Teknik Perangsangan Klitoral

Dalam hal kepekaan seksual, klitoris memegang peranan yang sangat penting. Klitoris terletak di ujung atas vagina, tepat di antara bibir dalam dan bibir luarnya, serta tersembunyi dalam lapisan seperti daging tipis.

Bagian yang tampak dari luar sebenarnya hanyalah ujung klitoris saja, sehingga berukuran kecil. Kelenjar ini berhubungan dengan crura (yang panjangnya sekitar 6 sampai 7 cm), yang juga berhubungan dengan tulang panggul. Tiga bagian inilah sesungguhnya yang disebut klitoris.

Bila seorang perempuan terangsang secara seksual, klitoris akan membengkak dan menjadi tegang. Perempuan akan menikmati orgasme dengan rangsangan langsung maupun tidak langsung pada klitorisnya. Saat intercourse dengan pasangan, bagian inilah yang harus mendapat perhatian ekstra. Saat ingin melakukan 'swalayan' atau bermasturbasi, perempuan bisa merangsang klitoris dengan jari.

Agar tak ada gangguan, carilah tempat yang tenang, sehingga Anda dapat santai dan sekaligus berkonsentrasi menikmati sensasi.

Mulailah dengan membayangkan hal hal yang merangsang nafsu anda sambil menggosok-gosok klitoris. Cara ataupun intensitasnya bisa Anda sesuaikan dengan keinginan. Saat mulai terangsang, kemaluan Anda akan mulai basah. Sementara melakukan perangsangan pada klitoris, dalam waktu bersamaan Anda juga bisa merangsang puting buah dada.

Cobalah membuka penutup klitoris anda agar gosokan jari Anda makin terasa pada klitoris. Bacalah juga bacaan bacaan erotis untuk semakin melambungkan fantasi.

Cara lain untuk bermasturbasi adalah memanfaatkan pancuran air dari shower. Aturlah panas air serta tekanan semprotan sesuai selera Anda. Dimulai dengan semprotan dengan tekanan ringan, selanjutnya ditingkatkan. Makin keras semprotan air, makin terasa rangsangannya pada klitoris Anda.

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Menjaga Kesehatan Vagina

Perempuan harus berhati-hati menjaga kebersihan organ kewanitaan. Sebab, masalah kebersihan bisa menjadi pintu masuk berbagai macam penyakit. Ada banyak hal yang harus diperhatikan:

1. Saat menstruasi, usahakan sesering mungkin mengganti pembalut. Darah yang keluar bisa menjadi media tumbuhnya kuman.
2. Sesudah berhubungan seks, bagian luar vagina sebaiknya selalu dibersihkan. Sebaiknya gunakan sabun pembersih khusus vagina. Jika perlu, gunakan cairan pembersih vagina bila memang ada infeksi di daerah kemaluan.
3. Saat membersihkan vagina, bilas dari arah depan ke belakang. Hal ini untuk menghindari terbawanya kuman dari anus ke vagina. Lebih baik gunakan air yang langsung ditadah dari keran biasa atau dengan keran semprot. Air yang terkumpul di ember atau bak mandi bisa saja terkontaminasi air kencing orang lain, spora, jamur, atau kuman.
4. Bila menggunakan kertas tisu, Anda harus hati-hati. Lendir dan air memang terserap, tetapi hendaknya diingat bahwa tidak semua tisu terjamin kualitasnya. Tisu yang terbuat dari serbuk kayu ada yang tercemar jamur kalau proses pembuatannya kurang baik.
5. Jaga organ intim agar tidak lembab setelah buang air kecil atau buang air besar. Bilas vagina sampai bersih, kemudian keringkan sebelum memakai celana dalam. Usahakan agar daerah kemaluan dan selangkangan selalu kering, lebih-lebih bagi yang bertubuh gemuk. Lingkungan yang lembab sangat disukai jamur.
6. Gantilah celana dalam sekurang-kurangnya dua sampai tiga kali sehari. Jangan biarkan celana basah atau lembab karena memberi peluang tumbuhnya jamur.
7. Sebaiknya tidak mengenakan celana terlalu ketat, berbahan nilon, jins, dan kulit. Pakai celana dalam berbahan katun yang menyerap keringat. Bila menggunakan panty liner, ganti setiap 2-3 jam.
8. Perempuan yang pernah melahirkan dan berhubungan seks, lakukan pap smear sekali setahun. Untuk mereka yang sudah menopause, lakukan 2-3 tahun sekali.
9. Jaga berat badan normal. Jangan sampai kegemukan karena menyebabkan vagina tertutup lipatan lemak sehingga lembab.

