DR MIJUL'S HOMOEOPATHY

What types of Diseases & Conditions can

2010-01-06T10:11:00.000-08:00

What types of Diseases & Conditions can
Homeopathic Medicine Treat?

I think most people don't have any idea, so I will list just a few right here. Cancers of all kinds (do NOT require chemotherapy, surgery and radiation), HIV/AIDS, autoimmune disorders, heart disease including arteriosclerosis (does NOT require balloon angioplasty or open heart surgery), hypertension, stroke, etc. Continuing the list, though it is endless and these are just some common ailments that people suffer from and will never be told by their Medical Doctor that there are safe, natural, inexpensive and effective therapies available. Neurological diseases including epilepsy, petite mal, twitchings, jerkings, convulsions, anxiety disorders, panic attacks, and so on. Parkinsonism, Alzheimer's, senile dementia, incontinence, premature old age, seminal emissions, infertility (in both sexes), mercury poisoning from dental amalgams, skin diseases including eczema, psoriasis, boils, acne, blackheads, warts, moles, brown spots, dry or oily skin, etc. Hormonal imbalances including mannish women with hair and masculine features, effeminine men, underdeveloped penis or breasts, PMS, menstrual problems. Emaciation, obesity, diabetes, overweight, bulimia, anorexia. Addictions: crystal meth., cocaine, alcohol, heroine, cannabis, any addiction. Mental disorders, developmental disorders, such as Downe's Syndrome, Autism, Mental Retardation, etc. Varicose veins, varices, vertigo, dizziness, pneumonia, bronchitis, influenza, manic-depression, Bipolar Syndrome, agoraphobia, hepatitis, jaundice, fevers, chronic weakness, chronic diarrhea, chronic constipation, emotion disorders, delusions, hypertension, phebitis, non-healing wounds, hot flashes, menopausal symptoms, vertigo, dizziness, disorientation, paralysis, hemiplegia, chronic respiratory infections, emphazema, alcoholism, violent behaviors, apathy, sexual dysfunction, sterility, osteoporosis, injuries, emaciation, anorexia, bulemia, CPOD, chest pain, macula, precancerous growths, Post Traumatic Stress Disorder, hyperactivity, ADHD, ADD, coma, mental insanity...this list is to be continued...

PNEUMOTHORAX

2010-01-06T08:38:00.000-08:00

PNEUMOTHORAX

Definition of Pneumothorax

Pneumothorax is a collection of air or gas in the pleural space of the lung, causing the lung to collapse. Pneumothorax may be the result of an open chest wound that permits the entrance of air, the rupture of an emphysematous vesicle on the surface of the lung, a severe bout of coughing, or it may occur spontaneously without evident cause.

Pneumothorax is a lung disorder in which air in the lungs leaks out through holes in the lung tissue into the spaces outside the lung airways. Pneumothorax is one type of lung disorders called air leak syndrome. A baby can have more than one form of air leak. Types of air leaks include the following:

· Pneumothorax - air leaks into the space between the chest wall and the outer tissues of the lungs.

· Pneumomediastinum - air leaks into the mediastinum (the space in the thoracic cavity behind the sternum and between the two pleural sacs containing the lungs).

· Pneumopericardium - air leaks into the sac surrounding the heart.

· Pulmonary interstitial emphysema (PIE) - air leaks and becomes trapped between the alveoli, the tiny air sacs of the lungs.

Air leaks may occur suddenly or may develop gradually. The degree of illness depends on the location of the leak and the amount of air.

Right-sided pneumothorax on CT scan of the chest or abdomen. A chest tube is in place--side of chest, the lumen (black) can be seen adjacent to the pleural cavity (black) and ribs (white). The heart can be seen in the centre.

In medicine (pulmonology), a pneumothorax is a potential medical emergency wherein air or gas is present in the pleural cavity. A pneumothorax can occur spontaneously. It can also occur as the result of disease or injury to the lung, or due to a puncture to the chest wall. A pneumothorax can result in a collapsed lung, or can be created therapeutically to collapse a lung.

Etiology

It most commonly arises:

· Spontaneously (most commonly in tall slim young males and in Marfan syndrome)

· Following a penetrating chest wound

· Following Barotrauma to the lungs

· It may also be due to:

· Chronic lung pathologies including emphysema, asthma

· Acute infections

· Chronic infections, such as tuberculosis

· Lung aggravation caused by Cystic Fibrosis

· Cancer

Pneumothoraces are divided into tension and non-tension pneumathoraces. A tension pneumothorax is a medical emergency as air accumulates in the pleural space with each breath. The increase in intrathoracic pressure results in massive shifts of the mediastinum away from the affected lung compressing intrathoracic vessels. A non-tension pneumothorax by contrast is of lesser concern because there is no ongoing accumulation of air and hence no increasing pressure on the organs within the chest.

The accumulation of blood in the thoracic cavity (hem thorax) exacerbates the problem, creating a hemopneumothorax

The following babies are most at risk for pneumothorax:

· babies with other lung diseases such as hyaline membrane disease (HMD)

· babies on mechanical ventilators

· premature babies whose lung tissues are more fragile

· babies with me conium aspiration because the me conium plugs the airways and can weaken the tissues

What causes pneumothorax?

Air leaks occur when the alveoli (tiny air sacs) become overdistended and burst. Pressure of the air delivered by mechanical ventilators (breathing machines) is the most common cause. Meconium aspiration (inhalation of the first stools passed in utero) can also trap air and lead to overdistention (the lungs expand too much) and air leaks. Air leaks often occur in the first 24 to 36 hours when lung disease is at its peak. Some otherwise healthy babies can develop a "spontaneous" air leak that does not cause symptoms or distress.

Description of Pneumothorax

The major types of pneumothorax are:

v Open pneumothorax results when a penetrating chest wound enables air to rush in and cause the lungs to collapse.

v Closed pneumothorax results when the chest wall is punctured or air leaks from a ruptured bronchus (or a perforated esophagus) and eventually ruptures into the pleural space.

v Spontaneous pneumothorax occurs in a previously healthy individual with no prior trauma. This is thought to be due to rupture of a bleb (a blister containing air) on the surface of the lung. This spontaneous pneumothorax is most frequent in people under the age of 40.

v Pulmonary Barotrauma occurs when a patient whose lung function is being maintained mechanically may have air forced into the lungs, which may rupture the pleural space.

Other things can cause pneumothorax. Air can enter the mediastinum (the space in the center of the chest between the lungs), especially during an asthmatic attack, and then rupture into the pleural space, causing a pneumothorax. When a lung biopsy specimen is taken at the time of bronchoscopy or during thoracentesis (removal of fluid from the pleural space), the pleura lining the lung may be penetrated, causing a leak of air which may then cause a pneumothorax.

Signs and symptoms

The following are the most common symptoms of pneumothorax. However, each baby may experience symptoms differently. Symptoms may include:

· Increasing respiratory distress, including rapid breathing, grunting, nostril flaring, and chest wall retractions

· Difficulty hearing breath sounds when listening with a stethoscope

· Change in the location of heart or lung sounds when the organs are moved by the presence of air

· Changes in arterial blood gas levels

The symptoms of pneumothorax may resemble other conditions or medical problems. Always consult your baby's physician for a diagnosis.

There may be no symptoms if the pneumothorax is small (a small amount of air in the pleural space) or there may be shortness of breath if a large amount of air is in that space. If a physician suspects a pneumothorax, a chest x-ray may be taken to confirm the diagnosis and to determine the amount of air present.

Pneumothorax presents mainly as a sudden shortness of breath, dry coughs, cyanosis (turning blue) and pain felt in the chest, back and/or arms. In penetrating chest wounds, the sound of air flowing through the puncture hole may indicate pneumothorax, hence the term "sucking" chest wound. The flopping sound of a punctured lung is also occasionally heard. Subcutaneous emphysema is another symptom.

If untreated, hypoxia may lead to loss of consciousness and coma. In addition, shifting of the mediastinum away from the site of the injury can obstruct the superior and inferior vena cava resulting in reduced cardiac preload and decreased cardiac output. Untreated, a severe pneumothorax can lead to death within several minutes

Spontaneous Pneumothoraces are reported in young people with a tall, skinny stature. There is a preponderance among men, possibly because men are in general taller than women. The reason for this association, while unknown, is hypothesized to be the presence of subtle abnormalities in connective tissue. Some spontaneous Pneumothoraces, however, are results of "blebs", blister like structures on the surface of the lung, that rupture allowing the escape of air into the pleural cave

Pneumothorax can also occur as part of medical procedures, such as the insertion of a central venous catheter (an intravenous catheter) in the subclavian vein or jugular While rare, it is considered a serious complication and needs immediate treatment. Other causes include mechanical ventilation, emphysema and quite rarely other lung diseases (p Tuberculosis

· Pneumonia

· Asthma

· Cystic fibrosis

· Lung cancer

· Interstitial lung disease

· Marfan syndrome

· Lymphangioleiomyomatosis

Investigations

In addition to a complete medical history and physical examination, diagnostic procedures for pneumothorax may include:

· Chest x-rays - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film. X-rays may show the following:

o air in places outside the normal lung airways

o collapse of the lung

o movement or shifting of other organs in the chest away from the air leak sick

· Tran illumination - a fiber optic light probe placed on the baby's chest wall (the side of the chest with the air leak transmits brighter light). This procedure is often used in an emergency.

AEM: Emergency Bedside Ultrasound to Detect Pneumothorax

A relatively new application of emergency ultrasound is its use in the diagnosis of pneumothorax. In patients with major trauma, early detection and treatment of pneumothorax are vital.

Diagnosis

The absence of audible breath sounds through a stethoscope can indicate that the lung is not unfolded in the pleural cavity. This accompanied by hyper resonance (higher pitched sounds than normal) to percussion of the chest wall is suggestive of the diagnosis. The "coin test" may be positive. Two coins when tapped on the affected side, produce a tinkling resonant sound which is audible on auscultation.

If the signs and symptoms are doubtful, an X-ray of the chest can be performed, but in severe hypoxia, or evidence of tension pneumothorax emergency treatment has to be administered first.

In a supine chest X-ray the deep sulcus sign is diagnostic^[, which is characterized by a low lateral costophrenic angle on the affected side. In layman's terms, the place where rib and diaphragm meet appears lower on an X-ray with a deep sulcus sign and suggests the diagnosis of pneumothorax.

Differential diagnosis

When presented with this clinical picture, other possible causes include:

· Acute Myocardial Infarction: presents with shortness of breath and chest pain, though MI chest pain is characteristically crushing, central and radiating to the jaw, left arm or stomach. Whilst not a lung condition, patients having an MI often happen to also have lung disease.

· Emphysema: here, delicate functional lung tissue is lost and replaced with air spaces, giving shortness of breath, and decreased air entry and increased resonance on examination. However, it is usually a chronic condition, and signs are diffuse (not localized as in pneumothorax).

Careful history taking and examination and a chest X-ray will allow accurate diagnosis.

Pathophysiology

Mechanics of a sucking chest wound. A. Air enters the chest through the opening in the chest wall during inspiration (a). The lung collapses on the affected side (b), air passes out of affected bronchus. Air enters the bronchus from the collapsed lung (c) and passes to the intact lung. The mediastinum shifts toward the uninvolved side (d), and hemothorax occurs (e). B. During expiration, air escapes through the wound (a). The collapsed lung expands (b). Air passes from the uninvolved side to the lung on involved side and out the trachea (c). The mediastinum shifts to the involved side (d), and hemothorax occurs (e).

The lungs are located inside the chest cavity, which is a hollow space. Air is drawn into the lungs by the diaphragm (a powerful abdominal muscle). The pleural cavity is the region between the chest wall and the lungs. If air enters the pleural cavity, either from the outside (open pneumothorax) or from the lung (closed pneumothorax), the lung collapses and it becomes mechanically impossible for the injured person to breathe, even with an open airway. If a piece of tissue forms a one-way valve that allows air to enter the pleural cavity from the lung but not to escape, overpressure can build up with every breath; this is known as tension pneumothorax. It may lead to severe shortness of breath as well as circulatory collapse, both life-threatening conditions. This condition requires urgent intervent

FIRST AID

Chest wound

Wounds (also known as 'sucking chest wounds') require immediate coverage with an occlusive dressing, field dressing, or pressure bandage made air-tight with petroleum jelly or clean plastic sheeting. The sterile inside of a plastic bandage packaging is good for this purpose; however in an emergency situation any airtight material, even the cellophane of a cigarette pack, can be used. A small opening, known as a flutter valve, may be left open so the air can escape while the lung reinflates. Any patient with a penetrating chest wound must be closely watched at all times and may develop a tension pneumothorax or other immediately life-threatening respiratory emergency at any moment. They cannot be left alone.

Blast injury or tension

If the air in the pleural cavity is due to a tear in the lung tissue (in the case of a blast injury or tension pneumothorax), it needs to be released. A thin needle can be used for this purpose, to relieve the pressure and allow the lung to reinflate.

Pre-hospital care

Many paramedics can perform needle thoracocentesis to relieve intrathoracic pressure. Incubation may be required, even of a conscious patient, if the situation deteriorates. Advanced medical care and immediate evacuation are strongly indicated.

An untreated pneumothorax is an absolute contraindication of evacuation or transportation by flight.

Clinical treatment

If the lung is less than 20 to 25 percent collapsed, the physician may choose to watch the progress by a series of chest x-rays until the air is completely absorbed or the lung completely re-expands.

