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ASKEP TONSILITIS PADA ANAK TONSILITIS PADA ANAK. KONSEP PENYAKIT. 1.1 PENGERTIAN. Tonsilitis adalah massa jaringan limfoid yang terletak di rongga faring. Tetapi abses peritonsil lebih sering terjadi pada orang dewasa sebagai komplikasi tonsillitis. Kesimpulannya seorang anak yang pernah mendapat serangan tonsillitis akut, katakanlah 5-6.

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Askep Epilepsy Pada Orang Dewasa Pdf Gratis

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Autisme adalah gangguan perkembangan syaraf ditandai dengan gangguan interaksi sosial dan komunikasi, dan dengan perilaku terbatas dan berulang. Tanda-tanda ini semua dimulai sebelum seorang anak berusia tiga tahun [2] autism mempengaruhi pengolahan informasi di otak dengan mengubah cara sel-sel saraf dan sinapsis mereka terhubung dan mengatur;. Bagaimana hal ini terjadi adalah tidak dipahami dengan baik [3] Ini adalah salah satu dari tiga. diakui gangguan dalam spektrum autisme (ASDs), dua lainnya adalah sindrom Asperger, yang tidak memiliki keterlambatan dalam perkembangan kognitif dan bahasa, dan Perkembangan Disorder-Tidak Dinyatakan Tertentu (biasa disingkat PDD-NOS) Pervasif, yang didiagnosis ketika set lengkap kriteria untuk autis atau sindrom Asperger tidak dipenuhi. [4]

Autisme memiliki dasar genetika yang kuat, walaupun genetika autis sangat kompleks dan tidak jelas apakah ASD dijelaskan lebih oleh mutasi jarang, atau dengan kombinasi yang jarang dari varian genetik umum [5] Dalam kasus yang jarang terjadi,. Autisme sangat terkait dengan agen yang menyebabkan cacat lahir [6] Kontroversi surround penyebab lainnya lingkungan diusulkan, seperti logam berat, pestisida atau vaksin anak;.. [7] hipotesis vaksin secara biologis masuk akal dan meyakinkan kurangnya bukti ilmiah [8] Prevalensi autisme adalah sekitar 1 – 2 per 1.000 orang di seluruh dunia, namun Pusat Pengendalian dan Pencegahan Penyakit (CDC) melaporkan sekitar 9 per 1.000 anak-anak di Amerika Serikat yang didiagnosis dengan ASD [9] [10] Jumlah orang didiagnosis dengan autisme telah meningkat secara dramatis sejak. 1980-an, sebagian karena perubahan dalam praktek diagnosis; pertanyaan apakah prevalensi sebenarnya telah meningkat adalah belum terselesaikan [11].

Orangtua biasanya melihat tanda-tanda dalam dua tahun pertama kehidupan anak mereka. [12] Tanda-tanda biasanya berkembang secara bertahap, tetapi beberapa anak-anak autis pertama mengembangkan lebih normal dan kemudian mundur [13]. Awal intervensi perilaku atau kognitif dapat membantu anak-anak autis mendapatkan rasa keterampilan perawatan, sosial, dan komunikasi. [12] Meskipun tidak ada obat dikenal, [12] ada telah dilaporkan kasus anak-anak yang sembuh. [14] Tidak banyak anak-anak autis hidup mandiri setelah mencapai usia dewasa, meskipun beberapa menjadi sukses. [15] Budaya autis telah berkembang, dengan beberapa individu yang mencari obat dan lain-lain percaya autis harus diterima sebagai perbedaan dan tidak diperlakukan sebagai gangguan. [16]

Isi

1 Karakteristik
1.1 Pengembangan Sosial
1.2 Komunikasi
1.3 berulang perilaku
1.4 Gejala lainnya
2 Klasifikasi
3 Penyebab
4 Mekanisme
4.1 Patofisiologi
4.2 Neuropsikologi
5 Penyaringan
6 Diagnosis
7 Manajemen
8 Prognosis
9 Epidemiologi
10 Sejarah
11 Referensi
12 Pranala luar

Autism is a disorder of neural development characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old.^[2] Autism affects information processing in the brain by altering how nerve cells and their synapses connect and organize; how this occurs is not well understood.^[3] It is one of three recognized disorders in the autism spectrum (ASDs), the other two being Asperger syndrome, which lacks delays in cognitive development and language, and Pervasive Developmental Disorder-Not Otherwise Specified (commonly abbreviated as PDD-NOS), which is diagnosed when the full set of criteria for autism or Asperger syndrome are not met.^[4]

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.^[5] In rare cases, autism is strongly associated with agents that cause birth defects.^[6]Controversies surround other proposed environmental causes, such as heavy metals, pesticides or childhood vaccines;^[7] the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.^[8] The prevalence of autism is about 1–2 per 1,000 people worldwide; however, the Centers for Disease Control and Prevention (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD.^[9][10] The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.^[11]

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Parents usually notice signs in the first two years of their child’s life.^[12] The signs usually develop gradually, but some autistic children first develop more normally and then regress.^[13] Early behavioral or cognitive intervention can help autistic children gain self-care, social, and communication skills.^[12] Although there is no known cure,^[12] there have been reported cases of children who recovered.^[14] Not many children with autism live independently after reaching adulthood, though some become successful.^[15] An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.^[16]

Karakteristik
Autisme adalah gangguan perkembangan saraf sangat bervariasi [17] yang pertama muncul pada masa bayi atau masa kanak-kanak, dan umumnya mengikuti kursus mantap tanpa pengampunan [18] terbuka. Gejala secara bertahap mulai setelah usia enam bulan, menjadi didirikan oleh usia dua atau tiga tahun, [19] dan cenderung terus melalui dewasa, meskipun sering dalam bentuk diredam lebih [20] Hal ini dibedakan bukan suatu gejala tunggal, melainkan oleh sebuah triad karakteristik gejala:. gangguan dalam interaksi sosial, gangguan dalam komunikasi, dan kepentingan terbatas dan berulang perilaku. Aspek-aspek lain, seperti makan atipikal, juga umum namun tidak penting untuk diagnosis [21] gejala individu Autism’s terjadi. pada populasi umum dan tampaknya tidak mengasosiasikan tinggi, tanpa garis tajam memisahkan patologis parah dari ciri-ciri umum. [22]

Pembangunan sosial
Sosial defisit membedakan autisme dan gangguan spektrum autisme terkait (ASD; Klasifikasi lihat) dari gangguan perkembangan lain [20] Orang-orang dengan autis memiliki gangguan sosial dan sering kekurangan intuisi tentang orang lain bahwa banyak orang yang mengambil untuk diberikan.. Tercatat autistik Temple Grandin menggambarkan ketidakmampuannya untuk memahami komunikasi sosial neurotypicals, atau orang dengan perkembangan syaraf normal, dengan meninggalkan perasaan “seperti seorang antropolog di Mars”. [23]

pembangunan sosial yang tidak biasa menjadi jelas pada awal masa kanak-kanak. Autistic bayi menunjukkan kurang memperhatikan rangsangan sosial, tersenyum dan melihat orang lain lebih jarang, dan kurang merespon nama mereka sendiri. Autistic balita lebih mencolok berbeda dari norma-norma sosial;. sebagai contoh, mereka memiliki kontak mata kurang dan berbalik mengambil, dan tidak memiliki kemampuan untuk menggunakan gerakan sederhana untuk mengekspresikan diri, seperti kekurangan untuk menunjuk hal-hal [24] Tiga-ke anak-anak autis lima tahun cenderung menunjukkan pemahaman sosial, pendekatan yang lain secara spontan, meniru dan merespon emosi, berkomunikasi nonverbal, dan bergantian dengan orang lain. Namun, mereka lakukan lampiran formulir ini untuk pengasuh utama mereka. [25] Sebagian besar anak-anak autis menampilkan keamanan lampiran agak kurang dari anak-anak non-autis, walaupun perbedaan ini menghilang pada anak-anak dengan perkembangan mental yang lebih tinggi atau kurang ASD parah [26] Lanjut Usia anak-anak dan. Dewasa dengan ASD melakukan buruk pada tes pengenalan wajah dan emosi. [27]

