Brain Surgrey

Neurosurgery is the surgical discipline focused on treating those central and peripheral nervous system diseases amenable to mechanical intervention.

Definition and scope
According to the U.S. Accreditation Council of Graduate Medical Education (ACGME),

“ Neurological Surgery is a discipline of medicine and that specialty of surgery which provides the operative and nonoperative management (ie, prevention, diagnosis, evaluation, treatment, critical care, and rehabilitation) of disorders of the central, peripheral, and autonomic nervous systems, including their supporting structures and vascular supply; the evaluation and treatment of pathological processes that modify the function or activity of the nervous system, including the hypophysis: and the operative and nonoperative management of pain. As such, neurological surgery encompasses the surgical, nonsurgical and stereotactic radiosurgical treatment of adult and pediatric patients with disorders of the nervous system: disorders of the brain, meninges, skull base, and their blood supply, including the surgical and endovascular treatment of disorders of the intracranial and extracranial vasculature supplying the brain and spinal cord; disorders of the pituitary gland; disorders of the spinal cord, meninges, and vertebral column, including those that may require treatment by fusion, instrumentation,or endovascular techniques; and disorders of the cranial and spinal nerves throughout their distribution. ”

Conditions
Neurosurgical conditions include primarily brain, spinal cord and peripheral nerve disorders.

Conditions treated by neurosurgeons include:
Spinal disc herniation
Spinal stenosis
Hydrocephalus
Head trauma (brain hemorrhages, skull fractures, etc.)
Spinal cord trauma
Traumatic injuries of peripheral nerves
Brain tumors
Tumors of the spine, spinal cord and peripheral nerves
Cerebral aneurysms
Some forms of hemorrhagic stroke, such as subarachnoid hemorrhages, as well as intraparenchymal and intraventricular hemorrhages
Some forms of pharmacologically resistant epilepsy
Some forms of movement disorders (advanced Parkinson's disease, chorea, hemiballism) - this involves the use of specially developed minimally invasive stereotactic techniques (functional, stereotactic neurosurgery)
Intractable pain of cancer or trauma patients and cranial/peripheral nerve pain
Some forms of intractable psychiatric disorders
Malformations of the nervous system
Carotid artery stenosis
Vascular malformations (i.e., arteriovenous malformations, venous angiomas, cavernous angiomas, capillary telangectasias) of the brain and spinal cord
Peripheral neuropathies such as Carpal Tunnel Syndrome and ulnar neuropathy
Moyamoya disease
Congenital malformations of the nervous system, including spina bifida and craniosynostosis

Job field
Neurosurgeons work in a variety of practice settings. Some neurosurgeons practice general neurosurgery, while others choose to limit their practice to specific subspecialties. Some areas of specialty include pediatric, spine, vascular/endovascular, tumor, peripheral nerve, functional, and skull base. Practices range from solo practices to large group practices with multidisciplinary components. Increasingly, neurosurgeons are working together with psychiatrists, neurologists and therapists to provide comprehensive care for patients with neurologic disorders such as back pain. About 20 percent of neurosurgeons practice under the auspices of a university practice plan, while the majority of neurosurgeons maintain private practices often with academic affiliations. Typical work schedules for a neurosurgeon include call coverage for one or more emergency rooms requiring sometimes frequent emergency surgeries. Most averages found online describing typical salary for a practicing neurosurgeon in the United States are between $300,000 and $500,000 annually, though these should be considered as weak small-survey estimates based on the values given by the AAMC. Also, it is fair to note that the Bureau of Labor Statistics has no recorded values for mean hourly, weekly, or annual wage.

Brain Surgrey

Meineres Disease

Ménière's disease is a disorder of the inner ear that can affect hearing and balance. It is characterized by episodes of dizziness and tinnitus and progressive hearing loss, usually in one ear. It is caused by an increase in volume and pressure of the endolymph of the inner ear. It is named after the French physician Prosper Ménière, who first reported that vertigo was caused by inner ear disorders in an article published in 1861.

Symptoms
The symptoms of Ménière's are variable; not all sufferers experience the same symptoms. However, so-called "classic Ménière's" is considered to comprise the following four symptoms:

Periodic episodes of rotary vertigo (the abnormal sensation of movement) or dizziness.
Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss, often initially in the lower frequency ranges.
Unilateral or bilateral tinnitus (the perception of noises, often ringing, roaring, or whooshing), sometimes variable.
A sensation of fullness or pressure in one or both ears.
Ménière's often begins with one symptom, and gradually progresses. A diagnosis may be made in the absence of all four classic symptoms.

Attacks of vertigo can be severe, incapacitating, and unpredictable. In some patients, attacks of vertigo can last for hours or days, and may be accompanied by an increase in the loudness of tinnitus and temporary, albeit significant, hearing loss in the affected ear(s). Hearing may improve after an attack, but often becomes progressively worse. Vertigo attacks are sometimes accompanied by nausea, vomiting, and sweating.

Some sufferers experience what are informally known as "drop attacks" — a sudden, severe attack of dizziness or vertigo that causes the sufferer, if not seated, to fall. Patients may also experience the feeling of being pushed or pulled (Pulsion). Some patients may find it impossible to get up for some time, until the attack passes or medication takes effect. There is also the risk of injury from falling.

In addition to hearing loss, sounds can seem tinny or distorted, and patients can experience unusual sensitivity to noises (hyperacusis). Some sufferers also experience nystagmus, or uncontrollable rhythmical and jerky eye movements, usually in the horizontal plane, reflecting the essential role of the balance system in coordinating eye movements.

Other symptoms include so-called "brain fog" (temporary loss of short term memory, forgetfulness, and confusion), exhaustion and drowsiness, headaches, vision problems, and depression. Many of these latter symptoms are common to many chronic diseases.

Cause
The exact cause of Ménière's disease is not known, but it is believed to be related to endolymphatic hydrops or excess fluid in the inner ear. It is thought that endolymphatic fluid bursts from its normal channels in the ear and flows into other areas causing damage. This may be related to swelling of the endolymphatic sac or other issues in the vestibular system of the inner ear, which is responsible for the body's sense of balance. The symptoms may occur in the presence of a middle ear infection, head trauma or an upper respiratory tract infection, or by using aspirin, smoking cigarettes or drinking alcohol. They may be further exacerbated by excessive consumption of caffeine and salt in some patients. Excessive levels of potassium in the body (usually caused by the consumption of potassium rich foods) may also exacerbate the symptoms.

Diagnosis
Many disorders have symptoms similar to Ménière's. The diagnosis is usually established by clinical findings and medical history. However, a detailed oto-neurological examination, audiometry and head magnetic resonance imaging (MRI) scan should be performed to exclude a tumour of the cranial nerve VIII (vestibulocochlear nerve) which would cause similar symptoms. Because there is no definitive test for Ménière's, it is only diagnosed when all other causes have been ruled out.

Ménière's typically begins between the ages of 30 and 60 and affects men slightly more than women.

Treatment
Initial treatment is aimed at both dealing with immediate symptoms and preventing recurrence of symptoms, and so will vary from patient to patient. Doctors may recommend vestibular training, methods for dealing with tinnitus, stress reduction, hearing aids to deal with hearing loss, and medication to alleviate nausea and symptoms of vertigo.

