Categories
Ailmemts & Remedies

Hammer Toe

Description:
A hammer toe or contracted toe is a deformity of the muscles and ligaments of the proximal interphalangeal joint of the second, third, or fourth toe causing it to be bent, resembling a hammer. In the early stage a flexible hammertoe is movable at the joints; a rigid hammertoe joint can’t be moved and usually requires surgery.

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Mallet toe is a similar condition affecting the distal interphalangeal joint.

Claw toe is another similar condition, with dorsiflexion of the proximal phalanx on the lesser metatarsophalangeal joint, combined with flexion of both the proximal and distal interphalangeal joints. Claw toe can affect the second, third, fourth, or fifth toes.

Signs and symptoms:
A hammer toe causes you discomfort when you walk. It can also cause you pain when you try to stretch or move the affected toe or those around it. Hammer toe symptoms may be mild or severe.

Other Symptoms:
*A toe that bends downward
*Corns or calluses
*Difficulty walking
*Inability to flex your foot or wiggle your toes
*Claw-like toes

Causes:
Woman soothing her feet after wearing high heels
Wearing high heels can cause hammertoe.
Hammer toe occurs from an imbalance in the muscles surrounding the middle toe joint. These muscles, tendons, and ligaments work together to bend and straighten the toes.

If one of the muscles weakens, it cannot bend or straighten the toe. If the toe stays bent long enough, the muscles tighten and the toe will not be able to straighten out.

These muscle weaknesses and imbalances are caused by a variety of factors. Because some of the causes for hammer toe are avoidable, it is possible to minimize risk of developing hammer toe.

Causes of hammer toe include the following:

*Certain shoes – wearing high heels or shoes that are too tight through the box can force toes into a flexed position. When worn repeatedly, the toes may not be able to straighten, even when barefoot.

*Sex – women are more likely to develop hammer toe than men.

*Injuries – When a toe is broken, stubbed, or jammed, it may be more likely to develop hammer toe.

*Age – risk increases with age.

*Toe length – if the second toe is longer than the big toe, hammer toe is more likely to occur.

*Certain diseases – people suffering from conditions like arthritis or diabetes are more likely to develop foot problems, including hammer toe

*Genetics – sometimes, hammer toe is hereditary and may run in families.

Due to footwear styles, women are more likely than men to develop hammer toe. The risk of hammer toe also rises with age.

Diagnosis:
A doctor can usually diagnose a hammer toe during a physical exam. Imaging tests, such as X-rays, may be necessary if you’ve had a bone, muscle, or ligament injury in your toe.

Treatment:
The severity of your condition determines the treatment options for a hammer toe.

Treatment for a mild hammer toe:
You can correct a hammer toe caused by inappropriate footwear by wearing properly fitting shoes. If a high arch caused the condition, wearing toe pads or insoles in your shoes can help. These pads work by shifting your toe’s position, which relieves pain and corrects the appearance of your toe.

Shop for shoe insoles.:
You can usually use over-the-counter (OTC) cushions, pads, or medications to treat bunions and corns. However, if they’re painful or if they cause your toes to become deformed, your doctor may opt to surgically remove them.

Don’t pop any blisters on your toes. Popping blisters can cause pain and infection. Use OTC creams and cushions to relieve pain and keep blisters from rubbing against the inside of your shoes.

Gently stretching your toes can also help relieve pain and reposition the affected toe.

Treatment for a severe hammer toe:
If you’re unable to flex your toe, surgery is the only option to restore movement. Surgery can reposition the toe, remove deformed or injured bone, and realign your tendons and joints. Surgery is normally done on an outpatient basis, so you can return home on the day of your surgery.

After treating the cause of your hammer toe, it usually goes away without complications. However, waiting too long to seek treatment can cause your surrounding toes to become deformed as the hammer toe forces them out of position. It’s best to get treatment as soon as the diagnosis is confirmed.

The 8 Best Hammer Toe Straighteners of 2019

Prevention:

Hammer toe, like many other foot problems, can be avoided with wearing proper footwear. Proper footwear should have the following:

Low heels – higher heels force the feet into unnatural positions and often bend the toes.

Enough toe room – shoes should be properly sized and pointy-toed shoes should be avoided. Shoes should accommodate for the longest toe, which may not always be the big toe.

Adjustability – shoes with adjustable laces and straps are best.

Proper arch support – arch support prevents a number of foot ailments.

Long-term outlook:
Hammer toe can be treated and prevented with simple exercises and footwear changes. However, if the toe becomes rigid, surgery may be needed to relieve the hammer toe.

