Habitat : Myrica pennsylvanica is native to eastern North America, from Newfoundland west to Ontario and Ohio, and south to North Carolina. It grows on dry or wet sterile soil near the coast. Coastal dunes, pine barrens, pine-oak forests, old fields, bogs, edges of streams, ponds, and swamps from sea level to 325 metres.
Myrica pensylvanica is a deciduous shrub growing to 4.5 m tall. The leaves are 2.5–7 cm long and 1.5-2.7 cm broad, broadest near the leaf apex, serrate, and sticky with a spicy scent when crushed. It is in flower from Apr to May, and the seeds ripen in October.The flowers are borne in catkins 3–18 mm long, in range of colors from green to red. The fruit is a wrinkled berry 3-5.5 mm diameter, with a pale blue-purple waxy coating; they are an important food for yellow-rumped warblers.
The flowers are monoecious (individual flowers are either male or female, but both sexes can be found on the same plant) and are pollinated by Wind.It can fix Nitrogen.
Suitable for: light (sandy), medium (loamy) and heavy (clay) soils and prefers well-drained soil. Suitable pH: acid and neutral soils and can grow in very acid and saline soils.
It can grow in semi-shade (light woodland) or no shade. It prefers dry or moist soil.
Prefers a moist soil. Grows well in an open position in a well-drained soil in sun or light shade. Thrives in any ordinary garden soil. Prefers a lime-free loamy or peaty soil. Does well in dry maritime sites. Hardy to about -40°c. Closely related to M. cerifera and perhaps no more than a hardier northern form of it, it has larger fruits than M. cerifera. Where their ranges overlap, Myrica pensylvanica hybridizes quite readily with both M . cerifera and M . Heterophylla. Tolerant of salt spread on roads. Plants in this genus are notably resistant to honey fungus. Many species in this genus have a symbiotic relationship with certain soil micro-organisms, these form nodules on the roots of the plants and fix atmospheric nitrogen. Some of this nitrogen is utilized by the growing plant but some can also be used by other plants growing nearby.
Seed – best sown as soon as it is ripe in the autumn in a cold frame. Barely cover the seed and keep it moist. Stored seed germinates more freely if given a 3 month cold stratification and then sown in a cold frame. Germination is usually good. Prick out the seedlings into individual pots when they are large enough to handle and grow on in the cold frame for the first winter. Plant out in late spring or early summer. Cuttings of half-ripe wood, 5 – 8cm with a heel, July/August in a frame. Pot up and overwinter in a cold frame. Fair to good percentage. Cuttings of mature wood in November/December in a frame. Layering in spring. Division of suckers in the dormant season. Plant them out direct into their permanent positions. Edible Uses:
Fruit – raw or cooked. The fruit is about 4mm in diameter and contains a single large seed. There is very little edible flesh and this is of poor quality. The leaves and fruit are used as a food flavouring in soups etc. A bay leaf substitute, imparting a delicate aroma and subtle flavour. The herb is removed before the food is served. Medicinal Uses:
The root bark is astringent and emetic in large doses. A tea made from the leaves is used in the treatment of fevers and externally as a wash for itchy skin. Other Uses:
A wax covering on the fruit is extracted by scalding the fruit with boiling water and immersing them for a few minutes, the wax floats to the surface and is then skimmed off. The fruit is then boiled in water to extract the wax from the pulp and once more the wax is skimmed off. It is then strained through a muslin cloth and can be used to make aromatic candles. Candles made from this wax are quite brittle but are less greasy in warm weather. They are slightly aromatic, with a pleasant balsamic odour, and do not smoke when put out, making them much more pleasant to use that wax or tallow candles. The wax is also used in making soaps. A green dye is obtained from the leaves. The plant is very wind hardy and can be grown as an informal hedge.