Anak-anak dengan autisme berfungsi tinggi menderita kesepian lebih intens dan sering dibandingkan dengan rekan-rekan non-autis, meskipun kepercayaan umum bahwa anak-anak autis lebih suka menyendiri. Membuat dan mempertahankan persahabatan seringkali terbukti sulit bagi mereka dengan autisme. Bagi mereka, kualitas persahabatan, bukan jumlah teman, memprediksi bagaimana mereka merasa kesepian. persahabatan Fungsional, seperti yang mengakibatkan undangan kepada pihak, dapat mempengaruhi kualitas hidup lebih mendalam. [28]

Ada laporan banyak anekdot, tetapi studi sistematis sedikit, agresi dan kekerasan pada individu dengan ASD. Data terbatas menunjukkan bahwa, pada anak dengan keterbelakangan mental, autisme dikaitkan dengan agresi, perusakan harta milik, dan tantrum. Sebuah studi 2007 mewawancarai orang tua dari 67 anak dengan ASD dan melaporkan bahwa sekitar dua-pertiga dari anak-anak periode amukan parah dan sekitar sepertiga memiliki sejarah agresi, dengan marah secara signifikan lebih umum dari pada anak-anak non-autis dengan gangguan bahasa [29] Sebuah penelitian di tahun 2008 Swedia menemukan bahwa, orang berusia 15 atau lebih tua keluar dari rumah sakit dengan diagnosis ASD, mereka yang melakukan kejahatan kekerasan secara bermakna lebih mungkin untuk memiliki kondisi psikopatologis lain seperti psikosis.. [30]

Komunikasi
Sekitar sepertiga sampai setengah individu dengan autisme tidak berkembang cukup ucapan yang alami untuk memenuhi kebutuhan sehari-hari mereka komunikasi [31] Perbedaan dalam komunikasi dapat hadir dari tahun pertama kehidupan,. Dan mungkin adalah munculnya keterlambatan mengoceh, gerak-gerik yang tidak biasa, berkurang tanggap, dan pola vokal yang tidak disinkronkan dengan wali tersebut. Pada tahun kedua dan ketiga, anak-anak autis memiliki mengoceh kurang sering dan kurang beragam, konsonan, kata, dan kombinasi kata, gerak tubuh mereka kurang sering diintegrasikan dengan kata-kata. Autis anak kecil kemungkinannya untuk membuat permintaan atau berbagi pengalaman, dan lebih mungkin untuk hanya mengulang kata-kata orang lain ‘(echolalia) [32] [33] atau kata ganti reverse [34] perhatian tampaknya Bersama. Perlu untuk berbicara fungsional, dan defisit dalam perhatian bersama tampaknya membedakan bayi dengan ASD: [4] misalnya, mereka mungkin melihat tangan menunjuk bukannya menunjuk-pada obyek, [24] [33] dan mereka konsisten gagal untuk menunjuk objek untuk mengomentari atau berbagi pengalaman [4] anak-anak. Autistic mungkin mengalami kesulitan dengan bermain imajinatif dan dengan simbol berkembang ke dalam bahasa [32] [33].

Dalam sepasang studi, berfungsi tinggi anak-anak autis usia 8-15 sama dilakukan juga, dan orang dewasa lebih baik daripada, secara individual cocok kontrol pada tugas-tugas dasar bahasa melibatkan kosakata dan ejaan. Kedua kelompok autis dilakukan lebih buruk daripada kontrol pada tugas-tugas kompleks seperti bahasa figuratif, pemahaman bahasa dan kesimpulan. Sebagai orang sering berukuran Facebook awalnya dari keterampilan dasar bahasa, studi-studi ini menunjukkan bahwa orang-orang berbicara kepada individu autistik lebih cenderung melebih-lebihkan apa memahami audiens mereka. [35]

Perilaku berulang
Autistic individu menampilkan berbagai bentuk perilaku berulang atau dibatasi, yang berulang Perilaku Skala-Revisi (RBS-R) [36] mengkategorikan sebagai berikut.

Seorang anak muda dengan autisme, dan garis tepat dari mainan ia membuat

Stereotypy adalah gerakan berulang, seperti mengepakkan tangan, membuat suara, rolling kepala, atau badan goyang.
perilaku kompulsif dimaksudkan dan muncul untuk mengikuti aturan, seperti mengatur obyek dalam tumpukan atau garis.
Kesamaan adalah resistensi terhadap perubahan, misalnya, bersikeras bahwa furnitur tidak dipindahkan atau menolak menjadi terganggu.
perilaku ritualistik melibatkan berubahnya pola aktivitas sehari-hari, seperti menu yang tidak berubah atau ritual ganti. Ini sangat erat kaitannya dengan persamaan dan validasi independen telah menyarankan menggabungkan dua faktor. [36]
Pembatasan perilaku terbatas dalam fokus, bunga, atau kegiatan, seperti keasyikan dengan program televisi tunggal, mainan, atau permainan.
Self-luka termasuk gerakan-gerakan yang melukai atau bisa melukai orang, seperti memukul-mukul mata menusuk, memetik kulit, tangan menggigit, dan kepala. [4] Sebuah studi 2007 melaporkan bahwa diri-luka di beberapa titik yang terkena dampak sekitar 30% anak-anak dengan ASD [29].
Tidak ada perilaku berulang atau merugikan diri tunggal tampaknya khusus untuk autis, tapi autis hanya muncul untuk memiliki pola peningkatan kejadian dan keparahan dari perilaku tersebut. [37]

Gejala lainnya
Autistic individu mungkin memiliki gejala yang independen terhadap diagnosis, tapi yang dapat mempengaruhi individu atau keluarga [21] Sebuah% 0,5% sampai 10 diperkirakan individu dengan ASD menunjukkan. kemampuan luar biasa, mulai dari keterampilan sempalan seperti menghafalkan trivia dengan bakat luar biasa langka sarjana autis luar biasa [38] Banyak orang dengan ASD menunjukkan. keterampilan unggul dalam persepsi dan perhatian, relatif terhadap populasi umum. [39] Sensory kelainan ditemukan di lebih dari 90% dari mereka yang autisme, dan dianggap fitur inti oleh beberapa, [40] meskipun tidak ada bukti yang baik bahwa gejala sensori membedakan autisme dari gangguan perkembangan lain. [41] Perbedaan yang lebih besar untuk di bawah-responsivitas (misalnya, berjalan ke hal-hal) daripada selama lebih-responsivitas (misalnya , marabahaya dari suara keras) atau untuk mencari sensasi (misalnya, gerakan berirama) [42] Sebuah% 60 -80% diperkirakan orang autis memiliki tanda-tanda motor yang meliputi tonus otot miskin, perencanaan motor miskin, dan berjalan kaki;. [40 defisit] dalam koordinasi motorik yang meresap di ASD dan lebih besar dalam autisme yang tepat. [43]

perilaku makan yang tidak biasa terjadi pada sekitar tiga-perempat dari anak-anak dengan ASD, sejauh itu sebelumnya sebuah indikator diagnostik. Selektivitas adalah masalah yang paling umum, meskipun ritual makan dan penolakan makanan juga terjadi; [29] hal ini tampaknya tidak mengakibatkan kekurangan gizi. Meskipun beberapa anak autis juga memiliki gastrointestinal (GI) gejala, ada kurangnya data ketat diterbitkan untuk mendukung teori bahwa anak-anak autis memiliki lebih atau berbeda gejala GI dari biasanya; [44] penelitian melaporkan hasil yang bertentangan, dan hubungan antara GI masalah dan ASD tidak jelas. [45]

Orang tua dari anak-anak dengan ASD memiliki tingkat stres yang lebih tinggi [46] Saudara anak-anak dengan ASD laporan kekaguman yang lebih besar dan konflik kalah dengan saudara saudara yang terkena dampak dari anak-anak atau mereka tidak terpengaruh dengan sindrom Down;. Bersaudara individu dengan ASD memiliki risiko yang lebih besar negatif saudara hubungan kesejahteraan dan miskin sebagai orang dewasa. [47]

