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Wednesday, August 18, 2010

MIGRAINE

Migraine is a neurological syndrome characterized by altered bodily perceptions, severe headaches, and nausea. Physiologically, the migraine headache is a neurological condition more common to women than to men. The word migraine was borrowed from Old French migraigne (originally as "megrim", but respelled in 1777 on a contemporary French model). The French term derived from a vulgar pronunciation of the Late Latin word hemicrania, itself based on Greek hemikrania, from Greek roots for "half" and "skull".
The typical migraine headache is unilateral (affecting one half of the head) and pulsating, lasting from 4 to 72 hours;symptoms include nausea, vomiting, photophobia (increased sensitivity to light), and phonophobia Approximately one-third of people who suffer from migraine headaches perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur. (increased sensitivity to sound).
Initial treatment is with analgesics for the headache, an antiemetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system.
There are migraine headache variants, some originate in the brainstem (featuring intercellular transport dysfunction of calcium and potassium ions) and some are genetically disposed.Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache. Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy.

Classification

The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches, in a document called "The International Classification of Headache Disorders, 2nd edition" (ICHD-2).[12]
According to ICHD-2, there are seven subclasses of migraines (some of which include further subdivisions):
  • Migraine without aura, or common migraine, involves migraine headaches that are not accompanied by an aura (visual disturbance, see below).
  • Migraine with aura usually involves migraine headaches accompanied by an aura. Less commonly, an aura can occur without a headache, or with a non-migraine headache. Two other varieties are Familial hemiplegic migraine and Sporadic hemiplegic migraine, in which a patient has migraines with aura and with accompanying motor weakness. If a close relative has had the same condition, it is called "familial", otherwise it is called "sporadic". Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, vertigo, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness.
  • Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo).
  • Retinal migraine involves migraine headaches accompanied by visual disturbances or even blindness in one eye.
  • Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion.
  • Probable migraine describes conditions that have some characteristics of migraines but where there is not enough evidence to diagnose it as a migraine with certainty.

Signs and symptoms

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same person:
  1. The prodrome, which occurs hours or days before the headache.
  2. The aura, which immediately precedes the headache.
  3. The pain phase, also known as headache phase.
  4. The postdrome.

Prodrome phase

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

Aura phase

For the 20–30% of migraine sufferers who experience migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely (see silent migraine). Symptoms of migraine aura can be visual, sensory, or motor in nature.
Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or formations of dazzling zigzag lines (scintillating scotoma; often arranged like the battlements of a castle, hence the alternative terms "fortification spectra" or "teichopsia"). Some patients complain of blurred or shimmering or cloudy vision, as though they were looking through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. The somatosensory aura of migraine consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the nose-mouth area on the same side. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue.
Other symptoms of the aura phase can include auditory, gustatory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.
Oliver Sacks's book Migraine describes "migrainous deliria" as a result of such intense migraine aura that it is indistinguishable from "free-wheeling states of hallucinosis, illusion, or dreaming."
 
Visual symptoms of migraine aura
Enhancements reminiscent of a zigzag fort structure
Negative scotoma, loss of awareness of local structures
Positive scotoma, local perception of additional structures
Mostly one-sided loss of perception

Pain phase

The typical migraine headache is unilateral, throbbing, and moderate to severe and can be aggravated by physical activity. Not all these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually it alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides and usually lasts 4 to 72 hours in adults and 1 to 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several a week, and the average sufferer experiences one to three headaches a month. The head pain varies greatly in intensity.
The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, and vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, and osmophobia and seek a dark and quiet room. Blurred vision, delirium, nasal stuffiness, diarrhea, polyuria, pallor, or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. The extremities tend to feel cold and moist. Vertigo may be experienced; a variation of the typical migraine, called vestibular migraine, has also been described. Lightheadedness, rather than true vertigo,[citation needed] and a feeling of faintness may occur.

Postdrome phase

The patient may feel tired or "hungover" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness.According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."

Triggers

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

Food and Drink

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

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

Aspartame While some people believe that aspartame triggers migraines, and anecdotal evidence is present, this has not been medically proven.

MSG MSG is frequently reported as a dietary trigger (12%).In a placebo-controlled trial, monosodium glutamate (MSG) in large doses (2.5 grams) taken on an empty stomach was associated with adverse symptoms including headache more often than was placebo. However another trial found no effect when 3.5g of MSG was given with food.

Tyramine The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers. However, a 2003 review article concluded that there was no scientific evidence for an effect of tyramine on migraine.