Even after treatment, hammer toe may return. The best way to make sure that hammer toe does not reoccur is through choosing proper footwear.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://search.yahoo.com/search?ei=utf-8&fr=aaplw&p=hammer+toe
https://www.healthline.com/health/hammer-toe#prevention
https://www.medicalnewstoday.com/articles/315600.php

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Categories
Ailmemts & Remedies

Agoraphobia

Description:
Agoraphobia is an anxiety disorder characterized by symptoms of anxiety in situations in which a person fears and avoid places or situations that might cause him or her to panic and make him or her feel trapped, helpless or embarrassed.As the person perceives their environment to be unsafe with no easy way to escape.These situations can include open spaces, public transit, shopping centers, or simply being outside their home. Peersons fear an actual or anticipated situation, such as using public transportation, being in open or enclosed spaces, standing in line, or being in a crowd. Being in these situations may result in a panic attack. The symptoms occur nearly every time the situation is encountered and last for more than six months. Those affected will go to great lengths to avoid these situations. In severe cases people may become completely unable to leave their homes.

Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger. In the DSM-5 agoraphobia is classified as a phobia along with specific phobias and social phobia. Other conditions that can produce similar symptoms include separation anxiety, posttraumatic stress disorder, and major depressive disorder. Those affected are at higher risk of depression and substance use disorder.

Without treatment it is uncommon for agoraphobia to resolve. Treatment is typically with a type of counselling called cognitive behavioral therapy (CBT). CBT results in resolution for about half of people. Women are affected about twice as often as men. The condition often begins in early adulthood and becomes less common in old age. It is rare in children.

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Symptoms:
Agoraphobia is a condition where sufferers become anxious in unfamiliar environments or where they perceive that they have little control.
Typical agoraphobia symptoms include fear of:

*Leaving home alone
*Crowds or waiting in line
*Enclosed spaces, such as movie theaters, elevators or small stores
*Open spaces, such as parking lots, bridges or malls
*Using public transportation, such as a bus, plane or train
*These situations cause anxiety because you fear you won’t be able to escape or find help if you start to feel panicked or have other disabling or embarrassing symptoms.

Panic disorder and agoraphobia:
Some people have a panic disorder in addition to agoraphobia. Panic disorder is a type of anxiety disorder in which you experience sudden attacks of extreme fear that reach a peak within a few minutes and trigger intense physical symptoms (panic attacks). You might think that you’re totally losing control, having a heart attack or even dying.

Fear of another panic attack can lead to avoiding similar circumstances or the place where it occurred in an attempt to prevent future panic attacks.

Signs and symptoms of a panic attack can include:

*Rapid heart rate
*Trouble breathing or a feeling of choking
*Chest pain or pressure
*Lightheadedness or dizziness
*Feeling shaky, numb or tingling
*Excessive sweating
*Sudden flushing or chills
*Upset stomach or diarrhea
*Feeling a loss of control
*Fear of dying

Causes:
Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger.

Research has uncovered a link between agoraphobia and difficulties with spatial orientation. Individuals without agoraphobia are able to maintain balance by combining information from their vestibular system, their visual system, and their proprioceptive sense. A disproportionate number of agoraphobics have weak vestibular function and consequently rely more on visual or tactile signals. They may become disoriented when visual cues are sparse (as in wide-open spaces) or overwhelming (as in crowds). Likewise, they may be confused by sloping or irregular surfaces. In a virtual reality study, agoraphobics showed impaired processing of changing audiovisual data in comparison with nonsuffering subjects.

Substance induced:
Chronic use of tranquilizers and sleeping pills such as benzodiazepines has been linked to onset of agoraphobia. In 10 patients who had developed agoraphobia during benzodiazepine dependence, symptoms abated within the first year of assisted withdrawal. Similarly, alcohol use disorders are associated with panic with or without agoraphobia; this association may be due to the long-term effects of alcohol misuse causing a distortion in brain chemistry. Tobacco smoking has also been associated with the development and emergence of agoraphobia, often with panic disorder; it is uncertain how tobacco smoking results in anxiety-panic with or without agoraphobia symptoms, but the direct effects of nicotine dependence or the effects of tobacco smoke on breathing have been suggested as possible causes. Self-medication or a combination of factors may also explain the association between tobacco smoking and agoraphobia and panic.

Attachment theory:
Some scholars have explained agoraphobia as an attachment deficit, i.e., the temporary loss of the ability to tolerate spatial separations from a secure base. Recent empirical research has also linked attachment and spatial theories of agoraphobia.

