1. Sleeping too late and waking up too late are main cause. 2. Not urinating in the morning. 3. Too much eating. 4. Skipping breakfast. 5. Consuming too much medication. 6. Consuming too much preservatives, additives, food colouring, and artificial sweetener. 7. Consuming unhealthycooking oil. As much as possible reduce cooking oil when frying, which includes even the best cooking oils like olive oil. Do not consume fried foods when you are tired, except if the body is very fit.
8. Consuming raw(overly done) foods also add to the burden of liver. Veggies should be eaten raw or cooked 3-5 parts. Fried veggies should be finished in one sitting, do not store.
We should prevent this without necessarily spending more. We just have to adopt a good daily lifestyle and eating habits. Maintaining good eating habits and time condition are very important for our bodies to absorb and get rid of unnecessary chemicals according to ‘schedule.’
Also high in the same sodium nitrates found inhot dogs, bacon, and other processed meats raise the risk of heart disease. The saturated fat in bacon also contributes to cancer.
3. Doughnuts…….CLICK & SEE .
Doughnuts are cancer-causing double trouble. First, they are made with white flour, sugar, andhydrogenated oils, then fried at high temperatures. Doughnuts may be the worst food you can possibly eat to raise your risk of cancer.
Like doughnuts, French fries are made withhydrogenated oils and then fried at high temperatures. They also contain cancer- causing acryl amides which occur during the frying process. They should be called cancer fries, not French fries.
Alternative Names::Morbus Charcot-Marie-Tooth, Charcot-Marie-Tooth neuropathy, hereditary motor and sensory neuropathy (HMSN), hereditary sensorimotor neuropathy (HSMN), or peroneal muscular atrophy.
Charcot–Marie–Tooth disease (CMT) is an inherited disorder of nerves (neuropathy) that takes different forms. It is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs but also in the hands and arms in the advanced stages of disease. Currently incurable, this disease is one of the most common inherited neurological disorders, with 36 in 100,000 affected.
In 1886, Professor Jean Martin Charcot of France (1825-1893) and his student Pierre Marie (1853-1940) published the first description of distal muscle weakness and wasting beginning in the legs, calling it peroneal muscular atrophy.
Howard Henry Tooth (1856-1926) described the same disease in his Cambridge dissertation in 1886, calling the condition peroneal progressive muscular atrophy. Tooth was the first to attribute symptoms correctly to neuropathy rather than to myelopathy, as physicians previously had done.
In 1912, Hoffman identified a case of peroneal muscular atrophy with thickened nerves. This disease was referred to as Hoffman disease and later was known as Charcot-Marie-Tooth-Hoffman disease.
In 1968, CMT disease was subdivided into 2 types, CMT 1 and CMT 2, based on pathologic and physiologic criteria. CMT disease has been subdivided further based on the genetic cause of the disease.
•In CMT type 1, the peripheral nerves’ axons – the part of the nerve cell that transmits electrical signals to the muscles – lose their protective outer coverings, their myelin sheaths. This disrupts the axons’ function.
•In CMT type 2, the axons’ responses are diminished due to a defect within the axons themselves. CMT type 2, the less common of the two classes, can be further separated into at least six subtypes, caused by defects in different genes.
Symptoms of the CMT usually begin in late childhood or early adulthood. Some people don’t experience symptoms until their early thirties or forties. Usually, the initial symptom is foot drop early in the course of the disease. This can also cause claw toe, where the toes are always curled. Wasting of muscle tissue of the lower parts of the legs may give rise to “stork leg” or “inverted bottle” appearance. Weakness in the hands and forearms occurs in many people later in life as the disease progresses.
Symptoms and progression of the disease can vary. Breathing can be affected in some; so can hearing, vision, and the neck and shoulder muscles. Scoliosis is common. Hip sockets can be malformed. Gastrointestinal problems can be part of CMT, as can chewing, swallowing, and speaking (as vocal cords atrophy). A tremor can develop as muscles waste. Pregnancy has been known to exacerbate CMT, as well as extreme emotional stress.