Other A 2005 literature review found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients.Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants, that dehydration deserved more attention, and that some patients report sensitivity to red wine. Little or no evidence associated notorious suspected triggers like chocolate, cheese, histamine, tyramine or nitrites with migraines. However, the review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine.

Weather

Several studies have found some migraines are triggered by changes in weather. One study noted 62% of the subjects thought weather was a factor but only 51% were sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:
  1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.
  2. Significant changes in weather
  3. Changes in barometric pressure
Another study examined the effects of warm chinook winds on migraines, with many patients reporting increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause was thought to be an increase in positive ions in the air.

Other

One study found that for some people who suffer from migraine in India, washing hair in a bath was a migraine trigger. The triggering effect also had to do with how the hair was later dried.
Strong fragrances have also been identified as potential triggers, and some sufferers report an increased sensitivity to scent as an aura effect.

Pathophysiology

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

Depolarization theory

Animation of cortical spreading depression.
 
A phenomenon known as cortical spreading depression can cause migraines.[40] In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.
This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. A study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.[41]

Vascular theory

Migraines can begin when blood vessels in the brain contract and expand inappropriately. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area.
When the constriction stops and the blood vessels dilate, they become too wide. The once solid walls of the blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain. The vascular theory of migraines is now seen as secondary to brain dysfunction.

Serotonin theory

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

Neural theory

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

Unifying theory

Both vascular and neural influences cause migraines.
  1. stress triggers changes in the brain
  2. these changes cause serotonin to be released
  3. blood vessels constrict and dilate
  4. chemicals including substance P irritate nerves and blood vessels causing neurogenic inflammation and pain
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BREAST CANCER

Breast cancer (malignant breast neoplasm) is cancers originating from breast tissue, most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk. Cancers originating from ducts are known as ductal carcinomas; those originating from lobules are known as lobular carcinomas. There are many different types of breast cancer, with different stages (spread), aggressiveness, and genetic makeup; survival varies greatly depending on those factors. Computerized models are available to predict survival.With best treatment and dependent on staging, 10-year disease-free survival varies from 98% to 10%. Treatment includes surgery, drugs (hormonal therapy and chemotherapy), and radiation.
Worldwide, breast cancer comprises 10.4% of all cancer incidence among women, making it the most common type of non-skin cancer in women and the fifth most common cause of cancer death. In 2004, breast cancer caused 519,000 deaths worldwide (7% of cancer deaths; almost 1% of all deaths). Breast cancer is about 100 times more common in women than in men, although males tend to have poorer outcomes due to delays in diagnosis.
Some breast cancers require the hormones estrogen and progesterone to grow, and have receptors for those hormones. After surgery those cancers are treated with drugs that interfere with those hormones, usually tamoxifen, and with drugs that shut off the production of estrogen in the ovaries or elsewhere; this may damage the ovaries and end fertility. After surgery, low-risk, hormone-sensitive breast cancers may be treated with hormone therapy and radiation alone. Breast cancers without hormone receptors, or which have spread to the lymph nodes in the armpits, or which express certain genetic characteristics, are higher-risk, and are treated more aggressively. One standard regimen, popular in the U.S., is cyclophosphamide plus doxorubicinCA; these drugs damage DNA in the cancer, but also in fast-growing normal cells where they cause serious side effects. Sometimes a taxane drug, such as docetaxel, is added, and the regime is then known as CAT; taxane attacks the microtubules in cancer cells. An equivalent treatment, popular in Europe, is cyclophosphamide, methotrexate, and fluorouracil (CMF). Monoclonal antibodies, such as trastuzumab (Herceptin), are used for cancer cells that have the HER2 mutation. Radiation is usually added to the surgical bed to control cancer cells that were missed by the surgery, which usually extends survival, although radiation exposure to the heart may cause damage and heart failure in the following years. (Adriamycin), known as

Signs and symptoms


Breast cancer showing an inverted nipple, lump, skin dimpling.
The first noticeable symptom of breast cancer is typically a lump that feels different from the rest of the breast tissue. More than 80% of breast cancer cases are discovered when the woman feels a lump. By the time a breast lump is noticeable, it has probably been growing for years. The earliest breast cancers are detected by a mammogram. Lumps found in lymph nodes located in the armpits can also indicate breast cancer.
Indications of breast cancer other than a lump may include changes in breast size or shape, skin dimpling, nipple inversion, or spontaneous single-nipple discharge. Pain ("mastodynia") is an unreliable tool in determining the presence or absence of breast cancer, but may be indicative of other breast health issues.
When breast cancer cells invade the dermal lymphatics—small lymph vessels in the skin of the breast—its presentation can resemble skin inflammation and thus is known as inflammatory breast cancer (IBC). Symptoms of inflammatory breast cancer include pain, swelling, warmth and redness throughout the breast, as well as an orange-peel texture to the skin referred to as peau d'orange.

