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Ailmemts & Remedies

Neuropathy

Definition:
Neuropathy is a general term that refers to diseases or malfunctions of the nerves. Any nerves at any location in the body can be damaged from injury or disease. Neuropathy is often classified according to the types or location of nerves that are affected. It is a disease caused by changes in the nerve cells. These changes may be age related. The degeneration is accelerated and aggravated if the patient suffers from diabetes, hypertension or has an abnormal lipid profile. Neuropathy can affect all three nervous systems — central, peripheral and autonomous.

If the central nervous system is affected, memory and cognitive skills decline. Forgetfulness becomes an accepted way of life. Peripheral neuropathy produces the most obvious, incapacitating, and distressing symptoms.

In some, the affected nerves may produce symptoms that are symmetrical (occurring in both limbs) and appear first in the furthest extremity. There may be paraesthesia (tingling, burning or numb sensation), hyperalgesia (abnormally acute pain sensation to innocuous stimuli) or deep aching. The symptoms tend to get worse at night and interfere with sleep.

Neuropathy can also be classified according to the disease causing it. (For example, neuropathy from the effects of diabetes is called diabetic neuropathy.)

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Types of Neuropathy::

Peripheral neuropathy: Peripheral neuropathy is when the nerve problem affects the nerves outside of the brain and spinal cord. These nerves are part of the peripheral nervous system. Accordingly, peripheral neuropathy is neuropathy that affects the nerves of the extremities- the toes, feet, legs, fingers, hands, and arms. The term proximal neuropathy has been used to refer to nerve damage that specifically causes pain in the thighs, hips, or buttocks.

Cranial neuropathy: Cranial neuropathy occurs when any of the twelve cranial nerves (nerves that exit from the brain directly) are damaged. Two specific types of cranial neuropathy are optic neuropathy and auditory neuropathy. Optic neuropathy refers to damage or disease of the optic nerve that transmits visual signals from the retina of the eye to the brain. Auditory neuropathy involves the nerve that carries signals from the inner ear to the brain and is responsible for hearing.

Autonomic neuropathy: Autonomic neuropathy is damage to the nerves of the involuntary nervous system, the nerves that control the heart and circulation (including blood pressure), digestion, bowel and bladder function, the sexual response, and perspiration. Nerves in other organs may also be affected.

Focal neuropathy: Focal neuropathy is neuropathy that is restricted to one nerve or group of nerves, or one area of the body. Symptoms of focal neuropathy usually appear suddenly.

Symptoms:
Neuropathy is associated with varied characteristic symptoms. Although some people with neuropathy may not have symptoms, certain symptoms are common. The degree to which an individual is affected by a particular neuropathy varies.

Damage to the sensory nerves is common in peripheral neuropathy. Symptoms often begin in the feet with a gradual onset of loss of feeling, numbness, tingling, or pain and progress toward the center of the body with time. The arms or legs may be involved. The inability to determine joint position may also occur, which can result in clumsiness or falls. Extreme sensitivity to touch can be another symptom of peripheral neuropathy. The sensation of numbness and tingling of the skin is medically known as paresthesia.

The loss of sensory input from the foot means that blisters and sores on the feet may develop rapidly and not be noticed. Because there is a reduced sensation of pain, these sores may become infected and the infection may spread to deeper tissues, including bone. In severe cases, amputation may be necessary.

When damage to the motor nerves (those that control movement) occurs, symptoms include weakness, loss of reflexes, loss of muscle mass, cramping, and/or loss of dexterity.

Autonomic neuropathy, or damage to the nerves that control the function of organs and glands, may manifest with a wide variety of symptoms, including:

•Nausea, vomiting, or abdominal bloating after meals

•Urinary symptoms, such as incontinence, difficulty beginning to urinate, or feeling that the bladder was not completely emptied

•Impotence (erectile dysfunction) in men

•Dizziness or fainting

•Constipation or diarrhea

•Blurred vision

•Heat intolerance or decreased ability to sweat

•Hypoglycemia unawareness: Low blood sugar levels (hypoglycemia) are associated with trembling, sweating, and palpitations. In people with autonomic neuropathy, these characteristic symptoms may not occur, making dangerously low blood sugar levels difficult to recognize.