If collapse of the lung exceeds 25 percent or if you are short of breath at rest, the physician may recommend removing the air through your chest wall. This can be done with a needle, but is better performed by inserting a tube and applying constant suction for 24 hours or more. The latter procedure also helps to prevent recurrence of pneumothorax

Small Pneumothoraces are often managed conservatively as they will resolve on their own. Repeat observation via chest X-rays and oxygen administered to speed the resolution is often carried out. Pneumothoraces which are too small to require tube thoracostomy and too large to leave untreated, have been aspirated with a needle.

Larger Pneumothoraces may require tube thoracostomy, also known as chest tube placement. If a thorough anesthetizing of the parietal pleura and the intercostals muscles is performed, the only major pain experienced should be either the injury that caused the pneumothorax or the re-expanding of the lung. Proper anesthetizing will come about by the following procedure: the needle should be inserted into the chest cavity and a negative pressure created in the syringe. While air bubbles rise into the syringe, the needle should be slowly pulled out of the cavity until the bubbles cease. The tip of the syringe that contains the anesthetic is now in the intercostals muscles. A proper and sizable injection should ensue. This will allow the patient to be fairly comfortable despite a hemostat or finger being inserted into the chest cavity. A tube is then inserted into the chest wall outside the lung and air is extracted using a simple one way valve or vacuum and a water valve device, depending on severity. This allows the lung to re-expand within the chest cavity. This re-expansion usually lasts for approximately 15–30 seconds depending on the size of the pneumothorax and feels as if your breath has been taken away. This response is normal and should pass fairly quickly. The pneumothorax is followed up with repeated X-rays. If the pneumothorax has resolved and there is no further air leak, the chest tube removed. If, during the time that the tube is still in the chest, the lung manages to sustain the re-expansion once suction is turned off, but the lung still diminishes if actually clamped off, a Heimlich valve may be used. This flutter valve allows air and fluid in the pleural cavity to escape the pleura into a drainage bag while not letting any air or fluid back in. This method was developed by the military in order to get soldiers with lung injuries stable and out of the battle field faster. It is a rarely used medical device in the treatment of patients these days, but may be used in order to allow the patient to leave the hospital.

It is critical that the chest tube be managed in such a way that it does not become occluded with clot or other fibrinous material. Chest tube clogging can result in build up of air in the pleural space. At the very least, this will lead to a recurrent pneumothorax. In the worse case, the patient can have a tension pneumothorax if the air builds up under pressure and impairs venous return to the heart. This can be fatal. The tubes have a tendency to form clot from blood and other fibrinous material that can occlude them. To keep them open they must be stripped, milked or even replaced if they totally occlude. Smaller tubes are more prone to clogging, although this can occur with larger tubes. One sign the chest tube is clogged is subcutaneous emphysema. Another is a loss of respiratory variation in the fluid in the tube to the drainage canister.

In the situation that the chest tube does not seem to be helping (for example a continued air leak despite chest tube drainage) the healing of the lung or if CAT scans show the presence of "blebs" on the surface of the lung thoracoscopic surgery, or video assisted thorascopic surgery (VATS), may be done in order to staple the leak shut. Two small incisions are made in the back, one for a small camera and one for the tool used to seal the lung. When finished the wound is covered with a steri-strip and bandaged up.

In case of penetrating wounds, these require attention, but generally only after the airway has been secured and a chest drain inserted. Supportive therapy may include mechanical ventilation.

Recurrent pneumothorax may require further corrective and/or preventive measures such as pleurodesis. If the pneumothorax is the result of bullae, then bullectomy (the removal or stapling of bullae or other faults in the lung) is preferred. Chemical pleurodesis is the injection of a chemical irritant that triggers an inflammatory reaction, leading to adhesion of the visceral pleura, which is in contact with the lung, to the parietal pleura. Substances used for pleurodesis include talc, blood, tetracycline and bleomycin. Mechanical pleurodesis does not use chemicals. The surgeon "roughs" up the inside chest wall ("parietal pleura") so the lung attaches to the wall with scar tissue. This can also include a "parietal" pleurectomy, which is the removal of the "parietal" pleura; "parietal" pleura is the serous membrane lining the inner surface of the thoracic cage and facing the "visceral" pleura, which lies all over the lung surface. Both operations can be performed using keyhole surgery to minimize discomfort to the patient. Sometimes pneumothorax occurs bilaterally in sequence or, more rarely, simultaneously; that is often associated to bilateral apical blebs and obviously requires bilateral treatment.

Specific treatment for pneumothorax and air leak syndrome will be determined by your baby's physician based on:

· Your baby's gestational age, overall health, and medical history

· Extent of the condition

· Your baby's tolerance for specific medications, procedures, or therapies

· Expectations for the course of the condition

· Your opinion or preference

Treatment for pneumothorax may include:

· Supplemental oxygen

· Removal of the collected air by insertion of a chest tube (a needle or catheter placed through the chest wall into the air space). The air may be withdrawn with a syringe or the tube connected to a drainage system to help remove the air until the leak can seal.

Spontaneous air leaks that do not cause symptoms or distress may get better on their own without treatment. As the leak seals over, air is absorbed into the body.

There are no specific treatments for pneumomediastinum and pulmonary interstitial emphysema (PIE), as these air leaks are in spaces that cannot be treated with chest tubes. High frequency ventilation is sometimes used for babies with PIE.

Possible Complications

· Recurrent pneumothorax

· Tension pneumothorax with shock

Tension pneumothorax

tension pneumothorax is a life-threatening condition that results from a progressive deterioration and worsening of a simple pneumothorax, associated with the formation of a one-way valve at the point of a rupture in the lung. Air becomes trapped in the pleural cavity between the chest wall and the lung, and builds up, putting pressure on the lung and keeping it from inflating fully.

Upon inspiration, when the pressure inside the chest and pleural cavity falls as a result of the respiratory muscles increasing chest dimensions, air is sucked in through the one way valve, into the pleural space. Because exhalation is a passive process, there is an insignificant amount of pressure created to force the air back out of the pleural cavity. This condition over time results in a gradual accumulation of air to the degree that it begins to put pressure on the mediastinum, compressing the heart and decreasing cardiac output due to the reduced amount of diastolic filling of the ventricles, and also putting pressure against the trachea, causing it to move away from the midline (the center). Because of the increased thoracic pressure, venous return to the heart is decreased, causing a backup of blood into the venous system, as evidenced by distended jugular veins

Signs and Symptoms

· Decreased or absent breath sounds on the affected side

· Tracheal deviation towards unaffected side

· Hyper resonance on percussion

· Unequal chest rise

· Dyspnea (difficulty breathing)

· Tachypnea (rapid breathing)

· Tachycardia (rapid heart rate)

· Hypotension (low blood pressure)

· Hypoxia (deficiency in the amount of oxygen reaching the tissues)

· Pale, cool, clammy skin

· Subcutaneous emphysema (air trapped beneath the skin)

· Cyanosis (bluish color of skin)

· Jugular venous distension (enlarged jugular veins; late sign)

Treatment

Initial treatment involves the insertion of a large bore cannula or needle into the second intercostals space on the mid-clavicular line (known as "needle thoracostomy", or more commonly, "needle decompression"), thereby releasing the pressure in the pleural cavity and converting the tension pneumothorax to a simple pneumothorax, which is then treated at the earliest opportunity by inserting a chest tube.

Tension pneumothorax represents a medical emergency which cannot often accommodate the time spent waiting for the capture and interpretation of a chest radiograph. Consequently, the decision to proceed with needle decompression must be made clinically (i.e., "at the bedside") by observing the acute presentation and reviewing relevant history. There is some debate on the topic of needle thoracostomy. There are risks associated with the process such as lung laceration, especially if no tension pneumothorax condition is present, and that relieved tension may reaccumulate undetected if the needle thoracostomy becomes dislodged. There is also the possibility that the cannula will not reach the pleural cavity due to a thick chest wall, especially in overweight individuals. Traditionally needle decompression has been attempted using a 4.5cm (2") to 5cm catheter. However, previous studies have shown a failure rate of up to 40% using this technique. Based on the clinical findings and failure rates, it is recommended that a 3.25" 14 gauge needle should be used in order to address the issue of the needle not reaching the pleural space.

Once the needle is placed, a chest tube is inserted. Almost always there is a rush of air released from the pleural space when the chest is entered, then the tube is slipped into the pleural space to drain the air and re-expand the lung. Nearly always, there will be a large air leak that will generally resolve over the subsequent days. If the chest tube becomes clogged or kinked, the tension pneumothorax will reoccur. This can be a life threatening event, especially when un recognized. Chest tubes are prone to clogging with fibrinous material or blood clot. Chest tube clogging can occur in the external portion of the chest tube, where it can be seen, at which point milking and stripping of the tubes can be carried out to try to re open or keep open the tubes. These techniques are controversial and of limited utility. Another option is to create a sterile field, open the chest tube and the connection to the drainage tubing, and introduce a external suction catheter to try to suck out the clogged chest tube. This has the disadvantage of breaking the sterile field, and air can be sucked back into the chest. If the chest tube clogging cannot be cleared, the tube has to be replaced. Often physicians will place large bore chest tubes or multiple chest tubes with the hope of minimizing the potential for chest tube clogging. Chest tube clogging can also occur in the non visible portion of the tube inside the chest, and go unrecognized. In the setting of ongoing air leak this can result in a return of the tension pneumothorax, which can be lethal if unrecognized.

Spontaneous Pneumothorax

Spontaneous Pneumothorax can be classified as primary spontaneous pneumothorax and secondary spontaneous pneumothorax. In primary spontaneous pneumothorax, it is usually characterized by a rupture of a bleb in the lung while secondary spontaneous pneumothorax mostly occurs due to chronic obstructive pulmonary disease (COPD).

Primary spontaneous pneumothorax

A primary spontaneous pneumothorax may occur without either trauma to the chest or any kind of blast injury. This type of pneumothorax is caused when a bleb (an imperfection in the lining of the lung) bursts causing the lung to deflate. The lung is reinflated by the surgical insertion of a chest tube. A minority of patients will suffer a second instance. In this case, thoracic surgeons often recommend thorascopic pleurodesis to improve the contact between the lung and the pleura. If multiple and/or bilateral occurrences continue, surgeons may opt for a far more invasive bullectomy and pleurectomy to permanently adhere the lung to the interior of the rib cage with scar tissue, making collapse of that lung physically impossible. Primary spontaneous pneumothorax is most common in tall, thin men between 17 and 40 years of age, without any history of lung disease. Though less common, it also occurs in women, usually of the same age and body type. The tendency for primary spontaneous pneumothorax sufferers to be tall and thin is not due to weight, diet or lifestyle, but because the genetic predisposition toward those traits often coincides with a genetic predisposition toward high volume lungs with large, burstable blebs. A small portion of primary spontaneous pneumothoraxes occur in persons outside the typical range of age and body type.

Secondary spontaneous pneumothorax

In secondary spontaneous pneumothorax, a known lung disease is the cause of the collapse The most common cause is chronic obstructive pulmonary disease (COPD). However, there are several other diseases that may also lead to spontaneous pneumothorax:

· Tuberculosis

· Pneumonia

· Asthma

· Cystic fibrosis

· Lung cancer

· Interstitial lung disease

· Marfan syndrome

· Lymphangioleiomyomatosis

Pneumothorax in the Newborn

Air leaks from the lungs into other parts of the chest cavity can occur in newborns, and it is a potentially serious problem. Small air leaks can occur in 1 to 2 percent of all births. Babies are normally born with collapsed lungs, and considerable pressure is generated as the newborn's body works to inflate them with the first few breaths. There is no problem whatsoever for 98 percent of all newborns, but in some babies, the lungs do not open completely at once, and the strong pressures generated to inflate the lung may cause small ruptures in the alveoli (the smallest, most plentiful breathing sacs). The leaked air may be removed from the chest cavity by the attending physician. Continuous removal of leaked air is necessary until the ruptures heal.

Prevention of pneumothorax and other air leaks:

Despite careful regulation of the air pressure and the settings on mechanical ventilators, air leaks can still occur. Your baby's physician and other healthcare providers in the newborn intensive care unit (NICU) will watch your baby carefully for signs of air leak so that treatment can be started as quickly as possible.

HOMOEOPATHIC MANAGEMENT

Arsenicum Album

Unable to lie down; fears suffocation. Air-passages constricted. Asthma worse midnight. Burning in chest. Suffocative catarrh. Cough worse after midnight; worse lying on back. Expectoration scanty, frothy. Darting pain through upper third of right lung. Wheezing respiration. Hæmoptysis with pain between shoulders; burning heat all over. Cough dry, as from sulphur fumes; after drinking.

Aconitum Napellus

Constant pressure in left chest; oppressed breathing on least motion. Hoarse, dry, croupy cough; loud, labored breathing. Child grasps at throat every time he coughs. Very sensitive to inspired air. Shortness of breath. Larynx sensitive. Stitches through chest. Cough, dry, short, hacking; worse at night and after midnight. Hot feeling in lungs. Blood comes up with hawking. Tingling in chest after cough.

Ammonium Muriaticum

Hoarseness and burning in larynx. Dry, hacking, scraping cough; worse lying on back or right side. Stitches in chest. Cough loose in afternoon, with profuse expectoration and rattling of mucus. Oppression of chest. Burning at small spots in chest. Scanty secretion. Cough with profuse salivation.