Known Hazards : There is a report that some of the constituents of the wax might be carcinogenic. Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider
Habitat : Gentiana decumbens is native to E. Asia – Himalayas to Siberia. It grows on the alpine slopes, 3300 – 4500 metres. Along streams, grassland slopes, clearings in forests, dry steppes at elevations of 1,200 – 2,700 metres in northern China. Along streams, grassland slopes, clearings in forests, dry steppes; 1200-2700 m. NE Nei Mongol, NW Xinjiang (Kazakhstan, E Mongolia, Russia; NE Europe). Description:
Gentiana decumbens is a perennial flowering plant. It grows 15-45 cm tall. Roots to 1.5 cm in diam. Stems ascending, stout, glabrous, simple. Basal leaves petiole 1-3 cm, membranous; leaf blade linear-lanceolate to linear-elliptic, 3.5-16 × 0.4-1.8 cm, base narrowed, margin scabrous, apex acuminate, veins 1-3. Stem leaves 2 or 3 pairs, smaller and with shorter petioles toward apex; petiole 1-1.5 cm; leaf blade linear to lanceolate, 1.7-5 cm × 3-6 mm, base obtuse, margin scabrous, apex acuminate, veins 1-3. Cymes axillary or terminal, forming a narrow panicle, axillary cymes sometimes on pedunclelike branches; peduncle to 5 cm. Pedicel to 1 cm. Calyx tube spathelike, 1-1.5 cm, split on 1 side to near base, membranous; lobes 1-5, subulate, 0.5-1 mm. Corolla dark blue, tubular-campanulate, 3-3.5 cm; lobes ovate-orbicular, 4-5 mm, margin entire, apex rounded; plicae ovate-triangular to truncate, 1-1.5 mm, oblique, margin entire. Stamens inserted just below middle of corolla tube; filaments 1-1.3 cm; anthers narrowly ellipsoid, 2-3 mm. Style 1.5-2 mm; stigma lobes linear. Capsules ovoid-ellipsoid to ovoid, 2-2.5 cm; gynophore to 2.2 cm. Seeds brown, ovoid-ellipsoid, 1.2-1.5 mm. Fl. and fr. Aug.
It is hardy to zone (UK) 4. It is in flower from Jul to August, and the seeds ripen from Aug to September. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Bumblebees, butterflies. Cultivation :
In general, gentians require a moist well-drained soil in a sheltered position, a certain minimum of atmospheric humidity, high light intensity but a site where temperatures are not too high. They are therefore more difficult to grow in areas with hot summers and in such a region they appreciate some protection from the strongest sunlight. Most species will grow well in the rock garden. Plants are intolerant of root disturbance.
Seed – best sown as soon as it is ripe in a light position in a cold frame. It can also be sown in late winter or early spring but the seed germinates best if given a period of cold stratification and quickly loses viability when stored, with older seed germinating slowly and erratically. It is advantageous to keep the seed at about 10°c for a few days after sowing, to enable the seed to imbibe moisture. Following this with a period of at least 5 – 6 weeks with temperatures falling to between 0 and -5°c will usually produce reasonable germination. It is best to use clay pots, since plastic ones do not drain so freely and the moister conditions encourage the growth of moss, which will prevent germination of the seed. The seed should be surface-sown, or only covered with a very light dressing of compost. The seed requires dark for germination, so the pots should be covered with something like newspaper or be kept in the dark. Pot up the seedlings into individual pots as soon as they are large enough to handle and grow on in light shade in the greenhouse for at least their first winter. The seedlings grow on very slowly, taking 2 – 7 years to reach flowering size. When the plants are of sufficient size, place them out into their permanent positions in late spring or early summer. Division in March. Most members of this genus have either a single tap-root, or a compact root system united in a single root head, and are thus unsuitable for division. Cuttings of basal shoots in late spring Medicinal Uses:….…Stomachic……..A tincture of the plant is used as a stomachic.
Habitat : These species are found worldwide in the tropics and subtropics. Several species also grow in temperate regions along water edges where it is shady and damp. Sunny places in moist woodland, water-logged lands at low to moderate elevations.