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The Unique Ngerebeg Ceremony

Hundreds of children, mostly of 3 to 15 years of age, gathered in the inner courtyard of Duwur Bingin Temple, in Tegalalang village on Wednesday (4/22/09). They dressed in traditional clothes some of them were bare-chested. They had painted their faces and bodies with colorful images and pattern and each of them carried a slender staff made from the branch of palm, decorated with colorful flowers and young coconut leaves. They are the participants of Ngerebeg ritual.

The Ngerebeg ritual began with distribution of deity’s blessing by magibung ritual (eating collectively); 6 to 8 participants formed a group, they sit together around a set of food and ate it together. After megibung, they lined up in front of the temple to receive purification ritual with sprinkling of holy water by the priest. Then the noisy procession of freakishly decorated children began to hit the street of Tegalalang village.

The screams of more than five hundreds children turned the quiet village into a wild hullabaloo. They paraded down the main street and stopped sometimes in front of temples to pay homage. The parents lined up on the side of the street, encouraging their children to scream and distributing refreshment to them. The procession lasted for three hours and ended up at Duwur Bingin temple.
Ngerebeg ritual is a preliminary ritual for the anniversary ceremony of Duur Bingin Temple. This ritual enacts the journey of Duwur Bingin Deity’s vassals. The children represent Panjak hana-tan hana (exist-non exist vassal). Panjak hana-tan hana refers to various supernatural beings, range from the Bhuta Kala (spirits of Nature) to the Wong Samar (human-like residents of isolated gorges and deep jungles). This ritual serves to purify the village through the noisy parade of scary-looking children it is believed that supernatural beings will be pacified so they will not disrupt the upcoming temple anniversary ceremony.

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Masalah Seputar Organ Intim

Karena sensitif, organ intim wanita perlu diperhatikan lebih seksama. Berikut ini jawaban atas pertanyaan seputar masalah kesehatan organ intim yang kerap melanda.

A. Keputihan bisa sembuh?
Keputihan, atau Fluor Albus, sering menimpa wanita. Penyebabnya bisa karena infeksi jamur, bakteri, atau virus. Jika tidak segera diobati, keputihan dapat menjalar ke daerah saluran kencing. Jika keputihan sudah menyababkan nyeri di daerah saluran kemih, segera ke dokter.

Bagaimana bakteri dan jamur masuk ke dalam vagina?
1. Kurang bersih
Kebersihan usai buang air kecil atau besar, sangat mutlak. Terlebih jika Anda buang air kecil atau besar di toilet umum. Bersihkan vagina dengan cairan khusus dengan kadar keasaman yang sama dengan vagina. Jangan bersihkan dengan sabun mandi biasa, karena tingkat keasamannya tinggi, karena akan membuat bakteri yang menguntungkan pada vagina mati.
2. Pakaian dalam lembap
Pakaian dalam yang lembap, akan memancing bakteri dan jamur hinggap. Bakteri dan jamur pun akan bersinggungan dengan vagina. Jangan memakai celana dalam dari bahan nilon (yang mengandung karet), karena tidak dapat menyerap keringat di daerah genital. Pakai pakaian dalam dari bahan katun yang dapat menyerap keringat dengan baik.
3. Bersih usai berhubungan
Tidak langsung membersihkan vagina setelah berhubungan seks. Usai bermesraan, segeralah buang air kecil dan membersihkannya dengan air, lalu keringkan hingga tidak lembap.
4. Memakai celana ketat
Celana panjang ketat, seperti jins, dapat menghambat sirkulasi darah di daerah vagina, perut, dan selangkangan. Hal ini juga akan memicu sekresi (pengeluaran cairan) berlebih karena terhambanya peredaran darah.

Tips:
1. Jangan digaruk, karena akan menyebabkan lecet dan perih.
2. Membersihkan dengan air rebusan daun sirih juga bisa menyembuhkan keputihan. Ambil kurang lebih 5 lembar daun sirih, lalu rebus hingga matang. Diamkan air sampai hangat, lalu segera gunakan.
3. Jika keputihan sudah dalam tingkat patologis, cepat ke dokter.

