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Sal sommige kinders per definisie altyd belemmer word?

Sal sommige kinders per definisie altyd belemmer word?


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Ek het 'n vraag gehad oor belemmering, dws lengte-vir-ouderdom. Die WGO definieer by as enige kind wie se lengte-vir-ouderdom 2 standaardafwykings onder die mediaan lengte-vir-ouderdom is.

Gegewe hierdie definisie, sou daar nie altyd belemmerde kinders wees nie? Ek moes die definisie verkeerd verstaan ​​het, want dit lyk na een van daardie uitdagings wat "opgelos" moet word, maar my huidige begrip beteken dat dit onoplosbaar is.

Enige insig word waardeer.


Jy is korrek, dat onder daardie definisie; tensy daar geen variasie was nie (wat onmoontlik sou wees), sou daar altyd individue wees wat onder 2 standaardafwykings val. "Vertraag" onder hierdie definisie sou egter nie 'n probleem wees as variasie uiters laag was nie. So ja, dit sou per definisie onoplosbaar wees, maar as variasie sou val, dan sou die "probleem" reggestel word, want dit sou nie meer 'n probleem wees nie.


Psigopate, Kinders en Bose

Dit het begin met Hierdie Amerikaanse lewe'se program hierdie week oor die psigopaattoets). En natuurlik die New York Times Sunday Magazine artikel, Kan jy 'n 9-jarige 'n psigopaat noem? En dan was daar die opiniestuk oor hoe ons nie verbaas moet wees dat 10 persent van die mense wat op Wall Street werk, "kliniese psigopate" is, getiteld, Capitalists and Other Psychopaths.

Hoe kan jy nie verkoel en verskrik word deur die verhaal van 'n 9-jarige wat 'n kleuter in 'n swembad sou gooi sodat hy sy nuuskierigheid kon bevredig oor hoe dit is om te verdrink nie? Dit is wat dit beteken om boos te wees.

Maar my denke oor gevaarlike, onemosionele en seergemaakte kinders het voor dit begin, twee weke gelede toe ek met 'n vriend van my gepraat het wat spesiale onderwys in 'n plaaslike laerskool gee. Sy het 'n student in haar klas vir wie sy bang is. Vir jare was hy moeilik om te hanteer - spoeg, slaan, hardloop rond, en sê die grofste en mees seksueel afstootlike dinge wat uit enigiemand se mond kan kom, maak nie saak dié van 'n kind wat nog nie naby puberteit is nie. En ook seer - 'n bors gryp en draai, 'n arm knyp of skop.

Maar skielik is hy baie erger. Kyk vir 'n oomblik eenkant en hy steek na 'n ander kind se oë. Medikasie wat veronderstel is om hom kalm te hou, maak hom meer gewelddadig en histeries. En dit lyk asof daar geen beddens - oral - vir 'n baie jong psigiatriese pasiënt is nie, selfs om hom dop te hou terwyl hulle die regte medikasiekombinasie probeer vind om sy gedrag binne hanteerbare vlakke te bring. Sy ma is by die verstand en bang vir haar jonger kinders.

Hoe hanteer sy ouers en sy onderwysers so 'n kind? Daar is geen maklike antwoorde nie.

Ek is ook getref deur mense se reaksies op die idee van 'n gevaarlike kind. Toe my suster die NY Times artikel oor "ongevoelige, onemosionele" kinders (soos kinderpsigopate genoem word) op haar Facebook-blad, het 'n vriendin gesê dat daardie kinders net "gebreek" moet word - dat hulle in beheer is van hul omgewing en dat hulle uitgeput moet wees tot die punt van voldoening. Het ons dit nie probeer nie? Is dit nie hoekom tronke buite verhouding vol volwasse psigopate is nie? En het dit gehelp? Wil ons nie mense keer voordat hulle by die punt gekom het waar hulle opgesluit moet word nie?

Die sterkpunte en grense van ouerskap

Ek is 'n ouerskapnavorser. Ek glo in omgewingsinvloed op menslike gedrag en glo dat vir die meeste kinders die enkele belangrikste invloed 'n ouer of ouer plaasvervanger is.

Ek glo ook in breine. As die skrywer van Die Amygdala het my dit laat doen geskryf het, is daar 'n magdom navorsing daar buite wat ons vertel dat:

  • Ons biologiese aanleg vorm hoe ons op ons omgewing reageer en hoe dit op ons reageer.
  • Ons interaksies met die omgewing vorm die strukturele en organisatoriese kenmerke van ons brein.

As ek sê goeie ouerskap maak kinders slimmer, meer vertrouend en vriendeliker teenoor ander, ek is nie verbaas dat neurowetenskaplikes vind dat daardie veranderinge gedokumenteer kan word met 'n fMRI wat strukturele en organisatoriese veranderinge in die brein toon nie. Trouens, in die laat 50's het ons veranderinge gevind in baie growwer maatstawwe van breingewig in studies met muise. Ek is ook nie verbaas wanneer ek verskille in ouerskap en kindergedrag kan sien wat weerspieël word in veranderinge in kortisol- en alfa-amilasevlakke tydens sosiale interaksies tussen ouers en hul kinders nie.

Wat dink jy veroorsaak gedrags- en kognitiewe verandering - feetjiestof? Waargenome gedrag het biologiese onderbou.

Maar dit beteken nie dat biologie die lot is nie. Dit beteken dat ons van mekaar verskil en dat gedrag moeilik is om te verander. Al ooit probeer om op te hou rook, gewig te verloor of op te hou om op jou kind te skree? Dan het jy dit reeds geweet.

Goeie konsekwente interaksies met volwassenes en kinders en gestruktureerde omgewings wat die reeks geleenthede vir negatiewe interaksies beperk en positiewe gedrag beloon, kan help om kinders nuwe, meer effektiewe en minder seermaak maniere te leer om met hul omgewings om te gaan. Maar dit neem tyd.

Programme wat kinders leer om emosies by ander te herken en gepas daarop te reageer (sien byvoorbeeld die PATHS-program) kan ook help om die vermoë van kinders wat nie natuurlik op ander se pyn reageer nie te ontwikkel om dit te doen. Dit is om die pyn te voel van diegene wat ons seergemaak het wat ons help keer om dit te doen.