Neuropathic pain is often a symptom of CMT though, like other symptoms of CMT, it’s presence and severity varies from case to case. For some people, pain can be significant to severe and interfere with daily life activities. However, pain is not experienced by all people with CMT. When pain is present as a symptom of CMT, it is comparable to that seen in other peripheral neuropathies, as well as Postherpetic neuralgia and Complex regional pain syndrome, among other diseases
The most common symptoms of Charcot-Marie-Tooth disease may include:
*Weakness in your legs, ankles and feet
*Loss of muscle bulk in legs and feet
*High foot arches
*Curled toes (hammertoes)
*Decreased ability to run
*Difficulty lifting your foot at the ankle (footdrop)
*Awkward or higher than normal step (gait)
*Frequent tripping or falling
*Decreased sensation in your legs and feet
*Numbness in the legs and feet
As Charcot-Marie-Tooth disease progresses, symptoms may not be limited to the feet and legs but may also involve the thighs, hands and arms. Charcot-Marie-Tooth disease generally doesn’t cause pain.
Charcot–Marie–Tooth disease is caused by mutations that cause defects in neuronal proteins. Nerve signals are conducted by an axon with a myelin sheath wrapped around it. Most mutations in CMT affect the myelin sheath. Some affect the axon.
The most common cause of CMT (70-80% of the cases) is the duplication of a large region in chromosome 17p12 that includes the gene PMP22. Some mutations affect the gene MFN2, which codes for a mitochondrial protein. Cells contain separate sets of genes in their nucleus and in their mitochondria. In nerve cells, the mitochondria travel down the long axons. In some forms of CMT, mutated MFN2 causes the mitochondria to form large clusters, or clots, which are unable to travel down the axon towards the synapses. This prevents the synapses from functioning.
Charcot-Marie-Tooth disease is hereditary, so you’re at higher risk of developing the disorder if anyone in your immediate family has had the disease. Other causes of neuropathies, such as diabetes, may cause symptoms of or worsen Charcot-Marie-Tooth disease.
Complications of Charcot-Marie-Tooth disease vary in severity from person to person, with foot abnormalities and difficulty walking generally being the most serious problems. Muscle weakness may also increase, and injury to areas of the body with decreased sensation may occur.
CMT can be diagnosed through symptoms, through measurement of the speed of nerve impulses (electromyography), through biopsy of the nerve, and through DNA testing. DNA testing can give a definitive diagnosis, but not all the genetic markers for CMT are known.CMT is first noticed when someone develops lower leg weakness and foot deformities such as foot drop, hammertoes and high arches. But signs alone do not lead to diagnosis. Patients must be referred to a neurologist or a physical medicine and rehabilitation physician (physiatrist). To see signs of muscle weakness the neurologist will ask patients to walk on their heels or to move part of their leg against an opposing force. In order to identify sensory loss the neurologist will test for deep tendon reflexes, such as the knee jerk, which are reduced or absent in CMT. The doctor will also ask about family history because CMT is hereditary. The lack of family history does not rule out CMT, but it will allow the doctor to rule out other causes of neuropathy such as diabetes or exposure to certain chemicals or drugs.
In 2010, CMT was one of the first diseases where the genetic cause of a particular patient’s disease was precisely determined by sequencing the whole genome of an affected individual. Two mutations were identified in a gene, SH3TC2, known to cause CMT. Researchers then compared the affected patient’s genome to the genomes of the patient’s mother, father, and seven siblings with and without the disease. The mother and father each had one normal and one mutant copy of this gene, and had mild or no symptoms. The offspring that inherited two mutant genes presented fully with the disease. Sequencing the initial patient’s whole genome cost $50,000, but researchers estimated that it would soon cost $5,000 and become common.
CMT is divided into the primary demyelinating neuropathies (CMT1, CMT3, and CMT4) and the primary axonal neuropathies (CMT2), with frequent overlap. Another cell involved in CMT is the Schwann cell, which creates the myelin sheath, by wrapping its plasma membrane around the axon in a structure that is sometimes compared to a Swiss roll.
Neurons, Schwann cells, and fibroblasts work together to create a working nerve. Schwann cells and neurons exchange molecular signals that regulate survival and differentiation. These signals are disrupted in CMT.
Demyelinating Schwann cells causes abnormal axon structure and function. They may cause axon degeneration. Or they may simply cause axons to malfunction.
The myelin sheath allows nerve cells to conduct signals faster. When the myelin sheath is damaged, nerve signals are slower, and this can be measured by a common neurological test, electromyography.
When the axon is damaged, on the other hand, this results in a reduced compound muscle action potential (CMAP).
There are many different genetic variants. Most cases are inherited as an autosomal dominant condition, but some are inherited in an autosomal recessive or x-linked pattern.