B. Kenapa Banyak Cairan?
Jika Anda stres, kelelahan, atau usai melahirkan, hormon Anda berubah tidak stabil. Hal ini akan memicu cairan pada vagina menjadi tidak terkontrol. Akibatnya, banyak pasangan mengeluhkan dampaknya terhadap hubungan seks. Untuk mengatasinya, coba bebera cara ini:

1. Totok vagina
Cara ini adalah dengan cara menekan titik-titik syaraf yang berhubungan dengan syaraf vagina. Gunanya adalah untuk membuat aliran darah menjadi lancar (tidak ada penyumbatan) dan menguatkan otot-otot di daerah panggul. Jika aliran darah lancar, maka cairan pada vagina pun keluar dengan normal, tidak berlebihan. Dan, jika otot-otot panggul kuat, maka kehidupan seksual Anda pun semakin berkualitas. Totok vagina biasanya dilakukan oleh orang yang sudah ahli.

2. Pengasapan atau V fogging (ratus)
Ratus kerap dilakukan perempuan jaman dulu. Caranya, dengan membakar rempah-rempah wangi di wadah yang disebut anglo. Guna pengasapan adalah untuk mematikan bakteri, dan menjaga vagina tetap kering. Anda pun dapat melakukan sendiri di rumah, dengan membeli perlengkapan berupa, anglo, kursi rotan khusus, dan rempah wangi yang kini banyak dijual. Jangan terlalu sering melakukan ratus, cukup 2 minggu sekali. Jika terlalu sering, bakteri yang berguna bagi vagina jadi ikut mati. Hal ini malah akan membuat daya tahan vagina terhadap penyakit menjadi menurun.

3. Perawatan dari dalam
Minum jamu-jamuan juga layak dilirik. Misalnya ramuan berupa racikan kunyit, asam dan daun sirih. Diminum seminggu 2-3 kali. Jika ingin praktis, sudah ada, kok, jamu yang berbentuk pil. Tetapi ingat, konsumsilah jamu-jamuan yang sudah terdaftar secara resmi.

C. Vagina Terasa ‘Lebar’
Seusai melahirkan secara normal, biasanya para wanita merasakan vaginanya tidak terlalu ‘rapat’ lagi. Ini dikarenakan otot-otot daerah panggul melemah. Bagi Anda yang sudah lama menikah, juga akan merasakah dinding dan rongga vagina semakin ‘lebar’. Untuk menguatkan kembali otot-otot daerah panggul, dan merapatkan dinding vagina, ada dua cara yang bisa Anda lakukan, yaitu:

1. Senam Kegel. Tujuannya untuk menguatkan otot panggul pubococcygeus (PC). Senam yang ditemukan oleh Dr. Arnold Kegel, dulu bertujuan untuk wanita yang tidak bisa menahan pipis. Karena gerakan-gerakannya menyebabkan otot-otot panggul kuat kembali, senam ini dianggap bagus juga untuk merapatkan vagina untuk kenikmatan seks. Gerakan senam ini seperti sedang menahan pipis. Sebaiknya dilakukan setiap hari, pagi, siang dan malam, masing-masing 15-20 menit. Jika dilakukan setiap waktu, maka otot-otot akan menguat lebih lama.

2. Minum jamu. Resep yang biasa dipakai para perempuan jaman dulu untuk “merapatkan” organ intim adalah campuran dari beberapa lembar daun sirih, buah gambir, irisan kulit pinang muda, dan kapur sirih secukupnya. Bahan-bahan tersebut dicampur jadi satu dan direbus sampai mendidih. Lalu, diamkan sampai hangat, dan siap diminum. Minumlah setiap pagi.

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Ronaldo Akan Bintangi Film Tentang Pengungsi Palestina

Bintang sepak bola terkenal asal Brazil - Ronaldo akan memerankan dirinya sendiri dalam sebuah film Iran yang diambil dari sebuah kisah nyata dari seorang gadis Palestina yang terbunuh, sebelum dirinya dapat mewujudkan impiannya bertemu dengan bintang sepak bola idolanya tersebut.

Film ini terinspirasi dari kisah nyata seorang gadis berumur 13 tahun bernama Alneyrab - yang memimpikan bertemu dengan bintang sepak bola terkenal Ronaldo selama kunjungannya dalam sebuah misi kemanusiaan pada tahun 2005 ke wilayah pengungsian Palestina, namun ia hanya dapat melihat bintang sepak bola pujaannya itu dari jauh.