Causes:
Neuropathy or nerve damage may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states.
Some of them are :-

•Diabetes: Diabetes is the condition most commonly associated with neuropathy. The characteristic symptoms of peripheral neuropathy often seen in people with diabetes are sometimes referred to as diabetic neuropathy. The risk of having diabetic neuropathy rises with age and duration of diabetes. Neuropathy is most common in people who have had diabetes for decades and is generally more severe in those who have had difficulty controlling their diabetes, or those who are overweight or have elevated blood lipids and high blood pressure.

•Vitamin deficiencies: Deficiencies of the vitamins B12 and folate as well as other B vitamins can cause damage to the nerves.

•Autoimmune neuropathy: Autoimmune diseases such as rheumatoid arthritis, systemic lupus, and Guillain-Barre syndrome can cause neuropathies.

•Infection: Some infections, including HIV/AIDS, Lyme disease, leprosy, and syphilis, can damage nerves.

•Post-herpetic neuralgia: Post-herpetic neuralgia, a complication of shingles (varicella-zoster virus infection) is a form of neuropathy.

•Alcoholic neuropathy: Alcoholism is often associated with peripheral neuropathy. Although the exact reasons for the nerve damage are unclear, it probably arises from a combination of damage to the nerves by alcohol itself along with the poor nutrition and associated vitamin deficiencies that are common in alcoholics.

•Genetic or inherited disorders: Genetic or inherited disorders can affect the nerves and are responsible for some cases of neuropathy. Examples include Friedreich’s ataxia and Charcot-Marie-Tooth disease.

•Amyloidosis: Amyloidosis is a condition in which abnormal protein fibers are deposited in tissues and organs. These protein deposits can lead to varying degrees of organ damage and may be a cause of neuropathy.

•Uremia: Uremia (a high concentration of waste products in the blood due to kidney failure) can lead to neuropathy.

•Toxins and poisons can damage nerves. Examples include, gold compounds, lead, arsenic, mercury, some industrial solvents, nitrous oxide, and organophosphate pesticides.

•Drugs or medication: Certain drugs and medications can cause nerve damage. Examples include cancer therapy drugs such as vincristine (Oncovin, Vincasar), and antibiotics such as metronidazole (Flagyl), and isoniazid (Nydrazid, Laniazid).

•Trauma/Injury: Trauma or injury to nerves, including prolonged pressure on a nerve or group of nerves, is a common cause of neuropathy. Decreased blood flow (ischemia) to the nerves can also lead to long-term damage.

•Tumors: Benign or malignant tumors of the nerves or nearby structures may damage the nerves directly, by invading the nerves, or cause neuropathy due to pressure on the nerves.

•Idiopathic: Idiopathic neuropathy is neuropathy for which no cause has been established. The term idiopathic is used in medicine to denote the fact that no cause is known.

Diagnosis:
The diagnosis of neuropathy and its cause involve a thorough medical history and physical examination to help your health care professional determine the cause and severity of neuropathy. A neurological examination, testing the reflexes and function of sensory and motor nerves, is an important component of the initial examination.

Although there are no blood tests that are specific for determining whether of not neuropathy is present, when neuropathy is suspected, blood tests are often used to check for the presence of diseases and conditions (for example, diabetes or vitamin deficiencies) that may be responsible for nerve damage.

Imaging studies such as X-rays, CT scans, and MRI scans may be performed to look for sources of pressure on or damage to nerves.

Exams and Tests:

Specific tests of nerve function include:

•Electromyography (EMG) is a test that measures the function of the nerves. For this test a very thin needle is inserted through the skin into the muscle. The needle contains an electrode that measures the electrical activity of the muscle.

•A nerve conduction velocity test (NCV) measures the speed at which signals travel through the nerves. This test is often done with the EMG. In the NCV test, patches containing surface electrodes are placed on the skin over nerves at various locations. Each patch gives off a very mild electrical impulse, which stimulates the nerve. The electrical activity of the nerves is measured and the speed of the electrical impulses between electrodes (reflecting the speed of the nerve signals) is calculated.

•In some cases, a nerve biopsy may be recommended. A biopsy is the surgical removal of a small piece of tissue for examination under a microscope. A pathologist, a physician specially trained in tissue diagnosis, examines the specimen and can help establish the cause of the neuropathy. The procedure is performed using a local anesthetic. The sural nerve (in the ankle), or the superficial radial nerve (wrist) are the sites most often used for biopsy.

