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Phonotactics

Phonotactics (from Ancient Greek "voice, sound" and  "having to do with arranging") is a branch of phonology that deals with restrictions in a language on the permissible combinations of phonemes. Phonotactics defines permissible syllable structure, consonant clusters and vowel sequences by means of phonotactic constraints.

Phonotactic constraints are highly language-specific. For example, in Japanese, consonant clusters like do not occur. Similarly, the clusters and  are not permitted at the beginning of a word in Modern English but are in German and Dutch (in which the latter appears as ) and were permitted in Old and Middle English. In contrast, in some Slavic languages and  are used alongside vowels as syllable nuclei.

Syllables have the following internal segmental structure:
 * Onset (optional)
 * Rhyme (obligatory, comprises nucleus and coda):
 * Nucleus (obligatory)
 * Coda (optional)

Both onset and coda may be empty, forming a vowel-only syllable, or alternatively, the nucleus can be occupied by a syllabic consonant. Phonotactics is known to affect second language vocabulary acquisition.

English phonotactics
The English syllable (and word) twelfths is divided into the onset, the nucleus  and the coda ; thus, it can be described as CCVCCCC (C = consonant, V = vowel). On this basis it is possible to form rules for which representations of phoneme classes may fill the cluster. For instance, English allows at most three consonants in an onset, but among native words under standard accents (and excluding a few obscure loanwords such as sphragistics), phonemes in a three-consonantal onset are limited to the following scheme:

 * + stop + approximant:
 * stream
 * + +  (not in most accents of American English)
 * stew
 * sputum
 * sprawl
 * splat
 * skew
 * scream
 * sclerosis
 * squirrel
 * scream
 * sclerosis
 * squirrel

This constraint can be observed in the pronunciation of the word blue: originally, the vowel of blue was identical to the vowel of cue, approximately. In most dialects of English, shifted to. Theoretically, this would produce. The cluster, however, infringes the constraint for three-consonantal onsets in English. Therefore, the pronunciation has been reduced to by elision of the  in what is known as yod-dropping.

Not all languages have this constraint; compare Spanish pliegue or French pluie.

Constraints on English phonotactics include:

 * All syllables have a nucleus
 * No geminate consonants
 * No onset
 * No in the syllable coda (except in Hiberno-English)
 * No affricates in complex onsets (except when underlying and  are analysed as  and )
 * No in complex onsets
 * The first consonant in a complex onset must be an obstruent (e.g. stop; combinations such as *ntat or *rkoop, with a sonorant, are not allowed)
 * The second consonant in a complex onset must not be a voiced obstruent (e.g. *zdop does not occur)
 * If the first consonant in a complex onset is not, the second must be a liquid or a glide
 * Every subsequence contained within a sequence of consonants must obey all the relevant phonotactic rules (the substring principle rule)
 * No glides in syllable codas (excluding the s of diphthongs)
 * The second consonant in a complex coda must not be, , , or (compare asthma, typically pronounced  or , but rarely )
 * If the second consonant in a complex coda is voiced, so is the first
 * An obstruent following or  in a coda must be homorganic with the nasal
 * Two obstruents in the same coda must share voicing (compare kids with kits )

Sonority Sequencing Principle
Segments of a syllable are universally distributed following the Sonority Sequencing Principle (SSP), which states that, in any syllable, the nucleus has maximal sonority and that sonority decreases as you move away from the nucleus. Sonority is a measure of the amplitude of a speech sound. The particular ranking of each speech sound by sonority, called the sonority hierarchy, is language-specific, but, in its broad lines, hardly varies from a language to another, which means all languages form their syllables in approximately the same way with regards to sonority.

To illustrate the SSP, the voiceless alveolar fricative is lower on the sonority hierarchy than the alveolar lateral approximant, so the combination  is permitted in onsets and  is permitted in codas, but  is not allowed in onsets and  is not allowed in codas. Hence slips and pulse  are possible English words while *lsips and *pusl are not.

The SSP expresses a very strong cross-linguistic tendency, however, it does not account for the patterns of all complex syllable margins, as there are both initial as well as final clusters violation the SSP, in two ways: the first occurs when two segments in a margin have the same sonority, which is known as a sonority plateau. Such margins are found in a few languages, including English, as in the words sphinx and fact (though note that phsinx and fatc both violate English phonotactics).

The second instance of violation of the SSP is when a peripheral segment of a margin has a higher sonority than a segment closer to the nucleus. These margins are known as reversals and occur in some languages including English (steal, bets  ) or French (dextre  but originally , strict ).

title: Phonotactics


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User:Jambe

James Brunskill
Currently I work at The University of Waikato.