Daar is 'n rede dat Elmo aan Sesame straat etiketteer emosies vir ons en wys ons hoe dit lyk. Sommige kinders weet nie hoe dit lyk om hartseer te wees of seer te kry nie. En sommige kinders voel nie hoe dit voel om hartseer of seergemaak te wees nie, so hulle weet nie wat daardie woorde beteken nie. Ons kan ook blind gebore word vir emosies.

Vir sommige kinders probeer programme soos PATH om hulle te leer wat hulle reeds weet – wat ander mense voel. Hulle weet dit omdat die spieëlneurone in hul eie brein reageer op die emosies van ander sodat hulle hul pyn voel. Om iemand anders se pyn te voel, maak dit vir jou pynlik om ander seer te maak.

Ander kinders voel dit nie. Hulle het min spieëlneurone en die pyn-, empatie- en vreessentrums in die amygdala is belemmer.

Korrektiewe ervaring in die omgewing kan daar nuttig wees.

  • Eerstens kan hulle kognitief leer om te herken wat hulle nie kan voel nie, net soos iemand wat nie rooi kan sien nie dalk kan leer om dit van ander kleure uit kontekstuele leidrade te onderskei. En hulle kan dalk strategieë geleer word wat hulle help om in hul behoeftes te voorsien – beloon hulle – sonder om ander seer te maak.
  • Tweedens, oefening help. Breine is nie oneindig smeebaar nie, maar hulle verander en groei na gelang van ervaring. As jy 'n area van jou brein gebruik, vergroot dit sy kapasiteit. Byvoorbeeld, die hippokampus van Londense taxibestuurders groei soos hulle dit gebruik om te navigeer. (Dit is die hippokampus wat die lokusse is om liggings te onthou.) Die hippokampus van voëls verander seisoenaal van grootte soos hulle dit gebruik om te onthou waar kos gestoor word. Die gebruik van 'n vermoë sal dit dus versterk en die ontwikkeling van breinstrukture en verbindings aanmoedig wat prestasie bevorder.
  • Derdens veroorsaak gebrek aan oefening atrofie. Ons begin die lewe met baie meer neurologiese verbindings as wat ons uiteindelik sal gebruik. Diegene wat nie gebruik word nie, word afgesny, wat ons doeltreffender maak. Maar dit beteken ook dat as ons nie normale omgewingservarings kry wat funksionering in 'n spesifieke area van die brein sal handhaaf nie, ons mettertyd al hoe slegter daarmee sal word. Mense wie se gedrag hulle weerhou van normale sosiale interaksies sal dus geneig wees om grond mettertyd te verloor.

Gene Omgewing Interaksie

Dit alles bring ons terug na kinderpsigopate.

In Waddington se bekende model van 'n geen-omgewing-interaksie het hy gepraat oor 'n kreode soos 'n heuwel gevul met klein valleie en riviertjies wat 'n bal afrol. Wie ons aan die einde was en waar ons geëindig het, was die pad van die bal. Die riviere het ons natuurlike genetiese (bv. biologiese) neigings verteenwoordig. Druk kan uitgeoefen word om ons van een pad na 'n ander te beweeg - veral by aansluitingspunte. As druk hard genoeg was - dink aan traumatiese breinbesering of aaklige omgewingsontneming - kon ons van een vallei na die volgende spring. Waar ons beland het, is wedersyds bepaal deur genetiese en omgewingsfaktore.

Een belangrike deel van Waddington se model is die diepte van daardie valleie. Sommige is vlak en verteenwoordig baie meer smeebare eienskappe. Sommige is baie diep en is moeilik of onmoontlik om uit te kom. Kinders wat in normale omgewings grootword en nie empatie het nie, is dalk nader aan laasgenoemde as eersgenoemde. Dit sal buitengewone pogings verg om hulle te laat verander. Aangesien hierdie mense dalk grootword om van die mees skadelike lede van ons samelewing te wees, kan dit egter tot ons voordeel wees om daardie poging aan te wend. Ons moet almal bid dat die sielkundiges wat hul lewens daaraan toegewy het om maniere te vind om daardie druk uit te oefen, suksesvol is om dit te doen.

Nog 'n belangrike deel van Waddington se model is dat daar verskeie maniere is om by dieselfde plek aan die onderkant van die heuwel uit te kom. So kan ons vind dat kinders wat gevoelloos en onemosioneel is nooit in staat is om die normale kapasiteit vir empatie te ontwikkel nie. Maar hulle kan kognitief leer hoe om op te tree op maniere wat nie skadelik vir ander of vir hulself is nie. En vanuit 'n samelewingsperspektief is dit dalk goed genoeg.


Nefrotiese sindroom by kinders

Kinders met te veel proteïene in hul urine, skielike gewigstoename en swelling in verskeie liggaamsdele kan 'n toestand hê wat nefrotiese sindroom genoem word. Nefrotiese sindroom in die kinderjare word ook nefrose genoem. Nefrotiese sindroom vind plaas wanneer klein strukture in die niere genoem glomeruli ophou werk behoorlik en laat te veel proteïen die niere binnedring.

Wat veroorsaak nefrotiese sindroom in die kinderjare?
In die meeste gevalle is die oorsaak nie bekend nie. 'n Aantal toestande kan egter die glomeruli beskadig en nefrotiese sindroom veroorsaak. By kinders is die mees algemene oorsaak as gevolg van minimale verandering siekte. Die oorsaak van minimale verandering siekte is nie bekend nie, maar dit kan verband hou met infeksies, gewasse, allergiese reaksies en oorgebruik van oor-die-toonbank medisyne soos ibuprofen en acetaminophen. Die meeste kinders ontgroei minimale verandering siekte teen die tyd dat hulle in hul tienerjare is.

Ander toestande kan die glomeruli beskadig, insluitend ander niertoestande, immuunstelselprobleme, infeksies of siektes soos kanker en diabetes. In sekere gevalle kan 'n allergiese reaksie op kos of die gebruik van sekere wettige en onwettige middels, of vetsug tot nefrotiese sindroom lei.