Antimonium Tartaricum

Great rattling of mucus, but very little is expectorated. Velvety feeling in chest. Burning sensation in chest, which ascends to throat. Rapid, short, difficult breathing; seems as if he would suffocate; must sit up. Emphysema of the aged. Coughing and gaping consecutively. Bronchial tubes overloaded with mucus. Cough excited by eating, with pain in chest and larynx. Edema and impending paralysis of lungs. Much palpitation, with uncomfortable hot feeling. Pulse rapid, weak, trembling. Dizziness, with cough. Dyspnea relieved by eructation. Cough and Dyspnea better lying on right side

Bacillinum Burnett

Catarrhal Dyspnea. Humid asthma. Bubbling rales and muco-purulent expectoration. Note. This mucous-purulent expectoration of bronchitis patients is equally poly-bacillary; it is a mixture of diverse species and hence Bacillinum is truly indicated (Cartier). Often relieves congestion of the lungs, thus paving way for other remedies in Tuberculosis.

Drosera Rotundifolia

Spasmodic, dry irritative cough, like whooping-cough, the paroxysms following each other very rapidly; can scarcely breathe; chokes. Cough very deep and hoarse; worse, after midnight; yellow expectoration, with bleeding from nose and mouth; retching. Deep, hoarse voice; hoarseness; laryngitis. Rough, scraping sensation deep in the fauces and soft palate. Sensation as if crumbs were in the throat, of feather in larynx. Laryngeal phthisis, with rapid emaciation. Harassing and titillating cough in children-not at all through the day, but commences as soon as the head touches the pillow at night. Clergyman's sore throat, with rough, scraping, dry sensation deep in the fauces; voice hoarse, deep, toneless, cracked, requires exertion to speak. Asthma when talking, with contraction of the throat at every word uttered.

Grindelia Robusta

An efficacious remedy for wheezing and oppression in bronchitis patients. The sibilant rales are disseminated with foamy mucus, very difficult to detach. Acts on the pulmonary circulation. Asthma, with profuse tenacious expectoration, which relieves. Stops breathing when falling asleep; wakes with a star, and gasps for breath. Must sit up to breathe. Cannot breathe when lying down. Pertussis, with profuse mucous secretion (Coccus). Bronchorrhœa, with tough, whitish, mucous expectoration. Sibilant rales. Weak heart and respiration. Cannot breathe lying down. Cheyne-Stokes respiration.

Justicia Adhatoda

Dry cough from sternal region all over chest. Hoarseness, larynx painful. Paroxysmal cough, with suffocative obstruction of respiration. Cough with sneezing. Severe Dyspnea with cough. Tightness across chest. Asthmatic attacks, cannot endure a close, warm room. Whooping-cough.

Hepar Sulphur

Loses voice and coughs when exposed to dry, cold wind. Hoarseness, with loss of voice. Cough troublesome when walking. Dry, hoarse cough. Cough excited whenever any part of the body gets cold or uncovered, or from eating anything cold. Croup with loose, rattling cough; worse in morning. Choking cough. Rattling, croaking cough; suffocative attacks; has to rise up and bend head backwards. Anxious, wheezing, moist breathing, asthma worse in dry cold air; better in damp. Palpitation of heart.

Ipecacuanha

Dyspnea; constant constriction in chest. Asthma. Yearly attacks of difficult shortness of breathing. Continued sneezing; coryza; wheezing cough. Cough incessant and violent, with every breath. Chest seems full of phlegm, but does not yield to coughing. Bubbling rales. Suffocative cough; child becomes stiff, and blue in the face. Whooping-cough, with nosebleed, and from mouth. Bleeding from lungs, with nausea; feeling of constriction; rattling cough. Croup. Hæmoptysis from slightest exertion (Millef). Hoarseness, especially at end of a cold. Complete aphonia

Phosphoricum Acidum

Chest troubles develop after brain-fag. Hoarseness. Dry cough from tickling in chest. Salty expectoration. Difficult respiration. Weak feeling in chest from talking (Stann). Pressure behind the sternum, rendering breathing difficult. -Better, from keeping warm. Worse, exertion, from being talked to; loss of vital fluids; sexual excesses. Everything impeding circulation causes aggravation of symptoms.

Belladonna

Drying in nose, fauces, larynx, and trachea. Tickling, short, dry cough; worse at night. Larynx feels sore. Respiration oppressed, quick, unequal. Cheyne-Stokes respiration (Cocaine; Opium). Hoarse; loss of voice. Painless hoarseness. Cough with pain in left hip. Barking cough, whooping cough, with pain in stomach before attack, with expectoration of blood. Stitches in chest when coughing. Larynx very painful; feels as if a foreign body were in it, with cough. High, piping voice. Moaning at every breath

Cactus Grandiflorus

Oppressed breathing as from a weight on chest. Constriction in chest, as if bound, hindering respiration. Inflammation of diaphragm

Veratrum Viride

Congestion of lungs. Difficult breathing. Sensation of a heavy load on chest. Pneumonia, with faint feeling in stomach and violent congestion. Croup. Menstrual colic before the appearance of the discharge with strangury.

Ferrum Phosphoricum

First stage of all inflammatory affections. Congestions of lungs. Hæmoptysis. Short, painful tickling cough. Croup. Hard, dry cough, with sore chest. Hoarseness. Expectoration of pure blood in pneumonia (Millefol). Cough better at night.

Ammonium Carbonicum

Cough every morning about three o'clock, with dyspnœa, palpitation, burning in chest; worse ascending. Chest feels tired. Emphysema. Much oppression in breathing; worse after any effort, and entering warm room, or ascending even a few steps. Asthenic Pneumonia. Slow labored, stertorous breathing; bubbling sound. Winter catarrh, with slimy sputum and specks of blood. Pulmonary œdema.

Apis Mellifica

Hoarseness; dyspnœa, breathing hurried and difficult. Œdema of larynx. Feels as if he could not draw another breath. Suffocation; short, dry cough, suprasternal. Hydrothorax.

The very characteristic effects of the sting of the bee furnish unerring indications for its employment in disease. Swelling or puffing up of various parts, œdema, red rosy hue, stinging pains, soreness, intolerance of heat, and slightest touch, and afternoon aggravation are some of the general guiding symptoms. Erysipelatous inflammations, dropsical effusions and anasarca, acute, inflammation.

Alopecia

2010-01-06T08:36:00.000-08:00

Alopecia

Introductlon

Alopecia or hair loss is the medical description of the loss of hair from the head or body, sometimes to the extent of baldness. Unlike the common aesthetic depilation of body hair, alopecia tends to be involuntary and unwelcome, e.g., androgenic alopecia. However, it may also be caused by a psychological compulsion to pull out one's own hair (trichotillomania) or the unforeseen consequences of voluntary hairstyling routines (mechanical "traction alopecia" from excessively tight ponytails or braids, or burns to the scalp from caustic hair relaxer solutions or hot hair irons).

ETIOLOGY

In some cases, alopecia is an indication of an underlying medical concern, such as iron deficiency.

Androgenetic alopecia (Male pattern baldness)
Fungal infection such as "black dot" tinea or tinea capitis
Chemical breakage such as over processing, or frequent use of chemical relaxer
Heat damage as from repeated hot comb use
Chronic exposure to traction on hair shaft such as Traction alopecia
Compulsive hair pulling such as trichotillomania
Hypothyroidism

Iron deficiency
Alopecia areata
Telogen effluvium resulting from physical or psychological stress
Hereditary disorder of the hair shaft or genodermatoses
Secondary syphillis can cause "moth eaten hairloss"
Discoid lupus erythematosus or chronic cutanous lupus erythematosus
Lichenplanopilaris
Pseudopelade of Brocq
Tufted folliculitis
Dissecting cellulitis
Alopecia mucinosa
Keratosis follicularis spinulosa decalvans
Androgenetic alopecia (Male pattern baldness)
Fungal infection such as "black dot" tinea or tinea capitis
Chemical breakage such as over processing, or frequent use of chemical relaxer
Heat damage as from repeated hot comb use
Chronic exposure to traction on hair shaft such as Traction alopecia
Compulsive hair pulling such as trichotillomania
Hypothyroidism
Testosterone booster tablets.

In s Adverse effect from certain drugs such as chemotherapy Alopecia or hair loss is the medical description of the loss of hair from the head or body, sometimes to the extent of baldness. Unlike the common aesthetic depilation of body hair, alopecia tends to be involuntary and unwelcome, e.g., androgenic alopecia. However, it may also be caused by a psychological compulsion to pull out one's own hair (trichotillomania) or the unforeseen consequences of voluntary hairstyling routines mechanical "traction alopecia" from excessively tight ponytails or braids, or burns to the scalp from caustic hair relaxer solutions or hot hair irons.

ome cases, alopecia is an indication of an underlying medical concern, such as iron deficiency.

When hair loss occurs in only one section, it is known as alopecia areata. Alopecia universalis is when complete hair loss on the body occurs, similar to how hair loss associated with chemotherapy sometimes affects the entire bod.

Epidemiology

The condition affects 0.1%–0.2% of humans, occurring in both males and females, though far more females than males.

Alopecia areata occurs in people who are apparently healthy and have no skin disorder.Initial presentation most commonly occurs in the late teenage years, early childhood, or young adulthood, but can happen with people of all ages.

Types

The most common type of alopecia areata involves hair loss in one or more round spots on the scalp.

Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata.
Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head.
Alopecia areata multilocularis refers to multiple areas of hair loss.
The disease may be limited only to the beard, in which case it is called Alopecia areata barbae.
If the patient loses all the hair on his/her scalp, the disease is then called Alopecia areata totalis.
If all body hair, including pubic hair, is lost, the diagnosis then becomes Alopecia areata universalis.

Alopecia areata

It is noncommunicable, or not contagious. It occurs more frequently in people who have affected family members, suggesting that heredity may be a factor,and at least one of the genes involved has been mapped to chromosome 8p21–22.In addition, it is slightly more likely to occur in people who have relatives with autoimmune diseases.

The condition is thought to be an autoimmune disorder in which the body attacks its own hair follicles and suppresses or stops hair growth.There is evidence that T cell lymphocytes cluster around these follicles, causing inflammation and subsequent hair loss. An unknown environmental trigger such as emotional stress or a pathogen is thought to combine with hereditary factors to cause the condition. There are a few recorded cases of babies being born with congenital alopecia areata; however, these are not cases of autoimmune disease because an infant is born without a fully developed immune system

First symptoms are small, soft, bald patches which can take just about any shape but are most usually round. It most often affects the scalp and beard but may occur on any hair-bearing part of the body.There may be different skin areas with hair loss and regrowth in the same body at the same time. It may also go into remission for a time, or permanently.

The area of hair loss may tingle or be very slightly painful. The hair tends to fall out over a short period of time, with the loss commonly occurring more on one side of the scalp than the other.

Another presentation of the condition are exclamation point hairs. Exclamation point hairs are hairs that become narrower along the length of the strand closer to the base, producing a characteristic "exclamation point" appearance.

One diagnostic technique applied by medical professionals is to gently tug at a handful of hair along the edge of a patch with less strength than would be required to pull out healthy hair. In healthy hair, no hair should fall out or ripped hair should be distributed evenly across the tugged portion of the scalp. In cases of alopecia areata hair will tend to pull out easier along the edge of the patch where the follicles are already being attacked by the body's immune system than away from the patch where they are still healthy. Professionals usually remind patients that the hair that is pulled out would eventually fall naturally. The test is conducted only once to identify the condition and rule out a simple localized hair loss condition.

Subterms for alopecia areata

ALOPECIA AREATA (AA) - The most commonly used term and covers all forms of the disease.
ALOPECIA PARTIALIS - The name given to specify patchy hair loss. Not often used as "alopecia areata" suffices
ALOPECIA TOTALIS (AT) - The name given to specify alopecia areata where all scalp hair is lost, but other body hair remains.
ALOPECIA UNIVERSALIS (AU) - The name given to specify alopecia areata where all scalp and body hair is lost.
ALOPECIA AREATA BARBAE - The term for an alopecia areata lesion found in the region of beard hair.
ALOPECIA AREATA OPHIASIS - The term used for an alopecia areata lesion limited to extension along the scalp margin (Occipital and temporal region - the strip of hair running from one ear around the back of the head to the other ear). Ophiasis comes from the latin "snake" due to the winding, snaking pattern the hair loss has over the back of the head. The term was originally used by Cornelius Celsus in 30AD
ALOPECIA AREATA DIFFUSA - A term occasionally used for an alopecia areata lesion of general thinning of hair on the scalp. It is usually simply called diffuse alopecia areata
RETICULAR ALOPECIA AREATA - The term used for the presence of numerous small, well defined patches of hair loss
SISAIPHO ALOPECIA AREATA - This is a new term so far only used by one clinical group in Seville, Spain (Munoz 1996). It is defined as entire loss of scalp hair except for a narrow ring of hair around the periphery.
TRIANGULAR ALOPECIA AREATA - A very rare form of alopecia areata where the hair loss lesion presents in a triangular shape
PERINAEVOID ALOPECIA AREATA - A very rare form of alopecia areata where hair is lost around nevi (moles or other skin growths)

Diagnosis

Treatment

About 50% of patients' hair will regrow in one year without any treatment. If the affected region is small, it is reasonable to observe the progression of the illness as the problem often spontaneously regresses and the hair grows back. In 90% of cases, the hair will, ultimately, grow back. In the other 10%, only some or no hair will regrow.