Several environmental and dietary changes are thought to reduce the frequency or severity of symptom outbreaks. Most patients are advised to adopt a low-sodium diet, typically one to two grams (1000-2000mg) at first, but diets as low as 400mg are not uncommon. Patients are advised to avoid caffeine, alcohol and tobacco, all of which can aggravate symptoms of Ménière's. Some recommend avoiding Aspartame. Patients are often prescribed a mild diuretic (sometimes vitamin B6). Many patients will have allergy testing done to see if they are candidate for allergy desensitization as allergies have been shown to aggravate Ménière's symptoms.

Women may experience increased symptoms during pregnancy or shortly before menstruation, probably due to increased fluid retention.

Lipoflavanoid is also recommended for treatment by some doctors.

Many patients consider fluorescent lighting to be a trigger for symptoms. The plausibility of this can be explained by how important a part vision plays in the overall mechanism of human balance.

Treatments aimed at lowering the pressure within the inner ear include antihistamines, anticholinergics, steroids, and diuretics. A medical device that provides transtympanic micropressure pulses is now showing some promise and is becoming more widely used as a treatment for Ménière's.

Surgery may be recommended if medical management does not control vertigo. Injection of steroid medication behind the eardrum, or surgery to decompress the endolymphatic sac may be used for symptom relief. Permanent surgical destruction of the balance part of the affected ear can be performed for severe cases if only one ear is affected. This can be achieved through chemical labyrinthectomy, in which a drug (such as gentamicin) that "kills" the vestibular apparatus is injected into the middle ear. The nerve to the balance portion of the inner ear can be cut (vestibular neurectomy), or the inner ear itself can be surgically removed (labyrinthectomy). These treatments eliminate vertigo, but because they are destructive, they are used only as a last resort. Typically balance returns to normal after these procedures, but hearing loss may continue to progress.

Progression
Progression of Ménière's is unpredictable: symptoms may worsen, disappear altogether, or remain the same.

Sufferers whose Ménière's began with one or two of the classic symptoms may develop others with time. Attacks of vertigo can become worse and more frequent over time, resulting in loss of employment, loss of the ability to drive, and inability to travel. Some patients become largely housebound. Hearing loss can become more profound and may become permanent. Some patients become deaf in the affected ear. Tinnitus can also worsen over time. Some patients with unilateral symptoms, as many as fifty percent by some estimates, will develop symptoms in both ears. Some of these will become totally deaf.

Yet the disease may end spontaneously and never repeat again. Some sufferers find that after eight to ten years their vertigo attacks gradually become less frequent and less severe; in some patients they disappear completely. In some patients, symptoms of tinnitus will also disappear, and hearing will stabilize (though usually with some permanent loss).

Famous sufferers
Alan B. Shepard, the first American astronaut, was diagnosed with Ménière’s disease in 1964, grounding him after only one brief spaceflight. Several years later, surgery (which was then at the experimental stage) was performed, allowing Shepard to fly to the Moon on Apollo 14.
The Ménière's Disease Information Center lists poet Emily Dickinson, author Jonathan Swift, NBA player Steve Francis, and many others as Ménière's disease sufferers.
According to his blog, Author and entrepreneur Guy Kawasaki has the illness.
Contemporary artist and graphic designer Doc Hammer, of The Venture Bros. fame, has Ménière's syndrome according to his May 16th, 2005 journal entry.
Paddy McAloon, the singer and songwriter for the British pop group Prefab Sprout, was diagnosed with Ménière's in 2004.
A paper by Arenberg et. al, 1990, suggests that Vincent Van Gogh, the Dutch Post-Impressionist, may have suffered from Ménière's, though this is now considered conjectural. See Vincent van Gogh's medical condition for a discussion of the range of possible alternative diagnoses. Some believe "The Starry Night" illustrates his dizziness. It's also speculated that ear pressure and deafness could have inspired him to cut off his own ear.

Charles Darwin may have suffered from Ménière’s disease. This idea is based on a common list of symptoms which were present in Darwin's case, such as tinnitus, vertigo, dizziness, motion sickness, vomiting, continual malaise and tiredness. The absence of hearing loss and 'fullness' of the ear (as far as known) excludes however a diagnosis of typical Ménière’s disease. Darwin himself had the opinion that most of his health problems had an origin in his 4-year bout with sea sickness. Later, he could not stand travelling by carriage, and only horse riding would not affect his health. One of the diagnoses that he received from his physicians at the time was that of "suppressed gout". The source of Darwin's illness is not known for certain. See Charles Darwin's illness for more details.
Fictional comic book villain Count Vertigo suffers from Ménière's disease and has the ability to inflict its symptoms on others.
Martin Luther and Julius Caesar also suffered from Ménière's disease.

Meineres Disease

Intermitent Explosive Disorder

Intermittent explosive disorder (IED) is a behavioral disorder characterized by extreme expressions of anger, often to the point of uncontrollable rage, that are disproportionate to the situation at hand. It is currently categorized in the Diagnostic and Statistical Manual of Mental Disorders as an impulse control disorder. IED belongs to the larger family of Axis I impulse control disorders listed in the DSM-IV-TR, along with kleptomania, pyromania, pathological gambling, and others. Impulsive aggression is unpremeditated, and is defined by a disproportionate reaction to any provocation, real or perceived. Some individuals have reported affective changes prior to an outburst (e.g., tension, mood changes, energy changes, etc.).

A 2006 study published by Harvard University researchers suggests that the disorder is considerably more prevalent than previously thought. In a study of almost 10,000 individuals 18 years or older, lifetime episodes were reported at 7.3%, while 12-month occurrences were reported at 3.9%. This suggests a mean lifetime occurrence of 43 instances, with an average of $1359 in property damage.

A 2005 study conducted in Rhode Island found the prevalence to be 6.3% (SE, +/- 0.7%) for lifetime DSM-IV IED in a study of 1300 patients under psychiatric evaluation. [4] The national prevalence has not been established, and the disorder is considered to be relatively rare, due at least in part to the fact that an IED diagnosis is usually given only if all other possible disorders and syndromes are ruled out. Prevalence is higher in men than in women. The disorder itself is not easily characterized and often exhibits comorbidity with other mood disorders, particularly bipolar disorder.

In this same study, 27 subjects exhibiting DSM-IV IED were recruited and interviewed to describe their symptomology and episodic behaviors. All subjects described outbursts as brief, lasting an average of 22 minutes ± SD of 23 minutes. One-third of the subjects reported experiencing somatization prior to an episode, e.g. “tingling, tremor, palpitations, chest tightness, head pressure, or hearing an echo”. Over half of the subjects reported an alteration in their awareness during the episode, but none reported amnesia of the outburst. Subjects generally reported an inability to resist the impulse to violence, and often reported a feeling of relief (88% reporting) or even pleasure (46% reporting) while committing the acts. After the acts, many subjects reported feelings of remorse at their actions. Remarkably, all 27 subjects reported their experiences with IED consistently.