Spatial theory:
In the social sciences, a perceived clinical bias[26] exists in agoraphobia research. Branches of the social sciences, especially geography, have increasingly become interested in what may be thought of as a spatial phenomenon. One such approach links the development of agoraphobia with modernity.Factors considered contributing to agoraphobia within modernity are the ubiquity of cars and urbanization. These have helped develop the expansion of public space, on one hand, and the contraction of private space on the other, thus creating in the minds of agoraphobic-prone people a tense, unbridgeable gulf between the two.

Evolutionary psychology:
An evolutionary psychology view is that the more unusual primary agoraphobia without panic attacks may be due to a different mechanism from agoraphobia with panic attacks. Primary agoraphobia without panic attacks may be a specific phobia explained by it once having been evolutionarily advantageous to avoid exposed, large, open spaces without cover or concealment. Agoraphobia with panic attack, though, may be an avoidance response secondary to the panic attacks due to fear of the situations in which the panic attacks occurred.

Risk factors:
Agoraphobia can begin in childhood, but usually starts in the late teen or early adult years — usually before age 35 — but older adults can also develop it. Women are diagnosed with agoraphobia more often than men are.

Risk factors for agoraphobia include:

*Having panic disorder or other phobias
*Responding to panic attacks with excessive fear and avoidance
*Experiencing stressful life events, such as abuse, the death of a parent or being attacked
*Having an anxious or nervous temperament
*Having a blood relative with agoraphobia

Agoraphobia can also lead to or be associated with:

*Depression
*Alcohol or drug abuse
*Other mental health disorders, including other anxiety disorders or personality disorders

Diagnosis:
Most people who present to mental health specialists develop agoraphobia after the onset of panic disorder. Agoraphobia is best understood as an adverse behavioral outcome of repeated panic attacks and subsequent anxiety and preoccupation with these attacks that leads to an avoidance of situations where a panic attack could occur. Early treatment of panic disorder can often prevent agoraphobia. Agoraphobia is typically determined when symptoms are worse than panic disorder, but also do not meet the criteria for other anxiety disorders such as depression. In rare cases where agoraphobics do not meet the criteria used to diagnose panic disorder, the formal diagnosis of agoraphobia without history of panic disorder is used (primary agoraphobia).

Treatment:
Agoraphobia treatment usually includes both psychotherapy and medication. It may take some time, but treatment can help you get better.

Psychotherapy:
Psychotherapy involves working with a therapist to set goals and learn practical skills to reduce your anxiety symptoms. Cognitive behavioral therapy is one of the most effective forms of psychotherapy for anxiety disorders, including agoraphobia.

Generally a short-term treatment, cognitive behavioral therapy focuses on teaching you specific skills to better tolerate anxiety, directly challenge your worries and gradually return to the activities you’ve avoided because of anxiety. Through this process, your symptoms improve as you build on your initial success.

Cognitive restructuring has also proved useful in treating agoraphobia. This treatment involves coaching a participant through a dianoetic discussion, with the intent of replacing irrational, counterproductive beliefs with more factual and beneficial ones.

Relaxation techniques are often useful skills for the agoraphobic to develop, as they can be used to stop or prevent symptoms of anxiety and panic.

Medications:
Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors. Benzodiazepines, monoamine oxidase inhibitor, and tricyclic antidepressants are also sometimes prescribed for treatment of agoraphobia. Antidepressants are important because some have antipanic effects. Antidepressants should be used in conjunction with exposure as a form of self-help or with cognitive behaviour therapy. A combination of medication and cognitive behaviour therapy is sometimes the most effective treatment for agoraphobia.

Benzodiazepines, antianxiety medications such as alprazolam and clonazepam, are used to treat anxiety and can also help control the symptoms of a panic attack. If taken for too long, they can cause dependence. Treatment with benzodiazepines should not exceed 4 weeks. Side effects may include confusion, drowsiness, light-headedness, loss of balance, and memory loss.

Alternative medicine:
Eye movement desensitization and reprocessing (EMDR) has been studied as a possible treatment for agoraphobia, with poor results.[39] As such, EMDR is only recommended in cases where cognitive-behavioral approaches have proven ineffective or in cases where agoraphobia has developed following trauma.