Treatment:
The treatment of neuropathy involves measures to control the symptoms as well as treatment measures that address the underlying cause of neuropathy, if appropriate. Medical treatments for diabetes, autoimmune diseases, infections, kidney disease, and vitamin deficiencies are varied and are directed at the specific underlying condition. In many cases, treatment of the underlying disease can reduce or eliminate the symptoms of neuropathy. Some cases, especially those involving compression or entrapment of nerves by tumors or other conditions, can be relieved by surgery.

Many adjuvant medications have been tried, such as mega doses of vitamins, iron, zinc, calcium, alpha lipoic acid, acetyl-L carnitine. Increasing doses of painkillers like tramadol are also used. Sometimes they are combined with anti histamines like diphendydramnine (Benadryl) and pain modifying drugs. Combinations with anti epileptics such as gabapentin and anti depressants like amitriptyline reduce the intensity of symptoms. None of these treatments has been 100 per cent successful. The pain is still present in 80 per cent of the patients 5-10 years later.

Control of blood glucose (sugar) levels is important in the treatment of diabetic neuropathy to help prevent further damage to nerves.

Clinical trials are underway to help find new and more effective treatments for neuropathy. For example, treatments that involve electrical nerve stimulation or magnetic nerve stimulation are being studied.

Self care at home:
Special and careful care of the feet is important in people with neuropathy to reduce the chance of developing sores and infections. The nerves to the feet are the nerves most commonly affected by neuropathy. Proper foot care includes:

•wash the feet with warm water each day and thoroughly dry feet after washing (especially between the toes);

•never go barefoot or wear improperly-fitting, damaged, or too-tight footwear;

•inspect the feet daily, looking for cuts, blisters, or other problems;

•cut and file toenails when needed;

•thick, seamless socks can help prevent irritation of the feet;

•call your health care practitioner if you have any problems with your feet;

•massaging the feet can improve circulation; and

•smoking cessation can further improve blood circulation, since smoking damages circulation to the extremities and may worsen foot problems.

.The intensity of the pain can be reduced by soaking the legs up to the knees in warm salted water for 10 minutes, half-an-hour before bed. Application of pain relieving ointments that contain capsaicin also provides relief. The ointment should be applied every 3-4 hours. Do not rub the ointment in too vigorously as it will damage the skin.

Prevention:

Neuropathy is preventable only to the extent that the underlying condition or cause is preventable. For those with diabetes, studies have conclusively shown that long-term control of blood glucose levels is critically important in preventing the development of neuropathy and other complications of diabetes. Neuropathy that arises due to poor nutrition or alcohol abuse may be preventable if these causes can be eliminated. Genetic or inherited causes of neuropathy are not preventable.

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

Resources:
http://www.emedicinehealth.com/neuropathy/article_em.htm
http://www.telegraphindia.com/1130211/jsp/knowhow/story_16546702.jsp

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Guillain-Barre syndrome

Definition:
Guillain-Barre syndrome is an uncommon disorder in which your body’s immune system attacks your nerves. Weakness and numbness in your extremities are usually the first symptoms. These sensations can quickly spread, eventually paralyzing your whole body.

Click to see the picture

The exact cause of Guillain-Barre syndrome is unknown, but it is often preceded by an infectious illness such as a respiratory infection or the stomach flu. Luckily, Guillain-Barre syndrome is relatively rare, affecting only 1 or 2 people per 100,000.

In its most severe form, Guillain-Barre syndrome is a medical emergency requiring hospitalization. There’s no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness.

GBS can cause symptoms that last for a few weeks. Most people recover fully from GBS, but some people have permanent nerve damage. In very rare cases, people have died of GBS, usually from difficulty breathing. In the United States, for example, an estimated 3,000 to 6,000 people develop GBS each year on average, whether or not they received a vaccination.

Guillain-Barre affects about 1,500 people every year in the UK, and about 150 develop CIDP. The exact mechanisms that cause the conditions aren’t clear, but about 60 per cent of those affected will have had a throat or intestinal infection, flu or major stress within the previous two weeks. This triggers the immune system, which then attacks the nerves.