Diagnosis & Treatment
The DSM-IV criteria for IED include: the occurrence of discrete episodes of failure to resist aggressive impulses that result in violent assault or destruction of property, the degree of aggressiveness expressed during an episode is grossly disproportionate to provocation or precipitating psychosocial stressor, and, as previously stated, diagnosis is made when other mental disorders that may cause violent outbursts (e.g., antisocial personality disorder, borderline personality disorder, attention deficit/hyperactivity disorder, etc.) have been ruled out (McElroy, 1999; McElroy, Soutullo, Beckman, Taylor Jr., & Keck Jr., 1998). Furthermore, the acts of aggression must not be due to a general medical condition, e.g., a head injury, Alzheimer’s disease, etc., or due to substance abuse or medication (Ibid.). Diagnosis is made using a psychiatric interview to affective and behavioral symptoms to the criteria listed in the DSM-IV.

Treatment is achieved through both cognitive behavioral therapy and psychotropic medication regimens. Therapy aids in helping the patient recognize the impulses in hopes of achieving a level of awareness and control of the outbursts, along with treating the emotional stress that accompanies these episodes. Multiple drug regimens are frequently indicated for IED patients. Tricyclic antidepressants and serotonin reuptake inhibitors (SRIs) such as fluoxetine, fluvoxamine, and sertraline appear to alleviate some pathopsychological symptoms; the reasons for such will be explained further in the subsequent section (Goodman, Ward, Kablinger, & Murphy, 1997; McElroy, 1999). GABAergic mood stabilizers and anticonvulsive drugs such as gabapentin, lithium, carbamazepine, and divalproex seem to aid in controlling the incidence of outbursts (Boyd, 2005; Bozikas, Bascilla, Yulis, & Savvidou, 2001; McElroy, 1999). Anxiolytics help alleviate tension and may help reduce explosive outbursts by increasing the provocative stimulus tolerance threshold, and are especially indicated in patients with comorbid obsessive-compulsive or other anxiety disorders (Boyd, 2005).

Pathophysiology
Impulsive behavior, and especially impulsive violence predisposition has been correlated to a low brain serotonin turnover rate, indicated by a low concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebral spinal fluid (CSF). This substrate appears to have important neurochemical properties, acting on the suprachiasmatic nucleus in the hypothalamus, which is the target for serotonergic output from the dorsal and median raphe nuclei. This site plays a role in the maintaining the circadian rhythm and regulation of glucose metabolism. A putative hereditary component to low CSF 5-HIAA and concordantly possibly to impulsive violence has been proposed upon observation that sons of alcoholic fathers who exhibit violent behavior also exhibit exceptionally low CSF 5-HIAA. Along with low CSF 5-HIAA concentration, vagal tone and increased insulin secretion has been observed in patients with confirmed DSM-IV IED.

Possible polymorphisms in the gene for tryptophan hydroxylase, which is responsible for the production of hydroxytryptophan, the precursor of serotonin. Within violent subjects, a significant relationship was observed between CSF 5-HIAA concentration and specific polymorphism genotypes. The phenotypes associated with these genotypes are extreme and it is hypothesized that these polymorphisms may only be significantly correlated to impulsive behavior (Virkkunen, Goldman, Nielsen, and Linnoila, 1995).

Additionally, lesions in the orbital/medial prefrontal cortex and related areas appear to be correlated to impulsively violent behavior, although currently no study has pinned down a specific area involved in IED. Research has shown, however, that damage in these areas, including the amygdale, increases the incidence of impulsive and aggressively violent behavior, and appears to decrease inhibition and ability to control emotion, as well as decreasing the ability to project consequences for their actions. Subjects who exhibit lesions in these regions may also exhibit decreased glucose metabolism, and concordantly decreased brain function in the prefrontal cortex, the region associated with decision making and action planning. More importantly is a reduced action in serotonergic neurons in this region as well as the amygdala (Best, Williams, & Coccaro, 2002).

Dr. Phil McGraw did a show on this disorder, and he had a doctor by the last name of Lawless who has a cutting edge clinic in Texas. This doctor said that metal toxicity in the body is part of the pathophysiology.

intermitent explosive disorder

Hemangiona

A hemangioma an abnormal build up of blood vessels in the skin or internal organs. It is also described as a congenital benign skin lesion consisting of dense, usually elevated masses of dilated blood vessels". In most cases, hemangiomas will disappear over time. They are formed either during gestation or appear during the first few weeks of life and may present as a birthmark. Hemangiomas occur in approximately ten percent of Caucasians, and are less prevalent in other races. Females are three to five times more likely to have hemangiomas than males. Hemangiomas can be vivid superficial lesions, known as capillary hemangiomas (often referred to as "Strawberry Marks"), or they can be deep bluish swelling, known as cavernous hemangiomas. Sometimes they can be both superficial and deep. Approximately eighty percent are located on the face and neck, with the next most prevalent location being the liver. Although hemangiomas are benign, some serious complications can occur.

Complications
The vast majority of hemangiomas are not associated with complications. Hemangiomas may break down on the surface to form ulcers. If the ulceration is deep, significant bleeding may rarely occur. Ulceration on the diaper area can be painful and problematic.

If an hemangioma develops in the larynx, breathing can be compromised. A hemangioma can grow and block one of the eyes, causing an occlusion amblyopia. Very rarely, extremely large hemangiomas can cause high-output heart failure due to the amount of blood that must be pumped to excess blood vessels. Lesions adjacent to bone can also cause erosion of the bone.

The most frequent complaints about hemangiomas, however, stem from psychosocial complications: the condition can affect a person's appearance and can provoke attention and malicious reactions from others. Particular problems occur if the lip or nose is involved, as distortion can be difficult to treat surgically.

Treatment
Most hemangiomas disappear without treatment, leaving minimal or no visible marks. Large hemangiomas can leave visible skin changes secondary to severe stretching of the skin or damage to surface texture. When hemangiomas interfere with vision, breathing, or threaten significant cosmetic injury, they are usually treated. The mainstay of treatment is oral corticosteroid therapy. Other drugs such as interferon or vincristine are sometimes considered if the corticosteroids do not work. If this fails, surgical removal often becomes necessary. Blockage of the airway will often require a tracheostomy to be performed (insertion of an external airway through the front of the neck into the trachea below the level of the obstruction). Smaller raised lesions are sometimes treated with injection of corticosteroid directly into the lesion. Pulsed dye laser can be useful for very early flat lesions if they appear in cosmetically significant areas or for those lesions that leave residual surface blood vessels in the case of incomplete resolution.

Ulceration will usually heal with topical medication and special dressings under medical supervision. Sometimes pulsed dye laser can be used to accelerate healing.

Prognosis
Hemangiomas go through three stages of development and decay:

In the proliferation stage, a hemangioma grows very quickly. This stage can last up to twelve months.
In the rest stage, there is very little change in a hemangioma's appearance. This usually lasts until the infant is one to two years old.
In the involution phase, a hemangioma finally begins to diminish in size. Fifty percent of lesions will have disappeared by age five with the vast majority gone by puberty.

hemangiona

Fiber Myalgia

Fibromyalgia (FM or FMS) is a chronic syndrome (constellation of signs and symptoms) characterized by diffuse or specific muscle, joint, or bone pain, fatigue, and a wide range of other symptoms. It is not contagious, and recent studies suggest that people with fibromyalgia may be genetically predisposed. It affects more females than males, with a ratio of 9:1 by ACR (American College of Rheumatology) criteria. Fibromyalgia is seen in 3% to 6% of the general population, and is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood. The disease is not life-threatening, though the degree of symptoms may vary greatly from day to day with periods of flares (severe worsening of symptoms) or remission. The syndrome is generally perceived as non-progressive, yet that issue is still debated. Fibromyalgia may actually be composed of several clinical entities, ranging from a mild, idiopathic inflammatory process in some individuals to a somatoform disorder resulting from clinical depression in others, with probable overlaps in between. Current diagnostic criteria are insufficient to differentiate these entities.