Klasifikasi
Autisme adalah salah satu dari lima gangguan perkembangan meluas (PDD), yang ditandai dengan kelainan luas interaksi sosial dan komunikasi, dan kepentingan sangat terbatas dan sangat perilaku berulang. [18] Gejala ini tidak berarti sakit, kerapuhan, atau gangguan emosional. [20]

Dari lima bentuk PDD, Asperger syndrome terdekat dengan autisme dalam tanda-tanda dan kemungkinan penyebab; sindrom Rett dan tanda-tanda gangguan disintegratif anak berbagi beberapa dengan autisme, tetapi mungkin memiliki penyebab yang tidak terkait; PDD tidak ditentukan (PDD-NOS, juga disebut autisme atipikal) didiagnosa apabila memenuhi kriteria tidak terpenuhi untuk kelainan yang lebih spesifik [48] Berbeda dengan autisme., orang dengan sindrom Asperger tidak memiliki keterlambatan substansial dalam perkembangan bahasa [2] Istilah autisme bisa. akan membingungkan, dengan autisme, sindrom Asperger dan PDD-NOS sering disebut gangguan spektrum autisme (ASD) [12] atau kadang-kadang gangguan autistik, [49] bahwa autisme sendiri sering disebut gangguan autistik, autis anak, atau autisme infantil. Pada artikel ini, autisme mengacu pada gangguan autistik klasik, dalam praktek klinis, meskipun, autisme, ASD, dan PDD sering digunakan secara bergantian [1] ASD, pada gilirannya, adalah bagian dari fenotipe autisme yang lebih luas, yang menggambarkan individu yang. mungkin tidak memiliki ASD tetapi memiliki sifat seperti autis, seperti menghindari kontak mata. [50]

Manifestasi dari autisme mencakup spektrum yang luas, mulai dari individu dengan gangguan berat-yang mungkin diam, cacat mental, dan terkunci ke dalam tangan mengepak dan goyang-untuk individu berfungsi tinggi yang mungkin memiliki pendekatan sosial yang aktif tapi khas aneh, sempit kepentingan fokus, dan verbose, komunikasi sombong. [51] Karena spektrum perilaku kontinu, batas-batas antara kategori diagnostik ini tentu agak sewenang-wenang. [40] Kadang-kadang sindrom dibagi menjadi rendah, menengah autisme atau tinggi berfungsi (LFA, MFA, dan HFA), berdasarkan ambang IQ, [52] atau pada berapa banyak dukungan individu membutuhkan dalam kehidupan sehari-hari; subdivisi ini tidak standar dan kontroversial. Autisme juga dapat dibagi menjadi autisme syndromal dan non-syndromal;. Yang autisme syndromal dikaitkan dengan keterbelakangan mental yang berat atau mendalam atau sindrom bawaan dengan gejala fisik, seperti sclerosis tuberous [53] Walaupun individu dengan sindrom Asperger cenderung berperforma lebih baik kognitif dibandingkan dengan autisme, sejauh mana tumpang tindih antara Sindrom Asperger, HFA, dan autis non-syndromal tidak jelas. [54]

Beberapa studi telah melaporkan diagnosa autisme pada anak-anak karena hilangnya kemampuan bahasa atau sosial, sebagai lawan dari kegagalan untuk membuat kemajuan, biasanya 15-30 bulan. Validitas dari perbedaan ini masih kontroversial;. Ada kemungkinan bahwa autisme regresif adalah subtipe tertentu, [13] [24] [32] [55] atau bahwa ada kontinum perilaku antara autisme dengan dan tanpa regresi [56]

Penelitian penyebab telah terhambat oleh ketidakmampuan untuk mengidentifikasi biologis sub-populasi yang berarti [57] dan dengan batas-batas tradisional antara disiplin ilmu psikiatri, neurologi psikologi, dan pediatri [58] yang lebih baru teknologi seperti fMRI dan difusi tensor imaging bisa. Membantu mengidentifikasi biologis fenotipe yang relevan (ciri-ciri yang dapat diamati) yang dapat dilihat di scan otak, untuk bantuan lebih lanjut studi neurogenetic autisme; [59] salah satu contoh diturunkan aktivitas di area wajah fusiform dari otak, yang berhubungan dengan persepsi gangguan orang versus obyek. [3] Hal ini telah diusulkan untuk mengklasifikasikan autisme menggunakan genetika serta perilaku.

Characteristics

Autism is a highly variable neurodevelopmental disorder^[17] that first appears during infancy or childhood, and generally follows a steady course without remission.^[18] Overt symptoms gradually begin after the age of six months, become established by age two or three years,^[19] and tend to continue through adulthood, although often in more muted form.^[20] 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.^[21] 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.^[22]

Social development

Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders.^[20] 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”.^[23]

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 do not have the ability to use simple movements to express themselves, such as the deficiency to point at things.^[24] 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.^[25] Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD.^[26] Older children and adults with ASD perform worse on tests of face and emotion recognition.^[27]

Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be 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 the quality of life more deeply.^[28]

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 non-autistic children with language impairments.^[29] 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.^[30]

Communication

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.^[31] 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)^[32][33] or reverse pronouns.^[34]Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:^[4] for example, they may look at a pointing hand instead of the pointed-at object,^[24][33] and they consistently fail to point at objects in order to comment on or share an experience.^[4] Autistic children may have difficulty with imaginative play and with developing symbols into language.^[32][33]

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well as, 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.^[35]

Repetitive behavior

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)^[36] categorizes as follows.

A young boy with autism, and the precise line of toys he made

• 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 stacks or lines.
• Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
• Ritualistic behavior involves an unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.^[36]
• Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.
• Self-injury includes movements that injure or can injure the person, such as eye poking, skin picking, hand biting, and head banging.^[4] A 2007 study reported that self-injury at some point affected about 30% of children with ASD.^[29]

No single repetitive or self-injurious behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.^[37]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.^[21] 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.^[38] Many individuals with ASD show superior skills in perception and attention, relative to the general population.^[39]Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some,^[40] although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.^[41] 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).^[42] An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking;^[40] deficits in motor coordination are pervasive across ASD and are greater in autism proper.^[43]

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;^[29] 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;^[44] studies report conflicting results, and the relationship between GI problems and ASD is unclear.^[45]

Parents of children with ASD have higher levels of stress.^[46] 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.^[47]

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.^[18] These symptoms do not imply sickness, fragility, or emotional disturbance.^[20]

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.^[48] Unlike with autism, people with Asperger syndrome have no substantial delay in language development.^[2] The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD)^[12] or sometimes the autistic disorders,^[49] 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.^[1] ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.^[50]

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.^[51] Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.^[40] Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds,^[52] 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.^[53] Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.^[54]

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,^{[13][24][32][55]} or that there is a continuum of behaviors between autism with and without regression.^[56]

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations^[57] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.^[58] Newer technologies such as fMRI and diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism;^[59] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.^[3] It has been proposed to classify autism using genetics as well as behavior.^[60]

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.^[61] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.^[61][62]

Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.^[63]

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.^[5][64] 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.^[20] Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.^[40] 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 fragile X syndrome, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.^[5] Numerous candidate genes have been located, with only small effects attributable to any particular gene.^[5] 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.^[65] 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.^[63]

Several lines of evidence point to synaptic dysfunction as a cause of autism.^[3] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.^[66] 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.^[67] 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.^[6]

Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,^[7] extensive searches are underway.^[68]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,^[11] and prenatal stress,^[69] although no links have been found, and some have been completely dis-proven.

Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine “overload”, a vaccine preservative or the MMR vaccine for causing autism.^[8] The latter theory was supported by litigation-funded study that has since been shown to have been “an elaborate fraud”.^[70] Although these theories lack convincing scientific evidence and are biologically implausible,^[8] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously-controlled childhood diseases in some countries, and the preventable deaths of several children.^[10][71]

Mechanism

Mekanisme
Gejala-gejala autisme hasil dari perubahan pematangan yang berhubungan dengan berbagai sistem otak. Bagaimana autisme terjadi belum dipahami dengan baik. Mekanisme dapat dibagi menjadi dua daerah: patofisiologi struktur otak dan proses yang terkait dengan autisme, dan hubungan neuropsikologi antara struktur otak dan perilaku [72] Perilaku tampaknya memiliki beberapa patofisiologi

Autism’s symptoms result from maturation-related changes in various systems of the brain. 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.^[72] The behaviors appear to have multiple pathophysiologies.^[22]

Pathophysiology

Autisme mempengaruhi amigdala, bagian lain otak kecil, dan banyak dari otak. [73]

Tidak seperti banyak gangguan otak lainnya seperti Parkinson, autis tidak memiliki mekanisme pemersatu yang jelas baik di tingkat molekuler, seluler, atau sistem, tetapi tidak diketahui apakah autisme adalah gangguan beberapa disebabkan oleh mutasi berkumpul di sebuah jalur beberapa molekul umum, atau adalah (seperti cacat intelektual) satu set besar gangguan dengan mekanisme yang beragam [17] autism muncul. untuk hasil dari faktor-faktor yang mempengaruhi perkembangan banyak atau semua sistem otak fungsional, [74] dan mengganggu perkembangan otak waktu lebih dari produk akhir [73] Neuroanatomical. kajian dan asosiasi dengan teratogen sangat menyarankan mekanisme yang autisme ini termasuk perubahan perkembangan otak segera setelah pembuahan [6] anomali ini muncul untuk memulai kaskade peristiwa patologis di otak yang secara signifikan dipengaruhi oleh faktor lingkungan.. [ 75] Hanya setelah lahir, otak anak-anak autis cenderung tumbuh lebih cepat dari biasanya, diikuti oleh pertumbuhan normal atau relatif lebih lambat di masa kecil. Hal ini tidak diketahui apakah pertumbuhan berlebih awal terjadi pada semua anak autis. Hal ini tampaknya paling menonjol di daerah otak yang mendasari perkembangan kognitif spesialisasi yang lebih tinggi [40] Hipotesis untuk basis selular dan molekul terlalu cepat awal patologis adalah sebagai berikut.:

Kelebihan neuron yang menyebabkan overconnectivity lokal di daerah otak kunci. [76]
Migrasi neuronal terganggu selama kehamilan awal. [77] [78]
Seimbang rangsang-hambat jaringan. [78]
Abnormal pembentukan sinapsis dan dendrit duri, [78] misalnya, dengan modulasi dari sistem sel-adhesi neurexin-neuroligin, [79] atau dengan sintesis protein buruk diatur sinaptik. [80] [81] pengembangan sinaptik terganggu juga dapat berkontribusi untuk epilepsi, yang dapat menjelaskan mengapa dua kondisi yang terkait. [82]
Interaksi antara sistem kekebalan tubuh dan sistem saraf mulai awal selama tahap embrionik kehidupan, dan neurodevelopment sukses tergantung pada respon imun seimbang. Ada kemungkinan bahwa aktivitas imun yang menyimpang selama periode kritis neurodevelopment adalah bagian dari mekanisme beberapa bentuk ASD [83] Meskipun beberapa kelainan pada sistem kekebalan tubuh telah. Telah ditemukan di sub kelompok individu spesifik autis, tidak diketahui apakah kelainan ini relevan atau sekunder untuk proses penyakit autisme’s [84] Sebagai autoantibodies ditemukan dalam kondisi selain ASD, dan tidak selalu hadir dalam ASD, [85] hubungan antara gangguan kekebalan tubuh dan autisme tetap tidak jelas dan kontroversial.. [77]

Hubungan zat kimia saraf untuk autisme belum dipahami dengan baik;. Beberapa yang telah diteliti, dengan bukti yang paling untuk peran serotonin dan perbedaan genetik transpornya [3] Orang lain telah menunjuk peran untuk kelompok I metabotropic reseptor glutamat (mGluR ) dalam patogenesis dari satu jenis autisme, Fragile X. [86] Beberapa data menunjukkan peningkatan beberapa hormon pertumbuhan, data lain berpendapat untuk faktor pertumbuhan berkurang [87] Juga, beberapa kesalahan metabolisme bawaan berhubungan dengan autisme tapi mungkin. akun kurang dari 5% dari kasus. [88]

Neuron cermin sistem (MNS) teori autisme hipotesis bahwa distorsi dalam pengembangan MNS mengganggu imitasi dan mengarah ke fitur inti autisme tentang kerusakan sosial dan kesulitan komunikasi. The MNS beroperasi saat hewan melakukan tindakan atau mengamati hewan lain melakukan tindakan yang sama. The MNS dapat berkontribusi untuk pemahaman individu orang lain dengan mengaktifkan pemodelan perilaku mereka melalui simulasi perwujudan tindakan mereka, niat, dan emosi. [89] Beberapa studi telah menguji hipotesis ini dengan menunjukkan kelainan struktural di daerah MNS individu dengan ASD , keterlambatan dalam aktivasi dalam rangkaian inti untuk imitasi pada individu dengan sindrom Asperger, dan hubungan antara aktivitas MNS berkurang dan keparahan dari sindrom pada anak dengan ASD [90] Namun,. individu dengan autisme juga memiliki aktivasi otak abnormal pada banyak sirkuit luar MNS [91] dan teori MNS tidak menjelaskan kinerja normal anak-anak autis pada tugas imitasi yang melibatkan tujuan atau benda. [92]

Autistic individu cenderung menggunakan berbagai wilayah di otak (kuning) untuk tugas gerakan dibandingkan dengan kelompok kontrol (biru). [93]

pola ASD-terkait fungsi rendah dan aktivasi menyimpang di otak berbeda tergantung pada tugas-tugas sosial atau nonsocial apakah otak lakukan. [94] Dalam autisme ada bukti untuk konektivitas fungsional berkurang dari jaringan default, jaringan otak skala besar yang terlibat dalam proses sosial dan emosional, dengan konektivitas utuh dari jaringan tugas-positif, yang digunakan dalam perhatian terus-menerus dan berpikir tujuan-diarahkan. Pada orang dengan autisme dua jaringan tidak berkorelasi negatif pada waktunya, menunjukkan ketidakseimbangan dalam Toggling antara dua jaringan, mungkin mencerminkan gangguan pemikiran diri-referensial [95] A 2008 otak-pencitraan studi menemukan. Pola tertentu sinyal di cingulate korteks yang berbeda pada individu dengan ASD. [96]

Teori underconnectivity autisme hipotesis bahwa autisme ditandai dengan underfunctioning hubungan saraf tingkat tinggi dan sinkronisasi, bersama dengan kelebihan dari proses low-level. [97] Bukti untuk teori ini telah ditemukan dalam penelitian neuroimaging fungsional pada individu autis [35] dan oleh sebuah studi gelombang otak yang menyarankan bahwa orang dewasa dengan ASD telah overconnectivity lokal di korteks dan koneksi fungsional lemah antara lobus frontal dan sisa korteks [98] Bukti lain menunjukkan. underconnectivity tersebut terutama dalam setiap belahan bumi korteks dan bahwa autisme adalah gangguan dari korteks asosiasi. [99]

Dari studi yang sesuai dengan potensi kejadian-terkait, perubahan sementara untuk aktivitas listrik otak dalam menanggapi rangsangan, ada bukti yang cukup untuk perbedaan pada individu autis sehubungan dengan perhatian, orientiation terhadap rangsangan auditori dan visual, deteksi kebaruan, bahasa dan pengolahan wajah, dan penyimpanan informasi, beberapa penelitian telah menemukan preferensi untuk rangsangan non-sosial [100] Sebagai contoh, studi magnetoencephalography telah menemukan bukti pada anak-anak autistik tanggapan tertunda dalam mengolah otak sinyal pendengaran [101]..