Another reported symptom complex of breast cancer is Paget's disease of the breast. This syndrome presents as eczematoid skin changes such as redness and mild flaking of the nipple skin. As Paget's advances, symptoms may include tingling, itching, increased sensitivity, burning, and pain. There may also be discharge from the nipple. Approximately half of women diagnosed with Paget's also have a lump in the breast.
In rare cases, what initially appears as a fibroadenoma (hard movable lump) could in fact be a phyllodes tumor. Phyllodes tumors are formed within the stroma (connective tissue) of the breast and contain glandular as well as stromal tissue. Phyllodes tumors are not staged in the usual sense; they are classified on the basis of their appearance under the microscope as benign, borderline, or malignant.

Occasionally, breast cancer presents as metastatic disease, that is, cancer that has spread beyond the original organ. Metastatic breast cancer will cause symptoms that depend on the location of metastasis. Common sites of metastasis include bone, liver, lung and brain. Unexplained weight loss can occasionally herald an occult breast cancer, as can symptoms of fevers or chills. Bone or joint pains can sometimes be manifestations of metastatic breast cancer, as can jaundice or neurological symptoms. These symptoms are "non-specific", meaning they can also be manifestations of many other illnesses.
Most symptoms of breast disorder do not turn out to represent underlying breast cancer. Benign breast diseases such as mastitis and fibroadenoma of the breast are more common causes of breast disorder symptoms. The appearance of a new symptom should be taken seriously by both patients and their doctors, because of the possibility of an underlying breast cancer at almost any age.

Risk factors

Main article: Risk factors of breast cancer
The primary risk factors that have been identified are sex, age, lack of childbearing or breastfeeding, and higher hormone levels.
In Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective, a 2007 report by American Institute for Cancer Research/ World Cancer Research Fund, it concluded women can reduce their risk by maintaining a healthy weight, drinking less alcohol, being physically active and breastfeeding their children. This was based on an review of 873 separate studies.
In 2009 World Cancer Research Fund announced the results of a further review review that took into account a further 81 studies published subsequently. This did not change the conclusions of the 2007 Report. In 2009, WCRF/ AICR published Policy and Action for Cancer Prevention, a Policy Report that included a preventability study.This estimated that 38% of breast cancer cases in the US are preventable through reducing alcohol intake, increasing physical activity levels and maintaining a healthy weight. It also estimated that 42% of breast cancer cases in the UK could be prevented in this way, as well as 28% in Brazil and 20% in China.
In a study published in 1995, well-established risk factors accounted for 47% of cases while only 5% were attributable to hereditary syndromes.Genetic factors usually increase the risk slightly or moderately; the exception is women and men who are carriers of BRCA mutations. These people have a very high lifetime risk for breast and ovarian cancer, depending on the portion of the proteins where the mutation occurs. Instead of a 12 percent lifetime risk of breast cancer, women with one of these genes has a risk of approximately 60 percent. In more recent years, research has indicated the impact of diet and other behaviors on breast cancer. These additional risk factors include a high-fat diet, alcohol intake, obesity, and environmental factors such as tobacco use, radiation, endocrine disruptors and shiftwork. Although the radiation from mammography is a low dose, the cumulative effect can cause cancer.
In addition to the risk factors specified above, demographic and medical risk factors include:
  • Personal history of breast cancer: A woman who had breast cancer in one breast has an increased risk of getting cancer in her other breast.
  • Family history: A woman's risk of breast cancer is higher if her mother, sister, or daughter had breast cancer. The risk is higher if her family member got breast cancer before age 40. Having other relatives with breast cancer (in either her mother's or father's family) may also increase a woman's risk.
  • Certain breast changes: Some women have cells in the breast that look abnormal under a microscope. Having certain types of abnormal cells (atypical hyperplasia and lobular carcinoma in situ [LCIS]) increases the risk of breast cancer.
  • Race: Breast cancer is diagnosed more often in women of European ancestry than those of African or Asian ancestry.
A National Cancer Institute (NCI) study of 72,000 women found that those who had a normal body mass index at age 20 and gained weight as they aged had nearly double the risk of developing breast cancer after menopause in comparison to women maintained their weight. The average 60 year-old woman's risk of developing breast cancer by age 65 is about 2 percent; her lifetime risk is 13 percent.
Abortion has not been found to be a risk factor for breast cancer. The breast cancer abortion hypothesis, however, continues to be promoted by some pro-life groups.
The United Kingdom is the member of International Cancer Genome Consortium that is leading efforts to map breast cancer's complete genome.