Cynanchum stauntonii is a perennial climbing herb,erect half-shrub, high 30 ~ 60cm. Stems cylindrical, with thin edges. 6-13cm,width of .03-0.5cmLeaves opposite, lanceolate or linear-lanceolate, long 6 ~ 13cm, width of 0.3 ~ 0.5cm, ends acuminate, midrib apparent. Cymes axillary, 3 to 8 flowers; Calyx 5 parted; Corolla purple, radial, inner surface is pilose, lobes narrowly triangular; Vice corolla lobes peltate, apex slightly thicker and the inner volume; stamens 5, and co-generation core column pistil, anther 2 rooms; stigma convex, including the films in the anther. Fruit solitary follicles. Flowering 5 to 8 months, the fruit of 9 to 10 months CLICK & SEE
Slender cylindrical roots, branching, slightly curved, long 4 ~ 15cm, diameter of 1.5 ~ 4mm; surface yellow-white or yellowish brown, for length of 1.5 ~ 4.5cm, the top of a residual stem; crisp, hollow cross section. Tufted slender curved section at the root, long up to 10cm, diameter of less than 1mm, there was hair to be like many branches, often twisting into the group. Gas micro, slightly sweet taste.
We have very little information on this species and do not know if it will be hardy in Britain, though judging by its native range it could succeed outdoors in many parts of this country. It probably does not have any special cultivation requirements and will probably succeed in most soils in a sunny position.
Seed – sow spring in the greenhouse. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division in spring.
The dried root, decocted with other herbs, is anodyne, antitussive and expectorant. A decoction of the root is used in the treatment of coughs and asthma. Decoctions of all parts are used as a febrifuge and for treating internal fever. The roots are used medicinally for pulmonary tuber-culosis, infantile malnutrition due to intestinal parasites, influenza, cough, and chronic bronchitis.
Known Hazards: There are some reports of toxins in this genus
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.
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.
Defenition: Autism is a brain development disorder that impairs social interaction and communication, and causes restricted and repetitive behavior, all starting before a child is three years old. This set of signs distinguishes autism from milder autism spectrum disorders (ASD) such as Asperger syndrome.
Most infants and young children are very social creatures who need and want contact with others to thrive and grow. They smile, cuddle, laugh, and respond eagerly to games like “peek-a-boo” or hide-and-seek. Occasionally, however, a child does not interact in this expected manner. Instead, the child seems to exist in his or her own world, a place characterized by repetitive routines, odd and peculiar behaviors, problems in communication, and a lack of social awareness or interest in others. These are characteristics of a developmental disorder called autism……….CLICK & SEE
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by multigene interactions or by rare mutations. In rare cases, autism is strongly associated with agents that cause birth defects. Other proposed causes, such as childhood vaccines, are controversial and the vaccine hypotheses lack convincing scientific evidence. Most recent reviews estimate a prevalence of one to two cases per 1,000 people for autism, and about six per 1,000 for ASD, with ASD averaging a 4.3:1 male-to-female ratio. The number of people known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.
Autism affects many parts of the brain; how this occurs is poorly understood. Parents usually notice signs in the first two years of their child’s life. Early behavioral or cognitive intervention can help children gain self-care, social, and communication skills. There is no cure. Few children with autism live independently after reaching adulthood, but some become successful, and an autistic culture has developed, with some seeking a cure and others believing that autism is a condition rather than a disorder.
Characteristics : Autism is distinguished by a pattern of symptoms rather than one single symptom. The main characteristics are impairments in social interaction, impairments in communication, restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis. Individual symptoms of autism occur in the general population and appear not to associate highly, without a sharp line separating pathological severity from common traits.
Autism is usually identified by the time a child is three years of age. It is often discovered when parents become concerned that their child may be deaf, is not yet talking, resists cuddling, and avoids interactions with others.
A preschool age child with “classic” autism is generally withdrawn, aloof, and fails to respond to other people. Many of these children will not even make eye contact. They may also engage in odd or ritualistic behaviors like rocking, hand flapping, or an obsessive need to maintain order.
Many children with autism do not speak at all. Those who do may speak in rhyme, have echolalia (repeating a person’s words like an echo), refer to themselves as “he” or “she”, or use peculiar language.
The severity of autism varies widely, from mild to severe. With proper supports, many of these children are able to perform well in a school setting and may be able to live independently when they grow up. Other children with autism function at a much lower level. Mental retardation is commonly associated with autism. Occasionally, a child with autism may display an extraordinary talent in art, music, or another specific area.
Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.
* Stereotypy is apparently purposeless movement, such as hand flapping, head rolling, or body rocking.
* Compulsive behavior is intended and appears to follow rules, such as arranging objects in a certain way.
* Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
* Ritualistic behavior involves the performance of daily activities the same way each time, such as an unvarying menu or dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.
* Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program.