I run a website which I call JAMBE Enterprises HQ, Associated with this site are the following :

 * http://www.jambe.co.nz
 * http://jambecorp.blogspot.com
 * http://awaw.blogspot.com

Beliefs
I am a Christian (as you will know if have visited my site). I believe that the bible is the word of God, an that "All Scripture is God-breathed and is useful for teaching, rebuking, correcting and training in righteousness, so that the man of God may be thoroughly equipped for every good work." 2 Timothy 3:16-17

Other Stuff

 * I sometimes visit the waikato linux users group wiki. My page there is http://www.wlug.org.nz/JamesBrunskill

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: User:Jambe


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Joseph François Dupleix

Joseph Marquis Dupleix (23 January 1697 – 10 November 1763) was Governor-General of French India and rival of Robert Clive.

Biography
Dupleix was born in Landrecies, on January 23, 1697. His father, François Dupleix, a wealthy fermier général, wished to bring him up as a merchant, and, in order to distract him from his taste for science, sent him on a voyage to India in 1715 on one of the French East India Company's vessels. He made several voyages to the Americas and India, and in 1720 was named a member of the superior council at Bengal. He displayed great business aptitude, and in addition to his official duties made large ventures on his own account, acquiring a fortune.

In 1730 he was made superintendent of French affairs in Chandernagore. In 1741, he married Jeanne Albert, widow of one of the councillors of the company. Albert was known to the Hindus as Joanna Begum and proved of great help to her husband in his negotiations with the native princes.

His reputation procured him in 1742 the appointment of governor general of all French establishments in India. Dupleix saw in the constant succession disputes among the Princes of India an opportunity to advance the interests of the French in India, and for this purpose he entered into relations with the native princes, and adopted a style of oriental splendour in his dress and surroundings. He built an army of native troops, called sepoys, who were trained as infantry men in his service and also included the famous Hyder Ali of Mysore.

The British were alarmed by this, but the danger to their settlements and power was partly averted by the bitter mutual jealousy which existed between Dupleix and Bertrand François Mahé de La Bourdonnais, French governor of the Isle of Bourbon (today's La Réunion).

When the city of Madras capitulated to the French following the Battle of Madras in 1746, Dupleix opposed that the town be returned under British rule, thus violating the treaty signed by La Bourdonnais. He then sent an expedition against Fort St David (1747), which won over the Nawab of Arcot, ally of the British. Dupleix again attempted the capture of Fort St David, and this time succeeded.

In 1748 Kolkata was besieged by the French, but in the course of the operations news arrived of the peace concluded between the French and the British at Aix-la-Chapelle. Dupleix next entered into negotiations about the subjugation of southern India. He sent a large body of troops to the aid of the two claimants of the sovereignty of the Carnatic and the Deccan. The British sided with their rivals to prevent the plans of Dupleix from materializing.

In 1750 the Subadar of Deccan gifted the Alamparai Fort to the French. This was a token of his appreciation of the services of Dupleix and the French forces to his services.

From 1751, Dupleix tried to expand French influence in Burma by sending the envoy Sieur de Bruno, and by providing military assistance the Mon in their conflict with the Burmese. Bruno proved remarkably successful in this effort, resulting in closer ties between the French and the Mon. However, the advent of the Seven Years' War meant that as French attentions were elsewhere this relationship came to nothing.

Commemoration
A number of things were named in his honour:
 * A square, road and metro station in the 15th arrondissement of Paris are named after him.
 * Four French warships have borne his name (beside two commercial ships):
 * The steam corvette FRENCH CORVETTE Dupleix (1861–1887), famous for her involvement in the Japanese revolution
 * A 7,700-tonne armoured cruiser (1897–1919)
 * A 10,000-tonne cruiser (1929–1942), scuttled in Toulon
 * The F70 type frigate FRENCH FRIGATE Dupleix
 * College Dupleix was the former name of Kanailal Vidyamandir and the Chandannagar College in Chandannagar, West Bengal.
 * A road in New Delhi near the Indian parliament named after him.
 * Rue Dupleix (Dupleix Street) was the former name of Nehru Street in Pondicherry.

Statue of Dupleix at Puducherry Beach
Dupleix left Puducherry in 1754, French recognition of his contribution came only in 1870, with the commissioning of two statues – one in Puducherry and the other in France. The former statue is now situated in Goubert Avenue at the end of Rock Beach. It was first installed on 16 July 1870. In 1979 the statue was moved from the middle of the current Bharathy park to its current location at the beach.