Although there is no current standard treatment, the use of ascorbic acid has been proposed, and has shown some benefit in animal models. A clinical trial to determine the effectiveness of high doses of ascorbic acid (vitamin C) in treating humans with CMT type 1A has been conducted. The results of the trial upon children have shown that a high dosage intake of ascorbic acid is safe but the efficacy endpoints expected were not met. In 2010, a study published in the Journal Science indicated that scientists had identified those proteins that control the thickness of myelin sheath. This discovery is expected to open the avenue to new treatments in the coming years.
The most important activity for patients with CMT is to maintain what movement, muscle strength and flexibility they have. Therefore, physical therapy and moderate activity are recommended but overexertion should be avoided. A physical therapist should be involved in designing a exercise program that fits a patient’s personal strengths and flexibility. Bracing can also be used to correct problems caused by CMT. Gait abnormalities can be corrected by the use of either articulated (hinged) or unarticulated, braces called AFOs (ankle-foot orthoses). These braces help control foot drop and ankle instability and often provide a better sense of balance for patients. Appropriate footwear is also very important for people with CMT, but they often have difficulty finding well-fitting shoes because of their high arched feet and hammer toes. Due to the lack of good sensory reception in the feet, CMT patients may also need to see a podiatrist for help in trimming nails or removing calluses that develop on the pads of the feet. A final decision a patient can make is to have surgery. Using a podiatrist or an orthopedic surgeon, patients can choose to stabilize their feet or correct progressive problems. These procedures include straightening and pinning the toes, lowering the arch, and sometimes, fusing the ankle joint to provide stability.
The Charcot-Marie-Tooth Association classifies the chemotherapy drug vincristine as a “definite high risk” and states that “vincristine has been proven hazardous and should be avoided by all CMT patients, including those with no symptoms.”
There are also several corrective surgical procedures that can be done to improve physical condition.
Genetic testing is available for many of the different types of Charcot-Marie-Tooth and may help guide treatment.
Lifestyle & Homeremedies:
Certain tactics may prevent complications caused by Charcot-Marie-Tooth disease and improve your ability to manage the effects of the disorder.
Started early and followed regularly, at-home activities can provide protection and relief:
*Stretch regularly. The goal of stretching is to improve or maintain the range of motion of your joints. Stretching improves your flexibility, balance and coordination. Stretching may also reduce your risk of injury. If you have Charcot-Marie-Tooth disease, regular stretching can prevent or reduce joint deformities that may result from uneven pulling of muscle on your bones.
*Exercise daily. Exercising every day keeps your bones and muscles strong. Low-impact exercises, such as biking and swimming, are less stressful on fragile muscles and joints. By strengthening your muscles and bones, you can improve your balance and coordination, reducing your risk of falls.
*Improve your stability. Muscle weakness associated with Charcot-Marie-Tooth disease may cause you to be unsteady on your feet, which can lead to falling and serious injury. Walking with a cane or a walker can increase your stability. Good lighting at night can help you avoid stumbling and falling.
Foot care is important
Because of foot deformities and loss of sensation, regular foot care is important to help relieve symptoms and to prevent complications:
*Inspect your feet. Daily inspection of your feet is important to prevent calluses, ulcers, wounds and infections.
*Take care of your nails. Cut your nails regularly. To avoid ingrown toenails and infections, cut straight across and avoid cutting into the nailbed edges. Consider regular professional pedicures.
*Wear the right shoes. Use shoes that fit properly and are roomy and protective. Consider wearing boots or high-top shoes for ankle support.
*Soak and moisturize the skin of your feet. Brief, daily cold and warm foot soaks followed by the application of moisturizing lotions keep the skin of the feet moist and pliable. This can be very effective in reducing neuropathic pain and foot discomfort.
Coping & Support:
Support groups, in conjunction with your doctor’s advice, can be valuable in dealing with Charcot-Marie-Tooth disease. Support groups bring together people who are coping with the same kinds of challenges, along with their families and friends, and offer a setting in which people can share their common problems.
Ask your doctor about support groups in your community. Your local health department, public library and telephone book and the Internet also may be good sources to find a support group in your area.
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.
The research was reported in the journal Neurology.
The volunteers, who had an average age of 78, were checked for signs of “cognitive impairment” or even dementia.
The Pittsburgh team also had access to brain scan results from four years previously which measured the amount of “grey matter” in their brains.
This is found at various parts of the brain and is known to diminish in many people as they get older.
Each of them had been quizzed in their 60s about the number of city blocks they walked each week as part of their normal routine.
The results showed that those who walked at least 72 blocks – six to nine miles – a week had a greater volume of grey matter.