Veroorsaak ander niersiektes swelling en proteïene in die urine?
Oedeem en proteïene in die urine is algemeen in ander tipes niersiekte, veral glomerulonefritis.

Wie kry dit?
Gewoonlik jong kinders tussen die ouderdomme van 1½ en 5, hoewel kinders van alle ouderdomme en selfs volwassenes dit kan kry. Dit gebeur twee keer so dikwels by seuns as by meisies.

Hoe kan ek weet of my kind dit het?
Jy sal dalk soggens swelling rondom jou kind se oë sien. Dikwels is dit die eerste teken. Soos die tyd verbygaan, kan die swelling die hele dag aanhou, en jy kan swelling in jou kind se enkels, voete of maag sien. Jou kind kan ook:

  • meer moeg wees
  • meer prikkelbaar wees
  • het 'n verminderde eetlus
  • lyk bleek.

Jou kind kan probleme ondervind om skoene aan te trek of klere te knoop as gevolg van swelling.

Hoe word nefrotiese sindroom gediagnoseer?
Jou kind se dokter sal kyk vir simptome, soos swelling en bleek vel. Daarbenewens kan 'n urinetoets kyk vir die hoeveelheid proteïen, bloed en ander dinge om te kyk vir nierskade. ’n Bloedtoets kan wys hoe goed jou kind se niere werk. Die dokter sal ook kyk vir ander siektes wat die nefrotiese sindroom kan veroorsaak. In sommige gevalle kan diagnose ook 'n nierbiopsie vereis.

Hoe word die nefrotiese sindroom behandel?
Nefrotiese sindroom is byna altyd behandelbaar, maar die behandeling hang af van die oorsaak. Die doel van die behandeling is om die verlies aan proteïen in die urine te stop en die hoeveelheid urine wat uit die liggaam beweeg, te verhoog. Jou dokter sal waarskynlik 'n middel genaamd prednisoon vir jou kind voorskryf. Die meeste kinders word beter met hierdie middel.

Wat doen prednisoon?
Prednisoon is 'n tipe kortikosteroïed (ook genoem "steroïede"), wat gebruik word om die verlies van proteïen uit die bloed te stop. Na een tot vier weke se behandeling moet u kind meer gereeld begin urineer. Soos jou kind meer urine vrystel, sal die swelling verdwyn.

Watter probleme kan met prednisoon voorkom?
Prednisoon kan 'n baie effektiewe middel wees, maar dit het 'n aantal newe-effekte. Sommige van hierdie newe-effekte kan insluit:

  • verhoogde honger
  • gewig optel
  • aknee (puisies)
  • buierigheid (baie gelukkig, dan baie hartseer)
  • ooraktiwiteit of "hiper" gedrag
  • 'n vertraagde groeitempo
  • hoër risiko van infeksie.

Newe-effekte is meer algemeen met groter dosisse en langdurige gebruik. Sodra prednisoon gestop is (en slegs met die dokter se bevele), verdwyn die meeste van hierdie newe-effekte.

Wat as prednisoon nie werk nie?
As prednisoon nie vir jou kind werk nie of as die newe-effekte te ongemaklik is, kan die dokter 'n ander soort medisyne bestel wat 'n immuunonderdrukker genoem word. Hierdie middel verminder die aktiwiteit van die liggaam se immuunstelsel en is effektief vir die meeste kinders. Jou dokter kan die goeie en slegte aspekte van immuunonderdrukkers in detail bespreek. Die newe-effekte van hierdie middels sluit in verhoogde vatbaarheid vir infeksie, haarverlies en verminderde bloedselproduksie.

Ouers moet ook bewus wees dat kinders wat immuunonderdrukkende middels gebruik, siek kan word as hulle aan waterpokkies blootgestel word. Daarom moet jy jou dokter dadelik in kennis stel as jou kind aan waterpokkies blootgestel word terwyl hy hierdie medikasie gebruik.

Jou kind kan dalk diuretika (waterpille) kry. Diuretika help die nier om die liggaam van sout en water ontslae te raak. Die mees algemene waterpil vir kinders word furosemied genoem.

Watter ander probleme gebeur met die nefrotiese sindroom?
Die meeste kinders sal slegs probleme hê met swelling. 'n Kind met die nefrotiese sindroom kan egter 'n ernstige infeksie in die maag of bloedklonte in die bene ontwikkel. Albei hierdie vereis onmiddellike mediese aandag.

Wat kan ouers doen?
Baie van jou kind se sorg sal deur jou verskaf word. Gee aandag aan jou kind se gesondheid, maar moenie jou kind oorbeskerm nie. Jou kind moet voortgaan met sy of haar gewone aktiwiteite, soos om skool by te woon en vriende te sien. Jy moet voortgaan om jou kind soos alle ander kinders in die gesin te behandel.

As jou kind siek is of prednisoon neem, sal die dokter 'n lae sout dieet aanbeveel, wat swelling sal verminder. Jou kind sal egter toegelaat word om soveel te drink wat hy of sy wil. Die eerste teken dat jou kind weer siek word, is die terugkeer van proteïene in die urine. As gevolg hiervan sal baie dokters vra dat jy jou kind se urine gereeld nagaan.

Gaan die siekte ooit weg?
Soms. Al het die nefrotiese sindroom nie 'n spesifieke genesing nie, "ontgroei" die meerderheid kinders hierdie siekte in hul laat tienerjare of in vroeë volwassenheid. Sommige kinders sal slegs een aanval van die sindroom hê. As jou kind vir drie jaar ná die eerste een nie weer ’n aanval kry nie, is die kans redelik goed dat hy of sy nie weer siek sal word nie.

Die meeste kinders sal egter dikwels twee of meer aanvalle hê. Die aanvalle kom meer gereeld voor in die eerste twee jaar nadat die sindroom toegeslaan het. Ná tien jaar ly minder as een uit elke vyf kind steeds aan aanvalle. Selfs al het 'n kind talle aanvalle, sal die meeste nie permanente nierskade ontwikkel nie. Om verdere aanvalle te voorkom, is die primêre taak van die versorger om die ophoping van vloeistof in die kind se liggaam met prednisoon en diuretika te beheer.