History
Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis. The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra (fiber) and the Greek words myo (muscle) and algos (pain).

Fibromyalgia was first recognized by the American Medical Association as a true illness and the cause of disability in 1987. In an article the same year, in the Journal of the American Medical Association, a physician named Dr. Don Goldenberg called the syndrome Fibromyalgia.

Symptoms
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch, and usually moderate to severe fatigue. Those affected may also experience heightened sensitivity of the skin (also called allodynia), tingling of the skin (often needle-like), achiness in the muscle tissues, prolonged muscle spasms, weakness in the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of fibromyalgia, and some studies suggest that these sleep disturbances are the result of a sleep disorder called alpha-delta sleep , a condition in which deep sleep (associated with delta EEG waves) is frequently interrupted by bursts of brain activity similar to wakefulness (i.e. alpha waves). Deeper stages of sleep (stages 3 & 4) are often dramatically reduced.

In addition, many patients experience cognitive dysfunction (known as "brain fog" or "fibrofog"), which may be characterized by impaired concentration and short-term memory consolidation, impaired speed of performance, inability to multi-task, and cognitive overload. Many experts suspect that "brain fog" is directly related to the sleep disturbances experienced by sufferers of fibromyalgia. However, the relationship has not been strictly established.

Other symptoms often attributed to fibromyalgia (possibly due to another comorbid disorder) may include myofascial pain syndrome, chronic paresthesia, physical fatigue, irritable bowel syndrome, genitourinary symptoms (such as those associated with the chronic bladder condition interstitial cystitis), dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although it is common in people with fibromyalgia for pain to be widespread, it may also be localized in areas such as the shoulders, neck, back, hips, or other areas. Many sufferers also experience varying degrees of temporomandibular joint disorder. Not all patients have all symptoms.

Fibromyalgia can, but does not always, start as a result of some trauma (such as a traffic accident), major surgery, or disease. Some evidence shows that Lyme Disease is a common trigger of fibromyalgia symptoms. However, there is currently no known strong correlation between any specific type of trigger and the subsequent initiation of symptoms. Symptoms can have a slow onset, and many patients have mild symptoms beginning in childhood, that are often misdiagnosed as growing pains. Symptoms are often aggravated by unrelated illness or changes in the weather. They can become more tolerable or less tolerable throughout daily or yearly cycles; however, many people with fibromyalgia find that, at least some of the time, the condition prevents them from performing normal activities such as driving a car or walking up stairs. The syndrome does not cause inflammation as is present in rheumatoid arthritis, although some anti-inflammatory treatments, such as Ibuprofen and Iontophoresis, may temporarily reduce pain symptoms in some patients.

Variability of symptoms
The following factors have been proposed to exacerbate symptoms of pain in patients:

Increased psychosocial stress
Excessive physical exertion (exercise seems to decrease the pain threshold of people with Fibromyalgia but increase it in healthy individuals)
Lack of slow-wave sleep
Changes in humidity and baromic pressure

Diagnosis
Strictly speaking, there are no "diagnostic criteria" for the disorder. Rather, there exist a widely accepted set of classification criteria for research purposes which were elaborated in 1990 by the Multicenter Criteria Committee of the the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990" define fibromyalgia according to the presence of the following criteria:

A history of widespread pain lasting more than three months—affecting all four quadrants of the body, i.e., both sides, and above and below the waist.
Tender points—there are 18 designated possible tender points (although a person with the syndrome may feel pain in other areas as well). During diagnosis, four kilograms-force (39 newtons) of force is exerted at each of the 18 points; the patient must feel pain at 11 or more of these points for fibromyalgia to be considered.[13] Four kilograms of force is about the amount of pressure required to turn fingernails white or to feel pain sensations on the forehead. This technique was developed by the American College of Rheumatology as a means of classifying an individual as having fibromyalgia for both clinical and research purposes. While these criteria for classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis, they have become the de facto diagnostic criteria in the clinical setting. It should be noted that the number of tender points that may be active at any one time may vary with time and circumstance.

Differentials
A number of other disorders can produce essentially the same symptoms as fibromyalgia. Other disorders known to produce similar symptoms are:

Chronic fatigue syndrome
Depression
Ehlers-Danlos Syndrome
Gulf War syndrome
Influenza
Lead poisoning
Lupus erythematosus (SLE)
Lyme disease
Mercury toxicity
Myofascial pain syndrome
Tendonitis
Tension myositis syndrome
Thyroid disease
Vitamin B12 deficiency
Vitamin D deficiency
Whiplash-associated disorder

Treatment
As with many other disorders, there is no universal cure for fibromyalgia. However, a steady interest in the disorder on the part of academic researchers as well as pharmaceutical interests has led to improvements in its treatment, which ranges from symptomatic prescription medication to alternative and complementary medicine.

Medications

Tricyclic antidepressants (TCAs)
Traditionally, low doses of sedating antidepressants (e.g. amitriptyline and trazodone) have been used to reduce the sleep disturbances that are associated with fibromyalgia and are believed by some practitioners to exacerbate the symptoms of the disorder. Because depression often accompanies chronic illness, these antidepressants may provide additional benefits to patients suffering from depression. Amitriptyline is often favoured as it can also have the effect of providing relief from neuralgenic or neuropathic pain.

Selective serotonin reuptake inhibitors (SSRIs)
Standard clinical doses of newer anti-depressants (SSRIs) like Citalopram (Celexa) have demonstrated good efficacy in some cases of Fibromyalgia.

Anti-seizure drugs
Anti-seizure drugs are also sometimes used, such as gabapentin and pregabalin (Lyrica). Pregabalin, originally used for the nerve pain suffered by diabetics, has been approved by the American Food and Drug Administration for treatment of fibromyalgia. A randomized controlled trial of pregabalin 450 mg/day found that a number needed to treat of 6 patients for one patient to have 50% reduction in pain.

Dopamine agonists
Dopamine agonists, such as Mirapex, are now being studied and used to treat fibromyalgia.

Combination therapy
Amitriptyline and fluoxetine can be combined according to a randomized crossover study.

Non-drug treatment
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Physical treatments
Studies have found gentle exercise, such as warm-water pool therapy, improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia. Stretching is recommended to ease muscle stiffness and fatigue, as is mild aerobic exercise. Because strenuous activity can exacerbate the muscle pain and fatigue already present, patients are advised to begin slowly and build their activity level gradually to avoid inducing additional pain. Exercise may be poorly tolerated in more severe cases with abnormal fatigue after exercise. Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy and/or massage may find them beneficial. Chiropractic care can also help relieve pain due to fibromyalgia.

A holistic approach—including managing diet, sleep, stress, activity, and pain—is used by many patients. Dietary supplements, massage, chiropractic care, managing blood sugar levels, and avoiding known triggers when possible means living as well as it is in the patient's power to do.

Mental treatments
As the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic. Although there is no universally accepted cure, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.

Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain. Neurofeedback has also shown to provide temporary and long-term relief.

Treatment for the "brain fog" has not yet been developed, however biofeedback and self-management techniques such as pacing and stress management may be helpful for some patients. The use of medication to improve sleep helps some patients, as does supplementation with folic acid and ginkgo biloba.

Investigational treatments
Milnacipran, a member of the new series of drugs known as serotonin-norepinephrine reuptake inhibitors (SNRIs), is available in parts of Europe where it has been safely prescribed for other disorders. On May 22nd, 2007, a Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as a treatment of fibromyalgia syndrome. At this time, only initial top-line results are available and further analyses will be completed in the coming weeks. If ultimately approved by the FDA, Milnacipran could be distributed in the United States as early as summer, 2008.

Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol the efficacy of guaifenesin in treating fibromyalgia has not been proven in properly designed research studies. Indeed, a controlled study conducted by researchers at Oregon Health Science University in Portland failed to demonstrate any benefits from this treatment, though these results have been contested.

Another drug being researched is the use of dextromethorphan, which is sold over the counter as a cough suppressant.

Living with fibromyalgia
Fibromyalgia can affect every aspect of a person's life. While neither degenerative nor fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can severely curtail social activity and recreation, and as many as 30% of those diagnosed with fibromyalgia are unable to maintain full-time employment. Like others with disabilities, individuals with FMS often need accommodations to fully participate in their education or remain active in their careers.

In the United States, those who are unable to maintain a full-time job due to the condition may apply for Social Security Disability benefits. Although fibromyalgia has been recognized as a genuine, severe medical condition by the government, applicants are often denied benefits. However, most are awarded benefits at the state judicial level; the entire process often takes two to four years.

In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistance.

Fibromyalgia is often referred to as an "invisible" illness or disability due to the fact that generally there are no outward indications of the illness or its resulting disabilities. The invisible nature of the illness, as well as its relative rarity and the lack of understanding about its pathology, often has psychosocial complications for those that have the syndrome. Individuals suffering from invisible illnesses in general often face disbelief or accusations of malingering or laziness from others that are unfamiliar with the syndrome.

There are a variety of support groups on the Web that cater to fibromyalgia sufferers. Some are offered at the bottom of this article.

Hypotheses on the cause of fibromyalgia
The cause of fibromyalgia is currently unknown. Over the past few decades, many hypotheses have been presented, and the understanding of the disorder has changed dramatically. Most current hypotheses explain only a few symptoms of the disorder and are thus incomplete.

Genetics
Using self-report of "Chronic Widespread Pain" (CWP) as a surrogate marker for fibromyalgia, the Swedish Twin Registry suggests a modest genetic contribution:
Monozygotic twins with CWP have a 15% chance that their twin sibling has CWP
Dizygotic twins with CWP have a 7% chance that their twin sibling has CWP

Stress
Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia, and that PTSD is linked with fibromyalgia. The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.

Dopamine abnormality
Dopamine is a neurotransmitter that is known to play a role in the pathogenesis of Parkinson's disease as well as restless leg syndrome. Pramipexole, a drug that stimulates dopamine D2/D3 receptors and is used to treat both Parkinson's disease and restless legs syndrome, has also been shown in controlled trials to have a positive effect on fibromyalgia. The National Fibromyalgia Association (NFA) recently circulated a press release describing a report that appears in the January 2007 Journal of Pain article which reports that fibromyalgia patients demonstrate a significant reduction in dopamine synthesis in the very areas of the brain wherein dopamine plays a role in fighting painful bodily sensations (i.e. analgesia).

Serotonin
Serotonin is a neurotransmitter that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration, digestion. One hypothesis of the pathophysiology fibromyalgia causation is a dysregulation of serotonin and norepinephrine in the neural synapse, contributing to many associated fibromyalgia symptoms.

The drug Cymbalta, originally used to treat depression, has been used successfully in treating fibromyalgia off-label. Cymbalta has not been approved by the FDA for fibromyalgia.

On October 19 2006, Eli Lilly issued a press release stating they had done trials which found Cymbalta, 60 mg once or twice daily, significantly reduced pain in more than half of women treated for fibromyalgia (FM), with and without major depression, according to 12-week data presented at the annual meeting of the American College of Rheumatology. Eli Lilly is in Phase III of its FM trials and is expected to submit a supplementary new drug application (sNDA) to the FDA for approval of Cymbalta for FM within the next 12 months.

Critics argue that randomized controlled trials of FM are difficult due to factors such as a lack of understanding of the pathophysiology and a heterogeneous FM patient population. Although there is a lack of understanding of what causes FM, it is estimated that approximately 5-7% of the U.S. population has FM, representing a large patient clientèle. Eli Lilly hopes Cymbalta will be the first FDA approved medication for FM and had been promoting Cymbalta for FM since 2004.

In the study testing the efficacy of Cymbalta for FM, participants completed several questionnaires to measure the amount of pain and discomfort the disease caused them at the beginning of the study, and then at the end of each of the first two weeks and every second week for the remaining 12 weeks of the study. Researchers also tested the participants for depression.

Women who took Cymbalta had significantly less pain and discomfort than those who took the placebo. For men, who made up only 11 percent of the study, there was no effect from taking the medication compared with a placebo. Reportedly, depression played no part in whether or not the drug worked to control pain. The change in the level of women's pain was particularly pronounced after a month of taking the drug, then levelled off a bit before dropping again near the end of the study.

However, in one of the primary measures of pain there was no significant difference between the two groups at the end of the 12-week trial. Also, because the trial lasted only 12 weeks, it is impossible to tell how well the drug would control treatment for a longer period of time. Lastly, the primary researcher on the project has received more than $10,000 in consulting fees from Eli Lilly, the manufacturer of Cymbalta, all other researchers also had ties to the company, reflecting a conflict of interest.

Sleep disturbance
Electroencephalography studies have shown that people with fibromyalgia lack of slow-wave sleep and circumstances that interfere with stage four sleep (such as drug use, pain, depression, serotonin deficiency, or anxiety) may cause or worsen the condition.[33] According to the sleep disturbance theory, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The theory supposes that stage 4 sleep is critical to the function of the nervous system, as it is during that stage that certain neurochemical processes in the body 'reset'. In particular, pain causes the release of the neuropeptide substance P in the spinal cord which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound to become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance theory holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect.

The sleep disturbance/substance P theory is could explains "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures.[citation needed] The theory posits that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. The theory could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system. The sleep disturbance theory could also provide a possible connection between fybromyalgia, chronic fatigue syndrome and post-polio syndrome through damage to the ascending reticular activating system of the reticular formation. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.

Critics of the theory argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.

HGH
An alternate theory suggests that stress-induced problems in the hypothalamus may lead to reduced sleep and reduced production of human growth hormone during slow-wave sleep. People with fibromyalgia tend to produce inadequate levels of HGH. Most patients with FM with low IGF-I levels failed to secrete GH after stimulation with clonidine and l-dopa.

This view is supported by the fact that those hormones under the direct or indirect control of HGH, including IGF-1, cortisol, leptin and neuropeptide Y are abnormal in people with fibromyalgia,[34] In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep though there is disagreement about the theory.