Dia meninggal dalam sebuah kamp pengungsian warga Palestina di Libanon selatan setelah kehilangan satu kakinya akibat menginjak ranjau darat yang ditebarkan Israel tanpa bisa mewujudkan impiannya bertemu dengan bintang idolanya itu.

Ronaldo bintang sepak bola dunia yang mendapat penghargaan selama tiga kali berturut-turut telah menandatangani kontrak awal untuk pembuatan film ini, agen dari Ronaldo mengatakan kepada situs Brazilian Sports - Globo. Namun Ronaldo masih harus mendapatkan ijin dari klubnya untuk keterlibatannya dalam film tersebut.

Ronaldo akan tampil di film ini dalam beberapa adegan 'mimpi', kata Farrokh Faradji Chadan, presiden dari komite kerjasama Brazil-Iran.

Film Iran ini sampai sekarang belum memiliki judul.

Pembuatan film ini akan dimulai pada awal September di Libanon, dimana Ronaldo hanya perlu menghabiskan beberapa hari suting saja, Ronaldo sendiri tidak menjelaskan berapa banyak bayaran yang akan ia terima dalam pembuatan film "kemanusiaan" ini.

Dia akan berada di Palestina pada September nanti dengan klub sepak bolanya Corinithians untuk bermain dalam sebuah pertandingan persahabatan melawan klub sepakbola Brazil lainnya - Fluminese. Tim sepak bolanya jauh-jauh hari telah menolak untuk bermain melawan tim sepak bola di Israel.

Ronaldo sebelumnya telah mengunjungi Israel dan tepi barat pada tahun 2005 sebagai duta kemanusiaan PBB.

Yah mudah-mudahan dengan keterlibatannya dalam film ini, Ronaldo bisa mendapat Hidayah untuk masuk Islam..Amiin.(fq/aby)

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Nikon D5000

Main Features


* New 2.7-in. 230k-dot Vari-angle monitor swings down approximately 90° and rotates 180°
* Nikon DX-format CMOS image sensor with 12.3 effective megapixels and Integrated Dust Reduction System
* Specially designed EXPEED image processing system
* One-touch access to Live View, which includes face priority AF and subject tracking

# D-SLR movie function: D-Movie, selectable from 320 x 216 pixels, 640 x 424 pixels or 1,280 x 720 pixels in AVI format
# 19 Scene Modes that automatically adjust exposure, image processing, Active D-Lighting and other settings for superior image quality
# Scene Recognition System, utilizing 420-pixel RGB sensor, improves autofocus, auto exposure and auto white balance performance and is also integrated with the Face Detection System
# Active D-Lighting for smooth tone reproduction in high-contrast environments
# Multi-CAM 1000 autofocus sensor module featuring 11 AF points provides fast and precise autofocus coverage across the frame
# Picture Control System offers Portrait and Landscape options for more vibrant customized colors
# Extensive palette of in-camera Retouch Menus including several new retouch options such as Soft Filter and Color Outline
# Incredibly low-noise performance throughout a wide sensitivity range of ISO 200 to 3200; can be set to ISO 100 and ISO 6400 equivalents
# Viewfinder with approx. 95% frame coverage and an easy-to-view 17.9 mm eyepoint (at -1.0 m-1)
# Up to 4 fps continuous shooting
# Built-in pop-up flash with Nikon's original i-TTL flash control
# Highly efficient energy-saving design that allows approx. 510 images on a single charge of the Rechargeable Li-ion Battery EN-EL9a (CIPA standard, with AF-S DX NIKKOR 18-55mm f/3.5-5.6G VR and flash fired at full power once every other shot.)
# Compatible with HDMI (High-Definition Multimedia Interface) output
# Included Nikon ViewNX software makes browsing and organizing your images easy
# Optional photo-editing software Capture NX 2 allows quick and easy photo editing
# Lightweight compact body

Specifications






Effective pixels

12.3 million

Image sensor

CMOS sensor, 23.6 x 15.8 mm; total pixels: 12.9 million; Nikon DX-format

Image size (pixels)

4,288 x 2,848 [L], 3,216 x 2,136 [M], 2,144 x 1,424 [S]

Sensitivity

ISO 200 to 3200 in steps of 1/3 EV. Can also be set to approx. 0.3, 0.7, or 1 EV (ISO 100 equivalent) below ISO 200, or to approx. 0.3, 0.7, or 1 EV (ISO 6400 equivalent) over ISO 3200, ISO sensitivity auto control available