Many people with anxiety disorders benefit from joining a self-help or support group (telephone conference-call support groups or online support groups being of particular help for completely housebound individuals). Sharing problems and achievements with others, as well as sharing various self-help tools, are common activities in these groups. In particular, stress management techniques and various kinds of meditation practices and visualization techniques can help people with anxiety disorders calm themselves and may enhance the effects of therapy, as can service to others, which can distract from the self-absorption that tends to go with anxiety problems. Also, preliminary evidence suggests aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided.

Certain dietary and herbal supplements claim to have calming and anti-anxiety benefits. Before one takes any of these for agoraphobia, should talk with the health care provider. Although these supplements are available without a prescription, they still pose possible health risks.

Yoga: Regular Yoga exercise with meditation under an expart improves self confidance and may get rid of Agoraphobia.

Prevention:
There’s no sure way to prevent agoraphobia. However, anxiety tends to increase the more you avoid situations that you fear. If you start to have mild fears about going places that are safe, try to practice going to those places over and over again before your fear becomes overwhelming. If this is too hard to do on your own, ask a family member or friend to go with you, or seek professional help.

If you experience anxiety going places or have panic attacks, get treatment as soon as possible. Get help early to keep symptoms from getting worse. Anxiety, like many other mental health conditions, can be harder to treat if you wait.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Agoraphobia
https://www.mayoclinic.org/diseases-conditions/agoraphobia/symptoms-causes/syc-20355987

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Ailmemts & Remedies

Mad Cow Disease

Other Names: Creutzfeldt-Jakob disease (CJD) or Bovine spongiform encephalopathy (BSE)

Description:
Mad cow disease is a degenerative brain disorder that leads to dementia and, ultimately, death. Symptoms of the disease is dementia-like brain disorders, such as Alzheimer’s. But mad cow disease usually progresses much more rapidly.

It captured public attention in the 1990s when some people in the United Kingdom developed a form of the disease after eating meat from diseased cattle.
Mad cow disease is thought to be due to an infection by a misfolded protein, known as a prion. Cattle are believed to have been infected by being fed meat-and-bone meal (MBM) that contained the remains of other cattle who spontaneously developed the disease or scrapie-infected sheep products. The outbreak increased throughout the United Kingdom due to the practice of feeding meat-and-bone meal to young calves of dairy cows. Cases are suspected based on symptoms and confirmed by examination of the brain. Cases are classified as classic or atypical, with the latter divided into H- and L types. It is a type of transmissible spongiform encephalopathy (TSE).

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The time between infection and onset of symptoms is generally four to five years. Time from onset of symptoms to death is generally weeks to months. Spread to humans is believed to result in variant Creutzfeldt–Jakob disease (vCJD)

Although serious, CJD is rare, and vCJD is the least common form. Worldwide, there is an estimated one case of CJD diagnosed per million people each year, most often in older adults.

Symptoms:
Mad cow disease is marked by rapid mental deterioration, usually within a few months. Initial signs and symptoms typically include:

  • Personality changes
  • Anxiety
  • Depression
  • Memory loss
  • Impaired thinking
  • Blurred vision or blindness
  • Insomnia
  • Difficulty speaking
  • Difficulty swallowing
  • Sudden, jerky movements

As the disease progresses, mental symptoms worsen. Most people eventually lapse into a coma. Heart failure, respiratory failure, pneumonia or other infections are generally the cause of death. Death usually occurs within a year.

In people with the rarer vCJD, psychiatric symptoms may be more prominent in the beginning, with dementia — the loss of the ability to think, reason and remember — developing later in the illness. In addition, this variant affects people at a younger age than classic CJD does and appears to have a slightly longer duration — 12 to 14 months.

Causes:
Mad cow disease is an infectious disease believed to be due to a misfolded protein, known as a prion. Cattle are believed to have been infected from being fed meat and bone meal (MBM) that contained the remains of other cattle who spontaneously developed the disease or scrapie-infected sheep products. The outbreak increased throughout the United Kingdom due to the practice of feeding meat-and-bone meal to young calves of dairy cows.

Prions replicate by causing other normally folded proteins of the same type to take on their misfolded shape, which then go on to do the same, leading to an exponential chain reaction. Eventually, the prions aggregate into an alpha helical, beta pleated sheet, which is thought to be toxic to brain cells.

The agent is not destroyed even if the beef or material containing it is cooked or heat-treated. Transmission can occur when healthy animals come in contact with tainted tissues from others with the disease. In the brain, the agent causes native cellular prion protein to deform into the misfolded state, which then goes on to deform further prion protein in an exponential cascade. This results in protein aggregates, which then form dense plaque fibers. Brain cells begin to die off in massive numbers, eventually leading to the microscopic appearance of “holes” in the brain, degeneration of physical and mental abilities, and ultimately death.