Dupleix is represented as a man of commanding stature. In the large nose and massive under jaw, some resemblance may be traced to Oliver Cromwell as commonly represented in his portraits. In the statue, Dupleix wears Court dress with bag wig and long riding boots; in his right hand is a plan of Puducherry, his left reposing on the hilt of his sword.

Restoration of the Dupleix statue was undertaken by the Public Works Department (PWD) of the government of Puducherry in 2014.

title: Joseph François Dupleix


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Autonomic neuropathy

Autonomic neuropathy (AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

Signs and symptoms
The signs and symptoms of autonomic neuropathy include the following:
 * Urinary bladder conditions: urinary incontinence or urinary retention which happens due to the uncoordinated contraction of the bladder. Neurogenic bladder is a broad term used to describe this dysfunction.
 * Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhea, constipation
 * Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion
 * Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).
 * Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.
 * Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).
 * Absence of signs of cerebellar dysfunction or parkinsonian symptoms as the presence of either would indicate the more serious disease of multiple system atrophy.

Causes
Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:
 * Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.
 * Injury to nerves caused by surgery or radiation to the neck.
 * Treatment with certain medications, including some drugs used in cancer chemotherapy.
 * Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.
 * An abnormal attack by the immune system (autoimmune autonomic ganglionopathy), sometimes as part of a paraneoplastic syndrome which can occur even when cancer has not yet been diagnosed.
 * Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.
 * Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.
 * Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjögren syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain–Barré syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.

Neurogenic Bladder
Depending on the symptoms and severity of the dysfunction, the doctor might suggest one of the following treatments

 * Behavioral changes: such as reducing water intake, kegel exercises, biofeedback training
 * Clean intermittent catheterization: insertion of a foley catheter to remove the urine every few hours and prevent retention, done in a sterile manner.
 * Pharmacological therapy, which includes anticholinergic drugs which reduce the contraction of the bladder
 * Botox injections into the bladder
 * Surgical treatment: Urinary diversion, Artificial Urinary Sphincter, Urethral sling, or insertion of electrical devices adjacent to the bladder to stimulate its contraction.

title: Autonomic neuropathy


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Basal rate

Basal rate, in biology, is the rate of continuous supply of some chemical or process. In the case of diabetes mellitus, it is a low rate of continuous insulin supply needed for such purposes as controlling cellular glucose and amino acid uptake.

Together with a bolus of insulin, the basal insulin completes the total insulin needs of an insulin-dependent person. An insulin pump and wristop controller is one way to arrange for a closely controlled basal insulin rate. The slow-release insulins (e.g., Lantus and Levemir) can provide a similar effect.

In healthy individuals, basal rate is monitored by the pancreas, which provides a regular amount of insulin at all times. The body requires this flow of insulin to enable the body to utilize glucose in the blood stream, so the energy in glucose can be used to carry out bodily functions. Basal rate requirements can differ for individuals depending on the activities they will carry out on that particular day. For example, if one is not highly active on a certain day, they will have a decreased basal rate because they are not using a lot of energy. On the other hand, basal rate increases dramatically when an individual is highly active.

Basal rates often even vary from hour to hour throughout the day. For example, one's insulin needs vary from activity to activity. Activities, such as sports, housework, shopping, gardening, tidying the house, and consuming alcohol all require a lowering in basal rate. These activities all require energy and, thus, use glucose; basal rate must decrease in order to keep glucose levels high enough to be used as fuel for the body. On the other hand, fevers, having a cold, taking a nap, taking cortisone-containing medication, and moments of excitement call for different basal rate needs. In these instances, the body has an overwhelming supply of glucose, and glucose levels need to decrease. To induce this decrease, basal rate needs to increase to increase insulin release to absorb some of the excess glucose from the blood stream.

Those with diabetes mellitus must be aware of their basal rates and regulate them accordingly. Basal rate can be raised and lowered through various methods. For example, individuals with diabetes mellitus often use an insulin pump to supply an increased amount of insulin into the blood stream. Those with diabetes also may eat carbohydrates or sugars to account for low blood sugar. However one monitors and regulates their blood sugar levels and basal rates, it is important to make changes gradually. An initial lowering in basal rate should be no more than 10% of the original. After the initial lowering point, one must note the factor by which one's blood sugar changes. If blood sugar levels decreased, one should lower their basal rate by 20% next time. If their blood sugar levels increased, a lowering of 10% was too great, and one should not lower their basal rate at all next time. If blood sugar levels remained relatively constant, a drop in basal rate of 10% was sufficient.

Just as the action to change basal rate should be gradual in nature, the actual response from changing basal rate does not happen instantly. A change in basal rate is felt around two hours after the action is done. This is especially important for those with diabetes to note, as it affects when they should act to monitor their basal rates. For example, if there is a particular time in the day when one notices a problem with blood glucose levels, they should act to change their basal rate accordingly two hours prior to when the problem was previously experienced.