Deposition disease
Another theory involves phosphate and calcium accumulation in cells that eventually reaches a level to impede the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the removal of excess phosphates from the blood stream. This theory posits that fibromyalgia is an inherited disorder, and that phosphate build-up in cells is gradual (but can be accelerated by trauma or illness). Calcium is required for the excess phosphate to enter the cells. The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.

Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the muscles to detect lumps and areas of spasm that are thought to be caused by an excess of calcium in the cytosol of the cells. This mapping approach is specific to deposition theory, and is not related to the trigger points of myofascial pain syndrome.

While this theory does not identify the causative mechanism in the kidneys, it proposes a treatment known as guaifenesin therapy. This treatment involves administering the drug guaifenesin to a patient's individual dosage, avoiding salicylic acid in medications or on the skin, and, if the patient is also hypoglycemic, a diet designed to keep insulin levels low.

The phosphate build-up theory explains many of the symptoms present in fibromyalgia and proposes an underlying cause. The guaifenesin treatment, based on this theory, has received mixed reviews, with some practitioners claiming many near-universal successes and others reporting no success. Only one controlled clinical trial has been conducted to date, and it showed no evidence of the efficacy of this treatment protocol. This study was criticized for not limiting the salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method. As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the theory. It should be noted that nothing in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.

Fibromyalgia as severe TMS
Another theory is that fibromyalgia is a severe form of Tension myositis syndrome (TMS) which is a mindbody disorder popularized in the books on healing back, neck, and other limb pain by Dr. John E. Sarno of the Howard A. Rusk Institute of Rehabilitation Medicine. Briefly the theory is that in many cases chronic pain is the result of physical changes (primarily mild oxygen deprivation) caused by the brain through the autonomic nervous system as a strategy for distracting you from painful or dangerous unconscious emotions such as repressed anger. Treatment is through a program of education and attitude change which stops the brain from using that chronic pain strategy. Psychotherapy is suggested in the minority of cases where education alone is not sufficient.

Other hypotheses
Other theories relate to various toxins from the patient's environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to intestinal bacteria, neurotransmitter disruptions in the central nervous system, and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule. This association has not repeated in a number of related studies, and the US-FDA concluded "the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants." Due to the multi-systemic nature of illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging branch of medical science called psychoneuroimmunology (PNI) is looking into how the various theories fit together.

Another hypothesis on the cause of symptoms in Fibromyalgia states that patients suffer from vasomotor dysregulation causing improper vascularflow and hypoperfusion (decreased blood flow to a given tissue or organ).

Comorbid diseases
Cutting across several of the above hypotheses is a hypothesis that proposes that fibromyalgia is almost always a comorbid disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia[50], and a large coeliac support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurance with chronic fatique.

By this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery. In other cases the two disorders coexist.

fiber myalgia

Manegment de Diabetic

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which could eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all diabetics who have had diabetes for 15 years or more[citation needed]. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes.

Signs and symptoms
Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read and drive. In some cases, the vision will get better or worse during the day.

As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (haemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours.

These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs vision. In extreme cases, a person will only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.

On fundoscopic exam, a doctor will see cotton wool spots, flame hemorrhages, and dot-blot hemorrhages.

Diabetes mellitus
Types of Diabetes
Diabetes mellitus type 1
Diabetes mellitus type 2
Gestational diabetes
Pre-diabetes:
Impaired fasting glycaemia
Impaired glucose tolerance

Disease Management
Diabetes management:
•Diabetic diet
•Anti-diabetic drugs
•Conventional insulinotherapy
•Intensive insulinotherapy
Other Concerns
Cardiovascular disease
Diabetic comas:
•Diabetic hypoglycemia
•Diabetic ketoacidosis
•Nonketotic hyperosmolar

Diabetic myonecrosis
Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy

Diabetes and pregnancy

Blood tests
Blood sugar
Fructosamine
Glucose tolerance test
Glycosylated hemoglobin

Pathogenesis
Diabetic retinopathy is result of microvascular retinal changes. Hyperglycemia-induced pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damage change the formation of blood retinal barrier and also make retinal blood vessel become more permiable.

Small blood vessels – such as those in the eye – are especially vulnerable to poor blood glucose control. An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any changes in their vision.

Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.

As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage. The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause Neovascular Glaucoma. Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative diabetic retinopathy (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.

Risk factors
All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset). The longer a person has diabetes, the higher the risk of developing some ocular problem. Between 40 to 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. [2] After 20 years of diabetes, nearly all patients with type 1 diabetes and >60% of patients with type 2 diabetes have some degree of retinopathy.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes. It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.


Diagnosis
Diabetic retinopathy is detected during an eye examination that includes:
Visual acuity test: This test uses an eye chart to measure how well a person sees at various distances (i.e., visual acuity).
Pupil dilation: The eye care professional places drops into the eye to widen the pupil. This allows him or her to see more of the retina and look for signs of diabetic retinopathy. After the examination, close-up vision may remain blurred for several hours.
Ophthalmoscopy: This is an examination of the retina in which the eye care professional: (1) looks through a device with a special magnifying lens that provides a narrow view of the retina, or (2) wearing a headset with a bright light, looks through a special magnifying glass and gains a wide view of the retina. Note that hand-held ophthalmoscopy is insufficient to rule out significant and treatable diabetic retinopathy.
Ocular Coherence Tomography or OCT:This is a scan similar to an ultrasound which is used to measure the thickness of the retina. It produces a cross section of the retina and can determine if there is any swelling or leakage.
Tonometry: A standard test that determines the fluid pressure (intraocular pressure) inside the eye. Elevated pressure is a possible sign of glaucoma, another common eye problem in people with diabetes.
Digital Retinal Screening Programs: Systematic programs for the early detection of eye disease including diabetic retinopathy are becoming more common, such as in the UK, where all people with diabetes mellitus are offered retinal screening at least annually. This involves digital image capture and transmission of the images to a digital reading center for evaluation and treatment referral. See Vanderbilt Ophthalmic Imaging Center and the English National Screening Programme for Diabetic Retinopathy
Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs for the early detection of diabetic retinopathy using slit-lamp biomicroscopy. These exist either as a standalone scheme or as part of the Digital program (above) where the digital photograph was considered to lack enough clarity for detection and/or diagnosis of any retinal abnormality.
Of the 18 million to 20 million diabetics in the United States, only about half receive annual eye examinations for retinopathy risk. In an effort to increase diabetic patient’s compliance for regular eye exams, Digital Healthcare, a Wake Forest, NC company specializing in retinal risk assessment, today announced the introduction of Retasure, a new retinal imaging risk assessment solution that connects primary care physicians with ophthalmic specialists to perform retinal imaging.

Retasure allows primary care physicians to capture digital images of diabetic patients’ retinas in a non-invasive procedure that takes just a few minutes. The images are then transmitted over a secure, HIPPA compliant network to a board certified ophthalmologist at an accredited reading center for examination. Results are returned to the primary care physician within 72 hours.

Retasure has been available throughout Europe, and more than one million people have are benefiting from the system annually.

The eye care professional will look at the retina for early signs of the disease, such as: (1) leaking blood vessels, (2) retinal swelling, such as macular edema, (3) pale, fatty deposits on the retina (exudates) – signs of leaking blood vessels, (4) damaged nerve tissue (neuropathy), and (5) any changes in the blood vessels.