Dit is belangrik om te onthou dat kinders met hierdie siekte 'n uitstekende langtermyn-uitkyk het en lang, gesonde lewens kan lei.


Voorbeelde van poligeniese eienskappe

Hoogte

Menslike lengte word in werklikheid deur baie gene beheer, daar is meer as 400 gene wat met lengte verband hou, en al hierdie gene is in wisselwerking om 'n persoon se fenotipe te vorm. Dit is 'n baie groot getal, maar dit maak sin omdat hoogte 'n samestelling is van die lengtes van baie verskillende liggaamsdele, soos beenbene, die bolyf en selfs die nek. Poligeniese eienskappe kan ook deur 'n organisme se omgewing beïnvloed word. As 'n persoon onvoldoende voeding tydens die kinderjare kry, kan hulle groei belemmer en uiteindelik kleiner en korter wees as wat hulle andersins sou. Daar word beraam dat 90% van 'n persoon se volwasse lengte deur genetika beheer word, en 10% word deur die omgewing beïnvloed.

Hierdie diagram toon die gemiddelde nageslaghoogte gebaseer op die gemiddelde lengte van beide ouers. Alhoewel lang ouers geneig is om lang kinders te hê, is daar 'n groot variasie in die lengte wat elke kind kan wees. Met ander woorde, lang ouers kan ook kort kinders hê, en omgekeerd. Dit word verteenwoordig deur die baie datapunte wat vir elke gemiddelde hoogte gewys word, met groter datapunte wat 'n groter aantal mense verteenwoordig.

Velkleur

By mense word velkleur deur baie dinge beïnvloed, maar die pigment melanien beïnvloed die meeste van 'n persoon se fenotipe. Oor die algemeen, hoe meer melanien 'n persoon het, hoe donkerder is hul vel. Albino mense produseer glad nie melanien nie. Die liggaam skep meer melanien om teen die son se UV-strale te beskerm, en daarom word die vel donkerder na langdurige sonblootstelling. Die hoeveelheid en tipe melanien wat 'n persoon produseer, soos eumelanien, feomelanien en neuromelanien, word deur veelvuldige gene beheer, en die verskillende tipes melanien tree in wisselwerking om die finale fenotipe te vorm. Mense met rooi hare het byvoorbeeld meer feomelanien en het dikwels 'n pienkerige velkleur.

Oogkleur

Daar is 2 hoof menslike oogkleurgene, OCA2 en HERC2, maar ten minste 13 ander gene speel ook 'n rol. Die gekleurde deel van 'n persoon se oog is die iris. Dit is 'n spier wat die grootte van die pupil verander om die hoeveelheid lig wat deur die retina geabsorbeer word, te verander. 'n Persoon se oogkleur word bepaal deur die pigmentasie van hul irisse, maar ook deur die manier waarop die selle in hul irisse lig verstrooi. Soos met velkleur, word oogkleur beïnvloed deur die teenwoordigheid van melanien. Mense met bruin oë het baie melanien, terwyl mense met blou oë lae melanien in die voorste deel van die iris het wat sigbaar is. Groen oë word veroorsaak deur verskeie faktore hulle is die gevolg van 'n ligbruin iris gekombineer met 'n blou toon wat deur ligverstrooiing gegee word.


Psigoanalitiese teorie van drome

Sigmund Freud se psigoanalitiese teorie van drome neem in ag dat wanneer ons slaap, ons brein ons gedagtes herorganiseer. Of ons ons drome onthou of nie, ons almal droom. Freud het dit gesien as 'n voortsetting van sy psigoanalitiese teorie droominterpretasie kan dus individuele gedrag verklaar.

Freud verdeel drome in twee komponente – materiale en hul interaksies. Om van 'n blom te droom het nie 'n universele betekenis nie aangesien almal 'n ander perspektief het en herinneringe aan 'n voorwerp geheg het. Dit is dus belangrik om eers die persoonlike betekenisse agter drome uit te vind.

Aangesien die meeste drome persoonlike ervarings, begeertes en eienskappe weerspieël, het Freud droominterpretasie gebruik om meer insig in 'n persoon se denkprosesse te gee. Hy het geglo dat oop kommunikasie met betrekking tot die id, ego en superego geestesongesteldheid kan help om moderne kognitiewe en gedragsterapieë saam te stem.

In die psigoanalitiese teorie van drome het Freud geglo dat elke droom "die vervulling van 'n wens" is. Hy het die belangrikheid van die latente droom beklemtoon - of die deel van 'n droom wat 'n sielkundige betekenis het en dikwels vir die bewuste verstand verborge is.

Die deel van 'n droom wat jy onthou wanneer jy wakker word, het hy na verwys as 'n manifeste droom. Volgens Freud kan slegs 'n latente droom ware insigte gee in die werking van die individuele verstand.


Inhoud

Outisme is 'n hoogs veranderlike, neuro-ontwikkelingsversteuring [28] waarvan die simptome die eerste keer tydens baba- of kinderjare verskyn, en oor die algemeen 'n bestendige kursus volg sonder remissie. [29] Outistiese mense kan in sommige opsigte ernstig gestremd wees, maar gemiddeld, of selfs meerderwaardig, in ander. [30] Openbare simptome begin geleidelik na die ouderdom van ses maande, word gevestig teen die ouderdom van twee of drie jaar [31] en is geneig om deur volwassenheid voort te gaan, hoewel dikwels in meer gedempte vorm. [32] Dit word onderskei deur 'n kenmerkende drietal van simptome: gestremdhede in sosiale interaksie, gestremdhede in kommunikasie en herhalende gedrag. Ander aspekte, soos atipiese eetgewoontes, is ook algemeen, maar is nie noodsaaklik vir diagnose nie. [33] Individuele simptome van outisme kom in die algemene bevolking voor en blyk nie hoogs te assosieer nie, sonder 'n skerp lyn wat patologies ernstig van algemene eienskappe skei. [34]