It rarely occurs in first-degree relatives, but familial cases have been reported and genetic similarities noted. For example, a study of Japanese people with Guillain-Barre following an intestinal infection with the bacteria Campylobacter jejuni found they were more likely to have a rare version of the gene for an immune system chemical known as tumour necrosis factor.

Symptoms:
Guillain-Barre syndrome often begins with weakness, tingling or loss of sensation starting in your feet and legs and spreading to your upper body and arms. These symptoms may begin — often not causing much notice — in your fingers and toes. In some people, symptoms begin in the arms or even the face. As the disorder progresses, muscle weakness can evolve into paralysis.

Signs and symptoms of Guillain-Barre syndrome may include:

*Prickling, “pins and needles” sensations in your fingers, toes or both
*Weakness or tingling sensations in your legs that spread to your upper body
*Unsteady walking or inability to walk
*Difficulty with eye movement, facial movement, speaking, chewing or swallowing
*Severe pain in your lower back
*Difficulty with bladder control or intestinal functions
*Very slow heart rate or low blood pressure
*Difficulty breathing
.
Most people with Guillain-Barre syndrome experience their most significant weakness within three weeks after symptoms begin. In some cases, signs and symptoms may progress very rapidly with complete paralysis of legs, arms and breathing muscles over the course of a few hours.

The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and André Strohl diagnosed two soldiers with the illness and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count.

GBS is also known as acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French polio, Landry’s ascending paralysis and Landry Guillain Barré syndrome.

Canadian neurologist C. Miller Fisher described the variant that bears his name in 1956

Causes:
Many things can cause GBS; about two-thirds of people who develop GBS symptoms do so several days or weeks after they have been sick with diarrhea or a respiratory illness. Infection with the bacterium Campylobacter jejuni is one of the most common risk factors for GBS. People also can develop GBS after having the flu or other infections (such as cytomegalovirus and Epstein Barr virus). On very rare occasions, they may develop GBS in the days or weeks after getting a vaccination.

Click to see picture of Neuron Hand-tuned

Typically, Guillain-Barre develops as an autoimmune reaction following an acute infection. It’s not inherited, although it’s thought that genetic factors may make some people more likely to develop autoimmune conditions.

Risk Factors:
Anyone can develop GBS; however, it is more common among older adults. The incidence of GBS increases with age, and people older than 50 years are at greatest risk for developing GBS.

.
Guillain-Barre may be triggered by:

*Most commonly, infection with campylobacter, a type of bacteria often found in undercooked food, especially poultry
*Surgery
*Epstein-Barr virus
*Hodgkin’s disease
*Mononucleosis
*HIV, the virus that causes AIDS
*Rarely, rabies or influenza immunizations

Diagnosis:
The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS.

*cerebrospinal fluid:
Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dL), without an accompanying increased cell count pleocytosis. A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.

.
*Electrodiagnostics
Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.

Diagnostic criteria Required:

*Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy
*Areflexia
*Disorder course < 4 weeks
*Exclusion of other causes (see below)

.
Supportive:
*relatively symmetric weakness accompanied by numbness and/or tingling
*mild sensory involvement
*facial nerve or other cranial nerve involvement
*absence of fever
*typical CSF findings obtained from lumbar puncture
*electrophysiologic evidence of demyelination from electromyogram

.
Differential diagnosis:
*acute myelopathies with chronic back pain and sphincter dysfunction
*botulism with early loss of pupillary reactivity and descending paralysis
*diphtheria with early oropharyngeal dysfunction
*Lyme disease polyradiculitis and other tick-borne paralyses
*porphyria with abdominal pain, seizures, psychosis
*vasculitis neuropathy
*poliomyelitis with fever and meningeal signs
*CMV polyradiculitis in immunocompromised patients
*critical illness neuropathy
*myasthenia gravis
*poisonings with organophosphate, poison hemlock, thallium, or arsenic
*intoxication with Karwinskia humboldtiana leaves or seeds
*paresis caused by West Nile virus
*spinal astrocytoma
*motor neurone disease
*West Nile virus can cause severe, potentially fatal neurological illnesses, which include encephalitis, meningitis, Guillain-Barré syndrome, and anterior myelitis.