Should the doctor suspect macular edema, he or she may perform a test called fluorescein angiography. In this test, a special dye is injected into the arm. Pictures are then taken as the dye passes through the blood vessels in the retina. This test allows the doctor to find the leaking blood vessels.


Management
There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease. In fact, even people with advanced retinopathy have a 90 percent chance of keeping their vision when they get treatment before the retina is severely damaged. Still, the best way of addressing diabetic retinopathy is to monitor it vigilantly and ensure that it does not happen in the first place by careful blood glucose control and limitation of dietary fructose.

These three treatments are laser surgery, injection of triamcinolone into the eye and vitrectomy. It is important to note that although these treatments are very successful, they do not cure diabetic retinopathy. Caution should be exercised in treatment with laser surgery since it causes a loss of retinal tissue. It is often more prudent to inject triamcinolone. In some patients it results in a marked increase of vision, especially if there is an edema of the macula.

Avoiding tobacco use and correction of associated hypertension are important therapeutic measures in the management of diabetic retinopathy.

Laser surgery
A type of laser surgery called panretinal photocoagulation, or PRP, is used to treat severe macular edema and proliferative retinopathy. The goal is to create 1 000 - 2 000 burns in the retina with the hope of reducing the retina's oxygen demand, and hence the possibility of ischemia. In treating advanced diabetic retinopathy, the burns are used to destroy the abnormal blood vessels that form at the back of the eye.

Before the surgery, the ophthalmologist dilates the pupil and applies anesthetic drops to numb the eye. In some cases, the doctor also may numb the area behind the eye to prevent any discomfort. The lights in the office are also dimmed to aid in dilating the pupil. The patient sits facing the laser machine while the doctor holds a special lens to the eye. During the procedure, the patient may see flashes of light. These flashes may eventually create an uncomfortable stinging sensation for the patient. After the laser treatment, patients should be advised not to drive for a few hours while the pupils are still dilated. Vision may remain a little blurry for the rest of the day, though there should not be much pain in the eye.

Scatter laser treatment
Rather than focus the light on a single spot, the eye care professional may make hundreds of small laser burns away from the center of the retina, a procedure called scatter laser treatment or panretinal photocoagulation. The treatment shrinks the abnormal blood vessels. Patients may lose some of their peripheral vision after this surgery, but the procedure saves the rest of the patient's sight. Laser surgery may also slightly reduce colour and night vision.

A person with proliferative retinopathy will always be at risk for new bleeding as well as glaucoma, a complication from the new blood vessels. This means that multiple treatments may be required to protect vision.

Vitrectomy
Instead of laser surgery, some people need an eye operation called a vitrectomy to restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous. It involves removing the cloudy vitreous and replacing it with a saline solution made up of salt and water. Because the vitreous is mostly water, there should be no change between the saline solution and the normal vitreous.

Studies show that people who have a vitrectomy soon after a large hemorrhage are more likely to protect their vision than someone who waits to have the operation. Early vitrectomy is especially effective in people with insulin-dependent diabetes, who may be at greater risk of blindness from a hemorrhage into the eye.

Vitrectomy is often done under local anesthesia. The doctor makes a tiny incision in the sclera, or white of the eye. Next, a small instrument is placed into the eye to remove the vitreous and insert the saline solution into the eye.

Patients may be able to return home soon after the vitrectomy, or may be asked to stay in the hospital overnight. After the operation, the eye will be red and sensitive, and patients usually need to wear an eyepatch for a few days or weeks to protect the eye. Medicated eye drops are also prescribed to protect against infection.

manegment de diabetic

Celiac Disese

Coeliac disease or celiac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed individuals in all age groups after early infancy. Symptoms may include diarrhoea, failure to thrive (in children) and fatigue, but these may be absent and associated symptoms in all other organ systems have been described. It affects approximately 1% of Indo-European populations, though it is significantly underdiagnosed. A growing portion of diagnoses are being made in asymptomatic persons as a result of increasing screening.

Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat (and similar proteins of the tribe Triticeae which includes other cultivars such as barley and rye). Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the bowel tissue, causing an inflammatory reaction. That leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrients. The only effective treatment is a lifelong gluten-free diet.

This condition has several other names, including: cœliac disease (with ligature), c(o)eliac sprue, non-tropical sprue, endemic sprue, gluten enteropathy or gluten-sensitive enteropathy, and gluten intolerance. The term coeliac derives from the Greek κοιλιακος (koiliakos, abdominal), and was introduced in the 19th century in a translation of what is generally regarded as an ancient Greek description of the disease by Aretaeus of Cappadocia.

Signs and symptoms
Classic symptoms of coeliac disease include diarrhoea, weight loss (or stunted growth in children), and fatigue, but while coeliac disease is primarily a bowel disease, bowel symptoms may also be limited or even absent. Some patients are diagnosed with symptoms related to the decreased absorption of nutrients or with various symptoms which, although statistically linked, have no clear relationship with the malfunctioning bowel. Given this wide range of possible symptoms, the classic triad is no longer a requirement for diagnosis.

Children between 9 and 24 months tend to present with bowel symptoms and growth problems shortly after first exposure to gluten-containing products. Older children may have more malabsorption-related problems and psychosocial problems, while adults generally have malabsorptive problems. Many adults with subtle disease only have fatigue or anaemia.

Gastrointestinal
The diarrhoea characteristic of coeliac disease is pale, voluminous and malodorous. Abdominal pain and cramping, bloatedness with abdominal distention (thought to be due to fermentative production of bowel gas) and mouth ulcers[4] may be present. As the bowel becomes more damaged, a degree of lactose intolerance may develop. However, the variety of gastrointestinal symptoms that may be present in patients with coeliac disease is great, and some may have a normal bowel habit or even tend towards constipation. Frequently the symptoms are ascribed to irritable bowel syndrome (IBS), only later to be recognized as coeliac disease; a small proportion of patients with symptoms of IBS have underlying coeliac disease, and screening may be justified.

Coeliac disease leads to an increased risk of both adenocarcinoma and lymphoma of the small bowel, which returns to baseline with diet. Longstanding disease may lead to other complications, such as ulcerative jejunitis (ulcer formation of the small bowel) and stricturing (narrowing as a result of scarring).

Malabsorption-related
The changes in the bowel make it less able to absorb nutrients, minerals and the fat-soluble vitamins A, D, E, and K.

The inability to absorb carbohydrates and fats may cause weight loss (or failure to thrive/stunted growth in children) and fatigue or lack of energy.
Anaemia may develop in several ways: iron malabsorption may cause iron deficiency anaemia, and folic acid and vitamin B12 malabsorption may give rise to megaloblastic anaemia.
Calcium and vitamin D malabsorption (and compensatory secondary hyperparathyroidism) may cause osteopenia (decreased mineral content of the bone) or osteoporosis (bone weakening and risk of fragility fractures).
A small proportion (10%) have abnormal coagulation due to deficiency of vitamin K, and are slightly at risk for abnormal bleeding.
Coeliac disease is also associated with bacterial overgrowth of the small intestine, which can worsen malabsorption, or cause malabsorption after treatment.

Miscellaneous
Coeliac disease has been linked with a number of conditions. In many cases it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.