Four years after the scans, 40% of the group had measurable cognitive impairment or even dementia.
Those who walked the most were half as likely to have these problems compared with those who walked the least.
Dr Kirk Erickson, who led the study, said: “If regular exercise in midlife could improve brain health and improve thinking and memory in later life, it would be one more reason to make regular exercise in people of all ages a public health imperative.”
Susanne Sorensen, from the Alzheimer’s Society, said that the study was further evidence that a healthy heart could lead to a healthy brain.
She added: “One of the benefits of this research is that it eliminates the impact other socio-economic factors may play and focuses specifically on walking rather than exercise more generally.
“Although a link has been found between lack of exercise and brain shrinkage, we need more research to find out why physical activity may affect the brain.
“The best way to reduce your risk is to take regular exercise, eat healthily, don’t smoke and get your blood pressure and cholesterol checked.”
Prosopagnosia (sometimes known as face blindness) is a disorder of face perception where the ability to recognize faces is impaired, while the ability to recognize other objects may be relatively intact. The term originally referred to a condition following acute brain damage, but recently a congenital form of the disorder has been proposed, which may be inherited by about 2.5% of the population. The specific brain area usually associated with prosopagnosia is the fusiform gyrus.
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It is often accompanied by other types of recognition impairments (place recognition, car recognition, facial expression of emotion, etc.) though sometimes it appears to be restricted to facial identity. Not surprisingly, prosopagnosia can create serious social problems. Prosopagnosics often have difficulty recognizing family members, close friends, and even themselves. They often use alternative routes to recognition, but these routes are not as effective as recognition via the face.
Few successful therapies have so far been developed for affected people, although individuals often learn to use ‘piecemeal’ or ‘feature by feature’ recognition strategies. This may involve secondary clues such as clothing, hair color, body shape, and voice. Because the face seems to function as an important identifying feature in memory, it can also be difficult for people with this condition to keep track of information about people, and socialize normally with others.
Some also use the term prosophenosia, which refers to the inability to recognize faces following extensive damage of both occipital and temporal lobes.
There are a variety of explanations for prosopagnosia. Of course, all these explanations propose that the procedures necessary for normal face recognition are not working properly. However, the explanations differ in their characterization of the impaired procedures. It appears that prosopagnosia actually refers to a number of different types of impairments, so no one explanation will account for all cases of prosopagnosia.
Selective inabilities to recognize faces were reported throughout the 19th century, and included case studies by Hughlings Jackson and Charcot. However, it was not named until the term prosopagnosia was first used in 1947 by Joachim Bodamer, a German neurologist. He described three cases, including a 24-year old man who suffered a bullet wound to the head and lost his ability to recognise his friends, family, and even his own face. However, he was able to recognize and identify them through other sensory modalities such as auditory, tactile, and even other visual stimuli patterns (such as gait and other physical mannerisms). Bodamer gave his paper the title Die Prosop-Agnosie, derived from classical Greek (prosopon) meaning “face” and (agnosia) meaning “non-knowledge”.
The study of prosopagnosia has been crucial in the development of theories of face perception. Because prosopagnosia is not a unitary disorder (i.e., different people may show different types and levels of impairment) it has been argued that face perception involves a number of stages, each of which can be separately damaged.This is reflected not just in the amount of impairment displayed but also in the qualitative differences in impairment that a person with prosopagnosia may present with.
This sort of evidence has been crucial in supporting the theory that there may be a specific face perception system in the brain. This is counter-intuitive to many people as they do not experience faces as ‘special’ or perceived in a different way from the rest of the world.
A recent case report described a closely related condition called prosopamnesia, in which the subject, from birth, could perceive faces normally but had a severely impaired ability to remember them.
It has also been argued that prosopagnosia may be a general impairment in understanding how individual perceptual components make up the structure or gestalt of an object. Psychologist Martha Farah has been particularly associated with this view.
Until early in the 21st century, prosopagnosia was thought to be quite rare and solely associated with brain injury or neurological illness affecting specific areas of the brain. However, recently a form of congenital prosopagnosia has been proposed, in which people are born with an impairment in recognising and perceiving faces, as well as other objects and visual scenes. The cases that have been reported suggest that this form of the disorder may be heritable and much more common than previously thought (about 2.5% of the population may be affected), although this congenital disorder is commonly accompanied by other forms of visual agnosia, and may not be “pure” prosopagnosia. It has been suggested that very mild cases of face blindness are much more common, perhaps affecting 10% of the population, although there have not been any studies confirming this. The inability to keep track of the identity of characters in movies is a common complaint.