Storage media

SD memory cards, SDHC compliant

Monitor

Vari-angle type, 2.7-in., approx. 230k-dot TFT LCD, approx. 100% frame coverage, and brightness adjustment

Exposure metering

3D Color Matrix Metering II, Center-Weighted and Spot Metering

Exposure modes

Auto modes (auto, auto [flash off]), Advanced Scene Modes (Portrait, Landscape, Child, Sports, Close up, Night portrait, Night landscape, Party/indoor, Beach/snow, Sunset, Dusk/dawn, Pet portrait, Candlelight, Blossom, Autumn colors, Food, Silhouette, High key, and Low key), programmed auto with flexible program (P), shutter-priority auto (S), aperture-priority auto (A), manual (M)

Interface

Hi-Speed USB

Power sources

One Rechargeable Li-ion Battery EN-EL9a, AC Adapter EH-5a

Dimensions (W x H x D)

Approx. 127 x 104 x 80 mm (5.0 x 4.1 x 3.1 in.)

Weight

Approx. 560 g (1 lb. 4 oz.) without battery, memory card, or body cap

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This blog is created by Sujana Yahya. I was born on April 11, 1970 in Indramayu - West Java, Indonesia. I have finished my study in SMA Muhammadiyah Cirebon - West Java in 1990.

Iam graduated from Nursing Academy - Banjarbaru, South Kalimantan. In 1998 I have joined to INTP-3 ( Indonesian Nurse Training Program) in The Netherlands for about 15 months. Since 2000 upto now Iam working in Physical Medicine & Rehabilitation Hospital Kuwait as a nursing staff under ministry of health.

My regards
Sujana Yahya
Physical Medicine & Rehabilitation Hospital
PO. BOX 4079 Safat 13041
Kuwait
email : indramayu_kuwait@yahoo.com

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AUTISM

Autism is a brain development disorder characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old.[1] Autism affects many parts of the brain; how this occurs is not understood.[2] The autism spectrum disorders (ASD) also include the related conditions Asperger syndrome and PDD-NOS, which have fewer signs and symptoms.[3]

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations, or by rare combinations of common genetic variants.[4] In rare cases, autism is strongly associated with agents that cause birth defects.[5] Controversies surround other proposed environmental causes, such as heavy metals, pesticides or childhood vaccines;[6] the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.[7] The prevalence of ASD is about 6 per 1,000 people, with about four times as many males as females. The number of people known to have autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.[8]

Parents usually notice signs in the first two years of their child's life. Although early behavioral or cognitive intervention can help children gain self-care, social, and communication skills, there is no known cure.[9] Not many children with autism live independently after reaching adulthood, though some become successful.[10] An autistic culture has developed, with some individuals seeking a cure and others believing autism should be tolerated as a difference and not treated as a disorder.[11]

Characteristics

Autism is a highly variable brain development disorder[12] that first appears during infancy or childhood, and generally follows a steady course without remission.[13] Overt symptoms gradually begin after the age of six months, become established by age two or three years,[14] and tend to continue through adulthood, although often in more muted form.[15] It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.[16] Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.[17]

Social development

Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders.[15] People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling "like an anthropologist on Mars".[18]

Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn taking, and are more likely to communicate by manipulating another person's hand.[19] Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers.[20] They display moderately less attachment security than usual, although this feature disappears in children with higher mental development or less severe ASD.[21] Older children and adults with ASD perform worse on tests of face and emotion recognition.[22]

Contrary to common beliefs, autistic children do not prefer being alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect their quality of life more deeply.[23]

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in children with a history of language impairment.[24] A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.[25]

Communication

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.[26] Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)[27][28] or reverse pronouns.[29] Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:[3] for example, they may look at a pointing hand instead of the pointed-at object,[19][28] and they consistently fail to point at objects in order to comment on or share an experience.[3] Autistic children may have difficulty with imaginative play and with developing symbols into language.[27][28]

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.[30]

Repetitive behavior

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)[31] categorizes as follows.