Sosiale ontwikkeling

Sosiale tekorte onderskei outisme en die verwante outismespektrumafwykings (ASD sien Klassifikasie) van ander ontwikkelingsafwykings. [32] Outistiese mense het sosiale gestremdhede en kort dikwels die intuïsie oor ander wat baie mense as vanselfsprekend aanvaar. Die bekende outistiese Temple Grandin het haar onvermoë om die sosiale kommunikasie van neurotipiese mense, of mense met tipiese neurale ontwikkeling, te verstaan, beskryf as dat sy haar "soos 'n antropoloog op Mars" laat voel. [35]

Ongewone sosiale ontwikkeling word vroeg in die kinderjare duidelik. Outistiese babas toon minder aandag aan sosiale stimuli, glimlag en kyk minder gereeld na ander, en reageer minder op hul eie naam. Outistiese kleuters verskil meer treffend van sosiale norme byvoorbeeld, hulle het minder oogkontak en beurte maak, en het nie die vermoë om eenvoudige bewegings te gebruik om hulself uit te druk nie, soos om na dinge te wys. [36] Drie- tot vyfjarige outistiese kinders is minder geneig om sosiale begrip te toon, ander spontaan te nader, emosies na te boots en daarop te reageer, nieverbaal te kommunikeer en beurte met ander te maak. Hulle vorm egter aanhangsels met hul primêre versorgers. [37] Die meeste outistiese kinders vertoon matig minder aanhegtingsekuriteit as neurotipiese kinders, alhoewel hierdie verskil verdwyn by kinders met hoër verstandelike ontwikkeling of minder uitgesproke outistiese eienskappe. [38] Ouer kinders en volwassenes met OSV presteer swakker op toetse van gesig- en emosieherkenning [39] alhoewel dit deels te wyte kan wees aan 'n laer vermoë om 'n persoon se eie emosies te definieer. [40]

Kinders met hoë funksionering outisme het meer intense en gereelde eensaamheid in vergelyking met nie-outistiese eweknieë, ten spyte van die algemene oortuiging dat outistiese kinders verkies om alleen te wees. Om vriendskappe te maak en in stand te hou, blyk dikwels moeilik te wees vir diegene met outisme. Vir hulle voorspel die kwaliteit van vriendskappe, nie die aantal vriende nie, hoe eensaam hulle voel. Funksionele vriendskappe, soos dié wat uitnodigings na partytjies tot gevolg het, kan die lewenskwaliteit dieper beïnvloed. [41]

Daar is baie anekdotiese verslae, maar min sistematiese studies, van aggressie en geweld by individue met OSV. Die beperkte data dui daarop dat outisme by kinders met intellektuele gestremdheid geassosieer word met aggressie, vernietiging van eiendom en ineenstortings. [42]

Kommunikasie

Ongeveer 'n derde tot 'n helfte van outistiese mense ontwikkel nie genoeg natuurlike spraak om in hul daaglikse kommunikasiebehoeftes te voorsien nie. [43] Verskille in kommunikasie kan vanaf die eerste lewensjaar teenwoordig wees, en kan vertraagde aanvang van gebabbel, ongewone gebare, verminderde responsiwiteit en vokale patrone insluit wat nie met die versorger gesinchroniseer is nie. In die tweede en derde jaar het outistiese kinders minder gereelde en minder diverse gebabbel, konsonante, woorde en woordkombinasies hul gebare word minder dikwels met woorde geïntegreer. Outistiese kinders is minder geneig om versoeke te rig of ervarings te deel, en is meer geneig om bloot ander se woorde te herhaal (echolalia) [44] [45] of omgekeerde voornaamwoorde. [46] Gesamentlike aandag blyk nodig te wees vir funksionele spraak, en tekorte in gesamentlike aandag blyk babas met OSV te onderskei. [20] Hulle kan byvoorbeeld na 'n wysende hand kyk in plaas van die aangewysde voorwerp, [36] [45] en hulle versuim konsekwent om na voorwerpe te wys om kommentaar te lewer op of 'n ervaring te deel. [20] Outistiese kinders kan probleme ondervind met verbeeldingspel en met die ontwikkeling van simbole in taal. [44] [45]

In 'n paar studies het hoëfunksionerende outistiese kinders tussen die ouderdomme van 8-15 ewe goed presteer as, en as volwassenes beter as, individueel ooreenstemmende kontroles by basiese taaltake wat woordeskat en spelling behels. Beide outistiese groepe het slegter gevaar as kontroles by komplekse taaltake soos figuurlike taal, begrip en afleiding. Aangesien mense aanvanklik aanvanklik groot is uit hul basiese taalvaardighede, dui hierdie studies daarop dat mense wat met outistiese individue praat, meer geneig is om te oorskat wat hul gehoor verstaan. [ beter bron nodig ] [47]

Herhalende gedrag

Outistiese individue kan baie vorme van herhalende of beperkte gedrag vertoon, wat die Herhalende Behavior Scale-Revised (RBS-R) soos volg kategoriseer. [48]

    : Herhalende bewegings, soos hand klap, kop rol of liggaam wieg. : Tydrowende gedrag wat bedoel is om die angs te verminder wat 'n individu verplig voel om herhaaldelik of volgens rigiede reëls uit te voer, soos om voorwerpe in 'n spesifieke volgorde te plaas, dinge na te gaan of hande te was.
  • Eendersheid: Weerstand teen verandering, byvoorbeeld, dring daarop aan dat die meubels nie geskuif word nie of weier om onderbreek te word. : Onveranderlike patroon van daaglikse aktiwiteite, soos 'n onveranderlike spyskaart of 'n aantrekritueel. Dit is nou geassosieer met eendersheid en 'n onafhanklike validering het voorgestel dat die twee faktore gekombineer word. [48]
  • Beperkte belangstellings: Belangstellings of fiksasies wat abnormaal is in tema of intensiteit van fokus, soos beheptheid met 'n enkele televisieprogram, speelding of speletjie. : Gedrag soos oogpoking, vel-pluk, handbyt en kopstamp. [20]