In cases where there is severe hair loss, there has been limited success treating alopecia areata with clobetasol or fluocinonide, steroid injections, or cream. Steroid injections are commonly used in sites where there are small areas of hair loss on the head or especially where eyebrow hair has been lost. Some other medications used are minoxidil, irritants (anthralin or topical coal tar), and topical immunotherapy cyclosporine, each of which are sometimes used in different combinations.

Oral corticosteroids decrease the hair loss, but only for the period during which they are taken, and these drugs have adverse side effects.

For small patches on the beard or head it is possible to suppress with topical tacrolimus ointments like Protopic. Symptoms may remain suppressed until aggravated by stress or other factors. Treatment with tacrolimus is recommended only for short periods of time due to adverse side effects.

Initial stages may be kept from increasing by applying topical corticosteroids. However, topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target.

In terms of adapting to the disease rather than treating in an effort to cure, there are also many options available. Wigs are often used by those with Alopecia, particularly Alopecia Totalis, in which hair is entirely lost from the scalp. Wigs are available at many levels of development and technology, including wigs with suction mechanisms to keep it firmly attached to the scalp. Most of the wigs available are so well made that it is impossible without close investigation to tell whether they are a person's actual hair, or a wig.

Prognosis

In most cases that begin with a small number of patches of hair loss, hair grows back after a few months to a year. In cases with a greater number of patches, hair can either grow back or progress to alopecia totalis or, in rare cases, universalis.

Effects of alopecia areata are mainly psychological (loss of self image due to hair loss). However, patients also tend to have a slightly higher incidence of asthma, allergies, atopic dermal ailments, and even hypothyroidism. Loss of hair also means that the scalp burns more easily in the sun. Loss of nasal hair increases severity of hay fever and similar allergic conditions. Patients may also have aberrant nail formation because keratin forms both hair and nails.

Episodes of alopecia areata before puberty predispose chronic recurrence of the condition. Pitting of the fingernails can hint at a more severe or prolonged course.

Hair may grow back and then fall out again later

Psychosocial issues

Alopecia can certainly be the cause of psychological stress. Because hair loss can lead to significant appearance changes, individuals may experience social phobia, anxiety, and depression. Some psychologists have even gone as far as to describe the feelings of loss and depression felt at the onset of the disease as being similar to those felt by people afflicted with terminal illness. Sometimes people with alopecia may find it difficult to meet or date others due to social phobia but places like make it easier for people to meet others alike and also people who do not mind dating alopecia singles. In severe cases where the chance of hair regrowth is slim, individuals need to adapt to the condition, rather than look for a cure. There is currently little provision for psychological treatment for people afflicted with alopecia.

Alopecia totalis

Alopecia totalis is the loss of all head hair. Its causes are unclear, but it is an autoimmune disorder. Stress is sometimes thought to be a contributor to the hair loss caused by alopecia, however many people leading relatively stress-free lives have experienced the symptoms.

Alopecia Totalis is one of a group of three main conditions. Those three are Alopecia Areata, Alopecia Universalis, and of course Alopecia Totalis (AT). AT is an auto-immune disorder which results in the total loss of hair, but only on the scalp. It is somewhat of an intermediary condition between Alopecia Areata which is patchy scalp hair loss, and Alopecia Universalis which extends to total body hair loss. AT usually appears in two types: One being a fairly sudden and complete loss of all head hair. The other being a slower form which originates as Alopecia Areata (patchy loss) and advances to complete scalp hair loss. In this sense it is sometimes tied to Alopecia Areata but not all the time.

Most sufferers are children and young adults under the age of 40, though it can affect people of all ages. It can also affect the the nails, giving them a ridged, pitted or brittle appearance. According to statistics, 2% of men and 1% of women in western society suffer from some form of Alopecia Areata. About 2% of those have Totalis or Universalis. This means that about 1 in every 125,000 men and 1 in every 250,000 women have Alopecia Totalis or Universalis.

Causes Alopecia Totalis

This condition comes about as a result of an autoimmune disorder which causes your immune system to attack your hair follicles. In most cases there is small chance of hair recovery, however there have been cases of complete restoration as well. Consider it a genetic auto immune condition that has an unknown trigger, and which can sometimes be "un-triggered" for unknown reasons. They are still researching why hair follicles are the target of the autoimmune activities.

Treatments for Alopecia Totalis

The main treatment for Alopecia Totalis are therapies which focus on immunomodulation, such as glucocorticoid injections, anthralin, or glucocorticoids taken orally. We have heard reports from some that years of steroid therapy can put the condition into remission. Years of steroid therapy is not always enjoyable however, as there are side effects. It is important to comment that Rogaine (Minoxidil) is not effective for those with Alopecia Totalis. Some treatments which have been considered include Methotrexate, a treatment for autoimmune disorders, and corticosteroids have been proposed as treatments.

Several genes have been studied and quite a bit of research has focused on the human leukocyte antigen. Two studies demonstrated that human leukocyte antigen DQ3 (DQB1*03) was found in more than 80% of patients with Alopecia Areata, which suggests that it can be a marker for general susceptibility to Alopecia Areata. The studies also found that HLA DQ7 (DQB1*0301) and human leukocyte antigen DR4 (DRB1*0401) were found quite a bit more often in patients with Alopecia Totalis (AT) and Alopecia Universalis (AU).

Alopecia Universalis

The most advanced form in a series of conditions all related to the same disease, alopecia universalis is characterized by total a loss of body hair.

A member of the group of hair loss conditions called alopecia areata, the only difference between alopecia universalis and its variants is the extent of hair loss.

Normally, sufferers are otherwise healthy, but are more likely than the general population to experience thyroid disease and vitiligo (patchy loss of skin color). Those with vitiligo may eventually develop AU over time. Many individuals with Alopecia Universalis are born with some hair but begin losing it very quickly. The disorder is inherited as an autosomal recessive trait. It is caused by a mutation in a gene dubbed HR in chromosome band 8p21.2 -- the human version of the gene that is responsible for hairlessness in mice.

Is the "hairless" gene only found in people with alopecia universalis? Most likely. Based on the known research, we can safely assume that only individuals with this rare and severe form of alopecia areata carry the gene. Unfortunately, there have not been enough studies to verify that this is true of all those afflicted. Aside from genetic tendencies, the contributing causes of Alopecia Universalis are not known.

As lack of body hair leaves areas like the scalp, eyes and nasal cavity particularly vulnerable, it is important that those with Alopecia Universalis take extra care to protect themselves from the sun, bacteria and other potentially harmful elements.

According to the National Alopecia Areata Foundation, fingernails and toenails can also be affected. Symptoms in the nails can range from pinprick-like indentations to severe distortion of the entire nail. Alopecia Universalis may be acute and short-lived or remain permanently. Regrowth is always a possibility, even for those with 100% hair loss over many years. However, it is not possible to predict when regrowth will occur.

Treatment

There is no standard treatment for alopecia universalis. Many treatments have been explored, including immunomodulatory agents such as imiquimod.

Alopecia Universalis may be acute and short-lived or remain permanently. Regrowth is always a possibility, even for those with 100% hair loss over many years. However, it is not possible to predict when regrowth will occur.

Noncicatricial alopecia

Noncicatricial alopecia is a nonscarring hair loss.

Causes of noncicatricial alopecia include

Alopecia areata
Anagen effluvium
Androgenetic alopecia
Dermatopathia pigmentosa reticularis
Telogen effluvium
Trichotillomania (Trichotillosis)

Cicatricial alopecia

Cicatricial alopecia presents clinically with the effacement/scarring of follicular orifices, always in a patchy or focal distribution.

Acne necrotica
Alopecia mucinosa
Atrichia with papular lesions
Central centrifugal cicatricial alopecia
Erosive pustular dermatitis of the scalp (Erosive pustular dermatosis of the scalp)
Folliculitis decalvans
Hot comb alopecia
Keratosis pilaris atropicans
Lichen planopilaris
Lupus erythematosus
Perifolliculitis capitis abscedens et suffodiens (Dissecting cellulitis of the scalp, Dissecting folliculitis, Perifolliculitis capitis abscedens et suffodiens of Hoffman)
Pressure alopecia
Pseudopelade of Brocq (Alopecia cicatrisata)
Sarcoidosis
Traction alopecia
Tufted folliculitis
Tumor alopecia

Baldness

Baldness involves the state of lacking hair where it often grows, especially on the head. The most common form of baldness is a progressive hair thinning condition called androgenic alopecia or "male pattern baldness" that occurs in adult male humans and other species. The amount and patterns of baldness can vary greatly; it ranges from male and female pattern alopecia (androgenic alopecia, also called androgenetic alopecia or alopecia androgenetica), alopecia areata, which involves the loss of some of the hair from the head, and alopecia totalis, which involves the loss of all head hair, to the most extreme form, alopecia universalis, which involves the loss of all hair from the head and the body.

Background, cause and incidence

Incidence of pattern baldness varies from population to population based on genetic background, Environmental factors do not seem to affect this type of baldness greatly. One large scale study in Maryborough, Victoria, Australia showed the prevalence of mid-frontal hair loss increases with age and affects 57% of women and 73.5% of men aged 80 and over.

According to Medem Medical Library's website, male pattern baldness affects roughly 40 million men in the United States. Approximately 25 percent of men begin balding by age 30; two-thirds begin balding by age 60. There is a 4 in 7 chance of getting the baldness gene.

Male pattern is characterized by hair receding from the lateral sides of the forehead, known as "receding hairline". Receding hairlines are usually seen in males above the ages of 20 but can be seen as early as late teens as well.

An additional bald patch may develop on top The trigger for this type of baldness (called androgenetic alopecia) is DHT, a powerful sex hormone, body, and facial hair growth promoter that can adversely affect the prostate as well as the hair located on the headmechanism by which DHT accomplishes this is not yet understood.

In genetically-prone scalps, DHT initiates a process of follicular miniaturization. Through the process of follicular miniaturization, hair shaft width is progressively decreased until scalp hair resembles fragile vellus hair or "peach fuzz" or else becomes non-existent. Onset of hair loss sometimes begins as early as end of puberty, and is mostly genetically determined. Male pattern baldness is classified on the Hamilton-Norwood scale I-VII.

It was previously believed that baldness was inherited from the maternal grandfather. While there is some basis for this belief, both parents contribute to their offspring's likelihood of hair loss. Most likely, inheritance is technically "autosomal dominant with mixed penetrance

There are several other kinds of baldness:

Traction alopecia is most commonly found in people with ponytails or cornrows who pull on their hair with excessive force.
Trichotillomania is the loss of hair caused by compulsive pulling and bending of the hairs. It tends to occur more in children than in adults. In this condition the hairs are not absent from the scalp but are broken. Where they break near the scalp they cause typical, short, "exclamation mark" hairs.
Traumas such as chemotherapy, childbirth, major surgery, poisoning, and severe stress may cause a hair loss condition known as telogen effluvium.
Worrisome hair loss often follows childbirth without causing actual baldness. In this situation, the hair is actually thicker during pregnancy due to increased circulating oestrogens. After the baby is born, the oestrogen levels fall back to normal pre-pregnancy levels and the additional hair foliage drops out. A similar situation occurs in women taking the fertility-stimulating drug clomiphene.
Iron deficiency is a common cause of thinning of the hair, though frank baldness is not usually seen.
Radiation to the scalp, as happens when radiotherapy is applied to the head for the treatment of certain cancers there, can cause baldness of the irradiated areas.
Some mycotic infections can cause massive hair loss.

Alopecia areata is an autoimmune disorder also known as "spot baldness" that can result in hair loss ranging from just one location (Alopecia areata monolocularis) to every hair on the entire body (Alopecia areata universalis).
Localized or diffuse hair loss may also occur in cicatricial alopecia (lupus erythematosus, lichen plano pilaris, folliculitis decalvans, central centrifugal cicatricial alopecia, postmenopausal frontal fibrosing alopecia, etc.). Tumours and skin outgrowths also induce localized baldness (sebaceous nevus, basal cell carcinoma, squamous cell carcinoma).
Hypothyroidism can cause hair loss, typically frontal, and is particularly associated with thinning of the outer third of the eyebrows (syphilis also can cause loss of the outer third of the eyebrows)
Hyperthyroidism can also cause hair loss, which is parietal rather than frontal.
Temporary loss of hair can occur in areas where sebaceous cysts are present for considerable duration; normally one to several weeks in length.

Pathophysiology

This genetically determined disorder is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients have a reduction in the terminal-to-vellus hair ratio, normally at least 2:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical distribution of hair loss.

Preventing and reversing hair loss

Treatments for the various forms of alopecia have limited success. Some hair loss sufferers make use of clinically proven treatments such as finasteride and topically applied minoxidil (in solution) in an attempt to prevent further loss and regrow hair. As a general rule, it is easier to maintain remaining hair than it is to regrow; however, the treatments mentioned may prevent hair loss from Androgenetic alopecia, and there are new technologies in cosmetic transplant surgery and hair replacement systems that can be completely undetectable.

In the USA, there are only two drug-based treatments that have been approved by the U.S. Food and Drug Administration (FDA) and one product that has been cleared by the FDA for the treatment of androgenetic alopecia, otherwise known as male or female pattern hair loss. The two FDA approved treatments are finasteride (marketed for hair loss as Propecia) and minoxidil.