The agent can be transmitted to humans by eating food contaminated with it. The highest risk to humans is believed to be from eating food contaminated with the brain, spinal cord, or digestive tract though any tissue may be involved.

However, “classic”mad cow disease hasn’t been linked to contaminated beef.

Diagnosis:
Diagnosis of mad cow disease continues to be a practical problem. It has an incubation period of months to years, during which no signs are noticed, though the pathway of converting the normal brain prion protein (PrP) into the toxic, disease-related PrPSc form has started. At present, virtually no way is known to detect PrPSc reliably except by examining post mortem brain tissue using neuropathological and immunohistochemical methods. Accumulation of the abnormally folded PrPSc form of PrP is a characteristic of the disease, but it is present at very low levels in easily accessible body fluids such as blood or urine. Researchers have tried to develop methods to measure PrPSc, but no methods for use in materials such as blood have been accepted fully.[by whom?]

The traditional method of diagnosis relies on histopathological examination of the medulla oblongata of the brain, and other tissues, post mortem. Immunohistochemistry can be used to demonstrate prion protein accumulation.

In 2010, a team from New York described detection of PrPSc even when initially present at only one part in a hundred billion (10?11) in brain tissue. The method combines amplification with a novel technology called surround optical fiber immunoassay and some specific antibodies against PrPSc. After amplifying and then concentrating any PrPSc, the samples are labelled with a fluorescent dye using an antibody for specificity and then finally loaded into a microcapillary tube. This tube is placed in a specially constructed apparatus so it is totally surrounded by optical fibres to capture all light emitted once the dye is excited using a laser. The technique allowed detection of PrPSc after many fewer cycles of conversion than others have achieved, substantially reducing the possibility of artifacts, as well as speeding up the assay. The researchers also tested their method on blood samples from apparently healthy sheep that went on to develop scrapie. The animals’ brains were analysed once any signs became apparent. The researchers could, therefore, compare results from brain tissue and blood taken once the animals exhibited signs of the diseases, with blood obtained earlier in the animals’ lives, and from uninfected animals. The results showed very clearly that PrPSc could be detected in the blood of animals long before the signs appeared. After further development and testing, this method could be of great value in surveillance as a blood- or urine-based screening test for BSE or mad cow disease.

Treatmen:
No effective treatment exists for mad cow disease or Creutzfeldt-Jakob disease or any of its variants. A number of drugs have been tested and have not shown benefits. For that reason, doctors focus on alleviating pain and other symptoms and on making people with these diseases as comfortable as possible.

Prevention:
A ban on feeding meat and bone meal to cattle has resulted in a strong reduction in cases in countries where the disease has been present. In disease-free countries, control relies on import control, feeding regulations, and surveillance measures.

In UK and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils from cattle are classified as specified risk materials, and must be disposed of appropriately.

An enhanced BSE-related feed ban is in effect in both the United States and Canada to help improve prevention and elimination of BSE.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Bovine_spongiform_encephalopathy
https://www.mayoclinic.org/diseases-conditions/creutzfeldt-jakob-disease/symptoms-causes/syc-20371226

Categories
Ailmemts & Remedies

Clubfoot

Description:
Clubfoot describes a range of foot abnormalities usually present at birth (congenital) in which your baby’s foot is twisted out of shape or position. In clubfoot, the tissues connecting the muscles to the bone (tendons) are shorter than usual. Clubfoot is a fairly common birth defect.

Clubfoot can be mild or severe. Most babies who are born with clubfoot are healthy in all other ways; about 1 in 3 of them have it in both feet.

Clubfoot doesn’t cause pain, but if it’s not treated, it can make it hard for a child to walk without a limp. It’s easy to correct in most cases, so most children don’t have long-lasting effects. Doctors generally recommend treating it soon after birth.

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Doctors are usually able to treat clubfoot successfully without surgery, though sometimes children need follow-up surgery later on.

Symptoms:

If your child has clubfoot, here’s what it might look like:

  • The top of the foot is usually twisted downward and inward, increasing the arch and turning the heel inward.
  • The foot may be turned so severely that it actually looks as if it’s upside down.
  • The affected leg or the foot may be smaller than a normal foot by up to a half-inch.
  • The calf muscles in the affected leg are usually underdeveloped.
  • The foot may have a limited range of motion.
  • Despite its look, clubfoot itself doesn’t cause any discomfort or pain.