Geen enkele herhalende of selfbeserende gedrag blyk spesifiek vir outisme te wees nie, maar outisme blyk 'n verhoogde patroon van voorkoms en erns van hierdie gedrag te hê. [49]

Ander simptome

Outistiese individue kan simptome hê wat onafhanklik van die diagnose is, maar wat die individu of die gesin kan beïnvloed. [33] 'n Geskatte 0,5% tot 10% van individue met OSV toon ongewone vermoëns, wat wissel van splintervaardighede soos die memorisering van onbenullighede tot die buitengewoon seldsame talente van wonderlike outistiese geleerdes. [50] Baie individue met OSV toon superieure vaardighede in persepsie en aandag, relatief tot die algemene bevolking. [51] Sensoriese abnormaliteite word in meer as 90% van outistiese mense gevind, en word deur sommige as kernkenmerke beskou, [52] hoewel daar geen goeie bewyse is dat sensoriese simptome outisme van ander ontwikkelingsafwykings onderskei nie. [53] Verskille is groter vir onderresponsiwiteit (byvoorbeeld om in dinge in te loop) as vir oorresponsiwiteit (byvoorbeeld benoudheid van harde geluide) of vir sensasiesoek (byvoorbeeld ritmiese bewegings). [54] 'n Geskatte 60-80% van outistiese mense het motoriese tekens wat swak spiertonus, swak motoriese beplanning en toneloop insluit [52] tekorte in motoriese koördinasie is deurdringend oor OSV en is groter in outisme. [55] Ongewone eetgedrag kom by ongeveer driekwart van kinders met OSV voor, in die mate dat dit voorheen 'n diagnostiese aanwyser was. Selektiwiteit is die algemeenste probleem, hoewel eetrituele en voedselweiering ook voorkom. [56]

Daar is tentatiewe bewyse dat geslagsdisforie meer gereeld by outistiese mense voorkom. [57] [58]

Gastrointestinale probleme is een van die mees algemeen geassosieerde mediese afwykings by outistiese mense. [59] Dit word gekoppel aan groter sosiale gestremdheid, geïrriteerdheid, gedrag en slaapprobleme, taalgestremdheid en gemoedsveranderinge. [59] [60]

Ouers van kinders met OSV het hoër vlakke van stres. [36] Broers en susters van kinders met OSV rapporteer groter bewondering van en minder konflik met die geaffekteerde broer of suster as broers en susters van onaangeraakte kinders en was soortgelyk aan broers en susters van kinders met Down-sindroom in hierdie aspekte van die broers en sustersverhouding. Hulle het egter laer vlakke van nabyheid en intimiteit gerapporteer as broers en susters van kinders met Down-sindroom broers en susters van individue met ASD het groter risiko van negatiewe welstand en swakker broers en sustersverhoudings as volwassenes. [61]

Daar word lankal aanvaar dat daar 'n algemene oorsaak op die genetiese, kognitiewe en neurale vlakke is vir outisme se kenmerkende drietal van simptome. [62] Daar is egter toenemende vermoede dat outisme eerder 'n komplekse afwyking is waarvan die kernaspekte duidelike oorsake het wat dikwels saam voorkom. [62] [63]

Outisme het 'n sterk genetiese basis, alhoewel die genetika van outisme kompleks is en dit onduidelik is of ASD meer verklaar word deur seldsame mutasies met groot effekte, of deur seldsame multigene interaksies van algemene genetiese variante. [65] [66] Kompleksiteit ontstaan ​​as gevolg van interaksies tussen veelvuldige gene, die omgewing en epigenetiese faktore wat nie DNS-volgordebepaling verander nie, maar oorerflik is en geenuitdrukking beïnvloed. [32] Baie gene is met outisme geassosieer deur opeenvolging van die genome van geaffekteerde individue en hul ouers. [67] Studies van tweelinge dui daarop dat oorerflikheid 0,7 is vir outisme en so hoog as 0,9 vir ASD, en broers en susters van diegene met outisme is ongeveer 25 keer meer geneig om outisties te wees as die algemene bevolking. [52] Die meeste van die mutasies wat outismerisiko verhoog, is egter nie geïdentifiseer nie. Outisme kan tipies nie na 'n Mendeliese (enkel-geen) mutasie of na 'n enkele chromosoomafwyking herlei word nie, en daar is getoon dat geen van die genetiese sindrome wat met OSV's geassosieer word, selektief ASD veroorsaak nie. [65] Talle kandidaatgene is opgespoor, met slegs klein effekte wat aan enige spesifieke geen toegeskryf kan word. [65] Die meeste lokusse verklaar individueel minder as 1% van gevalle van outisme. [68] Die groot aantal outistiese individue met onaangeraakte familielede kan die gevolg wees van spontane strukturele variasie—soos delesies, dupliserings of inversies in genetiese materiaal tydens meiose. [69] [70] Gevolglik kan 'n aansienlike fraksie van outismegevalle naspeurbaar wees na genetiese oorsake wat hoogs oorerflik is, maar nie oorgeërf nie: dit wil sê, die mutasie wat die outisme veroorsaak, is nie teenwoordig in die ouergenoom nie. [64] Outisme kan ondergediagnoseer word by vroue en meisies as gevolg van 'n aanname dat dit hoofsaaklik 'n manlike toestand is, [71] maar genetiese verskynsels soos inprenting en X-koppeling het die vermoë om die frekwensie en erns van toestande by mans te verhoog, en teorieë is voorgehou om 'n genetiese rede waarom mans meer gereeld gediagnoseer word, soos die ingeprente breinhipotese en die ekstreme manlike breinteorie. [72] [73] [74]

Maternale voeding en inflammasie tydens voorkonsepsie en swangerskap beïnvloed fetale neuro-ontwikkeling. Intrauteriene groeibeperking word geassosieer met ASD, in beide termyn en premature babas. [15] Moederlike inflammatoriese en outo-immuun siektes kan fetale weefsels beskadig, 'n genetiese probleem vererger of die senuweestelsel beskadig. [16]