Treatment :
Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Early intubation should be considered in any patient with a vital capacity (VC) <20 ml/kg, a negative inspiratory force (NIF) that is less negative (i.e., closer to zero) than -25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.

Once the patient is stabilized, treatment of the underlying condition should be initiated as soon as possible. Either high-dose intravenous immunoglobulins (IVIg) at 400 mg/kg for 5 days or plasmapheresis can be administered, as they are equally effective and a combination of the two is not significantly better than either alone. Therapy is no longer effective two weeks after the first motor symptoms appear, so treatment should be instituted as soon as possible. IVIg is usually used first because of its ease of administration and safety profile, with a total of five daily infusions for a total dose of 2 g/kg body weight (400 mg/kg each day). The use of intravenous immunoglobulins is not without risk, occasionally causing hepatitis, or in rare cases, renal failure if used for longer than five days. Glucocorticoids have not been found to be effective in GBS. If plasmapheresis is chosen, a dose of 40-50 mL/kg plasma exchange (PE) can be administered four times over a week.

Following the acute phase, the patient may also need rehabilitation to regain lost functions. This treatment will focus on improving ADL (activities of daily living) functions such as brushing teeth, washing, and getting dressed. Depending on the local structuring on health care, a team of different therapists and nurses will be established according to patient needs. An occupational therapist can offer equipment (such as wheelchair and special cutlery) to help the patient achieve ADL independence. A physiotherapist would plan a progressive training program and guide the patient to correct functional movement, avoiding harmful compensations which might have a negative effect in the long run. There is also some evidence supporting physiotherapy in helping patients with Guillain–Barré syndrome regain strength, endurance, and gait quality,[23] as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties. A speech and language therapist would be essential in the patient regaining speaking and swallowing ability if they were intubated and received a tracheostomy. The speech and language therapist would also offer advice to the medical team regarding the swallowing abilities of the patient and would help the patient regain their communication ability pre-dysarthria. There would also be a doctor, nurse and other team members involved, depending on the needs of the patient. This team contribute their knowledge to guide the patient towards his or her goals, and it is important that all goals set by the separate team members are relevant for the patient’s own priorities. After rehabilitation the patient should be able to function in his or her own home and attend necessary training as needed.

Prognosis:
Most of the time recovery starts after the fourth week from the onset of the disorder. Approximately 80% of patients have a complete recovery within a few months to a year, although minor findings may persist, such as areflexia. About 5–10% recover with severe disability, with most of such cases involving severe proximal motor and sensory axonal damage with inability of axonal regeneration. However, this is a grave disorder and despite all improvements in treatment and supportive care, the death rate among patients with this disorder is still about 2–3% even in the best intensive care units. Worldwide, the death rate runs slightly higher (4%), mostly from a lack of availability of life support equipment during the lengthy plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is needed in the worst cases. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy (CIDP).

Poor prognostic factors include: 1) age, over 40 years, 2) history of preceding diarrheal illness, 3) requiring ventilator support, 4) high anti-GM1 titre and 5) poor upper limb muscle strength

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

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/guillainbarre1.shtml
http://www.riversideonline.com/health_reference/Nervous-System/DS00413.cfm
http://en.wikipedia.org/wiki/Guillain%E2%80%93Barr%C3%A9_syndrome
http://www.cdc.gov/flu/protect/vaccine/guillainbarre.htm

Guillain-Barré Syndrome

http://nursingcomments.com/tag/guillain-barre-syndrome/

http://www.ami20.com/tag/guillain-barre

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Ailmemts & Remedies

Strabismus

Alternative Names: Crossed eyes; Esotropia; Exotropia; Squint; Walleye.

One eye moves normally, while the other points in (esotropia or “crossed eyes”), out (exotropia), up (hypertropia) or down (hypotropia).

Strabismus is often incorrectly referred to as “lazy eye” (which in fact refers to the associated condition amblyopia). It is also referred to as “squint”, “crossed eye”, “codeye” and “wall eye”.

“Cross-eyed” means that when a person with strabismus looks at an object, one eye fixates the object and the other fixates with a convergence angle less than zero, that is the optic axes overconverge. “Wall-eyed” means that when a person with strabismus looks at an object, one eye fixates the object and the other fixates with a convergence angle greater than zero, that is the optic axes diverge from parallel.