Most doctors can spot clubfoot simply by looking at your baby when he or she is born. If you have an ultrasound done late in your pregnancy, your doctor may notice it then.

Causes:
The cause of clubfoot is unknown (idiopathic), but it may be a combination of several factors.

There are many hypotheses about how clubfoot develops. Some hypothesis include: environmental factors, genetics, or a combination of both. Research has not yet pinpointed the root cause, but many findings agree that “it is likely there is more than one different cause and at least in some cases the phenotype may occur as a result of a threshold effect of different factors acting together.

Some researchers hypothesize, from the early development stages of humans, that clubfoot is formed by a malfunction during gestation. Early amniocentesis (11–13 wks) is believed to increase the rate of clubfoot because there is an increase in potential amniotic leakage from the procedure. Underdevelopment of the bones and muscles of the embryonic foot may be another underlying cause. In the early 1900s, it was thought that constriction of the foot by the uterus contributed to the occurrence of clubfoot.

Underdevelopment of the bones also affects the muscles and tissues of the foot. Abnormality in the connective tissue causes “the presence of increased fibrous tissue in muscles, fascia, ligaments and tendon sheaths”.

Genetics:
Mutations in genes involved in muscle development are risk factors for clubfoot, specifically those encoding the muscle contractile complex (MYH3, TPM2, TNNT3, TNNI2 and MYH8). These can cause congenital contractures, including clubfoot, in distal arthrogryposis (DA) syndromes.[6] Clubfoot can also be present in people with genetic conditions such as Loeys–Dietz syndrome.

Genetic mapping and the development of models of the disease have improved understanding of developmental processes. Its inheritance pattern is explained as a heterogenous disorder using a polygenic threshold model. The PITX1-TBX4 transcriptional pathway has become key to the study of clubfoot. PITX1 and TBX4 are uniquely expressed in the hind limb.

Risk Factors:

  • Gender. Two-thirds of babies with clubfoot are male.
  • Family history. Babies with a parent or sibling who had clubfoot are twice as likely to get it.
  • Lifestyle choices. If you smoke or use illegal drugs while you’re pregnant, you raise your baby’s chances of being born with it.
  • Other birth defects. In some cases, it’s linked with other another condition a baby is born with, such as spina bifida.
  • Environment. Smoking during pregnancy can significantly increase the baby’s risk of clubfoot

Too little amniotic fluid during pregnancy. This surrounds your baby in the womb. If there’s not enough, your baby’s chances of being born with clubfoot are higher.

Diagnosis:

Diagnosis of clubfoot deformity is by physical examination. Typically, a newborn is examined shortly after delivery with a head to toe assessment. Examination of the lower extremity and foot reveals the deformity, which may affect one or both feet. Examination of the foot shows four components of deformity.

  • First, there is a higher arch on the inside of the foot. This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called cavus deformity.
  • Second, the forefoot is curved inward or medially (toward the big toe). This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called metatarsus adductus.
  • Third, the heel is turned inward. This is a natural motion of the heel and subtalar joint, typically referred to as inversion. In clubfoot deformity, the turning in (inversion) of the heel is fixed (not passively correctable) and considered a varus deformity.
  • Fourth, and finally, the ankle is pointed downward. This is a natural motion of the ankle referred to as plantar flexion. In clubfoot deformity, this position is fixed (not correctable) and is referred to as equinus deformity.

A foot that shows all four components is diagnosed as having clubfoot deformity. These four components of a clubfoot deformity can be remembered with the acronym CAVE (cavus, forefoot adductus, varus and equinus).

The severity of the deformity can also be assessed on physical exam, but is subjective to quantify. One way to assess severity is based on the stiffness of the deformity or how much it can be corrected with manual manipulation of the foot to bring it into a corrected position. Other factors used to assess severity include the presence of skin creases in the arch and at the heel and poor muscle consistency.

In some cases, it may be possible to detect the disease prior to birth during a prenatal ultrasound. Prenatal diagnosis by ultrasound can allow parents the opportunity to get information about this condition and make plans for treatment after their baby is born.

Other testing and imaging is typically not needed. Further testing may be needed if there are concerns for other associated conditions.

Treatment:
Because your newborn’s bones, joints and tendons are very flexible, treatment for clubfoot usually begins in the first week or two after birth. The goal of treatment is to improve the way your child’s foot looks and works before he or she learns to walk, in hopes of preventing long-term disabilities.