Di bidang genetik, hubungan telah ditemukan antara autisme dan skizofrenia berdasarkan duplikasi dan penghapusan kromosom; penelitian menunjukkan bahwa skizofrenia dan autisme secara signifikan lebih umum dalam kombinasi dengan 1q21.1 sindrom penghapusan. Penelitian tentang autisme / hubungan skizofrenia untuk kromosom 15 (15q13.3), kromosom 16 (16p13.1) dan kromosom 17 (17p12) tidak dapat disimpulkan. [102]

Autism affects the amygdala, cerebellum, and many other parts of the brain.^[73]

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.^[17] Autism appears to result from developmental factors that affect many or all functional brain systems,^[74] and to disturb the timing of brain development more than the final product.^[73]Neuroanatomical studies and the associations with teratogens strongly suggest that autism’s mechanism includes alteration of brain development soon after conception.^[6] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.^[75] Just after birth, the brains of autistic children tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.^[40] Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:

• An excess of neurons that causes local overconnectivity in key brain regions.^[76]
• Disturbed neuronal migration during early gestation.^[77][78]
• Unbalanced excitatory–inhibitory networks.^[78]
• Abnormal formation of synapses and dendritic spines,^[78] for example, by modulation of the neurexin–neuroligincell-adhesion system,^[79] or by poorly regulated synthesis of synaptic proteins.^[80][81] Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.^[82]

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. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.^[83] Although some abnormalities in the immune system have been found in specific subgroups of autistic individuals, it is not known whether these abnormalities are relevant to or secondary to autism’s disease processes.^[84] As autoantibodies are found in conditions other than ASD, and are not always present in ASD,^[85] the relationship between immune disturbances and autism remains unclear and controversial.^[77]

The relationship of neurochemicals to autism is not well understood; several have been investigated, with the most evidence for the role of serotonin and of genetic differences in its transport.^[3] Others have pointed to a role for group I metabotropic glutamate receptors(mGluR) in the pathogenesis of one type of autism, Fragile X.^[86] Some data suggest an increase in several growth hormones; other data argue for diminished growth factors.^[87] Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.^[88]

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.^[89] 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 syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.^[90] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS^[91] and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.^[92]

Autistic individuals tend to use different areas of the brain (yellow) for a movement task compared to a control group (blue).^[93]

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.^[94] 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.^[95] A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.^[96]

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.^[97] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals^[35] and by a brainwave 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.^[98] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.^[99]

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.^[100] For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain’s processing of auditory signals.^[101]

In the genetic area, relations have been found between autism and schizophrenia based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with 1q21.1 deletion syndrome. Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.^[102]

Neuropsychology

Dua kategori utama teori kognitif telah diusulkan mengenai hubungan antara otak autis dan perilaku.

Kategori pertama berfokus pada defisit dalam kognisi sosial. Teori berempati-systemizing mendalilkan bahwa individu autis dapat systemize-yaitu, mereka dapat mengembangkan aturan-aturan internal operasi untuk menangani event di dalam otak-tapi kurang efektif berempati dengan menangani event yang dihasilkan oleh agen lainnya. Perpanjangan, teori otak ekstrim laki-laki, hipotesis autisme yang merupakan kasus ekstrim dari otak laki-laki, yang didefinisikan psychometrically sebagai individu dalam siapa systemizing lebih baik daripada berempati; [103] perpanjangan ini kontroversial, karena banyak studi bertentangan dengan gagasan bahwa bayi laki-laki dan perempuan merespon secara berbeda terhadap orang dan objek. [104]

Teori ini agak terkait dengan teori sebelumnya pendekatan pikiran, yang hipotesis bahwa perilaku autistik muncul dari ketidakmampuan untuk menganggap kondisi mental untuk diri sendiri dan orang lain. Teori hipotesis pikiran didukung oleh tanggapan atipikal anak-anak autis untuk uji Sally-Anne untuk penalaran tentang motivasi orang lain ‘, [103] dan neuron cermin teori sistem autisme digambarkan dalam peta Patofisiologi baik hipotesis [90]. Namun, kebanyakan studi tidak menemukan bukti kerusakan pada individu autistik ‘kemampuan untuk memahami maksud dasar orang lain atau tujuan, sebaliknya, data menunjukkan bahwa gangguan yang ditemukan dalam memahami emosi sosial yang lebih kompleks atau dalam mempertimbangkan orang lain’. sudut pandang [105]

Kategori kedua berfokus pada pengolahan nonsocial atau umum. disfungsi Eksekutif hipotesis bahwa hasil perilaku autistik sebagian dari defisit dalam memori kerja, perencanaan, hambatan, dan bentuk lain dari fungsi eksekutif [106] Pengujian eksekutif inti proses. seperti mata tugas gerakan menunjukkan peningkatan dari masa kanak-kanak terlambat untuk remaja, namun performa tidak pernah mencapai tingkat dewasa khas [107] Kekuatan dari teori ini memprediksi perilaku stereotip dan kepentingan sempit;. [108] dua kelemahan adalah bahwa fungsi eksekutif sulit untuk mengukur [106] dan bahwa defisit fungsi eksekutif belum ditemukan pada anak-anak autis muda [27].

teori lemah koherensi pusat hipotesis bahwa kemampuan terbatas untuk melihat gambaran besar mendasari gangguan sentral dalam autisme. Salah satu kekuatan teori ini adalah memprediksi bakat khusus dan puncak kinerja pada orang autis [109] A berfungsi terkait persepsi teori-disempurnakan-berfokus lebih pada keunggulan operasional yang berorientasi lokal dan persepsi pada individu autistik.. [110] Teori ini juga peta dari teori underconnectivity autisme.

kategori Baik yang memuaskan sendiri; teori kognisi sosial buruk menangani perilaku autisme yang kaku dan berulang, sementara teori-teori nonsocial mengalami kesulitan menjelaskan kerusakan sosial dan kesulitan komunikasi [[62] Sebuah teori gabungan berdasarkan defisit beberapa mungkin terbukti lebih bermanfaat.. 111

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;^[103] this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.^[104]

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,^[103] and the mirror neuron system theory of autism described in Pathophysiology maps well to the hypothesis.^[90] However, most studies have found no evidence of impairment in autistic individuals’ ability to understand other people’s basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others’ viewpoints.^[105]

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.^[106] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.^[107] A strength of the theory is predicting stereotyped behavior and narrow interests;^[108] two weaknesses are that executive function is hard to measure^[106] and that executive function deficits have not been found in young autistic children.^[27]

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.^[109] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.^[110] 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.^[62] A combined theory based on multiple deficits may prove to be more useful.^[111]

Screening

Sekitar setengah dari orang tua anak-anak dengan ASD pemberitahuan perilaku yang tidak biasa anak-anak mereka pada usia 18 bulan, dan sekitar empat-perlima pemberitahuan pada usia 24 bulan. [55] Menurut sebuah artikel dalam Journal of Autism dan Pembangunan Gangguan, kegagalan untuk memenuhi salah satu tonggak berikut “adalah indikasi mutlak untuk melanjutkan dengan evaluasi lebih lanjut Keterlambatan rujukan untuk pengujian tersebut. dapat menunda diagnosis dini dan pengobatan dan mempengaruhi hasil jangka panjang.” [21]

Tidak mengoceh dengan 12 bulan.
Tidak ada isyarat (menunjuk, melambai bye-bye, dll) dengan 12 bulan.
Tidak ada satu kata dengan 16 bulan.
No 2-kata spontan (tidak hanya echolalic) frasa dengan 24 bulan.
Kerugian dari setiap bahasa atau keterampilan sosial, pada usia berapa pun.
AS dan praktek Jepang adalah untuk menyaring semua anak-anak untuk ASD pada 18 dan 24 bulan, dengan menggunakan autis-spesifik tes skrining formal. Sebaliknya, di Inggris, anak-anak yang keluarga atau dokter mengenali tanda-tanda kemungkinan autisme disaring. Hal ini tidak diketahui pendekatan yang lebih efektif [3] alat Pemutaran meliputi Modified Checklist for Autism di Balita (M-CHAT), yang Pemutaran Awal Autistic Traits Kuesioner, dan Tahun Pertama Inventarisasi;. data awal di M-CHAT dan CHAT pendahulunya pada anak usia 18-30 bulan menunjukkan bahwa yang terbaik adalah digunakan dalam setting klinis dan bahwa ia memiliki kepekaan yang rendah (banyak false-negatif) tetapi spesifisitas yang baik (beberapa false-positif) [55] Ini mungkin lebih akurat. mendahului tes dengan screener broadband yang tidak membedakan ASD dari gangguan perkembangan lain [112] alat Skrining dirancang untuk norma satu budaya untuk perilaku seperti kontak mata mungkin tidak sesuai untuk budaya yang berbeda.. [113] Walaupun genetika untuk autisme adalah umumnya masih tidak praktis, dapat dipertimbangkan dalam beberapa kasus, seperti anak-anak dengan gejala-gejala neurologis dan fitur dismorfik. [114]

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.^[55] According to an article in the Journal of Autism and Developmental Disorders, failure to meet any of the following milestones “is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome.”^[21]

• No babbling by 12 months.
• No gesturing (pointing, waving bye-bye, etc.) by 12 months.
• No single words by 16 months.
• No 2-word spontaneous (not just echolalic) phrases by 24 months.
• Any loss of any language or social skills, at any age.