* Stereotypy is repetitive movement, such as hand flapping, making sounds, 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.[32]
* Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program or toy.
* Self-injury includes movements that injure or can injure the person, such as eye poking, skin picking, hand biting, and head banging.[3] A 2007 study reported that self-injury at some point affected about 30% of children with ASD.[24]

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.[31]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.[16] An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.[33] Many individuals with ASD show superior skills in perception and attention, relative to the general population.[34] Unusual responses to sensory stimuli are more common and prominent in autistic children, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.[35] Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).[36] Several studies have reported associated motor problems that include poor muscle tone, poor motor planning, and toe walking; ASD is not associated with severe motor disturbances.[37]

Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur;[24] this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual;[38] studies report conflicting results, and the relationship between GI problems and ASD is unclear.[9]

At some point in childhood, about two-thirds of individuals with ASD are affected by sleep problems; these most commonly include symptoms of insomnia such as difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. Sleep problems are associated with difficult behaviors and family stress, and are often a focus of clinical attention over and above the primary ASD diagnosis.[39]

Parents of children with ASD have higher levels of stress.[40] Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.[41]

Classification

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.[13] These symptoms do not imply sickness, fragility, or emotional disturbance.[15]

Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) is diagnosed when the criteria are not met for a more specific disorder.[42] Unlike autism, Asperger's has no substantial delay in language development.[1] The terminology of autism can be bewildering, with autism, Asperger's and PDD-NOS often called the autism spectrum disorders (ASD)[9] or sometimes the autistic disorders,[43] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder; in clinical practice, though, autism, ASD, and PDD are often used interchangeably.[44] ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[45]

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.[46] Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds,[47] or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into syndromal and non-syndromal autism; the syndromal autism is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis.[48] Although individuals with Asperger's tend to perform better cognitively than those with autism, the extent of the overlap between Asperger's, HFA, and non-syndromal autism is unclear.[49]

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype,[19][27][50][51] or that there is a continuum of behaviors between autism with and without regression.[52]

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations[53] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.[54] Newer technologies such as fMRI can help identify biologically-relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism.[55] It has been proposed to classify autism using genetics as well as behavior, with the name Type 1 autism denoting rare autism cases that test positive for a mutation in the CNTNAP2 gene.[56]

Causes

It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms.[57] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[57][58]
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants.[4] Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA but are heritable and influence gene expression.[15] Early studies of twins estimated heritability explains more than 90% of the risk of autism, assuming a shared environment and no other genetic or medical syndromes.[43] However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality like Angelman syndrome or fragile X syndrome, and none of the genetic syndromes associated with ASDs has been shown to selectively cause ASD.[4] Numerous candidate genes have been located, with only small effects attributable to any particular gene.[4] The large number of autistic individuals with unaffected family members may result from copy number variations—spontaneous deletions or duplications in genetic material during meiosis.[60] Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.[59]

Autism caused by some rare mutations may disrupt some synaptic pathways, such as those involved with cell adhesion.[61] Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.[62] All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.[5] Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,[6] extensive searches are underway.[63] Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[8] and prenatal stress.[64] Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and this has given rise to theories that vaccines or their preservatives cause autism. Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about autism has led to lower rates of childhood immunizations and higher likelihood of measles outbreaks.[7]

Mechanism

Autism's symptoms result from maturation-related changes in various systems of the brain.[65] Despite extensive investigation, how autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.[65] The behaviors appear to have multiple pathophysiologies.[17]

Pathophysiology

Unlike many other brain disorders such as Parkinson's, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms.[12] Autism appears to result from developmental factors that affect many or all functional brain systems,[66] and to disturb the timing of brain development more than the final product.[2] Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.[5] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[67] Although many major structures of the human brain have been implicated, almost all postmortem studies have been of individuals who also had mental retardation, making it difficult to draw conclusions.[2] Brain weight and volume and head circumference tend to be greater in autistic children.[68] The cellular and molecular bases of pathological early overgrowth are not known, nor is it known whether the overgrown neural systems cause autism's characteristic signs. Current hypotheses include:

* An excess of neurons that causes local overconnectivity in key brain regions.[69]
* Disturbed neuronal migration during early gestation.[70][71]
* Unbalanced excitatory–inhibitory networks.[71]
* Abnormal formation of synapses and dendritic spines,[71] for example, by modulation of the neurexin–neuroligin cell-adhesion system,[72] or by poorly regulated synthesis of synaptic protein.[73] Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.[74]

Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.[75] As autoantibodies have not been associated with pathology, are found in conditions other than ASD, and are not always present in ASD,[76] the relationship between immune disturbances and autism remains unclear and controversial.[70]

Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these cause structural or behavioral abnormalities is unclear.[65] Some data suggest an increase in several growth hormones; other data argue for diminished growth factors.[77] Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.[78]

The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions.[79] Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.[80] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS[81] and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.[82]
ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.[85] In autism there is evidence for reduced functional connectivity of the default network, a large-scale brain network involved in social and emotional processing, with intact connectivity of the task-positive network, used in sustained attention and goal-directed thinking. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought.[86] A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.[87]

The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[88] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals[30] and by a brain wave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex.[89] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.[90]

From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli.[91] For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.[92]

Neuropsychology

Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in social cognition. The empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing;[93] this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects[94].