Stress reduction

Stress reduction can be helpful in slowing hair loss.

Immunosuppressants

Immunosuppressants applied to the scalp have been shown to temporarily reverse alopecia areata, though the side effects of some of these drugs make such therapy questionable.

Saw palmetto

Saw palmetto extract has been demonstrated to inhibit both isoforms of alpha-5-reductase and does not interfere with the cellular capacity to secrete PSA

Polygonum multiflorum

Polygonum multiflorum is a traditional Chinese cure for hair loss. P. multiflorum contains stilbene glycosides similar to resveratrol.

Other factors to be considered

Alopecia of senescence
Alopecia associated with virilizing disorders of women, in whom it may be seen in association with hirsutism and menstrual problems
Anagen effluvium after exposure to toxic chemicals, including chemotherapeutic agents
Alopecia associated with hypothyroidism or hyperthyroidism
Telogen effluvium: This condition may accelerate androgenetic alopecia, and causes, such as iron deficiency and papulosquamous diseases of the scalp, must be considered.
Hypertension and/or smoking: A strong association of androgenetic alopecia with hypertension was noted in a study of 250 white men aged 35-65 years. In this French study, a definite familial tendency to androgenetic alopecia was also described, but no association was noted with diabetes mellitus, hyperlipidemia, or smoking. However, a study of 740 Taiwanese men aged 40-91 years indicated an association between androgenetic alopecia and smoking. Smoking status, current amount of cigarette smoking, and smoking intensity were statistically significant in this report.

Alopecia Mucinosa

Alopecia mucinosa, often referred to as follicular mucinosis, was first reported by Pinkus in 1957.The dermatologic eruptions consist of follicular papules and/or indurated plaques that demonstrate distinct histologic changes in the hair follicles that lead to hair loss. The accumulation of mucinous material in the damaged hair follicles and sebaceous glands creates an inflammatory condition and subsequent degenerative process. The face, the neck, and the scalp are the most frequently affected sites, although lesions may appear on any part of the body.

Pathophysiology

Alopecia mucinosa is a disease process defined histopathologically by mucin deposition in hair follicles and sebaceous glands, which undergo epithelial reticular degeneration. The exact pathogenesis is unknown, although the role of circulating immune complexes and cell-mediated immunity has been considered. The 3 clinical variants of the disease consist of a primary acute disorder of young persons, a primary chronic disorder of older persons, and a secondary disorder associated with benign or malignant disease.

The primary disorder of young persons consists of focal cutaneous lesions with limited progression. Lesions are typically limited to the head, the neck, and the shoulders (see Media File 1). Most lesions spontaneously resolve between 2 months and 2 years. Pediatric cases comprise most of this type of alopecia mucinosa, with the remainder of patients being younger than 40 years. Neonatal follicular mucinosis has also been reported.

Primary chronic alopecia mucinosa of older persons affects people older than 40 years. Lesions have a widespread distribution, and they may persist or recur indefinitely. No associated disorders are identified.

The secondary alopecia mucinosa may be associated with either benign disease or malignant disease. These patients are usually aged 40-70 years, and the lesions are widespread and numerous.

Alopecia mucinosa can occur secondary to benign disease including the inflammatory conditions lupus erythematosus, lichen simplex chronicus, and angiolymphoid hyperplasia. Secondary alopecia mucinosa is also associated with malignant disease, including mycosis fungoides, Kaposi sarcoma, and Hodgkin disease; mycosis fungoides is by far the most common association.

In most patients who exhibit both alopecia mucinosa and mycosis fungoides, these conditions appear to develop concomitantly; however, the concern exists that individuals exhibiting only alopecia mucinosa may also be at risk for subsequent development of lymphoma.

Drug-induced alopecia mucinosa has been associated with the use of adalimumaand imatinib.The clinical manifestations of alopecia mucinosa are grouped follicular papules and alopecia.

Nodules, plaques, and patches of follicular papules may exist.
Occasionally, mucinous material can be expressed from active lesions, and erythema and scaling are usually present.
The face and the scalp are the most common sites of involvement.
The alopecia that develops on hair-bearing skin is of the nonscarring type
Usually, the alopecia is reversible unless follicular destruction has occurred due to excess mucin in the outer root sheath and sebaceous glands. In patients with permanent alopecia, the whole follicle degenerates, and the cystic cavity becomes blocked with keratinous debris. When the plugs persist, they are obvious features on healed, hairless patches of alopecia mucinosa.

Causes

Alopecia mucinosa represents various stages of follicular damage leading to hair loss. The reactive process is of unknown etiology. The role of circulating immune complexes and cell-mediated immunity has been considered.

Histologic Findings

In pattern alopecia, hairs are miniaturized. In evolving-pattern alopecia, the diameter of hair shafts varies. Fibrous tract remnants (so-called streamers) can be found below miniaturized follicles. Although androgenetic alopecia is considered a noninflammatory form of hair loss, at times, a superficial, perifollicular, inflammatory infiltrate is noted. A mildly increased telogen-to-anagen ratio is often observed.

INVESTIGATIONS

Investigations are unnecessary in most cases of alopecia areata. When the diagnosis is in doubt appropriate tests may include:

Fungal culture
Skin biopsy
Serology for lupus erythematosus
Serology for syphilis

The increased frequency of autoimmune disease in patients with alopecia areata is probably insufficient to justify routine screening

Differential diagnosis

· Penile Squamous Cell Carcinoma (Dermatology)tumors present a difficult diagnostic and therapeutic issue, mainly because of their psychological implications. The diagnosis may be delayed because many ...

· Lymphomas of the Head and Neck (Otolaryngology and Facial Plastic Surgery)Otolaryngologists are frequently involved in the diagnosis of lymphoma. A quarter of all extranodal lymphomas occur in the head and neck, and 8% of ...

· Dermatologic Manifestations of Cardiac Disease (Dermatology)Cardiovascular disorders and therapies are often associated with a variety of dermatologic manifestations. Frequently, these cutaneous signs can be used in ...

· Leukemia Cutis (Dermatology)Leukemia cutis is the infiltration of neoplastic leukocytes or their precursors into the epidermis, the dermis, or the subcutis, resulting in clinically ... · Lupus Erythematosus, Bullous (Dermatology)that occurs in patients with systemic lupus erythematosus (SLE).1 The diagnosis of bullous systemic lupus erythematosus requires the following ...

· Anxiety Disorder (Pediatrics: Developmental and Behavioral)an anxiety disorder characterized by the persistent and excessive pulling of one's own hair, resulting in noticeable hair loss. In 1889, Hallopeau, a ...

· Pyoderma Gangrenosum (Dermatology)Pyoderma gangrenosum (PG) is an uncommon ulcerative cutaneous condition of uncertain etiology. Pyoderma gangrenosum was first described in 1930. It is ...

· Polycystic Ovarian Syndrome (Pediatrics: General Medicine)In 1935, Stein and Leventhal first described the association of polycystic ovaries, amenorrhea, hirsutism, and obesity.1 However, the key features ...

· Metastatic Carcinoma of the Skin (Dermatology)are very important to recognize. Cutaneous metastasis may herald the diagnosis of internal malignancy. Early recognition can lead to accurate and ...

· Ulerythema (Dermatology)keratotic facial papules that may result in scars, atrophy, and alopecia. This disorder has been described in association with other congenital ...

· Acrodermatitis Enteropathica (Dermatology)recessive disorder characterized by periorificial and acral dermatitis, alopecia, and diarrhea. Pathophysiology The genetic mutation of SLC39A4 on 8q24.3 ...

· Breast Cancer (Oncology)frequently diagnosed life-threatening cancer in women and the leading cause of cancer death among women. Over the last two decades, breast cancer research ...

· Paraneoplastic Diseases (Dermatology)A wide range of cutaneous signs may be related to internal malignancy. Cancer may manifest in the skin as metastasis (eg, leukemia cutis, cutaneous T-cell ...

MIGRAINE

2010-01-06T08:29:00.000-08:00

MIGRAINE

Definition

Migraine is a neurological syndrome characterized by altered bodily perceptions, headaches, and nausea. Physiologically, the migraine headache is a neurological condition more common to women than to men. Etymologically, the French word migraine derives from the Old English megrim (severe headache) and the Greek hemicrania (half skull). The latter term was in turn simply a translation of an ancient Egyptian name for migraine (literally "half head")

The typical migraine headache is unilateral and pulsating, lasting from 4 to 72 hours symptoms include nausea, vomiting, photophobia (increased sensitivity to bright light), and hyperacusis (increased sensitivity to noise); approximately one third of people who suffer migraine headache perceive an — unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.

Initial treatment is with analgesics for the head-ache, an anti-emetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the accepted theory is a disorder of the control system, as PET scan has demonstrated the aura coincides with diffusion of cortical depression consequent to increased blood flow (up to 300% greater than baseline). There are migraine headache variants, some originate in the brainstem (featuring intercellular transport dysfunction of calcium and potassium ions) and some are genetically disposed. Studies of twins indicate a 60 to 65 percent genetic influence upon their developing propensity to migraine headache. Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy.

Classification

The International Headache Society (IHS) classifies migraine headache

The IHS defines the intensity of pain with a verbal, four-point scale:

Number	Name	Annotations
0	no pain
1	mild pain	does not interfere with usual activities
2	moderate pain	inhibits, but does not wholly prevent usual activities
3	severe pain	prevents all activities

Migraine without aura

The common form of migraine headache; the patient primarily suffers migraine without aura, and might also suffer migraine with aura. The International Classification of Headache Disordersdefinition is:

Description: Recurrent headache disorder manifesting in attacks lasting 4–72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and photophobia. Diagnostic criteria:

A. At least five attacks fulfilling criteria B-D

B. Headache attacks lasting 4-72 hours [when untreated]

C. Headache has at least two of the following characteristics:

1. Unilateral location

2. Pulsating quality

3. Moderate or severe pain intensity

4. Aggravation by or causing avoidance of routine physical activity

D. During the headache at least one of the following:

1. Nausea and/or vomiting

2. Photophobia and photophobia

E. Not attributed to another disorder

Migraine with Aura

The second-most common form of migraine headache: the patient primarily suffers migraine with aura, and might also suffer migraine without aura. The International Classification of Headache Disorders definition is:

Description: Recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes. Headache with the features of "migraine without aura" usually follows the aura symptoms. Less commonly, headache lacks migrainous feature or is completely absent [i.e., the aura may occur without any subsequent headache].

Diagnostic criteria:

A. At least two attacks fulfilling criterion B

B. Migraine aura fulfilling criteria

C. Not attributed to another disorder. ... [Criteria for "Typical aura":]
Aura consisting of at least one of the following, but no motor weakness:

1. Fully reversible visual symptoms including positive features (e.g. flickering lights, spots or lines) and/or negative features (i.e., loss of vision)

2. Fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (i.e., numbness)

3. Fully reversible dysphasic speech disturbance
[Aura also has] at least two of the following:

1. Homonymous visual symptoms [i.e., affecting just one side of the field of vision] and/or unilateral sensory symptoms [i.e., affecting just one side of the body]

2. At least one aura symptom develops gradually over [at least] 5 minutes and/or different aura symptoms occur [one after the other] over [at least] 5 minutes

3. Each symptom lasts [from] 5 [to] 60 minutes ...

Other potential aura criteria:

· Fully reversible motor weakness...

· Each aura symptom lasts [from] 5 minutes [to] 24 hours...

· [In the case of a "Basilar-type" migraine], Dysarthria [difficulty speaking], vertigo [dizziness], tinnitus [ringing in the ears], [and other symptoms].

Basilar type Migraine

Basilar type migraine (BTM) previously basilar artery migraine [BAM] and basilar migraine [BM]) is an uncommon, complicated migraine with symptoms caused by brainstem dysfunction. Serious episodes of BTM can lead to stroke, coma, and death. Using trip tans and other vasoconstrictors as abortive treatments for BTM is contraindicated. Abortive treatments for BTM address vasodilatation and restoration of normal blood flow to the vertebrobasilar territory to restore normal brainstem function.

Familial hemiplegics migraine

Familial hemiplegics migraine (FHM) is migraine with a possible polygenetic cause. An FHM episode might last 4–72 hours ^[ and appear caused by ion channel mutations; FHM is in three types. The patient experiences typical migraine headache either preceded or accompanied with unilateral, reversible limb weakness and sensory and speech difficulties. There also exists the "sporadic hemiplegics migraine" (SHM) a non-familial form. Affecting a differential diagnosis, between basilar migraine and hemiplegics migraine, is difficult; often, the decisive symptom is either motor weakness or unilateral paralysis that occurs in FHM and SHM; basilar migraine can present tingling and numbness, true motor weakness and paralysis occur only in hemiplegics migraine.

Abdominal migraine

Abdominal migraine is a recurrent disorder of unknown origin, principally affecting children; episodes feature nausea, vomiting, and moderate-to-severe central, abdominal pain (ca. 1–72 hrs); the child is well between episodes. Formal diagnosis requires at least five (5) episodes (unattributable to another cause) and fulfillment of these criteria:

1. Episodes last 4–72 hours, untreated

2. Pain must feature ALL these characteristics:

o Location in the mid-abdomen, around the umbilicus; or poorly localized

o Dull pain; 'just sore' quality

o Moderate-to-severe intensity

3. An episode must feature at least two of these symptoms:

o Loss of appetite

o Nausea

o Vomiting

o Pallor

o Moody

Most children suffering abdominal migraine will develop propensity to migraine headache in adult life; the two propensities might co-exist during the child's adolescence.