* Self-injury includes movements that injure or can injure the person, such as biting oneself. Dominick et al. reported that self-injury at some point affected about 30% of children with ASD.
No single repetitive behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.
* Lack of pointing to direct others’ attention to objects (occurs in the first 14 months of life)
* Does not adjust gaze to look at objects that others are looking at
* Cannot start or sustain a social conversation
* Develops language slowly or not at all
* Repeats words or memorized passages, such as commercials
* Does not refer to self correctly (for example, says “you want water” when the child means “I want water”)
* Uses nonsense rhyming
* Communicates with gestures instead of words
* Shows a lack of empathy
* Does not make friends
* Is withdrawn
* Prefers to spend time alone, rather than with others
* May not respond to eye contact or smiles
* May actually avoid eye contact
* May treat others as if they are objects
* Does not play interactive games
Response to sensory information:
* Has heightened or low senses of sight, hearing, touch, smell, or taste
* Seems to have a heightened or low response to pain
* May withdraw from physical contact because it is overstimulating or overwhelming
* Does not startle at loud noises
* May find normal noises painful and hold hands over ears
* Rubs surfaces, mouths or licks objects
* Shows little pretend or imaginative play
* Doesn’t imitate the actions of others
* Prefers solitary or ritualistic play
* Has a short attention span
* Uses repetitive body movements
* Shows a strong need for sameness
* “Acts up” with intense tantrums
* Has very narrow interests
* Demonstrates perseveration (gets stuck on a single topic or task)
* Shows aggression to others or self
* Is overactive or very passive
The cause of autism remains unknown, although current theories indicate a problem with function or structure of the central nervous system. What we do know, however, is that parents or “inadequate parenting” do not cause autism.
Genetic factors seem to be important. For example, identical twins are much more likely than fraternal twins or siblings to both have autism. Similarly, language abnormalities are more common in relatives of autistic children. Chromosomal abnormalities and other neurological problems are also more common in families with autism.
A number of other possible causes have been suspected, but not proven. They involve digestive tract changes, diet, mercury poisoning, vaccine sensitivity, and the body’s inefficient use of vitamins and minerals.
The exact number of children with autism is not known. A report released by the U.S. Centers for Disease Control and Prevention (CDC) suggests that autism and related disorders are more common than previously thought, although it is unclear if this is due to an increasing rate of the illness or an increased ability to diagnose the illness.
Autism affects boys 3 to 4 times more often than girls. Family income, education, and lifestyle do not seem to affect the risk of autism.
Some parents have heard that the MMR vaccine that children receive may cause autism. This theory was based, in part, on two facts. First, the incidence of autism has increased steadily since around the same time the MMR vaccine was introduced. Second, children with the regressive form of autism (a type of autism that develops after a period of normal development) tend to start to show symptoms around the time the MMR vaccine is given. This is likely a coincidence due to the age of children at the time they receive this vaccine.
Several major studies have found NO connection between the vaccine and autism, however. The American Academy of Pediatrics and the Center for Disease Control and Prevention report that there is no proven link between autism and the MMR vaccine.
Some doctors attribute the increased incidence in autism to newer definitions of autism. The term “autism” now includes a wider spectrum of children. For example, a child who is diagnosed with high-functioning autism today may have been thought to simply be odd or strange 30 years ago.
Screening & Diagnosis:
:All children should have routine developmental exams by their pediatrician. Further testing may be needed if there is concern on the part of the clinician or the parents. This is particularly true whenever a child fails to meet any of the following language milestones:
* Babbling by 12 months
* Gesturing (pointing, waving bye-bye) by 12 months
* Single words by 16 months
* Two-word spontaneous phrases by 24 months (not just echoing)
* Loss of any language or social skills at any age.
These children might receive a hearing evaluation, a blood lead test, and a screening test for autism (such as the Checklist for Autism in Toddlers (CHAT) or the Autism Screening Questionnaire).
A health care provider experienced in the diagnosis and treatment of autism is usually necessary for the actual diagnosis. Because there is no biological test for autism, the diagnosis will often be based on very specific criteria laid out in a book called the Diagnostic and Statistical Manual IV.