These theories are somewhat related to the earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by autistic children's atypical responses to the Sally–Anne test for reasoning about others' motivations,[93] and the mirror neuron system theory of autism described in Pathophysiology maps well to the hypothesis.[80] However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic emotions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.[95]

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function.[96] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.[97] A strength of the theory is predicting stereotyped behavior and narrow interests;[98] two weaknesses are that executive function is hard to measure[96] and that executive function deficits have not been found in young autistic children.[22]

Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people.[99] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[100] These theories map well from the underconnectivity theory of autism.

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties.[58] A combined theory based on multiple deficits may prove to be more useful.[101]

Screening

About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months.[51] As postponing treatment may affect long-term outcome, any of the following signs is reason to have a child evaluated by a specialist without delay:

* No babbling by 12 months.
* No gesturing (pointing, waving goodbye, etc.) by 12 months.
* No single words by 16 months.
* No two-word spontaneous phrases (other than instances of echolalia) by 24 months.
* Any loss of any language or social skills, at any age.[16]

The American Academy of Pediatrics recommends that all children be screened for ASD at the 18- and 24-month well-child doctor visits, using autism-specific formal screening tests.[3] In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.[102] Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor CHAT on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives).[51] It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.[103] Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.[104] Genetic screening for autism is generally still impractical.[105]

Diagnosis

Diagnosis is based on behavior, not cause or mechanism.[17][106] Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder.[1] ICD-10 uses essentially the same definition.[13]

Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.[19]

A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions.[107] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.[108] A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment[107] such as Landau–Kleffner syndrome.[109] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.[110]

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.[44] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,[111] consensus guidelines in the U.S. and UK are limited to high-resolution chromosome and fragile X testing.[44] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.[112] As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.[105] Metabolic and neuroimaging tests are sometimes helpful, but are not routine.[44]

ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later.[51] In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice.[107] A 2009 U.S. study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years.[113] Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek 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.[114]

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.[115] 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.[116]

Management

The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs.[9] Studies of interventions have methodological problems that prevent definitive conclusions about efficacy.[117] Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of systematic reviews of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options.[118] Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills,[9] and often improve functioning and decrease symptom severity and maladaptive behaviors;[119] claims that intervention by around age three years is crucial are not substantiated.[120] Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[9] Educational interventions have some effectiveness in children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children[121] and is well-established for improving intellectual performance of young children.[119] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[108] It is not known whether treatment programs for children lead to significant improvements after the children grow up,[119] and the limited research on the effectiveness of adult residential programs shows mixed results.[122]

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.[15][123] More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[124] Aside from antipsychotics,[125] there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[126] A person with ASD may respond atypically to medications, the medications can have adverse effects,[9] and no known medication relieves autism's core symptoms of social and communication impairments.[127] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function after birth,[62] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.[61]

Although many alternative therapies and interventions are available, few are supported by scientific studies.[22][128][129] Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.[23] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[130] Though most alternative treatments, such as melatonin, have only mild adverse effects[131] some may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets;[132] in 2005, botched chelation therapy killed a five-year-old child with autism.[133]

Treatment is expensive; indirect costs are more so. For someone born in 2000, a U.S. study estimated an average lifetime cost of $3.75 million (net present value in 2009 dollars, inflation-adjusted from 2003 estimate[134]), with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.[135] Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems;[136] one 2008 U.S. study found a 14% average loss of annual income in families of children with ASD,[137] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.[138] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[129]

Prognosis

There is no known cure.[9] Children recover occasionally, so that they lose their diagnosis of ASD;[139] this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;[119] reported rates in unselected samples of children with ASD have ranged from 3% to 25%.[139] A few autistic children have acquired speech at age 5 or older.[140] Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.[23] Although core difficulties tend to persist, symptoms often become less severe with age.[15] 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.[141] Acquiring language before age six, having an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.[142] 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.[10] A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.[143] 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%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or part-time work.[144] Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.[8]

Epidemiology

Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD;[8] because of inadequate data, these numbers may underestimate ASD's true prevalence.[44] PDD-NOS's prevalence has been estimated at 3.7 per 1,000, Asperger's at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000.[145] The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness,[145][146] though unidentified environmental risk factors cannot be ruled out.[6] The available evidence does not rule out the possibility that autism's true prevalence has increased;[145] a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.[63]

