borne encephalitis virus, a member of the genus Flavivirus in the family Flaviviridae. It was first isolated in 1937. Three virus sub-types also exist: European or Western tick-borne encephalitis virus (transmitted by Ixodes ricinus), Siberian tick-borne encephalitis virus (transmitted by I. persulcatus), and Far-Eastern tick-borne encephalitis virus, formerly known as Russian spring summer encephalitis virus (transmitted by I. persulcatus).The former Soviet Union conducted research on tick-borne diseases, including the TBE viruses.

Transmission
It is transmitted by the bite of several species of infected woodland ticks, including Ixodes scapularis, I. ricinus and I. persulcatus, or (rarely) through the non-pasteurized milk of infected cows.Infection acquired through goat milk consumed as raw milk or raw cheese (Frischkäse) has been documented in 2016 and 2017 in the German state of Baden-Württemberg. None of the infected had neurological disease.

Diagnosis
Detection of specific IgM and IgG antibodies in patients sera combined with typical clinical signs, is the principal method for diagnosis. In more complicated situations, e.g. after vaccination, testing for presence of antibodies in cerebrospinal fluid may be necessary. It has been stated that lumbar puncture always should be performed when diagnosing TBE and that pleocytosis in cerebrospinal fluid should be added to the diagnostic criteria.PCR (polymerase chain reaction) method is rarely used, since TBE virus RNA is most often not present in patient sera or cerebrospinal fluid at the time of neurological symptoms.

Prevention
Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis in the form of a vaccination. Tick-borne encephalitis vaccines are very effective and available in many disease endemic areas and in travel clinics. Trade names are Encepur N and FSME-Immun CC.

Treatment
There is no specific antiviral treatment for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary.

Epidemiology
As of 2011, the disease was most common in Central and Eastern Europe, and Northern Asia. About ten to twelve thousand cases are documented a year but the rates vary widely from one region to another. Most of the variation has been the result of variation in host population, particularly that of deer. In Austria, an extensive vaccination program since the 1970s reduced the incidence in 2013 by roughly 85%.In Germany, during the 2010s, there have been a minimum of 95 (2012) and a maximum of 584 cases (2018) of TBE  (or FSME as it is known in German) </s>