The other pervasive developmental disorders include:
* Asperger syndrome (like autism, but with normal language development)
* Rett syndrome (very different from autism, and only occurs in females)
* Childhood disintegrative disorder (rare condition where a child acquires skills, then loses them by age 10)
* Pervasive developmental disorder – not otherwise specified (PDD-NOS), also called atypical autism.
An evaluation of autism will often include a complete physical and neurologic examination. It may also include a specific diagnostic screening tool, such as:
Children with known or suspected autism will often have genetic testing (looking for chromosome abnormalities) and perhaps metabolic testing.
Autism encompasses a broad spectrum of symptoms. Therefore, a single, brief evaluation cannot predict a child’s true abilities. Ideally, a team of different specialists will evaluate the child. They might evaluate speech, language, communication, thinking abilities, motor skills, success at school, and other factors.
Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis. It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.
The symptoms of autism and ASD begin early in childhood but are occasionally missed. Adults may seek retrospective diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.
Sometimes people are reluctant to have a child diagnosed because of concerns about labeling the child. However, failure to make a diagnosis can lead to failure to get the treatment and services the child needs.
An early, intensive, appropriate treatment program will greatly improve the outlook for most young children with autism. Most programs will build on the interests of the child in a highly structured schedule of constructive activities. Visual aids are often helpful.
Treatment is most successful when geared toward the child’s particular needs. An experienced specialist or team should design the individualized program. A variety of effective therapies are available, including applied behavior analysis (ABA), speech-language therapy, medications, occupational therapy, and physical therapy. Sensory integration and vision therapy are also common, but there is little research supporting their effectiveness. The best treatment plan may use a combination of techniques.
APPLIED BEHAVIORAL ANALYSIS (ABA)
This program is for younger children with an autism spectrum disorder. It highly effective in many cases. ABA uses a one-on-one teaching approach that relies on reinforced practice of various skills. The goal is to get the child close to typical developmental functioning.
ABA programs are usually conducted within a child’s home, under the supervision of a behavioral psychologist. Unfortunately, these programs can be very expensive and have not been widely adopted by school systems. Parents often must seek funding and staffing from other sources, which can be hard to find in many communities.
Another program is called the Treatment and Education of Autistic and Related Communication Handicapped Children (TEACCH). TEACCH, developed as a statewide program in North Carolina, uses picture schedules and other visual cues. These help the child work independently and to organize and structure their environments. Though TEACCH tries to enhance a child’s adaptation and skills, there is also an acceptance of the deficits associated with autism spectrum disorders. In contrast to ABA programs, TEACCH programs do not anticipate that children will achieve typical developmental progress in response to the treatment.
Medicines are often used to treat behavior or emotional problems that people with autism may have. These include hyperactivity, impulsiveness, attention problems, irritability, mood swings, outbursts, tantrums, aggression, extreme compulsions that the child finds it impossible to suppress, sleep difficulty, and anxiety. Currently, only risperidone is approved for treatment of children ages 5-16 with irritability and aggression associated with autism.
Some children with autism appear to respond to a gluten-free or a casein-free diet. Gluten is found in foods containing wheat, rye, and barley. Casein is found in milk, cheese, and other dairy products. Not all experts agree that dietary changes will make a difference, and not all reports studying this method have shown positive results.
If considering these or other dietary changes, seek guidance from both a gastroenterologist (doctor who specializes in the digestive system) and a registered dietitian. You want to be sure that the child is still receiving adequate calories, nutrients, and a balanced diet.
Beware that there are widely publicized treatments for autism that do not have scientific support, and reports of “miracle cures” that do not live up to expectations. If your child has autism, it may be helpful to talk with other parents of children with autism, talk with autism specialists, and follow the progress of research in this area, which is rapidly developing.
At one time, there was enormous excitement about using secretin infusions. Now, after many studies have been conducted in many laboratories, it’s possible that secretin is not effective after all, but research is ongoing.
For organizations that can provide additional information and help on autism, see autism resources.
There is no cure. Children recover occasionally, sometimes after intensive treatment and sometimes not; it is not known how often this happens. Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination. Although core difficulties remain, symptoms often become less severe in later childhood. Few high-quality studies address long-term prognosis. Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife. Acquiring language before age six, having IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism. A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care. A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence. A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); only 56% had ever been employed, most in volunteer, sheltered or part time work. Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.
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