Treating an abdominal migraine can often be difficult; medications used to treat other forms of migraines are usually employed. These include Elavil (75-150 mg), Wellbutrin SR (400 mg), and Topamax (200-400 mg). In some cases, the abdominal migraine is a symptom linked to cyclic vomiting syndrome there may be a history of migraines in the family of the sufferer.

Acephalgic Migraine

Acephalgic migraine is a neurological syndrome. It is a variant of migraine in which the patient may experience aura symptoms such as scintillating scotoma, nausea, photophobia, hemi paresis and other migraine symptoms but does not experience headache. Encephalic migraine is also referred to as amigrainous migraine, ocular migraine, or optical migraine.

Sufferers of encephalic migraine are more likely than the general population to develop classical migraine with headache.

The prevention and treatment of encephalic migraine is broadly the same as for classical migraine. However, because of the absence of "headache", diagnosis of encephalic migraine is apt to be significantly delayed and the risk of misdiagnosis significantly increased.

Visual snow might be a form of encephalic migraine.

If symptoms are primarily visual, it may be necessary to consult an ophthalmologist or optometrist to rule out potential eye disease before considering this diagnosis.

Menstrual migraine

Menstrual migraine is distinct from other migraines. Approximately 21 million women in the US suffer from migraines, and about 60% of them suffer from menstrual migraines. There are two types of menstrual migraine – Menstrually Related Migraine (MRM) and Pure Menstrual Migraine (PMM)

· MRM is a headache of moderate-to-severe pain intensity that happens around the time of a woman’s period and at other times of the month as well.

· PMM is similar in every respect but only occurs around the time of a woman’s period. The exact causes of menstrual migraine are uncertain but evidence suggests there may be a link between menstruation and migraine tdue to the drop in estrogen levels that normally occurs right before the period starts. Menstrual migraine has been reported to be more likely to occur during a five-day window, from two days before to two days after menstruation. Signs and symptoms

Signs and Symptoms

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same migraineur:

1. The prodrome, which occurs hours or days before the headache.

2. The aura, which immediately precedes the headache

3. The pain phase, also known as headache phase.

Diagnosis

Migraines are under diagnosed and misdiagnosed The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

· 5 or more attacks

· 4 hours to 3 days in duration

· 2 or more of - unilateral location, pulsating quality, moderate to severe pain, aggravation by or avoidance of routine physical activity

· 1 or more accompanying symptoms - nausea and/or vomiting, photophobia, phonophobia

For migraine with aura, only two attacks are required to justify the diagnosis.

The mnemonic pounding (Pulsating, duration of 4–72 hours, Unilateral, Nausea, and Disabling) can help diagnose migraine. If 4 of the 5 criteria are met, then the positive likelihood ratio for diagnosing migraine is 24. The presence of either disability, nausea or sensitivity, can diagnose migraine with:^[34]

· sensitivity of 81%

· specificity of 75%

Migraine should be differentiated from other causes of headaches such as cluster headaches. These are extremely painful, unilateral headaches of a piercing quality. The duration of the common attack is 15 minutes to three hours. Onset of an attack is rapid, and most often without the preliminary signs that are characteristic of a migraine.

Prodrome Phase

Prodromal symptoms occur in 40–60% of migraineurs (migraine sufferers). This phase may consist of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g. chocolate), stiff muscles (especially in the neck), constipation or diarrhea, increased urination, and other visceral symptoms. These symptoms usually precede the headache phase of the migraine attack by several hours or days, and experience teaches the patient or observant family how to detect that a migraine attack is near.

Aura Phase

For the 20–30% of individuals who suffer migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely. Symptoms of migraine aura can be visual, sensory, or motor in nature

Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white and/or black or rarely of multicolored lights (photopia) or formations of dazzling zigzag lines (scintillating scotoma; often arranged like the battlements of a castle, hence the alternative terms "fortification spectra" or "teichopsia Some patients complain of blurred or shimmering or cloudy vision, as though they were looking through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. The somatosensory aura of migraine consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the nose-mouth area on the same side. Paresthesia migrates up the arm and then extend to involve the face, lips and tongue.

Other symptoms of the aura phase can include auditory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Pain phase

The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity. Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides, and usually lasts between 4 and 72 hours in adults and 1 and 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from one to three headaches a month. The head pain varies greatly in intensity.

The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, while vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, polyuria, pallor or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist.Postdrome phase

Postdrome phase

The patient may feel tired, have head pain, cognitive difficulties, "hungover", gastrointestinal symptoms, mood changes and weakness. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness. For some patients, a 5 to 6 hour nap may reduce the pain, but slight headaches may still occur when standing or sitting quickly. Normally these symptoms go away after a good night's rest

Migraines are under diagnosed and misdiagnosed. The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

· 5 or more attacks

· 4 hours to 3 days in duration

· 2 or more of - unilateral location, pulsating quality, moderate to severe pain, aggravation by or avoidance of routine physical activity

· 1 or more accompanying symptoms - nausea and/or vomiting, photophobia, phonophobia

Pathophysiology

Migraines were once thought to be initiated exclusively by problems with blood vessels. The vascular theory of migraines is now considered secondary to brain dysfunction and claimed to have been discredited by others. Trigger points can be at least part of the cause, and perpetuate most kinds of headaches. The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.

Depolarization Theory

A phenomenon known as cortical spreading depression can cause migraines In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.

This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.

Vascular Theory

Migraines can begin when blood vessels in the brain contract and expand inappropriately. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area.

When the constriction stops and the blood vessels dilate, they become too wide. The once solid walls of the blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain.

Rotonin is a type of neurotransmitter, or "communication chemical" which passes messages between nerve cells. It helps to control mood, pain sensation, sexual behaviors, sleep, as well as dilation and constriction of the blood vessels among other things. Low serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. Trip tans activate serotonin receptors to stop a migraine attack.

Neural theory

When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. Substance P is one of the substances released with first irritation. Pain then increases because substance P aids in sending pain signals to the brain.

Unifying theory

Both vascular and neural influences cause migraines.

1. stress triggers changes in the brain

2. these changes cause serotonin to be released

3. blood vessels constrict

4. chemicals including substance P irritate nerves and blood vessels causing pain

Migraine is an extremely common condition which will affect 12–28% of people at some point in their lives however this figure — the lifetime prevalence — does not provide a very clear picture of how many patients there are with active migraine at any one time. Typically, therefore, the burden of migraine in a population is assessed by looking at the one-year prevalence — a figure that defines the number of patients who have had one or more attacks in the previous year. The third figure, which helps to clarify the picture, is the incidence — this relates to the number of first attacks occurring at any given age and helps understanding of how the disease grows and shrinks over time

Based on the results of a number of studies, one year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women. These figures vary substantially with age: approximately 4–5% of children aged fewer than 12 suffer from migraine, with little apparent difference between boys and girls. There is then a rapid growth in incidence amongst girls occurring after puberty, which continues throughout early adult life.^] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men After menopause, attacks in women tend to decline dramatically, so that in the over 70s there are approximately equal numbers of male and female sufferers, with prevalence returning to around 5%.At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1 Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds. There is a strong relationship between age, gender and type of migraine. Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low, but they do not fall outside the range of values seen in European and North American studies. The incidence of migraine is related to the incidence of epilepsy in families, with migraine twice as prevalent in family members of epilepsy sufferers, and more common in epilepsy sufferers themselves.

Triggers

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal. In the medical literature, these factors are known as 'precipitants.'

The Medline Plus Medical Encyclopedia, for example, offers the following list of migraine triggers:

Migraine attacks may be triggered by:

· Allergic reactions

· Bright lights, loud noises, and certain odors or perfumes

· Physical or emotional stress

· Changes in sleep patterns

· Smoking or exposure to smoke

· Skipping meals

· Alcohol

· Menstrual cycle fluctuations, birth control pills, hormone fluctuations during the menopause transition

· Tension headaches

· Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate (MSG) or nitrates (like bacon, hot dogs, and salami)

· Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.

Sometimes the migraine occurs with no apparent "cause". The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors and keeping a "headache diary" recording migraine incidents and diet to look for correlations in order to avoid trigger foods. It must be mentioned, that some trigger factors are quantitative in nature, i.e., a small block of dark chocolate may not cause a migraine, but half a slab of dark chocolate almost definitely will, in a susceptible person. In addition, being exposed to more than one trigger factor simultaneously will more likely cause a migraine, than a single trigger factor in isolation, e.g., drinking and eating various known dietary trigger factors on a hot, humid day, when feeling stressed and having had little sleep will probably result in a migraine in a susceptible person, but consuming a single trigger factor on a cool day, after a good night's rest with minimal environmental stress may mean that the sufferer will not develop a migraine after all. Migraines can be complex to avoid, but keeping an accurate migraine diary and making suitable lifestyle changes can have a very positive effect on the sufferer's quality of life. Some trigger factors are virtually impossible to avoid, e.g. the weather or emotions, but by limiting the avoidable trigger factors, the unavoidable ones may have less of an impact on the sufferer.

Food

Many migraine sufferers report reduced incidence of migraines due to identifying and avoiding their individual food triggers. However, more studies are needed.

Gluten

One food elimination that has proven to reduce or eliminate migraines in a percentage of patients is gluten. For those with (often undiagnosed) celiac disease or other forms of gluten sensitivity, migraines may be a symptom of gluten intolerance. One study found that migraine sufferers were ten times more likely than the general population to have celiac disease, and that a gluten-free diet eliminated or reduced migraines in these patients. Another study of 10 patients with a long history of chronic headaches that had recently worsened or were resistant to treatment found that all 10 patients were sensitive to gluten. MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Seven out of nine of these patients that went on a gluten-free diet stopped having headaches completely.

Aspartame

Some people may develop migraines from consuming aspartame. In a University of Parkinson's-Florida study, the incidence of migraine doubled for the majority of participants when they took aspartame, and their headaches lasted longer and were marked by increased signs of shakiness and diminished vision. Headaches are the most common side effect cited by those who consume aspartame-containing products.

MSG

In a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo.

Tyramine

The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers.

Weather

Several studies have found some migraines are triggered by changes in weather. One study noted 62% of the subjects thought weather was a factor but only 51% were sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.

2. Significant changes in weather

3. Changes in barometric pressure

Another study examined the effects of warm Chinook winds on migraines, with many patients reporting increased incidence of migraines immediately before and/or during the Chinook winds. The number of people reporting migrainous episodes during the Chinook winds was higher on high-wind Chinook days. The probable cause was thought to be an increase in positive ions in the air.

Other

One study found that for some migraineurs in India, washing hair in a bath was a migraine trigger. The triggering effect also had to do with how the hair was later dried.

Treatment

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and prophylactic pharmacological drugs. Patients who experience migraines often find that the recommended migraine treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all. Pharmological treatments are considered effective if they reduce the frequency or severity of migraine attacks by 50%.Children and adolescents are often first given drug treatment, but the value of diet modification should not be overlooked. The simple task of starting a diet journal to help modify the intake of trigger foods like hot dogs, chocolate, cheese and ice cream could help alleviate symptoms. For patients who have been diagnosed with recurring migraines, migraine abortive medications can be used to treat the attack, and may be more effective if taken early, losing effectiveness once the attack has begun. Treating the attack at the onset can often abort it before it becomes serious, and can reduce the near-term frequency of subsequent attacks

Paracetamol or non-steroidal anti-inflammatory drug (NSAIDs)

The first line of treatment is over-the-counter abortive medication.

· Regarding non-steroidal anti-inflammatory drugs, a randomized controlled trial found that naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan.

· Paracetamol, at a dose of 1000 mg, benefited over half of patients with mild or moderate migraines in a randomized controlled trial.

· Simple analgesics combined with caffeine may help.^] During a migraine attack, emptying of the stomach is slowed, resulting in nausea and a delay in absorbing medication. Caffeine has been shown to partially reverse this effect. Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. Food and Drug Administration as an Over The Counter Drug (OTC) treatment for migraine when compounded with aspirin and paracetamol

· Patients themselves often start off with paracetamol (known as acetaminophen in North America), aspirin, ibuprofen, or other simple analgesics that are useful for tension headaches. OTC drugs may provide some relief, although they are typically not effective for most sufferers.

Analgesics combined with antiemetics

Anti-emetics by mouth may help relieve symptoms of nausea and help prevent vomiting, which can diminish the effectiveness of orally taken analgesia. In addition some antiemetics such as metoclopramide are prokinetics and help gastric emptying which is often impaired during episodes of migraine. In the UK there are three combination antiemetic and analgesic preparations available: MigraMax (aspirin with metoclopramide), Migraleve (paracetamol/codeine for analgesia, with buclizine as the antiemetic) and paracetamol/metoclopramide). The earlier these drugs are taken in the attack, the better their effect.