Causes of Basal Rate
The liver is the primary contributing organ which produces glucose continuously even when nothing is being eaten. The liver will supply glucose either from fats or from previously eaten foods. Therefore, the basal rate can be thought of as a sort of "second bolus" after the initial bolus intake of insulin.

Modelling the Basal Rate
Most adult diabetics (over the age of 21) will have a fairly constant ratio of bolus:basal of 60%:40%, where 60% of all insulin intake in a single 24-hour period will be attributed to meals (bolus) and 40% should then be attributed to the basal rate. This ratio will fluctuate from person to person depending on their size, activity level, and caloric intake as well but is a good baseline for determining the correct basal rate for an adult diabetic. Thus, the basal rate could theoretically be set based on an averaged bolus insulin intake of several days. Averaging the total bolus, and then dividing this number by 36 would then give the required hourly basal rate intake for any individual with a 60:40 ratio established.

title: Basal rate


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Dupleix

Dupleix could refer to one of the following:

People:
 * Joseph François Dupleix, governor general of the French establishment in India in the 18th century

Naval ships:
 * French corvette Dupleix (1861) (1856–1887) famous for her involvement in the Japanese revolution
 * French ship Dupleix, a 7700 tonne armoured cruiser (1897–1919): built in Rochefort and launched on 28 April 1900
 * French cruiser Dupleix, French heavy cruiser of the Suffren class, launched 9 October 1930
 * Dupleix (D 641), the latest Dupleixis a F70 typ anti-submarine frigate

Commercial ships:
 * a steamship built at La Ciotat in 1862, which between 1883 and 1888 operated between Sydney and Nouméa, was sold, refurbished and subsequently operated between Australia and New Zealand.
 * a three-masted barque (1901–1917) sunk by the German commerce raider Seeadler on 5 March 1917
 * a cargo ship (1914–1942) sunk in the Pacific by a Japanese submarine.

In transport:
 * Dupleix (Paris Métro), a station in the 15th arrondissement of Paris

title: Dupleix


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Bunion

A bunion, also known as hallux valgus, is a deformity of the MTP joint connecting the big toe to the foot. The big toe often bends towards the other toes and the joint becomes red and painful. The onset of bunions is typically gradual. Complications may include bursitis or arthritis.

The exact cause is unclear. Proposed factors include wearing overly tight shoes, high-heeled shoes, family history, and rheumatoid arthritis. Diagnosis is generally based on symptoms and supported by X-rays. A similar condition of the little toe is referred to as a bunionette.

Treatment may include proper shoes, orthotics, or NSAIDs. If this is not effective for improving symptoms, surgery may be performed. It affects about 23% of adults. Females are affected more often than males. Usual age of onset is between 20 and 50 years old. The condition also becomes more common with age. It was first clearly described in 1870. Archaeologists have found a high incidence of bunions in skeletons from 14th- and 15th-century England, coinciding with a fashion for pointy shoes.

Signs and symptoms

Symptoms may include irritation of the skin around the bunion, and blisters may form more easily at the site. Pain may be worse when walking.

Bunions can lead to difficulties finding properly fitting footwear and may force a person to buy a larger size shoe to accommodate the width of the bunion. If the bunion deformity becomes severe enough, the foot can hurt in different places even without the constriction of shoes. It is then considered as being a mechanical function problem of the forefoot.

Cause

The exact cause is unclear. It may be due to a combination of internal and external causes. Proposed factors include wearing overly tight shoes, high-heeled shoes, family history and rheumatoid arthritis. The American College of Foot and Ankle Surgeons states that footwear only worsens a problem caused by genetics.

Excessive pronation of the foot causes increased pressure on the inside of the big toe that can result in a deformation of the medial capsular structures of the joint, subsequently increasing the risk of developing bunions.

Pathophysiology
The bump itself is partly due to the swollen bursal sac or an osseous (bony) anomaly on the metatarsophalangeal joint. The larger part of the bump is a normal part of the head of the first metatarsal bone that has tilted sideways to stick out at its distal (far) end (metatarsus primus varus).

Bunions are commonly associated with a deviated position of the big toe toward the second toe, and the deviation in the angle between the first and second metatarsal bones of the foot. The small sesamoid bones found beneath the first metatarsal (which help the flexor tendon bend the big toe downwards) may also become deviated over time as the first metatarsal bone drifts away from its normal position. Osteoarthritis of the first metatarsophalangeal joint, diminished and/or altered range of motion, and discomfort with pressure applied to the bump or with motion of the joint, may all accompany bunion development. Atop of the first metatarsal head either medially or dorso-medially, there can also arise a bursa that when inflamed (bursitis), can be the most painful aspect of the process.