Blootstelling aan lugbesoedeling tydens swangerskap, veral swaar metale en deeltjies, kan die risiko van outisme verhoog. [75] [76] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines, [25] and prenatal stress. Some, such as the MMR vaccine, have been completely disproven. [77] [78] [79] [80]

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. [81] The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud". [82] Although these theories lack convincing scientific evidence and are biologically implausible, [81] 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. [83] [84]

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. [85] The behaviors appear to have multiple pathophysiologies. [34]

There is evidence that gut–brain axis abnormalities may be involved. [59] [60] [86] A 2015 review proposed that immune dysregulation, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction. [60] A 2016 review concludes that enteric nervous system abnormalities might play a role in neurological disorders such as autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain. [86]

Several lines of evidence point to synaptic dysfunction as a cause of autism. [19] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion. [87] 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. [88] 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, there is strong evidence that autism arises very early in development. [89]

Diagnosis is based on behavior, not cause or mechanism. [34] [90] Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, typically before age three, and lead to clinically significant functional impairment. [3] Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with unusual objects. The disturbance must not be better accounted for by Rett syndrome, intellectual disability or global developmental delay. [3] ICD-10 uses essentially the same definition. [29]

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) [91] 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. [36] The Diagnostic interview for social and communication disorders (DISCO) may also be used. [92]

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. [93] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions. [94] A differential diagnosis for ASD at this stage might also consider intellectual disability, hearing impairment, and a specific language impairment [93] such as Landau–Kleffner syndrome. [95] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression. [96]

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause. [97] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes, [98] consensus guidelines in the US and UK are limited to high-resolution chromosome and fragile X testing. [97] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations. [99] 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. [100] Metabolic and neuroimaging tests are sometimes helpful, but are not routine. [97]

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. [1] 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. [93] 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.

Signs of autism may be more challenging for clinicians to detect in females. [ beter bron nodig ] [101] Autistic females have been shown to engage in masking more frequently than autistic males. [101] Masking may include making oneself perform normative facial expressions and eye contact. [ beter bron nodig ] [102] A notable percentage of autistic females may be misdiagnosed, diagnosed after a considerable delay, or not diagnosed at all. [101]

Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis. [103] 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. [104]

Klassifikasie

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, severely restricted interests, and highly repetitive behavior. [29] These symptoms do not imply sickness, fragility, or emotional disturbance. [32]

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. [105] Unlike with autism, people with Asperger syndrome have no substantial delay in language development. [106] The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD) [6] or sometimes the autistic disorders, [107] whereas autism itself is often called autistic disorder, childhood autism, of infantile autism. In this article, autism refers to the classic autistic disorder in clinical practice, though, autism, ASD, en PDD are often used interchangeably. [97] 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. [108]

Research into causes has been hampered by the inability to identify biologically meaningful subgroups within the autistic population [109] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics. [110] 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 [111] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects. [19] It has been proposed to classify autism using genetics as well as behavior. [112]

Spectrum

Autism has long been thought to cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, developmentally disabled, and prone to frequent repetitive behavior such as hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. [113] Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary. [52]

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. [1] According to an article, 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". [33]

  • No response to name (or eye-to-eye gaze) by 6 months. [114]
  • No babbling by 12 months.
  • No gesturing (pointing, waving, etc.) by 12 months.
  • No single words by 16 months.
  • No two-word (spontaneous, not just echolalic) phrases by 24 months.
  • Loss of any language or social skills, at any age.

The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there is no concern. [ unbalanced? – discuss ] [115] The 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. [19] 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, the Checklist for Autism in Toddlers (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). [1] It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders. [116] Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture. [117] 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. [118]

While infection with rubella during pregnancy causes fewer than 1% of cases of autism, [119] vaccination against rubella can prevent many of those cases. [120]

The main goals when treating autistic children are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes. [122] [123] No single treatment is best and treatment is typically tailored to the child's needs. [6] Families and the educational system are the main resources for treatment. [19] Services should be carried out by behavior analysts, special education teachers, speech pathologists, and licensed psychologists. Studies of interventions have methodological problems that prevent definitive conclusions about efficacy. [124] However, the development of evidence-based interventions has advanced in recent years. [122] 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. [125] Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, communication, and job skills, [6] and often improve functioning and decrease symptom severity and maladaptive behaviors [126] claims that intervention by around age three years is crucial are not substantiated. [127] While medications have not been found to help with core symptoms, they may be used for associated symptoms, such as irritability, inattention, or repetitive behavior patterns. [9]

Onderwys

Educational interventions often used include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy and cognitive behavioral interventions in adults without intellectual disability to reduce depression, anxiety, and obsessive-compulsive disorder. [6] [128] Among these approaches, interventions either treat autistic features comprehensively, or focalize treatment on a specific area of deficit. [122] The quality of research for early intensive behavioral intervention (EIBI)—a treatment procedure incorporating over thirty hours per week of the structured type of ABA that is carried out with very young children—is currently low, and more vigorous research designs with larger sample sizes are needed. [129] Two theoretical frameworks outlined for early childhood intervention include structured and naturalistic ABA interventions, and developmental social pragmatic models (DSP). [122] One interventional strategy utilizes a parent training model, which teaches parents how to implement various ABA and DSP techniques, allowing for parents to disseminate interventions themselves. [122] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation. Despite the recent development of parent training models, these interventions have demonstrated effectiveness in numerous studies, being evaluated as a probable efficacious mode of treatment. [122]

Early, intensive ABA therapy has demonstrated effectiveness in enhancing communication and adaptive functioning in preschool children [6] [130] it is also well-established for improving the intellectual performance of that age group. [6] [126] [130] Similarly, a teacher-implemented intervention that utilizes a more naturalistic form of ABA combined with a developmental social pragmatic approach has been found to be beneficial in improving social-communication skills in young children, although there is less evidence in its treatment of global symptoms. [122] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided. [94] It is not known whether treatment programs for children lead to significant improvements after the children grow up, [126] and the limited research on the effectiveness of adult residential programs shows mixed results. [131] 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. [132]