Some patients find relief from taking other sedative antihistamines which have anti-nausea properties, such as Benadryl which in the US contains diphenhydramine

Serotonin agonists

Sumatriptan and related selective serotonin receptor agonists are excellent for severe migraines or those that do not respond to NSAIDsor other over-the-counter drugs Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Anti-depressants

In addition to SSRIs, anti-depressant drugs such as tricyclics have been long established as highly efficacious prophylactic treatments. Despite not being approved by the FDA for this purpose, these drugs are widely prescribed Other anti-depressant drugs, such as bupropion and venlafaxine, have also been shown to be clinically efficacious These drugs, however, may give rise to undesirable side effects, such as insomnia, sedation or sexual dysfunction. They do offer advantages for treating patients with coexistent depression.

Ergot alkaloids

Until the introduction of sumatriptan in 1991, ergot derivatives were the primary oral drugs available to abort a migraine once it is established.

Ergot drugs can be used either as a preventive or abortive therapy, though their relative expense and cumulative side effects suggest reserving them as an abortive rescue medicine. However, ergotamine tartrate tablets (usually with caffeine), though highly effective, and long lasting (unlike triptans), have fallen out of favour due to the problem of egotisms. Oral ergotamine tablet absorption is reliable unless the patient is nauseated. Anti-nausea administration is available by ergotamine suppository (or Ergostat sublingual tablets made until circa 1992). Ergot drugs themselves can be so nauseating it is advisable for the sufferer to have something at hand to counteract this effect when first using this drug. Ergotamine-caffeine 1/100 mg fixed ratio tablets (like Cafergot, Ercaf, etc.) are much less expensive per headache than triptans, and are commonly available in Asia. They are difficult to obtain in the USA. Ergotamine-caffeine can't be regularly used to abort evening or night onset migraines due to debilitating caffeine interference with sleep. Pure ergotamine tartrate is highly effective for evening-night migraines, but is rarely or never available in the USA. Dihydroergotamine (DHE), which must be injected or inhaled, can be as effective as ergotamine tartrate,

Other agents

If over-the-counter medications do not work, or if triptans are unaffordable, the next step for many doctors is to prescribe Fioricet or Fiorinal, which is a combination of butalbital (a barbiturate), paracetamol (in Fioricet) or acetylsalicylic acid (more commonly known as aspirin and present in Fiorinal), and caffeine. While the risk of addiction is low, butalbital can be habit-forming if used daily, and it can also lead to rebound headaches. Barbiturate-containing medications are not available in many European countries.

Amidrine, Duradrin, and Midrin is a combination of acetaminophen, dichloralphenazone, and isometheptene often prescribed for migraine headaches. Some studies have recently shown that these drugs may work better than sumatriptan for treating migraines.

Anti-emetics may need to be given by suppository or injection where vomiting dominates the symptoms.

Recently it has been found that calcitonin gene related peptides (CGRPs) play a role in the pathogenesis of the pain associated with migraine as triptans also decrease its release and action. CGRP receptor antagonists such as olcegepant and telcagepant are being investigated both in vitro and in clinical studies for the treatment of migraine.

Status migrainosus

Status migrainosus is characterized by migraine lasting more than 72 hours, with not more than four hours of relief during that period. It is generally understood that status migrainosus has been refractory to usual outpatient management upon presentation.

Treatment of status migrainosus consists of managing comorbidities (i. e. correcting fluid and electrolyte abnormalities resulting from anorexia and nausea/vomiting often accompanying status migr.), and usually administering parenteral medication to "break" (abort) the headache.

Although the literature is full of many case reports concerning treatment of status migrainosus, first line therapy consists of intravenous fluids, metoclopramide, and triptans

Herbal treatment

The herbal supplement feverfew is marketed by the as an OTC migraine abortive, administered sublingually (under the tongue) in a mixture with ginger. An open-label study found some tentative evidence of the treatment's effectiveness, but no scientifically sound study has been done. Cannabis in addition to prevention is also known to relieve pain during the onset of a migraine.

Preventive treatment

Preventive treatment of migraines can be an important component of migraine management. Such treatments can take many forms, including everything from taking certain drugs or nutritional supplements, to lifestyle alterations such as increased exercise and avoidance of migraine triggers. One such book that outlines these preventative measures quite well is "7 Steps To A Healthy Brain" by Dr. Winner.

The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy Another reason to pursue these goals is to avoid medication overuse headache (MOH), otherwise known as rebound headache, which is a common problem among migraneurs. This is believed to occur in part due to overuse of pain medications, and can result in chronic daily headache

Many of the preventive treatments described below are quite effective: Even with a placebo (sham treatment), one-quarter of patients find that their migraine frequency is reduced by half or more and actual treatments often far exceed this figure

Trigger avoidance

Patients should attempt to identify and avoid factors that promote or precipitate migraine episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and regular meals may be helpful. General dietary restriction has not been demonstrated to be an effective approach to treating migraine. However, eliminating particular foods that are known to trigger migraines in an individual can be very effective.

Gluten-Free Diet

Some individuals have a condition called celiac disease that results in the body incorrectly processing gluten. Studies have suggested that many migraine sufferers have celiac disease, and for those who do, decreasing gluten intake may significantly reduce migraine frequency. Celiac disease and gluten sensitivity may be an underlying cause of migraines in some patients, and a gluten-free diet has been demonstrated to reduce, if not completely eliminate, migraines in these individuals. A study of 10 patients with a long history of chronic headaches that had recently worsened or were resistant to treatment found that all 10 patients were sensitive to gluten. MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Seven out of nine of these patients that went on a gluten-free diet stopped having headaches completely Another study showed that migraneurs were 10 times more likely than the general population to have celiac disease, and that for migraneurs with celiac disease, a gluten-free diet improved blood-flow to the brain and either eliminated migraines or reduced migraine frequency, duration, and intensity

Prescription drugs

A 2006 review article by S. Modi and D. Lowder offers some general guidelines on when a physician should consider prescribing drugs for migraine prevention:

Following appropriate management of acute migraine, patients should be evaluated for initiation of preventive therapy. Factors that should prompt consideration of preventive therapy include the occurrence of two or more migraines per month with disability lasting three or more days per month; failure of, contraindication for, or adverse events from acute treatments; use of abortive medication more than twice per week; and uncommon migraine conditions (e.g., hemiplegic migraine, migraine with prolonged aura, migrainous infarction). Patient preference and cost also should be considered.

...Therapy should be initiated with medications that have the highest levels of effectiveness and the lowest potential for adverse reactions; these should be started at low dosages and titrated slowly. A full therapeutic trial may take two to six months. After successful therapy (e.g., reduction of migraine frequency by approximately 50 percent or more) has been maintained for six to 12 months, discontinuation of preventive therapy can be considered.

Preventive medication has to be taken on a daily basis, usually for a few weeks, before the effectiveness can be determined. Supervision by a neurologist is advisable. A large number of medications with varying modes of action can be used. Selection of a suitable medication for any particular patient is a matter of trial and error, since the effectiveness of individual medications varies widely from one patient to the next. Often preventive medications do not have to be taken indefinitely. Sometimes as little as six months of preventive therapy is enough to "break the headache cycle" and then they can be discontinued.

The most effective prescription medications include several drug classes:

· Beta blockers such as propranolol and atenolol. A meta-analysis by the Cochrane Collaboration of nine randomized controlled trials or crossover studies, which together included 668 patients, found that propranolol had an "overall relative risk of response to treatment (here called the 'responder ratio')" was 1.94. Anticonvulsants such as valproic acid and topiramate. A meta-analysis by the Cochrane Collaboration of ten randomized controlled trials or crossover studies, which together included 1341 patients, found anticonvulsants had an "2.4 times more likely to experience a 50% or greater reduction in frequency with ^{anticonvulsants than with placebo" and a number needed to treat of 3.8.} However, concerns have been raised about the marketing of gabapentin. Antidepressants include tricyclic antidepressants (TCAs) such as amitriptyline and the newer selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine. A meta-analysis by the Cochrane Collaboration found selective serotonin reuptake inhibitors are no more effective than placebo. Another meta-analysis found benefit from SSRIs among patients with migraine or tension headache; however, Sthe effect of SSRIs on only migraines was not separately reported. A randomized controlled trial found that amitriptyline was better than placebo and similar to propranolol. A wide range of pharmacological drugs have been evaluated to determine their efficacy in reducing the frequency or severity of migraine attacks. These drugs include beta-blockers, calcium antagonists, neurostabalizers, nonsteroidal anti-inflammatory drugs (NSAIDs),tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), other antidepressants, and other specialized drug therapies. The US Headache Consortium lists five drugs as having medium to high efficacy: amitriptyline, divalproex, timolol, propranolol and topiramate. Lower efficacy drugs listed include aspirin, atenolol, fenoprofen, flurbiprofen, fluoxetine, gabapentin, ketoprofen, metoprolol, nadolol, naproxen, nimodipine, verapamil and Botulinum A. Additionally, most antidepressants (tricyclic, SSRIs and others such as Bupropion) are listed as "clinically efficacious based on consensus of experience" without scientific support Many of these drugs may give rise to undesirable side-effects, or may be efficacious in treating comorbid conditions, such as depression.

Other drugs:

· Methysergide was withdrawn from the US market by Novartis, but is available in Canadian pharmacies. Although highly effective, it has rare but serious side effects, including retroperitoneal fibrosis.

· Memantine, which is used in the treatment of Alzheimer's disease, is beginning to be used off label for the treatment of migraines. It has not yet been approved by the FDA for the treatment of migraines.

· Aspirin can be taken daily in low doses such as 80 mg, the blood thinners in ASA have been shown to help some migrainures, especially those who have an aura.

HERBAL AND NUTRITIONAL SUPPLEMENTS

Butterbur

50 mg or 75 mg/day of butterbur (Petasites hybridus) rhizome extract was shown in a controlled trial to provide 50% or more reduction in the number of migraines to 68% of participants in the 75 mg dose group, 56% in the 50 mg dose group and 49% in the placebo group after four months. Native butterbur contains some carcinogenic compounds, but a purified version, Petadolex, does not.

Cannabis

Cannabis was a standard treatment for migraines from 1874 to 1942 has been reported to help people through an attack by relieving the nausea and dulling the head pain, as well as possibly preventing the headache completely when used as soon as possible after the onset of pre-migraine symptoms, such as aura.

Coenzyme Q10

Supplementation of coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraines. In an open-label trial Young and Silberstein found that 61.3% of patients treated with 100 mg/day had a greater than 50% reduction in number of days with migraine, making it more effective than most prescription prophylactics. Less than 1% reported any side effects. A double-blind placebo-controlled trial has also found positive results.

Feverfew

The plant feverfew (Tanacetum parthenium) is a traditional herbal remedy believed to reduce the frequency of migraine attacks. A number of clinical trials have been carried out to test this claim, but a 2004 review article concluded that the results have been contradictory and inconclusive However, since then, more studies have been carried out. As well as its prophylactic properties, feverfew is also touted as a migraine abortative.

Magnesium citrate

Magnesium citrate has reduced the frequency of migraine in an experiment in which the magnesium citrate group received 600 mg per day oral of trimagnesium dicitrate. In weeks 9–12, the frequency of attacks was reduced by 41.6% in the magnesium citrate group and by 15.8% in the placebo group.

Riboflavin

The supplement Riboflavin (also called Vitamin B₂) has been shown (in a placebo-controlled trial) to reduce the number of migraines, when taken at the high dose of 400 mg daily for three months

Vitamin B12

There is tentative evidence that Vitamin B₁₂ may be effective in preventing migraines In particular, in an open-label pilot study, 1 mg of intranasal hydroxocobalamin (a form of Vitamin B12), taken daily for three months, was shown to reduce migraine frequency by 50% or more in 10 of 19 participants Although the study was not placebo-controlled, this response is larger than the typical placebo effect in migraine prophylaxis.

Melatonin

Melatonin has been studied in migraine and other headache disorders. In an open label study, migraine patients taking melatonin 3 mg before bedtime with a good headache response and tolerability. Melatonin has multiple mechanisms affecting migraine

Surgical Treatments

Surgery may be used to treat migraines by severing the corrugators’ supercilious muscle and zygomaticotemporal nerve. The treatment may reduce or eliminate headaches in some individuals. In 2005, researchwas published indicating that some people with a patent foramen ovale (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines reduce in frequency if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.

Botulin toxin has been used to treat individuals with frequent or chronic migraines. It appears to be effective for chronic migraines but not useful in the treatment of episodic migraine. Spinal cord stimulators are an implanted medical device sometimes used for those who suffer severe migraines several days each month.

Behavioral treatments

Many physicians believe that exercise for 15–20 minutes per day is helpful for reducing the frequency of migraines Specific exercises have been developed that are believed to effectively reduce the severity and frequency of migrainesSleep is often a good solution if a migraine is not so severe as to prevent it, as when a person awakes the symptoms will have most likely subsided.

Diet, visualization, and self-hypnosis are also alternative treatments and prevention approaches.

Sexual activity has been reported by a proportion of male and female migraine sufferers to relieve migraine pain significantly in some cases

In many cases where a migraine follows a particular cycle, attempting to interrupt the cycle may prolong the symptoms. Letting a headache "run its course" by not using

Painkillers can sometimes decrease the length of an episode. This is especially true of cases where vomiting is common, as often the headache will subside immediately after vomiting. Curbing the pain may delay vomiting, and prolong the headache

Alternative medicine

A number of forms of alternative medicine, particularly bodywork, are used in preventing migraines.