Diagnosis

Bunion can be diagnosed and analyzed with a simple x-ray, which should be taken with the weight on the foot. The hallux valgus angle (HVA) is the angle between the long axes of the proximal phalanx and the first metatarsal bone of the big toe. It is considered abnormal if greater than 15–18°. The following HV angles can also be used to grade the severity of hallux valgus:

 * Mild: 15–20°
 * Moderate: 21–39°
 * Severe: ≥ 40°

The intermetatarsal angle (IMA) is the angle between the longitudinal axes of the first and second metatarsal bones, and is normally less than 9°. The IM angle can also grade the severity of hallux valgus as:

 * Mild: 9–11°
 * Moderate: 12–17°
 * Severe: ≥ 18°

Treatment
Conservative treatment for bunions include changes in footwear, the use of orthotics (accommodative padding and shielding), rest, ice, and pain medications such as acetaminophen or nonsteroidal anti-inflammatory drugs. These treatments address symptoms but do not correct the actual deformity. If the discomfort persists and is severe or when aesthetic correction of the deformity is desired, surgical correction by an orthopedic surgeon or a podiatric surgeon may be necessary.

Orthotics

Orthotics are splints or regulators while conservative measures include various footwear like toe spacers, valgus splints, and bunion shields. Toe spacers seem to be effective in reducing pain, but there is not evidence that any of these techniques reduces the physical deformity. There are a variety of available orthotics including off-the-shelf commercial products and custom-molded orthotics, which may be prescribed medical devices.

Surgery
Procedures are designed and chosen to correct a variety of pathologies that may be associated with the bunion. For instance, procedures may address some combination of:

At present there are many different bunion surgeries for different effects. The age, health, lifestyle and activity level of the patient may also play a role in the choice of procedure.
 * removing the abnormal bony enlargement of the first metatarsal,
 * realigning the first metatarsal bone relative to the adjacent metatarsal bone,
 * straightening the great toe relative to the first metatarsal and adjacent toes,
 * realigning the cartilaginous surfaces of the great toe joint,
 * addressing arthritic changes associated with the great toe joint,
 * repositioning the sesamoid bones beneath the first metatarsal bone,
 * shortening, lengthening, raising, or lowering the first metatarsal bone,
 * correcting any abnormal bowing or misalignment within the great toe,
 * connecting two parallel long bones side by side by syndesmosis procedure

Traditional bunion surgery can be performed under local, spinal or general anesthetic. A person who has undergone bunion surgery can expect a 6- to 8-week recovery period during which crutches are usually required to aid mobility. An orthopedic cast is much less common today as newer, more stable procedures and better forms of fixation (stabilizing the bone with screws and other hardware) are used. Hardware may even include absorbable pins that perform their function and are then broken down by the body over the course of months. After recovery long term stiffness or limited range of motion may occur in some patients. Visible or limited scarring may also occur for patients.

title: Bunion


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Callus

A callus (: calluses) is an area of thickened and sometimes hardened skin that forms as a response to repeated friction, pressure, or other irritation. Since repeated contact is required, calluses are most often found on the feet and hands, but they may occur anywhere on the skin. Some degree of callus, such as on the bottom of the foot, is normal.

Calluses are generally not harmful and help prevent blisters, as well as offering protection. However, excessive formation may sometimes lead to other problems, such as a skin ulceration or infection, or cause the affected person to try to offload the affected painful area, which can place excessive stress on the asymptomatic side.

Rubbing that is too frequent or forceful will cause blisters, as opposed to calluses, to form.

Cause
Normally, a callus will form on any part of the skin exposed to excess friction over a long period of time. Activities that are known for causing calluses include (but are not limited to) construction work and craftwork, the arts, food preparation, many sports and physical activities, and fashion choices like wearing high heels.

Although calluses can occur anywhere on the body as a reaction to moderate, constant "grinding" pressure, they are most often found on the foot (where the most pressure and friction are applied). On the feet (arguably the source of the most problematic calluses), they typically form on the metatarsal-phalangeal joint area ("balls of the foot"), heels and small toes due to the compression applied by tightly fitting shoes.

Biologically, calluses are formed by the accumulation of terminally differentiated keratinocytes in the outermost layer of skin. Though the cells of calluses are dead, they are quite resistant to mechanical and chemical damage due to extensive networks of cross-linked proteins and hydrophobic keratin intermediate filaments containing many disulfide bonds. It is the natural reaction of the palmar or plantar skin. Too much friction occurring too fast for the skin to develop a protective callus will cause a blister or abrasion instead.