IgA deficiency is present in 2% of patients with coeliac disease, and in turn this condition features a tenfold increased risk of coeliac disease. Other features of this condition are an increased risk of infections and autoimmune disease.
Dermatitis herpetiformis; this itchy cutaneous condition has been linked to a transglutaminase enzyme in the skin, features small bowel changes identical to those in coeliac disease and occurs more often (2%) in patients with coeliac disease.
Neurological associations: epilepsy, ataxia (coordination problems), myelopathy and peripheral neuropathy have all been linked with coeliac disease, but the strength of these associations and the causality is still subject of debate.
Growth failure and/or pubertal delay in later childhood can occur even without obvious bowel symptoms or severe malnutrition. Evaluation of growth failure often includes coeliac screening.
Miscarriage and infertility.
Hyposplenism (a small and underactive spleen) - it is unclear whether this actually increases infection risk in coeliacs.
Other auto-immune disorders: diabetes mellitus type 1, autoimmune thyroiditis, primary biliary cirrhosis and microscopic colitis.

Role of other grains
Wheat varieties or subspecies containing gluten such as spelt and Kamut®, and the rye/wheat hybrid triticale, also trigger symptoms.

Barley and rye also induce symptoms of coeliac disease. A small minority of coeliac patients also react to oats. Most probably oats produce symptoms due to cross contamination with other grains in the fields or in the distribution channels. There is at least one oat vendor (McCann's) which, while not claiming to be gluten-free, points out that the risk of contamination is low due to the processes they use. Other cereals, such as maize (corn), quinoa, millet, sorghum, rice are safe for a patient to consume. Other carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.

Diagnosis
There are several tests that can be used to assist in diagnosis. The level of symptoms may determine the order of the tests, but all tests lose their usefulness if the patient is already taking a gluten-free diet. Intestinal damage begins to heal within weeks of gluten being removed from the diet, and antibody levels decline over months. For those who have already started on a gluten-free diet, it may be necessary to perform a re-challenge with 10 g of gluten (four slices of bread) per day over 2–6 weeks before repeating the investigations. Those who experience severe symptoms (e.g. diarrhoea) earlier can be regarded as sufficiently challenged and can be tested earlier.

Combining findings into a prediction rule to guide use of endoscopy reported a sensitivity of 100% (it would identify all the cases) and specificity of 61% (it would be incorrectly positive in 39%). The prediction rule recommends that patients with high risk symptoms or positive serology should undergo endoscopy. The study defined high risk symptoms as weight loss, anaemia (haemoglobin less than 120 g/l in females and less than 130 g/l in males), or diarrhoea (more than three loose stools per day).

Blood tests
Serology by blood test is useful both in diagnosing coeliac disease (high sensitivity of about 98%, i.e. it misses 2 in 100 cases) and in excluding it (high specificity of over 95%, i.e. a positive test is most likely confirmative of coeliac disease rather than another condition). Because of the major implications of a diagnosis of coeliac disease, professional guidelines recommend that a positive blood test is still followed by an endoscopy. A negative test may still prompt a biopsy if the suspicion remains very high; this would pick up the remaining 2% undiagnosed cases, as well as offering alternative explanations for the symptoms. As such, endoscopy with biopsy is still considered the gold standard in the diagnosis of coeliac disease.

Due to its high sensitivity, serology has been proposed as a screening measure, because the presence of antibodies would detect previously undiagnosed cases of coeliac disease and prevent its complications in those patients. Serology may also be used to monitor adherence to diet: in those who still ingest gluten, antibody levels remain elevated.

Four serological blood tests exist for coeliac disease. The most widely used ones detect an antibody of the IgA type against particular antigens in the small bowel. Older tests detected antibodies against reticulin (ARA) or gliadin (AGA), but recent evidence supports the use of the more modern tests, namely those detecting IgA antibodies against endomysium (EMA) or tissue transglutaminase (TTG). Generally, serology may be unreliable in young children, with anti-gliadin performing somewhat better than other tests in children under five. Serology tests are based on indirect immunofluorescence (reticulin, gliadin and endomysium) or ELISA (gliadin or tissue transglutaminase).

Guidelines recommend that a total serum IgA level is checked in parallel, as coeliac patients with IgA deficiency may be unable to produce the antibodies on which these tests depend ("false negative"). In those patients, IgG antibodies against transglutaminase (IgG-TTG) may be diagnostic.

Endoscopy
Endoscopic still of duodenum of patient with coeliac disease showing scalloping of folds.
Schematic of the Marsh classification of upper jejunal pathology in coeliac diseaseAn upper endoscopy with biopsy of the duodenum (beyond the duodenal bulb) or jejunum is performed. It is important for the physician to obtain multiple samples (four to eight) from the duodenum. Not all areas may be equally affected; if biopsies are taken from healthy bowel, it would result in false negative results.

Most patients with coeliac disease have a small bowel that appears normal on endoscopy; however, five endoscopic findings have been associated with a high specificity for coeliac disease when all are found: scalloping of the small bowel folds (pictured), paucity in the folds, a mosaic pattern to the mucosa (described as a cracked-mud appearance), prominence of the submucosal blood vessels and a nodular pattern to the mucosa.

Until the 1970s, biopsies were obtained using metal capsules attached to a suction device. The capsule was swallowed and allowed to pass into the small intestine. After X-ray verification of its position, suction was applied to collect part of the intestinal wall inside the capsule. One much utilized capsule system is the Watson capsule. This method has now been largely replaced by fiberoptic endoscopy, which carries a higher sensitivity rate and a lower error frequency.

Pathology
The classic pathology changes of coeliac disease in the small bowel are categorized by the "Marsh classification":
Marsh stage 0: normal mucosa
Marsh stage 1: increased number of intra-epithelial lymphocytes, usually exceeding 20 per 100 enterocytes
Marsh stage 2: proliferation of the crypts of Lieberkuhn
Marsh stage 3: partial or complete villous atrophy
Marsh stage 4: hypoplasia of the small bowel architecture

The changes classically improve or reverse after gluten is removed from the diet, so many official guidelines recommend a repeat biopsy several (4–6) months after commencement of gluten exclusion.

In some cases a deliberate gluten challenge, followed by biopsy, may be conducted to confirm or refute the diagnosis. A normal biopsy and normal serology after challenge indicates the diagnosis may have been incorrect. Patients are warned that one does not "outgrow" coeliac disease in the same way as childhood food intolerances.

Other diagnostic tests
Other tests that may assist in the diagnosis are blood tests for a full blood count, electrolytes, calcium, renal function, liver enzymes, vitamin B12 and folic acid levels. Coagulation testing (prothrombin time and partial thromboplastin time) may be useful to identify deficiency of vitamin K, which predisposes patients to hemorrhage. These tests should be repeated on follow-up, as well as anti-tTG titres.

Some professional guidelines recommend screening of all patients for osteoporosis by DXA/DEXA scanning.

Screening and case finding
There is significant debate as to the benefits of screening. Some studies suggest that early detection would decrease the risk of osteoporosis and anaemia. In contrast, a cohort studied in Cambridge suggested that people with undetected coeliac disease had a beneficial risk profile for cardiovascular disease (less overweight, lower cholesterol levels).

Clinical scenarios in which screening may be justified include type 1 diabetes, unexplained iron-deficiency anemia, Down's syndrome, Turner's syndrome, irritable bowel syndrome, lupus, and autoimmune thyroid disease.

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