Boys are at higher risk for ASD than girls. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without.[8] Although the evidence does not implicate any single pregnancy-related risk factor as a cause of autism, the risk of autism is associated with advanced age in either parent, and with diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy.[147] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.[148]

Autism is associated with several other conditions:

* Genetic disorders. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,[149] and ASD is associated with several genetic disorders.[150]
* Mental retardation. The fraction of autistic individuals who also meet criteria for mental retardation has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence.[151] For ASD other than autism, the association with mental retardation is much weaker.[152]
* Anxiety disorders are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms.[153]
* Epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.[154]
* Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.[78]
* Minor physical anomalies are significantly increased in the autistic population.[155]
* Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for ADHD, Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.[156]

History

A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther contains the story of a 12-year-old boy who may have been severely autistic.[157] According to Luther's notetaker Mathesius, Luther thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated.[158] The earliest well-documented case of autism is that of Hugh Blair, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance.[159] The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.[160]

The New Latin word autismus (English translation autism) was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word autos (αὐτός, meaning self), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".[161]

The word autism first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler's terminology autistic psychopaths in a lecture in German about child psychology.[162] Asperger was investigating a form of ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981.[160] Leo Kanner of the Johns Hopkins Hospital first used autism in its modern sense in English when he introduced the label early infantile autism in a 1943 report of 11 children with striking behavioral similarities.[29] Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders.[58] It is not known whether Kanner derived the term independently of Asperger.[163]

Kanner's reuse of autism led to decades of confused terminology like infantile schizophrenia, and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.[164] As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions.[165] Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,[160] parents continue to feel social stigma in situations where their autistic children's behaviors are perceived negatively by others,[166] and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research.[167] The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely.[168] Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.[11][169]


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# ^ Lack of research on drug treatments:

* Angley M, Young R, Ellis D, Chan W, McKinnon R (2007). "Children and autism—part 1—recognition and pharmacological management" (PDF). Aust Fam Physician 36 (9): 741–4. PMID 17915375. http://www.racgp.org.au/afp/200709/200709angley.pdf.
* Broadstock M, Doughty C, Eggleston M (2007). "Systematic review of the effectiveness of pharmacological treatments for adolescents and adults with autism spectrum disorder". Autism 11 (4): 335–48. doi:10.1177/1362361307078132. PMID 17656398.

# ^ Buitelaar JK (2003). "Why have drug treatments been so disappointing?". Novartis Found Symp 251: 235–44; discussion 245–9, 281–97. doi:10.1002/0470869380.ch14. PMID 14521196.
# ^ Lack of support for interventions:

* Francis K (2005). "Autism interventions: a critical update" (PDF). Dev Med Child Neurol 47 (7): 493–9. doi:10.1017/S0012162205000952. PMID 15991872. http://journals.cambridge.org/production/action/cjoGetFulltext?fulltextid=313204.
* Rao PA, Beidel DC, Murray MJ (2008). "Social skills interventions for children with Asperger's syndrome or high-functioning autism: a review and recommendations". J Autism Dev Disord 38 (2): 353–61. doi:10.1007/s10803-007-0402-4. PMID 17641962.
* Schechtman MA (2007). "Scientifically unsupported therapies in the treatment of young children with autism spectrum disorders" (PDF). Pediatr Ann 36 (8): 497–8, 500–2, 504–5. PMID 17849608. http://pediatricsupersite.com/showPdf.aspx?rid=23083.

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# ^ Seltzer MM, Shattuck P, Abbeduto L, Greenberg JS (2004). "Trajectory of development in adolescents and adults with autism". Ment Retard Dev Disabil Res Rev 10 (4): 234–47. doi:10.1002/mrdd.20038. PMID 15666341.
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# ^ Billstedt E, Gillberg C, Gillberg C (2005). "Autism after adolescence: population-based 13- to 22-year follow-up study of 120 individuals with autism diagnosed in childhood". J Autism Dev Disord 35 (3): 351–60. doi:10.1007/s10803-005-3302-5. PMID 16119476.
# ^ Eaves LC, Ho HH (2008). "Young adult outcome of autism spectrum disorders". J Autism Dev Disord 38 (4): 739–47. doi:10.1007/s10803-007-0441-x. PMID 17764027.
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