Sometimes a callus occurs where there is no rubbing or pressure. These hyperkeratoses can have a variety of causes. Some toxic materials, such as arsenic, can cause thick palms and soles. Some diseases, such as syphilis, can cause thickening of the palms and soles as well as pinpoint hyperkeratoses. There is a benign condition called keratosis palmaris et plantaris, which produces corns in the creases of the fingers and non-weight bearing spaces of the feet. Some of this may be caused by actinic keratosis, which occurs due to overexposure to sun or with age and hormonal shifts.

Corns

A corn (or clavus, plural clavi) is a cone-shaped callus that penetrates into the dermis, usually on the feet or hands. Corns may form due to chronic pressure or rubbing at a pressure point (in this skin over a bone), or due to scar tissue from a healing wound creating pressure in a weight-bearing area such as the sole of the foot. If there is constant stimulation of the tissue producing the corns, even after the corn is surgically removed, the skin may continue to grow as a corn.

The hard part at the center of the corn resembles a funnel with a broad raised top and a pointed bottom. Because of their shape, corns intensify the pressure at the tip and can cause deep tissue damage and ulceration. The scientific name for a corn is heloma (plural helomata). A hard corn is called a heloma durum, while a soft corn is called a heloma molle.

The location of the soft corns tends to differ from that of hard corns. Hard corns occur on dry, flat surfaces of skin. Soft corns (frequently found between adjacent toes) stay moist, keeping the surrounding skin soft. The corn's center is not soft however, but indurated.

The specific diagnostic workup and treatments for corns may differ substantially from other forms of calluses.

Prevention
Corns and calluses are easier to prevent than to treat. When it is undesirable to form a callus, minimizing rubbing and pressure will prevent callus formation. Footwear should be properly fitted, gloves may be worn, and protective pads, rings or skin dressings may be used. People with poor circulation or sensation should check their skin often for signs of rubbing and irritation so they can minimize any damage.

Treatment

Calluses and corns may heal by themselves eventually, once the irritation is consistently avoided. They may also be dissolved with keratolytic agents containing salicylic acid, sanded down with a pumice stone or silicon carbide sandpaper or filed down with a callus shaver, or pared down by a professional such as a podiatrist.

Diabetes
People with diabetes face special skin challenges. Because diabetes affects the capillaries, the small blood vessels which feed the skin, thickening of the skin with callus increases the difficulty of supplying nutrients to the skin. Callus formation is seen in high numbers of patients with diabetes, and together with absent foot pulses and formation of hammer toe, this may be an early sign of individuals at an increased risk for foot ulcers.

The stiffness of a callus or corn, coupled with the shear and pressure that caused it, may tear the capillaries or adjoining tissue, causing bleeding within the callus or corn. This can often be result of trying to pick, cut, or shave off the callus by yourself at home. Although the bleeding can be small, sometimes small pools of blood or hematoma are formed. The blood itself is an irritant, a foreign body within the callus that makes the area burn or itch. If the pool of blood is exposed to the outside, infection may follow. Infection may also lead to ulceration. This process can be prevented at several places. Diabetic foot infections are the leading cause of diabetic limb amputation.

Society and culture
Calluses in the hands are frequently associated with manual labor and blue-collar workers. During the Gads Hill Train Robbery in 1874, the James–Younger Gang purportedly refrained from robbing men with calloused hands, assuming them to be working class laborers. Such notion is also present in Māori culture, where the words raupā and raupo refer to hands left cracked and chapped due to manual work, and are used as similes for someone deemed a hard worker.

Calluses have also been known to develop on the forehead from the frequent prostrations required in Muslim prayer; known as a prayer bump or zebiba, such calluses are considered marks of piety in some Muslim countries, and people have been known to take special steps, such as praying on straw mats, to encourage the callus to develop.

Calluses may also form on the fingertips from the repeated pressure and friction of playing stringed instruments. This formation of calluses allows the player to repeatedly depress the strings without causing pain. Because of this, callus formation is viewed as something of a rite of passage for beginner string players.

title: Callus


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Cerebrovascular disease

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension (high blood pressure) is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

A stroke usually presents with an abrupt onset of a neurologic deficit – such as hemiplegia (one-sided weakness), numbness, aphasia (language impairment), or ataxia (loss of coordination) – attributable to a focal vascular lesion. The neurologic symptoms manifest within seconds because neurons need a continual supply of nutrients, including glucose and oxygen, that are provided by the blood. Therefore, if blood supply to the brain is impeded, injury and energy failure is rapid.