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CATARACT

A cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in degree from slight to complete opacity and obstructing the passage of light. Early in the development of age-related cataract the power of the lens may be increased, causing near-sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially blinding if untreated. The condition usually affects both the eyes, but almost always one eye is affected earlier than the other.
A senile cataract, occurring in the elderly, is characterized by an initial opacity in the lens, subsequent swelling of the lens and final shrinkage with complete loss of transparency. Moreover, with time the cataract cortex liquefies to form a milky white fluid in a Morgagnian cataract, which can cause severe inflammation if the lens capsule ruptures and leaks. Untreated, the cataract can cause phacomorphic glaucoma. Very advanced cataracts with weak zonules are liable to dislocation anteriorly or posteriorly. Such spontaneous posterior dislocations (akin to the historical surgical procedure of couching) in ancient times were regarded as a blessing from the heavens, because some perception of light was restored in the cataractous patients.
Cataract derives from the Latin cataracta meaning "waterfall" and the Greek kataraktes and katarrhaktes, from katarassein meaning "to dash down" (kata-, "down"; arassein, "to strike, dash"). As rapidly running water turns white, the term may later have been used metaphorically to describe the similar appearance of mature ocular opacities. In Latin, cataracta had the alternate meaning "portcullis",so it is also possible that the name came about through the sense of "obstruction". Early Persian physicians called the term nazul-i-ah, or "descent of the water"—vulgarised into waterfall disease or cataract—believing such blindness to be caused by an outpouring of corrupt humour into the eye. In dialect English a cataract is called a pearl, as in "pearl eye" and "pearl-eyed".


Classification


Bilateral cataracts in an infant due to Congenital rubella syndrome
The following is a classification of the various types of cataracts. This is not comprehensive and other unusual types may be noted.
  • Classified by etiology
  • Age-related cataract
  • Cortical Senile Cataract
  • Immature senile cataract (IMSC): partially opaque lens, disc view hazy
  • Mature senile cataract (MSC): Completely opaque lens, no disc view
  • Hypermature senile cataract (HMSC): Liquefied cortical matter: Morgagnian cataract
  • Senile Nuclear Cataract
  • Cataracta brunescens
  • cataracta nigra
  • cataracta rubra
  • Congenital cataract

Slit lamp photo of anterior capsular opacification visible a few months after implantation of Intraocular lens in eye, magnified view
  • Drug-induced cataract (e.g. corticosteroids)
  • Traumatic cataract
  • Blunt trauma (capsule usually intact)
  • Penetrating trauma (capsular rupture & leakage of lens material—calls for an emergency surgery for extraction of lens and leaked material to minimize further damage)
  • Classified by opacities, cataract can be classified by using Lens Opacities Classification System III (LOCS III: Nuclear NC1-5, Cortical C1-5 and Posterior P1-5. By application planning in procedures of phacoemulsification, LCOS III can be converted in newer cataract grading system. Gede Pardianto (2009) introduced Optical Biometry Based Cataract Grading System (OBBCGS) that so helpful in cataract grading due to phacoemulsification planning. LOCS III's NC0, C0 and P0 acan be converted as OBBCGS' No cataract (NC), LOCS III's NC1-3, C1-3, P1-4 can be converted to OBBCGS' Optical Biometry Examined Cataract (OBEC) and LOCS III's NC4-5, C4-5, P4-5 can be converted to OBBCGS's Optical Biometry Un-examined Cataract (OBUC); that need examination by Applanation Ultrasound Biometry.
  • Classified by location of opacity within lens structure (However, mixed morphology is quite commonly seen, e.g. PSC with nuclear changes & cortical spokes of cataract)
  • Anterior cortical cataract
  • Anterior polar cataract
  • Anterior subcapsular cataract