Treatment options include:

  • Stretching and casting (Ponseti method)
  • French method:
  • Surgery

(Ponseti method :

Using the Ponseti method, the foot deformity is corrected in stages. These stages are as follows: manipulating the foot to an improved position and then holding it with a long leg cast, then removing the cast after a week, and then manipulating the foot again. The foot position usually improves over a course of 4–6 casts. The amount of casts varies from person to person to address each individual’s characteristic needs.

  • The initial cast focuses on aligning the forefoot with the hindfoot as Ponseti describes the forefoot as relatively pronated in comparison to the hindfoot. Supinating the forefoot and elevating the first metatarsal improves this alignment.
  • Subsequent casts are applied after stretching the foot with a focus on abducting the forefoot with lateral pressure at the talus, to bring the navicula laterally and improve the alignment of the talonavicular joint. In contrast to the Kite Method of casting, it is important to avoid constraining the calcanocuboid joint. With each additional cast, the abduction is increased and this moves the hindfoot from varus into valgus. It is important to leave the ankle in equinus until the forefoot and hindfoot are corrected.
  • The final stage of casting, is to correct the equinus. After fully abducting the forefoot with spontaneous correction of the hindfoot, an attempt is made to bring the ankle up and into dorsiflexion. For the majority of children, the equinus will not fully correct with casting and a procedure is done to facilitate this final aspect of the deformity correction. The procedure is a percutaneous achilles tendon release or tenotomy. Ponseti advocated for doing this in the clinic with a local anesthetic. For safety reasons, many centers perform this procedure with sedation or monitored anesthesia care. In this procedure, numbing medicine is applied, the skin is cleansed, and a small scalpel is used to divide the Achilles tendon. With a small scalpel there is minimal bleeding and no need for stitches. A small dressing is applied and a final clubfoot cast is applied with the foot in a fully corrected position. This cast is typically left in place for 3 weeks.

After correction has been achieved with casting, maintenance of correction starts with full-time (23 hours per day) use of a brace —also known as a foot abduction brace (FAB)—on both feet, regardless of whether the TEV is on one side or both, typically full-time for 3 months. After 3 months, brace wear is decreased and used mostly when sleeping for naps and at night-time. This part-time bracing is recommended until the child is 4 years of age.

Roughly 30% of children will have recurrence. A recurrence can usually be managed with repeating the casting process. Recurrence is more common when there is poor compliance with the bracing, because the muscles around the foot can pull it back into the abnormal position. Approximately 20% of infants successfully treated with the Ponseti casting method will have an imbalance between the muscles that invert the ankle (posterior tibialis and anterior tibialis muscles) and the muscles that evert the ankle (peroneal muscles). Patients with this imbalance are more prone to recurrence. After 18 months of age, this can be addressed with surgery to transfer the anterior tibialis tendon from its medial attachment (the navicula) to a more lateral position (the lateral cuneiform) to rebalance these muscle forces. While this requires a general anesthetic and subsequent casting while the tendon heals, it is a relatively minor surgery that corrects a persistent muscle imbalance while avoiding disturbance to the joints of the foot.

French method:
The French method for treatment of clubfoot is a conservative method of treatment of a newborn which requires daily physical therapy for the first two months. The goal of this treatment is to avoid future need of surgery, but the success rate varies and after release surgery may still be necessary. The treatment includes daily manipulations of the feet along with stretching of the feet, followed by taping in order to maintain the range of motion gains achieved at the end of each session. The French method differs from the Ponseti method in that the taping techniques allow some motion in the feet. Another focus is to strengthen the peroneal muscles which is thought to contribute towards long-term correction. After the two month mark physical therapy sessions can be weaned down to three times per week instead of daily until the child reaches six months old. Parents are required to continue on with home exercises and night splinting even after the program has achieved proper foot correction in order to maintain the correction. The Ponseti method is generally preferred.

Surgery:
If your baby’s clubfoot is severe or doesn’t respond to nonsurgical treatments, more-invasive surgery may be needed. An orthopedic surgeon can lengthen or reposition tendons and ligaments to help ease the foot into a better position. After surgery, your child will be in a cast for up to two months, and then need to wear a brace for a year or so to prevent the clubfoot from coming back.

Even with treatment, clubfoot may not be totally correctable. But in most cases, babies who are treated early grow up to wear ordinary shoes and lead full, active lives.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Clubfoot
https://www.mayoclinic.org/diseases-conditions/clubfoot/symptoms-causes/syc-20350860
https://www.webmd.com/a-to-z-guides/what-is-clubfoot#1

Categories
Ailmemts & Remedies Pediatric

Herpangina.

Other Names: Mouth blisters or Hand-foot-and-mouth disease (HFMD).