Clinical trials have suggested that chiropractic care may be an efficacious treatment for migraine headaches Likewise, Massage therapy, physical therapy, and Bowen Techniqueare often very effective forms of treatment to reduce the frequency and intensity of migraines^] These initial studies are limited by lack of control subjects, poor control subjects, lack of blind study design, small sample sizes, and other methodological flaws. Chiropractic researchers have argued that the current evidence for chiropractic treatment of migraines indicates that "evidence is steadily increasing to the point where there is now seen to be a moderate level of efficacy for chiropractic SMT in the treatment of headaches or migraines The effect of chiropractic treatment may be mediated by stress release, and may be more efficacious for tension-type headaches than migraines

A review of the literature until 2004 found that "Chiropractic manipulation demonstrated a trend toward benefit in the treatment of TTH, but evidence is weak. ... In the absence of clear evidence regarding their role in treatment, physicians and patients are advised to make cautious and individualized judgments about the utility of physical treatments for headache management; in most cases, the use of these modalities should complement rather than supplant better-validated forms of therapy." Frequent migraines can leave the sufferer with a stiff neck which can cause stress headaches that can then exacerbate the migraines. Claims have been made that Myofascial Release can relieve this tension and in doing so reduce or eliminate the stress headache element

Some migraine sufferers find relief through acupuncture, which is usually used to help prevent headaches from developing. Sometimes acupuncture is used to relieve the pain of an active migraine headache in one controlled trial of acupuncture with a sham control in migraine; the acupuncture was not more effective than the sham acupuncture but was

MIASMSMATIC BACKGROUND

Miasm is a Greek word. It means pollution or contagious foul exhalation from human body or any infective material.

There are three types of Miasms

v Psori

v Syphilis

v Sycotic

v Tubercular

In the case of Migrine the symptoms that covers,

v Frequent one sided headache even from moderate emotion disturbances - Psora, Tubercular.

v Vertige – Psora

v Dizziness inability to think or perform mental Labour – Psora

v Headache of various types Frontal, Temporil, Tempro parietal – Psora

v One sided headache – Psora

v Morning headache – Psora

v <>

v Visual Halluciladions – Psora

v Photophobia – Psora, Tubercular, Syphilis

v Nausea, Vomiting – Psora

v <>

v Frontal / Vertex headache - Tubercular

All most all of the symptoms covers Psora.

So DOMINANT MIASM – PSORA.

2009-11-02T10:55:00.000-08:00

2009-03-08T08:32:00.000-07:00

What types of Diseases & Conditions can
Homeopathic Medicine Treat?

Dr Mijul and his classmates

2009-02-07T08:34:00.000-08:00

2009-02-07T08:21:00.000-08:00

Calendula officinalis… the Antiseptic

Calendula Officinalis is native to Europe but because of its beauty and adaptability, gardeners have spread it around the world. The flowers range in color from mild yellow to deep orange, and because of their intensity have been called "Golden drops of Sunshine ". "Caleds" means first day of month. This flower blooms on the first day of the month or at least once in a month.

Shakespeare speaks in A Winter's Talc of Calendula "that goes to bed with sun and with him rises weeping ". Since ancient times the East Indian, Arabs, Romans, Greeks all noted how Calendula's flowers open in the morning and close in the evening and how the flowering seasons extends for many months. Calendula once held a prominent place in European Kitchen Gardens where it was grown for use in Soups and broths. For centuries the English and Germans believed that eating the flowers maintained health throughout the winter. Stevens, Author of 'Countrie Farme', in 17th century England, claims that "No broths are well made without dried Marigold". Sweet flower conserves were also served in the morning before breakfast.

Calendula officinalis is the chief homoeopathic medicine for wounds. It is magical in its ability to soothe pain, stop bleeding, promote rapid healing, and prevent scarring. It is also an excellent antiseptic, thereby preventing infections. It should be part of every midwife's bag of tricks.

Calendula preparations are widely used as an external application available in the market as liniments, lotions, and ointments. Cosmetically Calendula juice is used as a hair - coloring agent, which gives yellow and golden colour. Calendula is mixed with chamomile, lavender for making baby oil and creams. Many pharmaceutical preparations are available as talcum powder also! Calendula is used internally, preferably in low potency to treat many septic conditions.

Physiological action of calendula is mainly on circulatory system. Through vasomotor system the capillary vessels become partially paralyzed and consequently receive more blood, which attracts large amount white blood cells together with viscosity or adhesive qualities.

Dr. William Boericke has written

"A most remarkable healing agent, applied locally. Useful for open wounds; parts that will not heal, ulcers, etc. Promotes healthy granulations and rapid healing by first intention."

"Locally. Aqueous Calendula for all wounds, internally tincture, to third potency. Use Calendula Cerate for burns sores, fissures, and abrasions."

Calendula contains essential oil, flavonol glycosides, saponins, triterpene alcohols, sterols, carotenes, xanthophylls, polysaccharides, tannins and other constituents. Contains much nitrogen and phosphoric acid.

Calendula is indicated when the individual feels worse in damp, heavy, cloudy weather. There is a tendency to get cold easily and is greatly affected by the cold. As the season shifts from summer into chilly fall days, many people are susceptible to colds and flues. I think Calendula gives us an important hint by not only surviving, but also thriving through the shift in seasons.

2009-02-07T08:13:00.000-08:00

Alcoholism can fall into two separate categories: problem drinking and actual physical dependence on alcohol. Problem drinking is commonly emotional in its roots, whereby the alcoholic uses drink to avoid feeling. Alcohol dependence is where the person needs alcohol in order to function.

Generally four times as many men than women are affected, however, alcohol use and abuse is quickly on the rise with females and younger adults, even children. Women are more affected by alcohol than men due to lower body weight, lower water content, higher fat content and less of the enzyme that breaks down alcohol. Not only do women develop liver disease from a lesser amount of alcohol, they are at a higher risk of developing osteoporosis as alcohol adversely affects bone metabolism.

The overall rate of premature death related to alcoholism is 50 to 100 percent higher for women than for men. Women are also more likely to have psychological troubles such as anxiety, eating disorders and depression, which can often be occurring prior to drinking becoming a problem. Thus, treating the alcohol dependency does not mean the emotional and mental difficulties are immediately cured. Actually, as the person has lost her ?crutch?, dealing with the strains of life may even be more difficult than previously experienced.

Alcoholism tends to run in families, and this is for a couple of reasons. First, there is the physiological dependence alcohol can have on the body. Heredity is involved in almost fifty percent of the risk of becoming an alcoholic. Environment also plays a large role because too often the normal emotional development of a child has not been allowed, due to the constant upheaval caused by the alcoholic?s behaviour. There is little stability, and children of alcoholics can find themselves either taking on too much or too little responsibility, possibly leading to emotional or relationship troubles further on in life. Socially, the family may feel the need to hide the alcoholic?s problem, not speaking about it and leading to the ?enabling? behaviour that can affect the family?s ability to reach out and ask for help. There is a social stigma attached to alcoholism, which if properly understood, would be treated as a disease and not a result of poor willpower.


Quercus Glandium Spiritus - Spirit ditilled from Tincture of Acron Kernels, frequently used for alcoholism	Aven Sativa - Common Oat, used for detox and nervous system

The body sees alcohol as a poison. Some of the effects of chronic alcohol use include damage to the liver, brain, duodenum, pancreas and central nervous system. The brain is affected because the amount of oxygen is reduced to the brain in addition to alcohol harming the cells themselves. This can result in disorientation, amnesia, hallucinations, emotional swings and in severe cases, seizures and neurological complications. Every cell in the body is damaged metabolically and the immune system is depressed by alcohol. If an alcoholic continues to drink, the life span can be shortened by up to fifteen years.

95 percent of alcohol is processed by the liver at the rate of about ¼ to ½ ounce per hour. Continued use of alcohol reduces the liver?s ability to produce digestive enzymes, resulting in poor assimilation and use of proteins, fats, B vitamins and fat-soluble vitamins A, D, E and K. Amino acid deficiencies occur, reducing the body?s store of zinc, vital for immunity. Excessive amounts of fat are then accumulated in the liver, as they are not being metabolised. In time, the liver cells can become inflamed and may die, which is hepatitis. The final stage is cirrhosis, a disease whereby the liver is inflamed, hardens and scars, preventing the normal passage of blood through the liver. This impairs the vital function of detoxification, the liver?s primary function. An estimated one out of five alcoholics is affected by cirrhosis.

The liver is not the only organ to show damage from alcohol. The peripheral nervous system can be inhibited, resulting in a loss of sensation in the hands and feet, with difficulty walking. Chronic drinking inflames the pancreas, leading to an even further reduction in digestion and can lead to diabetes. There is an increased risk of mouth, throat, stomach and colon cancer due to the toxicity of alcohol. Add to the common partner in crime, smoking, and you increase the risk of cancer by 50 percent. High blood pressure, reduced testosterone, enlargement of the heart and visible dilation of blood vessels just beneath the skin?s surface are results of alcohol and can often lead to heart failure.

Nux Vomica - King of drinking and debauchery

Drinking while pregnant can lead to foetal alcohol syndrome. This can present with lower birth weight, stunted growth, smaller brains, lower intelligence and even retardation. The liver of the foetus is not developed and cannot handle the alcohol; therefore it remains in the circulation, depressing the central nervous system of the developing baby. In addition, joints, fingers, limbs, and facial features can be deformed, plus heart and kidney defects. Some children will become hyperactive and have learning disabilities - all this from even moderate amounts of alcohol taken during pregnancy, especially in the first three to four months.

Alcoholics who quit drinking suddenly may suffer withdrawal symptoms. Shaking, insomnia, hallucinations, convulsions, anxiety, rapid pulse, fever, profuse perspiration and emotional mood swings can occur. There are various medical terms for these stages of withdrawal. Delirium tremens (DTs) usually covers the symptom picture of anxiety, confusion, nightmares, and possibly terrors. The floor can feel as though it is moving, the walls are falling or the room is rotating. It is vital to recognize that delirium tremens can be fatal and should be treated under medical supervision. There can also be hepatic coma, as the alcohol-damaged liver cannot rid the body of toxic substances. It is suggested that patients be given Vitamin B injections, which will help support the nervous system while they are withdrawing. With proper nutritional supplementation, there is the possibility of liver regeneration, so long as the damage has not been too severe.

In the UK, there are one million registered alcoholics and drug addicts. Considering that only 1/5 of all addicts will register, the appropriate figure is somewhere around 5 million people with an addiction. Then multiply this number by five - the parent, spouse, child, friend or work colleague whose life is affected by the alcoholic?s disease, and you have roughly 25 million people trying to cope with this destructive behaviour. Half the population of the UK is directly involved and there is no sign of it slowing down.

Homeopathic remedies to help recover from alcohol addiction include Nux vomica and especially Avena sativa used for detox and nervous system support. Other support remedies to consider are Opium and Quercus if it fits the case. Use daily in a low potency such as a 6c with a liver support remedy in mother tincture such as Chelidonium, Carduus marianus, Taraxacum or Hydrastis. Deeply suppressed emotions will probably need to be addressed as well. Think of Carcinosin, Aurum, Staphysagria, the Natrums, Lycopodium, Lachesis and Sepia. If there is a family tendency towards alcoholism look at the nosodes, especially Syphilinum. The important thing to remember is that recovery is a process, and treating alcoholism is rarely straightforward.

2009-02-05T07:21:00.000-08:00

HI I AM Dr MIJUL A HOMOEOPATH FROM KOZHIKODE

DR MIJUL'S HOMOEOPATHY

What types of Diseases & Conditions can

PNEUMOTHORAX

PNEUMOTHORAX

Definition of Pneumothorax

//<![CDATA[ if (window.showTocToggle) { var tocShowText = "show"; var tocHideText = "hide"; showTocToggle(); } //]]> Etiology

What causes pneumothorax?

Description of Pneumothorax

Signs and symptoms

AEM: Emergency Bedside Ultrasound to Detect Pneumothorax

Differential diagnosis

Pathophysiology

Chest wound

Blast injury or tension

Pre-hospital care

Clinical treatment

Tension pneumothorax

Signs and Symptoms

Treatment

Spontaneous Pneumothorax

Primary spontaneous pneumothorax

Secondary spontaneous pneumothorax

Prevention of pneumothorax and other air leaks:

HOMOEOPATHIC MANAGEMENT

Arsenicum Album

Antimonium Tartaricum

Drosera Rotundifolia

Grindelia Robusta

Hepar Sulphur

Ipecacuanha

Alopecia

Epidemiology

Types

Diagnosis

Treatment

Prognosis

Psychosocial issues

Causes Alopecia Totalis

Treatments for Alopecia Totalis

Alopecia Universalis

Treatment

Noncicatricial alopecia

Background, cause and incidence

Pathophysiology

Preventing and reversing hair loss

Stress reduction

Saw palmetto

Polygonum multiflorum

Alopecia Mucinosa

Pathophysiology

Causes

Histologic Findings

MIGRAINE

Classification

Migraine without aura

Migraine with Aura

Basilar type Migraine

Familial hemiplegics migraine

Abdominal migraine

Acephalgic Migraine

Menstrual migraine

Diagnosis

Prodrome Phase

Aura Phase

Pain phase

Pathophysiology

Vascular Theory

Neural theory

Unifying theory

Triggers

Food

Weather

Other

Treatment

Paracetamol or non-steroidal anti-inflammatory drug (NSAIDs)

Analgesics combined with antiemetics

Serotonin agonists

Anti-depressants

Ergot alkaloids

Other agents

Etiology