US and Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective.^[3] 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).^[55] It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.^[112] Screening tools designed for one culture’s norms for behaviors like eye contact may be inappropriate for a different culture.^[113] Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.^[114]

Diagnosis

Diagnosis is based on behavior, not cause or mechanism.^[22][115] 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.^[2]ICD-10 uses essentially the same definition.^[18]

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.^[24]

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.^[116] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.^[117] A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment^[116] such as Landau–Kleffner syndrome.^[118] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.^[119]

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.^[1] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,^[120] consensus guidelines in the US and UK are limited to high-resolution chromosome and fragile X testing.^[1] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome’s copy number variations.^[121] 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.^[122]Metabolic and neuroimaging tests are sometimes helpful, but are not routine.^[1]

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.^[55] 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.^[116] A 2009 US 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.^[123] 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.^[124]

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.^[125] 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 or blindisms.^[126]

Management

A three-year-old with autism points to fish in an aquarium, as part of an experiment on the effect of intensive shared-attention training on language development.^[93]

seorang anak autism berumur tiga tahun menunjuk ikan didalam akuarium, sebagai bagian dari percobaan tentang pengaruh pelatihan bersama-perhatian intensif terhadap perkembangan bahasa. [93]

Tujuan utama saat merawat anak-anak dengan autisme untuk mengurangi defisit yang terkait dan kesusahan keluarga, dan untuk meningkatkan kualitas hidup dan kemandirian fungsional. Tidak ada pengobatan tunggal yang terbaik dan pengobatan biasanya disesuaikan dengan kebutuhan anak [12] Keluarga dan sistem pendidikan. Sumber daya utama untuk pengobatan. [3] Studi tentang intervensi memiliki masalah metodologis yang mencegah kesimpulan definitif tentang kemanjuran. [127] Meskipun intervensi psikososial banyak memiliki beberapa bukti yang positif, menunjukkan bahwa beberapa bentuk pengobatan adalah lebih baik untuk pengobatan tidak ada, kualitas metodologi tinjauan sistematis dari studi ini secara umum miskin, hasil klinis mereka kebanyakan tentatif, dan ada sedikit bukti untuk efektivitas relatif . dari pilihan pengobatan [128] intensif, berkelanjutan program pendidikan khusus dan terapi perilaku awal dalam hidup dapat membantu anak-anak memperoleh keterampilan perawatan diri, sosial, dan pekerjaan, [12] dan sering meningkatkan fungsi dan mengurangi keparahan gejala dan perilaku maladaptif; [129 ] mengklaim bahwa intervensi oleh sekitar usia tiga tahun sangat penting tidak dibuktikan [130] pendekatan yang tersedia termasuk analisis perilaku terapan (ABA), model pembangunan, pengajaran terstruktur, terapi bicara dan bahasa, sosial terapi keterampilan, dan terapi okupasi.. [12]

Pendidikan intervensi dapat efektif untuk derajat yang bervariasi pada anak-anak yang paling: ABA perawatan intensif telah menunjukkan efektivitas dalam meningkatkan fungsi global pada anak prasekolah [131] dan mapan untuk meningkatkan kinerja intelektual anak usia dini [129] laporan Neuropsikologi sering kurang dikomunikasikan. untuk pendidik, sehingga kesenjangan antara apa laporan merekomendasikan dan apa pendidikan yang diberikan [117] Tidak diketahui apakah program pengobatan untuk anak-anak mengarah kepada perbaikan yang signifikan setelah anak-anak tumbuh, [129] dan penelitian terbatas pada efektivitas. program perumahan orang dewasa menunjukkan hasil yang beragam [132] Kesesuaian termasuk anak-anak dengan berbagai tingkat keparahan gangguan spektrum autisme pada populasi pendidikan umum. adalah subyek perdebatan saat ini di kalangan pendidik dan peneliti. [133]

Banyak obat yang digunakan untuk mengobati gejala ASD yang mengganggu dengan mengintegrasikan seorang anak ke rumah atau sekolah ketika perawatan perilaku gagal [20] [134] Lebih dari. separuh anak didiagnosis AS dengan ASD diresepkan obat-obatan psikoaktif atau antikonvulsan, dengan obat yang paling umum kelas yang antidepresan, stimulan, dan antipsikotik [135] Selain dari antipsikotik,. [136] ada penelitian yang dapat diandalkan sedikit tentang efektivitas atau keamanan pengobatan obat untuk remaja dan orang dewasa dengan ASD [137] Seseorang dengan ASD dapat menanggapi atypically ke. obat, obat dapat memiliki efek samping, [12] dan tidak ada pengobatan autisme meringankan dikenal inti gejala gangguan sosial dan komunikasi. [138] Percobaan pada tikus telah membalikkan atau mengurangi beberapa gejala yang berhubungan dengan autisme dengan mengganti atau modulasi fungsi gen, [67 ] [86] menyarankan kemungkinan sasaran terapi untuk mutasi langka tertentu diketahui menyebabkan autisme. [66] [139]

Meskipun banyak alternatif terapi dan intervensi yang tersedia, hanya sedikit yang didukung oleh penelitian ilmiah [27] [140] Perawatan pendekatan memiliki sedikit dukungan empiris dalam konteks kualitas-of-hidup,. Dan banyak program fokus pada langkah-langkah kesuksesan yang kurang validitas prediktif dan real- relevansi dunia. [28] Bukti ilmiah tampaknya kurang peduli kepada service provider dari program pemasaran, ketersediaan pelatihan, dan permintaan orang tua [141] Beberapa pengobatan alternatif dapat menempatkan anak beresiko.. Sebuah studi 2008 menemukan bahwa dibandingkan dengan rekan-rekan mereka, anak-anak autis memiliki tulang secara signifikan lebih tipis jika pada diet bebas kasein; [142] pada tahun 2005, terapi khelasi gagal membunuh seorang anak lima tahun dengan autisme [143].

Pengobatan mahal biaya tidak langsung lebih begitu. Untuk orang yang lahir pada tahun 2000, sebuah studi AS memperkirakan biaya seumur hidup rata-rata $ 3.770.000 (nilai sekarang bersih pada tahun 2011 dolar, disesuaikan dengan inflasi dari tahun 2003 perkiraan), [144] dengan sekitar 10% perawatan kesehatan, pendidikan tambahan 30% dan perawatan lainnya , dan 60% kehilangan produktivitas ekonomi [145] program yang didukung publik sering tidak memadai atau tidak sesuai untuk anak tertentu, dan unreimbursed luar biaya-saku medis atau terapi yang berhubungan dengan kemungkinan masalah keluarga keuangan;. [146] satu 2008 AS studi menemukan kerugian rata-rata 14% dari pendapatan tahunan dalam keluarga anak dengan ASD, [147] dan sebuah studi yang terkait menemukan bahwa ASD dikaitkan dengan probabilitas tinggi bahwa masalah perawatan anak akan sangat mempengaruhi penyerapan tenaga kerja orang tua. [148] negara bagian AS semakin membutuhkan pribadi asuransi kesehatan untuk menutup layanan autisme, pergeseran biaya dari program pendidikan publik didanai untuk asuransi kesehatan yang didanai secara pribadi. [149] Setelah masa kanak-kanak, isu-isu kunci pengobatan termasuk perawatan perumahan, pelatihan kerja dan penempatan, seksualitas, keterampilan sosial, dan perencanaan perumahan