Besides hypertension, there are also many less common causes of cerebrovascular disease, including those that are congenital or idiopathic and include CADASIL, aneurysms, amyloid angiopathy, arteriovenous malformations, fistulas, and arterial dissections. Many of these diseases can be asymptomatic until an acute event, such as a stroke, occurs. Cerebrovascular diseases can also present less commonly with headache or seizures. Any of these diseases can result in vascular dementia due to ischemic damage to the brain.

Signs and symptoms
The most common presentation of cerebrovascular diseases is an acute stroke, which occurs when blood supply to the brain is compromised. Symptoms of stroke are usually rapid in onset, and may include weakness of one side of the face or body, numbness on one side of the face or body, inability to produce or understand speech, vision changes, and balance difficulties. Hemorrhagic strokes can present with a very severe, sudden headache associated with vomiting, neck stiffness, and decreased consciousness. Symptoms vary depending on the location and the size of the area of involvement of the stroke. Edema, or swelling, of the brain may occur which increases intracranial pressure and may result in brain herniation. A stroke may result in coma or death if it involves key areas of the brain.

Other symptoms of cerebrovascular disease include migraines, seizures, epilepsy, or cognitive decline. However, cerebrovascular disease may go undetected for years until an acute stroke occurs. In addition, patients with some rare congenital cerebrovascular diseases may begin to have these symptoms in childhood.

Congenital
Congenital diseases are medical conditions that are present at birth that may be associated with or inherited through genes. Examples of congenital cerebrovascular diseases include arteriovenous malformations, germinal matrix hemorrhage, and CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy). Arteriovenous malformations are abnormal tangles of blood vessels. Usually, a capillary bed separates arteries from veins, which protects the veins from the higher blood pressures that occur in arteries. In arteriovenous malformations, arteries are directly connected to veins, which increases the risk of venous rupture and hemorrhage. Cerebral arteriovenous malformations in the brain have a 2–4% chance of rupture each year. However, many arteriovenous malformations go unnoticed and are asymptomatic throughout a person's lifetime.

A germinal matrix hemorrhage is bleeding into the brain of premature infants caused by the rupture of fragile blood vessels within the germinal matrix of premature babies. The germinal matrix is a highly vascularized area within an unborn infant's brain from which brain cells, including neurons and glial cells, originate. Infants are at most risk to germinal matrix hemorrhages when they are born prematurely, before 32 weeks. The stresses exposed after birth, along with the fragile blood vessels, increase risk of hemorrhage. Signs and symptoms include flaccid weakness, seizures, abnormal posturing, or irregular respiration.

CADASIL is an inherited disorder caused by mutations in the NOTCH3 gene located on chromosome 19. NOTCH3 codes for a transmembrane protein whose function is not well-known. However, the mutation causes accumulation of this protein within small to medium-sized blood vessels. This disease often presents in early adulthood with migraines, stroke, mood disturbances, and cognitive deterioration. MRI shows white matter changes in the brain and also signs of repeated strokes. The diagnosis can be confirmed by gene testing.

Acquired
Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages. Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections. Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include: • Hypertension

• Smoking

• Obesity

• Diabetes

Controlling these risk factors can reduce the incidence of atherosclerosis and stroke. Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.

An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I.  However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.

Arterial dissections are tears of the internal lining of arteries, often associated with trauma. Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.

Idiopathic
Idiopathic diseases are those that occur spontaneously without a known cause. Moyamoya is an example of an idiopathic cerebrovascular disorder that results in narrowing and occlusion of intracranial blood vessels. The most common presentation is stroke or transient ischemic attack, but cognitive decline within children may also be a presenting symptom. The disease may begin to show symptoms beginning in adolescence, but some may not have symptoms until adulthood.

Mechanism of brain cell death
When a reduction in blood flow lasting seconds occurs, the brain tissue suffers ischemia, or inadequate blood supply. If the interruption of blood flow is not restored in minutes, the tissue suffers infarction followed by tissue death. When the low cerebral blood flow persists for a longer duration, this may develop into an infarction in the border zones (areas of poor blood flow between the major cerebral artery distributions). In more severe instances, global hypoxia-ischemia causes widespread brain injury leading to a severe cognitive sequelae called hypoxic-ischemic encephalopathy.

An ischemic cascade occurs where an energetic molecular problem arises due to lack of oxygen and nutrients. The cascade results in decreased production of adenosine triphosphate (ATP), which is a high-energy molecule needed for cells in the brain to function. Consumption of ATP continues in spite of insufficient production, this causes total levels of ATP to decrease and lactate acidosis to become established (ionic homeostasis in neurons is lost). The downstream mechanisms of the ischemic cascade thus begins. Ion pumps no longer transport Ca2+ out of cell, this triggers release of glutamate, which in turn allows calcium into cell walls. In the end the apoptosis pathway is initiated and cell death occurs.