A classic case of a prosopagnosia is presented by “Dr P” in Oliver Sacks‘ 1985 book The Man Who Mistook His Wife for a Hat. Although Dr P could not recognize his wife from her face, he was able to recognize her by her voice. His recognition of pictures of his family and friends appeared to be based on highly specific features, such as his brother’s square jaw and big teeth.
Subtypes Apperceptive prosopagnosia
Apperceptive prosopagnosia is thought to be a disorder of some of the earliest processes in the face perception system. People with this disorder cannot make any sense of faces and are unable to make same-different judgements when they are presented with pictures of different faces. They may also be unable to work out attributes such as age or gender from a face. However, they may be able to recognise people based on non-face clues such as their clothing, hairstyle or voice.
Associative prosopagnosia is thought to be an impairment to the links between early face perception processes and the semantic information we hold about people in our memories. People with this form of the disorder may be able to say whether photos of people’s faces are the same or different and derive the age and gender from a face (suggesting they can make sense of some face information) but may not be able to subsequently identify the person or provide any information about them such as their name, occupation or when they were last encountered. They may be able to recognise and produce such information based on non-face information such as voice, hair, or even particularly distinctive facial features (such as a distinctive moustache) that does not require the structure of the face to be understood. Typically such people do not report that ‘faces make no sense’ but simply that they do not look distinctive in any way.
Developmental prosopagnosia (DP) is a face recognition deficit that is lifelong, manifests itself in early childhood and that cannot be attributed to acquired brain damage. However, a number of studies have found functional deficits in DP both on the basis of EEG measures and fMRI. It has been suggested that a genetic factor is responsible for the condition.
There seem to be two categories of DP patients:
– patients who are impaired in basic face processing (age estimation, judgment of facial affect) and also show deficits on other forms of visual processing;
– patients with pure face recognition impairments in the presence of intact basic visual processing.
The first group of patients fail to obtain view-centered descriptions. According to the Bruce and Young model of face recognition, these are precursors of the more abstract expression-independent descriptions. View-centered descriptions do not seem to be specific for faces, as the patients with impairments of processing the physical aspects of faces also show difficulties in non-facial tasks like object recognition or tests of visuo-spatial abilities.
However, there is as yet only limited evidence for a classification into different subtypes.
There are many developmental disorders that incorporate within themselves an increased likelihood that the person will have differences in face perception, of which the person may or may not be aware. That is to say, the person may or may not have insight in the clinical sense of the word. However, the mechanism by which these effects take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Williams syndrome, and autism spectrum disorders in general. However, these types of disorders are very complicated, so arbitrary assumptions should be avoided.
Unconscious face recognition:-
One particularly interesting feature of prosopagnosia is that it suggests both a conscious and unconscious aspect to face recognition. Experiments have shown that when presented with a mixture of familiar and unfamiliar faces, people with prosopagnosia may be unable to successfully identify the people in the pictures, or even make a simple familiarity judgement (“this person seems familiar / unfamiliar”). However, when a measure of emotional response is taken (typically a measure of skin conductance), there tends to be an emotional response to familiar people even though no conscious recognition takes place.
This suggests emotion plays a significant role in face recognition, perhaps unsurprising when basic survival (particularly security) relies on identifying the people around you.
It is thought that Capgras delusion may be the reverse of prosopagnosia. In this condition people report conscious recognition of people from faces, but show no emotional response, perhaps leading to the delusional belief that their relative or spouse has been replaced by an impostor.
Everyone sometimes has trouble recognizing faces, and it is even more common for people to have trouble remembering other people’s names. Prosopagnosia is much more severe than these everyday problems that everyone experiences. Prosopagnosics often have difficulty recognizing people that they have encountered many times. In extreme cases, prosopagnosics have trouble recognizing even those people that they spend the most time with such as their spouses and their children.
One of the telltale signs of prosopagnosia is great reliance on non-facial information such as hair, gait, clothing, voice, and other information. Prosopagnosics also sometimes have difficulty imagining the facial appearance of acquaintances. One of the most common complaints of prosopagnosics is that they have trouble following the plot of television shows and movies, because they cannot keep track of the identity of the characters.
If you would like to assess your face recognition abilities, we currently have two tests of face recognition available. These tests include feedback on how your scores compare to the scores of people with normal face recognition.