Slit lamp photo of posterior capsular opacification visible a few months after implantation of Intraocular lens in eye, seen on retroillumination
  • Nuclear cataract—Grading correlates with hardness & difficulty of surgical removal
  • 1: Grey
  • 2: Yellow
  • 3: Amber
  • 4: Brown/Black (Note: "black cataract" translated in some languages (like Hindi) refers to glaucoma, not the color of the lens nucleus)
  • Posterior cortical cataract
  • Posterior polar cataract (importance lies in higher risk of complication—posterior capsular tears during surgery)
  • Posterior subcapsular cataract (PSC) (clinically common)
  • After-cataract: posterior capsular opacification (PCO) subsequent to a successful extracapsular cataract surgery (usually within three months to two years) with or without IOL implantation. Requires a quick & painless office procedure with Nd:YAG laser capsulotomy to restore optical clarity.

Signs and symptoms

As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted. Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare can be a problem as light is scattered by the cataract into the eye. The affected eye will have an absent red reflex. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is demonstrated an eye specialist consultation is recommended.
In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon appears to be confined to one eye only.
The symptoms of cataracts are very similar to the symptoms of ocular citrosis.

Causes

Cataracts develop for a variety of reasons, including long-term exposure to ultraviolet light, exposure to radiation, secondary effects of diseases such as diabetes, hypertension and advanced age, or trauma (possibly much earlier); they are usually a result of denaturation of lens protein. Genetic factors are often a cause of congenital cataracts and positive family history may also play a role in predisposing someone to cataracts at an earlier age, a phenomenon of "anticipation" in pre-senile cataracts. Cataracts may also be produced by eye injury or physical trauma. A study among Icelandair pilots showed commercial airline pilots are three times more likely to develop cataracts than people with non-flying jobs. This is thought to be caused by excessive exposure to radiation coming from outer space. Cataracts are also unusually common in persons exposed to infrared radiation, such as glassblowers who suffer from "exfoliation syndrome". Exposure to microwave radiation can cause cataracts. Atopic or allergic conditions are also known to quicken the progression of cataracts, especially in children. Cataracts can also be caused by iodine deficien
Cataracts may be partial or complete, stationary or progressive, hard or soft.
Some drugs can induce cataract development, such as corticosteroids and Seroquel.
There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also classified by their location, e.g. posterior (classically due to steroid use) and anterior (common (senile) cataract related to aging).

Associations with systemic conditions

  • Congenital
  • Others
  • Toxic substances introduced systemically

Prevention

Although cataracts have no scientifically proven prevention, it is sometimes said that wearing ultraviolet-protecting sunglasses may slow the development of cataracts.Regular intake of antioxidants (such as vitamin A, C and E) is theoretically helpful, but taking them as a supplement has been shown to have no benefit. The less well known antioxidant N-acetylcarnosine has been shown in randomized controlled clinical trials to treat cataracts, and can be expected to prevent their formation by similar mechanisms. N-acetylcarnosine is a proposed treatment for other ocular disorders that are instigated, or exacerbated by oxidative stress including glaucoma, retinal degeneration, corneal disordes, and ocular inflammation.

Treatment

Main article: Cataract surgery

Cataract surgery, using a temporal approach phacoemulsification probe (in right hand) and "chopper" (in left hand) being done under operating microscope at a Navy medical center

When a cataract is sufficiently developed to be removed by surgery, the most effective and common treatment is to make an incision (capsulotomy) into the capsule of the cloudy lens in order to surgically remove the lens. There are two types of eye surgery that can be used to remove cataracts: extra-capsular (extracapsular cataract extraction, or ECCE) and intra-capsular (intracapsular cataract extraction, or ICCE).
Extra-capsular (ECCE) surgery consists of removing the lens but leaving the majority of the lens capsuleHigh frequency sound waves (phacoemulsification) are sometimes used to break up the lens before extraction. intact.
Intra-capsular (ICCE) surgery involves removing the entire lens of the eye, including the lens capsule, but it is rarely performed in modern practice.
In either extra-capsular surgery or intra-capsular surgery, the cataractous lens is removed and replaced with a plastic lens (an intraocular lens implant) which stays in the eye permanently.
Cataract operations are usually performed using a local anaesthetic and the patient is allowed to go home the same day. Recent improvements in intraocular technology now allow cataract patients to choose a multifocal lens to create a visual environment in which they are less dependent on glasses. Under some medical systems multifocal lenses cost extra. Traditional intraocular lenses are monofocal.
Complications are possible after cataract surgery, including endophthalmitis, posterior capsular opacificationretinal detachment.




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