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Definition:-Strabismus  is a condition in which the eyes are not properly aligned with each other. It typically involves a lack of coordination between the extraocular muscles that prevents bringing the gaze of each eye to the same point in space and preventing proper binocular vision, which may adversely affect depth perception. Strabismus can be either a disorder of the brain coordinating the eyes or a disorder of one or more muscles, as in any process that causes a dysfunction of the usual direction and power of the muscle or muscles. Difficult strabismus problems are usually co-managed between orthoptists and ophthalmologists.

It is a disorder in which the eyes do not line up in the same direction when focusing. The condition is more commonly known as “crossed eyes.”

Causes:-
Strabismus is caused by a lack of coordination between the eyes. As a result, the eyes look in different directions and do not focus at the same time on a single point.

In most cases of strabismus in children, the cause is unknown. In more than half of these cases, the problem is present at or shortly after birth (congenital strabismus).

In children, when the two eyes fail to focus on the same image, the brain may learn to ignore the input from one eye. If this is allowed to continue, the eye that the brain ignores will never see well. This loss of vision is called amblyopia, and it is frequently associated with strabismus.

Some other disorders associated with strabismus in children include:

*Apert syndrome
*Cerebral palsy
*Congenital rubella
*Hemangioma near the eye during infancy
*Incontinentia pigmenti syndrome
*Noonan syndrome
*Prader-Willi syndrome
*Retinopathy of prematurity
*Retinoblastoma
*Traumatic brain injury
*Trisomy 18 (a child has 3 copies of chromosome 18, instead of the normal 2 copies)

Strabismus that develops in adults can be caused by:

*Botulism
*Diabetes (causes a condition known as acquired paralytic strabismus)
*Guillain-Barre syndrome
*Injuries to the eye
*Shellfish poisoning
*Stroke
*Traumatic brain injury
*Vision loss from any eye disease or injury

A family history of strabismus is a risk factor. Farsightedness may be a contributing factor. In addition, any other disease causing vision loss may cause strabismus.

Diagnosis:-
During eye examinations, orthoptists, ophthalmologists and optometrists typically use a cover test to aid in the diagnosis of strabismus. If the eye being tested is the strabismic eye, then it will fixate on the object after the “straight” eye is covered, as long as the vision in this eye is good enough. If the “straight” eye is being tested, there will be no change in fixation, as it is already fixated. Depending on the direction that the strabismic eye deviates, the direction of deviation may be assessed. Exotropic is outwards (away from the midline) and esotropic is inwards (towards the nose).

click to see

A simple screening test for strabismus is the Hirschberg test. A flashlight is shone in the patient’s eye. When the patient is looking at the light, a reflection can be seen on the front surface of the pupil. If the eyes are properly aligned with one another, then the reflection will be in the same spot of each eye. Therefore, if the reflection is not in the same place in each eye, then the eyes aren’t properly aligned.
Differential diagnosis: pseudostrabismus
Pseudostrabismus is the false appearance of strabismus. It generally occurs in infants and toddlers whose bridge of the nose is wide and flat, causing the appearance of strabismus. With age, the bridge of the child’s nose narrows and the folds in the corner of the eyes go away. To detect the difference between pseudostrabismus and strabismus, a Hirschberg test may be used.

click to see

Exams and Tests:
A physical examination will include a detailed examination of the eyes. Tests will be done to determine the strength of the eye muscles.

click to see

Eye tests include:

*Retinal exam
*Standard ophthalmic exam
*Visual acuity
*A neurological examination will also be performed.
Laterality
Strabismus may be classified as unilateral if the same eye consistently ‘wanders’, or alternating if either of the eyes can be seen to ‘wander’. Alternation of the strabismus may occur spontaneously, with or without subjective awareness of the alternation. Alternation may also be seen following the cover test, with the previously ‘wandering’ eye remaining straight while the previously straight eye is now seen to be ‘wandering’ on removal of the cover. The cover-uncover test is used to diagnose the type of strabismus (also known as tropia) present.

Onset
Strabismus may also be classified based on time of onset, either congenital, acquired or secondary to another pathological process, such as cataract. Many infants are born with their eyes slightly misaligned. The best time for physicians to assess this is between ages 3 and 6 months.