The main goals when treating children with autism 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.^[12] Families and the educational system are the main resources for treatment.^[3] Studies of interventions have methodological problems that prevent definitive conclusions about efficacy.^[127] 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.^[128] Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills,^[12] and often improve functioning and decrease symptom severity and maladaptive behaviors;^[129] claims that intervention by around age three years is crucial are not substantiated.^[130] Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.^[12]

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children^[131] and is well-established for improving intellectual performance of young children.^[129] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.^[117] It is not known whether treatment programs for children lead to significant improvements after the children grow up,^[129] and the limited research on the effectiveness of adult residential programs shows mixed results.^[132] The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.^[133]

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.^[20][134] More than half of US children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.^[135] Aside from antipsychotics,^[136] there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.^[137] A person with ASD may respond atypically to medications, the medications can have adverse effects,^[12] and no known medication relieves autism’s core symptoms of social and communication impairments.^[138] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,^[67][86] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.^[66][139]

Although many alternative therapies and interventions are available, few are supported by scientific studies.^[27][140] 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.^[28] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.^[141] Some alternative treatments 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;^[142] in 2005, botched chelation therapy killed a five-year-old child with autism.^[143]

Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $3.77 million (net present value in 2011 dollars, inflation-adjusted from 2003 estimate),^[144] with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.^[145] 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;^[146] one 2008 US study found a 14% average loss of annual income in families of children with ASD,^[147] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.^[148] US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.^[149] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.^[150]

Prognosis

Penyembuhkan tidak diketahui [3] [12] Anak-anak kadang-kadang pulih, sehingga mereka kehilangan diagnosis mereka ASD;. [14] ini kadang-kadang terjadi setelah perawatan intensif dan kadang-kadang tidak. Tidak diketahui seberapa sering pemulihan terjadi; [129] melaporkan angka dalam sampel yang tidak dipilih dari anak-anak dengan ASD telah berkisar antara 3% sampai 25% [14] Sebagian besar anak-anak autis dapat memperoleh bahasa dengan usia 5 tahun atau lebih muda, meskipun beberapa telah dikembangkan. keterampilan komunikasi dalam tahun kemudian [151] Kebanyakan anak autis dengan kurangnya dukungan sosial, hubungan yang bermakna, kesempatan kerja masa depan atau penentuan nasib sendiri.. [28] Walaupun kesulitan inti cenderung bertahan, gejala sering menjadi kurang berat dengan usia. [20] Sedikit penelitian berkualitas tinggi alamat prognosis jangka panjang. Beberapa orang dewasa menunjukkan peningkatan sederhana dalam keterampilan komunikasi, tapi sedikit penurunan, tidak ada penelitian yang difokuskan pada autisme setelah setengah baya [152] Mendapatkan bahasa sebelum usia enam, memiliki IQ di atas 50, dan memiliki keterampilan berharga semua memprediksi hasil yang lebih baik;. Hidup mandiri tidak mungkin dengan autisme parah. [153] Penelitian pada tahun 2004 Inggris 68 orang dewasa yang didiagnosis sebelum tahun 1980 sebagai anak-anak autis dengan IQ diatas 50 menemukan bahwa 12% mencapai tingkat tinggi kemerdekaan sebagai orang dewasa, 10% memiliki beberapa teman dan pada umumnya di bekerja tetapi diperlukan dukungan beberapa, 19% memiliki kemerdekaan beberapa tapi umumnya tinggal di rumah dan membutuhkan dukungan yang cukup dan pengawasan dalam kehidupan sehari-hari, 46% diperlukan penyediaan perumahan spesialis dari fasilitas yang mengkhususkan diri dalam ASD dengan tingkat dukungan dan otonomi sangat terbatas, dan . 12% dibutuhkan tinggi tingkat rumah sakit perawatan [15] Sebuah studi 2005 Swedia 78 orang dewasa yang tidak mengecualikan IQ rendah ditemukan prognosis yang buruk;. misalnya, hanya 4% mencapai kemerdekaan [154] Sebuah penelitian 2008 di Kanada 48 orang dewasa muda didiagnosis dengan ASD sebagai anak-anak prasekolah ditemukan hasil berkisar melalui miskin (46%), wajar (32%), baik (17%), dan sangat baik (4%), 56% dari orang dewasa muda telah bekerja pada beberapa titik selama hidup mereka, sebagian besar dalam pekerjaan sukarela, terlindung atau paruh waktu. [155] Perubahan dalam praktek diagnostik dan peningkatan ketersediaan intervensi awal yang efektif membuatnya jelas apakah temuan ini dapat digeneralisasi kepada anak-anak baru-baru ini didiagnosis. [11

No cure is known.^[3][12] Children recover occasionally, so that they lose their diagnosis of ASD;^[14] this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;^[129] reported rates in unselected samples of children with ASD have ranged from 3% to 25%.^[14] Most autistic children can acquire language by age 5 or younger, though a few have developed communication skills in later years.^[151] Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.^[28] Although core difficulties tend to persist, symptoms often become less severe with age.^[20] 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.^[152] 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.^[153] 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.^[15] A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.^[154] 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.^[155] Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.^[11]

Epidemiology

Laporan kasus autisme per 1.000 anak-anak tumbuh secara dramatis di Amerika Serikat 1996-2007. Tidak diketahui berapa banyak, jika ada, pertumbuhan berasal dari perubahan prevalensi autisme’s.

ulasan terakhir cenderung memperkirakan prevalensi 1-2 per 1.000 untuk autisme dan dekat dengan 6 per 1.000 untuk ASD; [11] karena data yang tidak memadai, angka-angka ini mungkin meremehkan prevalensi benar ASD’s [1] prevalensi PDD-NOS telah telah. diperkirakan sebesar 3,7 per 1.000, Asperger syndrome di sekitar 0,6 per 1.000, dan gangguan disintegratif masa kanak-kanak 0,02 per 1.000 [156]. Jumlah kasus yang dilaporkan autisme meningkat secara dramatis pada tahun 1990 dan awal 2000-an. Peningkatan ini terutama disebabkan perubahan dalam praktek diagnostik, pola rujukan, ketersediaan layanan, usia saat diagnosis, dan kesadaran masyarakat, [156] [157] meskipun tak dikenal faktor risiko lingkungan tidak dapat dikesampingkan. [7] bukti yang tersedia tidak mengesampingkan kemungkinan bahwa prevalensi autisme benar telah meningkat;. [156] peningkatan yang nyata akan menyarankan mengarahkan lebih banyak perhatian dan dana terhadap perubahan faktor lingkungan daripada terus fokus pada genetika [68]

Anak laki-laki berisiko lebih tinggi untuk ASD dibandingkan anak perempuan. Rasio rata-rata seks 4.3:1 dan sangat dimodifikasi oleh penurunan kognitif: mungkin dekat dengan 02:01 dengan keterbelakangan mental dan lebih dari 5.5:1 tanpa [11] Meskipun bukti tidak mengimplikasikan apapun faktor risiko yang berhubungan dengan kehamilan tunggal. sebagai penyebab autisme, risiko autisme dikaitkan dengan usia lanjut di salah satu orangtua, dan dengan diabetes, pendarahan, dan penggunaan obat psikiatrik pada ibu selama kehamilan. [158] Risikonya lebih besar dengan ayah yang lebih tua dibandingkan dengan ibu yang lebih tua ; dua penjelasan potensi peningkatan beban mutasi dikenal di dalam sperma yang lebih tua, dan hipotesis bahwa laki-laki menikah nanti jika mereka membawa kewajiban genetik dan menunjukkan beberapa tanda-tanda autisme [40] Kebanyakan profesional percaya bahwa ras, etnis, dan latar belakang sosial ekonomi tidak. mempengaruhi terjadinya autisme. [159]

Beberapa kondisi lain sering terjadi pada anak autis [3] Mereka termasuk.:

Genetik gangguan. Sekitar 10-15% kasus autis memiliki Mendel diidentifikasi (single-gen) kondisi, kelainan kromosom, atau sindrom genetik lainnya, [160] dan ASD dikaitkan dengan gangguan genetik. [161]
Keterbelakangan mental. Fraksi individu autis yang juga memenuhi kriteria untuk keterbelakangan mental telah dilaporkan sebagai mana saja dari 25% menjadi 70%, variasi lebar menggambarkan kesulitan menilai kecerdasan autistik. [162] Untuk ASD selain autisme, hubungan dengan keterbelakangan mental jauh lebih lemah. [163]
gangguan Kegelisahan adalah umum di antara anak-anak dengan ASD, tidak ada data perusahaan, namun studi telah melaporkan prevalensi berkisar antara 11% sampai 84%. Banyak gangguan kecemasan memiliki gejala yang lebih baik dijelaskan oleh ASD sendiri, atau sulit dibedakan dengan gejala ASD’s. [164]
Epilepsi, dengan variasi risiko epilepsi karena usia, tingkat kognitif, dan jenis gangguan bahasa. [165]
Beberapa cacat metabolik, seperti fenilketonuria, dikaitkan dengan gejala autis. [88]
anomali Minor fisik secara signifikan meningkat pada populasi autistik. [166]
Mendahului diagnosis. Meskipun aturan DSM-IV keluar diagnosa bersamaan banyak kondisi lain bersama dengan autisme, kriteria penuh untuk ADHD, sindrom Tourette, dan kondisi ini sering hadir dan diagnosa ini komorbid semakin diterima. [167]
Masalah tidur mempengaruhi sekitar dua pertiga dari individu dengan ASD di beberapa titik di masa kecil. Ini paling sering termasuk gejala insomnia seperti kesulitan dalam tidur, malam sering terbangun, dan terjaga pagi. Masalah tidur yang berhubungan dengan perilaku yang sulit dan stres keluarga, dan sering menjadi fokus perhatian klinis atas dan di atas diagnosis ASD utama. [168]

Reports of autism cases per 1,000 children grew dramatically in the US from 1996 to 2007. It is unknown how much, if any, growth came from changes in autism’s prevalence.

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;^[11] because of inadequate data, these numbers may underestimate ASD’s true prevalence.^[1]PDD-NOS‘s prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000.^[156] 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,^[156][157] though unidentified environmental risk factors cannot be ruled out.^[7] The available evidence does not rule out the possibility that autism’s true prevalence has increased;^[156] a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.^[68]

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.^[11] 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.^[158] The risk is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism.^[40] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.^[159]

Several other conditions are common in children with autism.^[3] They include:

• Genetic disorders. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,^[160] and ASD is associated with several genetic disorders.^[161]
• 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.^[162] For ASD other than autism, the association with mental retardation is much weaker.^[163]
• 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.^[164]
• Epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.^[165]
• Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.^[88]
• Minor physical anomalies are significantly increased in the autistic population.^[166]
• 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.^[167]
• Sleep problems affect about two-thirds of individuals with ASD at some point in childhood. 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.^[168]

Sejarah(History)

Leo Kanner introduced the label early infantile autism in 1943.

Beberapa contoh gejala autis dan perawatan yang digambarkan jauh sebelum autisme bernama. Talk Tabel Martin Luther, yang disusun oleh notetaker nya, Mathesius, berisi cerita seorang anak 12 tahun yang mungkin telah sangat autistik. [169] Luther dilaporkan pikir anak itu massa berjiwa daging kesurupan , dan menyarankan bahwa dia akan mati lemas, meskipun kritikus kemudian telah meragukan kebenaran laporan ini. [170] Kasus didokumentasikan dengan baik awal autisme adalah bahwa Hugh Blair Borgue, seperti yang dijelaskan dalam kasus pengadilan 1747 di mana saudaranya berhasil dimohonkan untuk membatalkan pernikahan Blair untuk mendapatkan warisan Blair [171] The Boy Liar dari Aveyron, anak liar tertangkap pada tahun 1798, menunjukkan beberapa tanda autisme;. para mahasiswa kedokteran Jean Itard memperlakukannya dengan program perilaku yang dirancang untuk membantu dia bentuk lampiran sosial dan untuk mendorong pidato melalui imitasi. [172]

The New autismus kata Latin (autisme terjemahan bahasa Inggris) ini diciptakan oleh psikiater Eugen Bleuler Swiss pada tahun 1910 karena ia mendefinisikan gejala skizofrenia. Dia berasal itu dari kata Yunani autos (αὐτός, berarti diri), dan menggunakannya untuk berarti sehat diri kekaguman, mengacu pada “penarikan autistik dari pasien untuk fantasinya, terhadap mana setiap pengaruh dari luar menjadi gangguan tak tertahankan”. [ 173]

Yang autisme Kata pertama mengambil pengertian modern pada tahun 1938 ketika Hans Asperger dari Vienna University Hospital mengadopsi psikopat terminologi Bleuler’s autistik dalam ceramah di Jerman tentang psikologi anak. [174] Asperger sedang menyelidiki sebuah ASD sekarang dikenal sebagai sindrom Asperger, meskipun karena berbagai alasan itu tidak secara luas diakui sebagai diagnosis terpisah sampai 1981 [172] Leo Kanner dari Rumah Sakit Johns Hopkins autisme digunakan pertama dalam pengertian modern dalam bahasa Inggris ketika ia memperkenalkan label autisme infantil awal dalam laporan 1943 dari 11 anak-anak dengan kemiripan perilaku mencolok. [34] Hampir semua karakteristik yang dijelaskan dalam makalah pertama Kanner pada subjek, terutama “kesendirian autistik” dan “desakan kesamaan”, adalah. masih dianggap sebagai khas spektrum autistik gangguan [62] Ini. Tidak diketahui apakah Kanner berasal istilah independen dari Asperger. [175]

kembali Kanner autisme menyebabkan puluhan tahun bingung terminologi seperti skizofrenia kekanak-kanakan, dan fokus anak psikiatri di perampasan ibu menyebabkan kesalahpahaman autisme sebagai respons bayi untuk “ibu lemari pendingin”. Dimulai pada 1960-an autisme didirikan sebagai sindrom terpisah dengan menunjukkan bahwa itu adalah seumur hidup, yang membedakannya dari keterbelakangan mental dan skizofrenia dan dari gangguan perkembangan lain, dan menunjukkan manfaat dari orang tua terlibat dalam program-program aktif terapi [176] Seperti terlambat. sebagai pertengahan 1970-an ada sedikit bukti peran genetik pada autisme, sekarang ini dianggap salah satu yang paling diwariskan dari semua kondisi kejiwaan [177] Meskipun Munculnya organisasi-organisasi induk dan destigmatization masa kanak-kanak ASD telah sangat terpengaruh. bagaimana kita memandang ASD, [172] orang tua tetap merasa stigma sosial dalam situasi di mana perilaku anak-anak autis mereka dianggap negatif oleh orang lain, [178] dan perawatan dokter banyak primer dan spesialis medis masih mengungkapkan beberapa keyakinan konsisten dengan penelitian autisme usang. [179 ]

Internet telah membantu individu autistik bypass isyarat-isyarat nonverbal dan berbagi emosional yang mereka menemukan begitu sulit untuk berurusan dengan, dan telah memberikan mereka cara untuk membentuk komunitas online dan bekerja jarak jauh [180] aspek sosiologis dan budaya autis telah mengembangkan:. Beberapa di masyarakat mencari penyembuhan, sementara yang lain percaya bahwa autisme hanyalah cara lain menjadi. [16] [181]

A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic.^[169] Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report.^[170] The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair’s marriage to gain Blair’s inheritance.^[171] 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.^[172]

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 autós (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”.^[173]

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.^[174] Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981.^[172]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.^[34] 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.^[62] It is not known whether Kanner derived the term independently of Asperger.^[175]

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.^[176] 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.^[177] Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,^[172] parents continue to feel social stigma in situations where their autistic children’s behaviors are perceived negatively by others,^[178] and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research.^[179]

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.^[180]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.^[16][181]

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