There are several arteries that supply oxygen to different areas of the brain, and damage or occlusion of any of them can result in stroke. The carotid arteries cover the majority of the cerebrum. The common carotid artery divides into the internal and the external carotid arteries. The internal carotid artery becomes the anterior cerebral artery and the middle central artery. The ACA transmits blood to the frontal parietal. From the basilar artery are two posterior cerebral arteries. Branches of the basilar and PCA supply the occipital lobe, brain stem, and the cerebellum. Ischemia is the loss of blood flow to the focal region of the brain. This produces heterogeneous areas of ischemia at the affected vascular region, furthermore, blood flow is limited to a residual flow. Regions with blood flow of less than 10 mL/100 g of tissue/min are core regions (cells here die within minutes of a stroke). The ischemic penumbra with a blood flow of <25 ml/100g tissue/min, remain usable for more time (hours).

Types of stroke
There are two main divisions of strokes: ischemic and hemorrhagic. Ischemic stroke involves decreased blood supply to regions of the brain, while hemorrhagic stroke is bleeding into or around the brain.

Ischemic

 * Ischemic stroke, the most common is caused by a blockage of a blood vessel in the brain, usually caused by thrombosis or emboli from a proximal arterial source or the heart, that leads to the brain being starved of oxygen. The neurologic signs and symptoms must last longer than 24 hours or the brain infarction is demonstrated, mainly by imaging techniques.
 * Transient ischemic attack (TIA) also called a mini-stroke. This is a condition in which the blood flow to a region of the brain is blocked, but blood flow is quickly restored and the brain tissue can fully recover. The symptoms are only transient, leaving no sequelae, or long-term deficits. In order to diagnose this entity, all neurologic signs and symptoms must have been resolved within 24 hrs without evidence of brain infarction on brain imaging.

Hemorrhagic

 * Subarachnoid haemorrhage occurs when blood leaks out of damaged vessels into the cerebrospinal fluid in the subarachnoid space around the brain. The most common cause of a subarachnoid hemorrhage is an aneurysm rupture due to the weakened blood vessel walls and increased wall stress. The neurologic symptoms are produced by the blood mass effect on neural structures, from the toxic effects of blood on the brain tissue, or by the increasing of intracranial pressure.
 * Intracerebral haemorrhage is bleeding directly into the brain rather than around the brain. Causes and risk factors include hypertension, blood thinning medications, trauma, and arteriovenous malformations.

Diagnosis
Diagnoses of cerebrovascular disease may include:
 * medical history
 * physical exam
 * neurological examination.
 * acute stroke imaging is generally performed in significant symptoms of new onset.

It is important to differentiate the symptoms caused by a stroke from those caused by syncope (fainting) which is also a reduction in cerebral blood flow, almost always generalized, but they are usually caused by systemic hypotension of various origins: cardiac arrhythmias, myocardial infarction, hemorrhagic shock, among others.

Treatment
Treatment for cerebrovascular disease may include medication, lifestyle changes, and surgery, depending on the cause.

Examples of medications are:
 * antiplatelets (aspirin, clopidogrel)
 * blood thinners (heparin, warfarin)
 * antihypertensives:
 * ACE inhibitors
 * beta blockers
 * calcium channel blockers - in particular Nimodipine reduces the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage (SAH)
 * anti-diabetic medications.

Surgical procedures include:
 * endovascular surgery and vascular surgery (for future stroke prevention).

Prognosis
Prognostics factors: Lower Glasgow Coma Scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.

Epidemiology

Worldwide, it is estimated there are 31 million stroke survivors, though about 6 million deaths were due to cerebrovascular disease (2nd most common cause of death in the world and 6th most common cause of disability).

Cerebrovascular disease primarily occurs with advanced age; the risk for developing it goes up significantly after 65 years of age. CVD tends to occur earlier than Alzheimer's Disease (which is rare before the age of 80). In some countries such as Japan, CVD is more common than AD.

In 2012, 6.4 million adults from the US had a stroke, which corresponds to 2.7% of the US. This is approximately 129,000 deaths in 2013.

Geographically, a "stroke belt" in the US has long been known, similar to the "diabetes belt" which includes all of Mississippi and parts of Alabama, Arkansas, Florida, Georgia, Kentucky, Louisiana, North Carolina, Ohio, Pennsylvania, South Carolina, Tennessee, Texas, Virginia, and West Virginia.

title: Cerebrovascular disease