Screening for prosopagnosia is not an easy task, as what most doctors would say. Because of this, a specific tool in the diagnosis for prosopagnosia was developed, called Cambridge Face Memory Test. This is a test that is much reliable and can effectively test for a person’s ability to recognize faces. There was previous a test called Benton which also aims in testing the person for face recognition problems.
The difference between the two tests is that the Cambridge Face Memory test uses faces alone; without hair, ears or neck. While Benton uses images of faces with hair, ears and neck making the test provide results as false-negative. But the Cambridge Face Memory test is not considered the gold standard of prosopagnosia since the brain is a very complex part of a person’s body, which can alter its way of functioning. According to reports, the test is not widely used for it’s still in the process of making it a good and viable test for prosopagnosia.
Other tests such as the EEG and fMRI can be of health in the diagnosis of the condition, most especially the developmental prosopagnosia.
Those at risk of this condition are the people who have a family history of prosopagnosia. Those with first degree family members who suffer from prosopagnosia are most likely to develop such condition. It has been reported that children of a person with prosopagnosia are at risk of the condition. Other risk factors include the following:
*People who suffered from brain injury.
*People who have had stroke.
Those who have neurodegenerative disorders are also at risk of developing prosopagnosia.
Most of the cases of prosopagnosia that have been documented have been due to brain damage suffered after maturity from head trauma, stroke, and degenerative diseases. These are examples of acquired prosopagnosia: these individuals had normal face recognition abilities that were then impaired. It seems likely that more cases of acquired prosopagnosia have been published for two reasons. First, their impairment with faces is usually quite apparent to these individuals, because they have experienced normal face recognition in the past and so they quickly notice their impairment. Second, because these individual have had brain damage, they are in contact with medical doctors who have assessed their face recognition abilities. (Note that if you have experienced a noticeable decline in your face recognition abilities, you should contact a neurologist immediately. Any sudden decline may indicate the existence of a condition that needs immediate attention.)
In contrast, in cases of developmental prosopagnosia, the onset of prosopagnosia occurred prior to developing normal face recognition abilities (adult levels of face recognition are reached during teenage years). Developmental prosopagnosia has been used to refer to individuals whose prosopagnosia is genetic in nature, individuals who experienced brain damage prior to experience with faces (prenatal brain damage or immediate brain damage), and individuals who experienced brain damage or severe visual problems during childhood. However, these etiologies should be differentiated, because they are different paths to prosopagnosia and so probably result in different types of impairment; they could be referred to as genetic prosopagnosia, preexperiential prosopagnosia, and postexperiential prosopagnosia, respectively. In some cases, it may be difficult to determine the cause of prosopagnosia, but many times individuals will either know that family members are also prosopagnosic or be aware of potential incidents that may have resulted in brain damage.
Individuals with developmental prosopagnosia often do not realize that they are unable to recognize faces as well as others. Of course, they have never recognized faces normally so their impairment is not apparent to them. It is also difficult for them to notice, because individuals with normal face recognition rarely discuss their reliance on faces. As a result, there are a number of individuals who have not recognized their prosopagnosia until well into adulthood. We have been contacted by far more developmental prosopagnosics than acquired prosopagnosics, and so it may be that this condition is more common than acquired prosopagnosia.
Prosopagnosia might be an enduring condition. However, patients may eventually recover if the damage is confined to their right hemisphere (Goldsmith and Liu, 2001). A study that tracked 18 people with prosopagnosia found that the time required for 50% of the people to recover was 9 weeks. Bilateral damage may be necessary in order for the people with prosopagnosia symptoms to endure past and acute period (Goldsmith and Liu, 2001).
However, for people whose prosopagnosia does not go away on it’s own, there is no real treatment. However, there are lifestyle changes that can help people to cope. Often learning to identify clothing, or distinctive features of people may help in recognition. Another helpful thing is to right down list of who you expect to see. Therefore, when you see someone you already have ideas about who they could be.
Cecilia Burman wrote about what it is like to have prosopagnosia. She knows from experience. Please visit her website and read as much as you can. The following link goes to a page where she talks about how she has adapted and learned to identify people as best and as fast as she can. She also points out that all people with prosopagnosia are not alike. They are as different as can be. Their only similarity is their face-blindness.
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.
An hour and a half after feeding mice a single dose of epicatechin, animals that had ingested the compound suffered significantly less brain damage following an induced stroke.
“While most treatments against stroke in humans have to be given within a two- to three-hour time window to be effective, epicatechin appeared to limit further neuronal damage when given to mice 3.5 hours after a stroke. Given six hours after a stroke, however, the compound offered no protection to brain cells.”