Description:
Herpangina is often seen in the pediatric population, with occasional outbreaks among adult patients. They are both caused primarily by enteroviral infections. Herpangina presents as a stereotypical vesicular/ulcerative enanthem on the oropharyngeal mucosa. Usually, herpangina is produced by one particular strain of coxsackie virus A (and the term “herpangina virus” refers to coxsackievirus A) but it can also be caused by coxsackievirus B or echoviruses. Most cases of herpangina occur in the summer, affecting mostly children. However, it occasionally occurs in adolescents and adults. It was first characterized in 1920.

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HFMD is identified by a similar rash on the oral mucous membranes, with additional characteristic exanthem on hands and feet. Both syndromes are highly contagious. Although these syndromes are usually benign, their symptoms can cause significant temporary discomfort for patients and distress for their parents. Rarely, they can present as a more severe disease, and patients develop long-term sequelae.

Symptoms:
Symptoms include sudden fever with sore throat, headache, loss of appetite, and often neck pain. Within two days of onset an average of four or five (but sometimes up to twenty) 1 to 2 mm diameter grayish lumps form and develop into vesicles with red surrounds, and over 24 hours these become shallow ulcers, rarely larger than 5 mm diameter, that heal in one to seven days. These lesions most often appear on the tonsillar pillars (adjacent to the tonsils), but also on the soft palate, tonsils, uvula, or tongue.

A small number of lesions (usually 2 – 6) form in the back area of the mouth, particularly the soft palate or tonsillar pillars. The lesions progress initially from red macules to vesicles and lastly to ulcerations which can be 2 – 4 mm in size.

Causes:
Herpangina is usually caused by group A coxsackieviruses. However, it can also be caused by group B coxsackieviruses, enterovirus 71, and echovirus. These viruses are highly contagious and can easily spread from person to person, especially in schools and childcare centers.

People who are infected with herpangina are most contagious during the first week of infection.

Herpangina is typically transmitted through contact with fecal matter. The infection may also be spread through contact with droplets from an infected person’s sneeze or cough.

This means that you can get herpangina if you touch your mouth after touching something that’s contaminated with fecal particles or droplets from an infected person. The virus can live on surfaces and objects, such as countertops and toys, for several days.

Risk Factors:
Herpangina can affect anyone, but it most commonly occurs in children under age 5. It’s particularly common in children who attend school, childcare facilities, or camps. In the United States, the risk of developing herpangina is higher during the summer and fall.

Diagnosis:
The diagnoses of HFMD and herpangina are usually made clinically. In mild cases, no imaging or laboratory testing is required. Laboratory studies are usually obtained to gain additional information about complications such as dehydration or to rule out alternative diagnoses. Confirmatory testing is usually required only in complicated disease, for the collection of epidemiological data during epidemics, or to differentiate herpangina or HFMD from more serious diseases such as eczema herpeticum. Viral culture is the “gold standard” for confirmatory testing. Unfortunately, it can often take longer than 1 week to obtain culture results. This makes it an impractical test for clinical practice. Polymerase chain reaction (PCR) testing is fast and highly sensitive for enteroviruses. Samples may be obtained from the stool, mucocutaneous ulcers, vesicular fluid, or cerebrospinal fluid. Enzyme-linked immunosorbent assays (ELISA) are also available. ELISA testing for enteroviruses is generally less sensitive than PCR and should be utilized only in cases where PCR is not available.

Treatment:
Treatment is usually supportive only, as the disease is self-limiting and usually runs its course in less than a week.

Since herpangina is a viral infection, antibiotics aren’t an effective form of treatment. Instead, your doctor may recommend:

Ibuprofen or acetaminophen: These medications can ease any discomfort and reduce fever. Do not use aspirin to treat symptoms of a viral infection in children or teenagers. This has been linked to Reye’s syndrome, a life-threatening illness that results in sudden swelling and inflammation in the liver and brain.

Topical anesthetics: Certain anesthetics, such as lidocaine, can provide relief for a sore throat and any other mouth pain associated with herpangina.

Increased fluid intake: It’s important to drink plenty of fluids during recovery, especially cold milk and water. Eating popsicles can also help soothe a sore throat. Avoid citrus drinks and hot beverages, as they may make symptoms worse.
With treatment, symptoms should disappear within seven days with no lasting effects.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://www.ncbi.nlm.nih.gov/books/NBK507792/
https://www.healthline.com/health/herpangina#causes
https://en.wikipedia.org/wiki/Herpangina