Pathophysiology:-
Strabismus can be an indication that a cranial nerve has a lesion. Particularly Cranial Nerve III (Occulomotor), Cranial Nerve IV (Trochlear) or Cranial Nerve VI (Abducens). A strabismus caused by a lesion in either of these nerves results in the lack of innervation to eye muscles and results in a change of eye position. A strabismus may be a sign of increased intracranial pressure, as CN III is particularly vulnerable to damage from brain swelling.

More commonly however, squints are termed concominant (i.e. non paralytic). This means the squint is not caused by a lesion reducing innervation. The squint in this example, is caused by a refractive error in one or both eyes. This refractive error causes poor vision in one eye and so stops the brain from being able to use both eyes together.
Treatment and management:-Treatment involves strategies to strengthen the weakened muscles and realign the eyes. Glasses and eye muscle exercises may be prescribed.

If the condition is caused by a lazy eye, the doctor may prescribe an eye patch. Some children may need surgery. For more information on treating lazy eye, see: Amblyopia

As with other binocular vision disorders, the primary therapeutic goal for those with strabismus is comfortable, single, clear, normal binocular vision at all distances and directions of gaze.

Whereas amblyopia, if minor and detected early, can often be corrected with use of an eyepatch on the dominant eye and/or vision therapy, the use of eyepatches is unlikely to change the angle of strabismus. Advanced strabismus is usually treated with a combination of eyeglasses or prisms, vision therapy, and surgery, depending on the underlying reason for the misalignment. Surgery does not change the vision; it attempts to align the eyes by shortening, lengthening, or changing the position of one or more of the extraocular eye muscles and is frequently the only way to achieve cosmetic improvement. Glasses affect the position by changing the person’s reaction to focusing. Prisms change the way light, and therefore images, strike the eye, simulating a change in the eye position.

Early treatment of strabismus and/or amblyopia in infancy can reduce the chance of developing amblyopia and depth perception problems. Most children eventually recover from amblyopia by around age 10, if they have had the benefit of patches and corrective glasses.

Eyes that remain misaligned can still develop visual problems. Although not a cure for strabismus, prism lenses can also be used to provide some comfort for sufferers and to prevent double vision from occurring.

In adults with previously normal alignment, the onset of strabismus usually results in double vision (diplopia).

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You may click to see:-Vision Screening Online Training Program
Prognosis:-With early diagnosis and treatment, the problem can usually be corrected. Delayed treatment may lead to permanent vision loss in one eye.

When strabismus is congenital or develops in infancy, it can cause amblyopia, in which the brain ignores input from the deviated eye. Strabismus can lead to a permanent weakening of vision in the strabismic eye called amblyopia (this may not always happen), sometimes referred to as lazy eye. The appearance of strabismus may also be a cosmetic problem. One study reported that 85% of adult strabismus patients “reported that they had problems with work, school and sports because of their strabismus.” The same study also reported that 70% said strabismus “had a negative effect on their self-image.”

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

Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/001004.htm
http://en.wikipedia.org/wiki/Strabismus

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Warning: Swine Flu Shot Linked to Killer Nerve Disease

A warning that the swine flu vaccine has been linked to a deadly nerve disease has been sent by the UK Government to senior neurologists in a confidential letter.
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The letter from the Health Protection Agency, the official body that oversees public health, was leaked to The Daily Mail, leading to demands to know why the information has not been given to the public before the vaccination of millions of people, including children, begins.

It tells the neurologists that they must be alert for an increase in a brain disorder called Guillain-Barre Syndrome (GBS), which could be triggered by the vaccine. GBS attacks the lining of the nerves, causing paralysis and inability to breathe, and can be fatal.

The letter refers to the use of a similar swine flu vaccine in the United States in 1976 when:

•More people died from the vaccination than from swine flu
•The vaccine may have increased the risk of contracting GBS by eight times
•The vaccine was withdrawn after just ten weeks when the link with GBS became clear
•The U.S. Government was forced to pay out millions of dollars to those affected
Concerns have already been raised that the new vaccine has not been sufficiently tested and that the effects, especially on children, are unknown.

Source: The Daily Mail August 15, 2009

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