Medikasie

Medications may be used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails. [7] They may also be used for associated health problems, such as ADHD or anxiety. [7] 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. [10] [11] The atypical antipsychotic drugs risperidone and aripiprazole are FDA-approved for treating associated aggressive and self-injurious behaviors. [9] [32] [133] However, their side effects must be weighed against their potential benefits, and people with autism may respond atypically. [9] Side effects, for example, may include weight gain, tiredness, drooling, and aggression. [9] SSRI antidepressants, such as fluoxetine and fluvoxamine, have been shown to be effective in reducing repetitive and ritualistic behaviors, while the stimulant medication methylphenidate is beneficial for some children with co-morbid inattentiveness or hyperactivity. [6] There is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD. [ mediese aanhaling nodig ] No known medication relieves autism's core symptoms of social and communication impairments. [ mediese aanhaling nodig ] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function, suggesting the possibility of targeting therapies to specific rare mutations known to cause autism. [ mediese aanhaling nodig ]

Alternative medicine

Although many alternative therapies and interventions are available, few are supported by scientific studies. [39] [ mediese aanhaling nodig ] 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. [41] Some alternative treatments may place the child at risk. The preference that children with autism have for unconventional foods can lead to reduction in bone cortical thickness with this being greater in those on casein-free diets, as a consequence of the low intake of calcium and vitamin D however, suboptimal bone development in ASD has also been associated with lack of exercise and gastrointestinal disorders. [134] In 2005, botched chelation therapy killed a five-year-old child with autism. [135] [136] Chelation is not recommended for autistic people since the associated risks outweigh any potential benefits. [137] Another alternative medicine practice with no evidence is CEASE therapy, a mixture of homeopathy, supplements, and 'vaccine detoxing'. [ mediese aanhaling nodig ]

Although popularly used as an alternative treatment for autistic people, as of 2018 there is no good evidence to recommend a gluten- and casein-free diet as a standard treatment. [138] [139] [140] A 2018 review concluded that it may be a therapeutic option for specific groups of children with autism, such as those with known food intolerances or allergies, or with food intolerance markers. The authors analyzed the prospective trials conducted to date that studied the efficacy of the gluten- and casein-free diet in children with ASD (4 in total). All of them compared gluten- and casein-free diet versus normal diet with a control group (2 double-blind randomized controlled trials, 1 double-blind crossover trial, 1 single-blind trial). In two of the studies, whose duration was 12 and 24 months, a significant improvement in ASD symptoms (efficacy rate 50%) was identified. In the other two studies, whose duration was 3 months, no significant effect was observed. [138] The authors concluded that a longer duration of the diet may be necessary to achieve the improvement of the ASD symptoms. [138] Other problems documented in the trials carried out include transgressions of the diet, small sample size, the heterogeneity of the participants and the possibility of a placebo effect. [140] [141] In the subset of people who have gluten sensitivity there is limited evidence that suggests that a gluten-free diet may improve some autistic behaviors. [142] [143] [144]

Results of a systematic review on interventions to address health outcomes among autistic adults found emerging evidence to support mindfulness-based interventions for improving mental health. This includes decreasing stress, anxiety, ruminating thoughts, anger, and aggression. [128] There is tentative evidence that music therapy may improve social interactions, verbal communication, and non-verbal communication skills. [145] There has been early research looking at hyperbaric treatments in children with autism. [146] Studies on pet therapy have shown positive effects. [147]

There is no known cure. [6] [19] The degree of symptoms can decrease, occasionally to the extent that people lose their diagnosis of ASD [148] this occurs sometimes after intensive treatment and sometimes not. It is not known how often this outcome happens [126] reported rates in unselected samples have ranged from 3% to 25%. [148] Most autistic children acquire language by age five or younger, though a few have developed communication skills in later years. [149] Many autistic children lack social support, future employment opportunities or self-determination. [41] Although core difficulties tend to persist, symptoms often become less severe with age. [32]

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. [150] 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. [151]

Many autistic people face significant obstacles in transitioning to adulthood. [152] Compared to the general population autistic people are more likely to be unemployed and to have never had a job. About half of people in their 20s with autism are not employed. [153]

People with autism tend to face increased stress levels related to psychosocial factors, such as stigma, which may increase the rates of mental health issues in the autistic population. [154]

As of 2007, reviews estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD. [25] A 2016 survey in the United States reported a rate of 25 per 1,000 children for ASD. [155] Globally, autism affects an estimated 24.8 million people as of 2015 [update] , while Asperger syndrome affects a further 37.2 million. [12] In 2012, the NHS estimated that the overall prevalence of autism among adults aged 18 years and over in the UK was 1.1%. [156] Rates of PDD-NOS's 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. [157] CDC estimates about 1 out of 59 (1.7%) for 2014, an increase from 1 out of every 68 children (1.5%) for 2010. [158]

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, [157] [159] [160] though unidentified environmental risk factors cannot be ruled out. [18] The available evidence does not rule out the possibility that autism's true prevalence has increased [157] a real increase would suggest directing more attention and funding toward psychosocial factors and changing environmental factors instead of continuing to focus on genetics. [161] It has been established that vaccination is not a risk factor for autism and is not behind any increase in autism prevalence rates, if any change in the rate of autism exists at all. [162]

Males are at higher risk for ASD than females. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with intellectual disability and more than 5.5:1 without. [25] Several theories about the higher prevalence in males have been investigated, but the cause of the difference is unconfirmed [163] one theory is that females are underdiagnosed. [164]

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. [163] [165] 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. [28] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism. [166]

Several other conditions are common in children with autism. [19] They include:

  • Genetiese afwykings. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome, [167] and ASD is associated with several genetic disorders. [168]
  • Intellectual disability. The percentage of autistic individuals who also meet criteria for intellectual disability has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing intelligence of individuals on the autism spectrum. [169] In comparison, for PDD-NOS the association with intellectual disability is much weaker, [170] and by definition, the diagnosis of Asperger's excludes intellectual disability. [171]
  • 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. [172]
  • Epilepsie, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder. [173]
  • Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms. [174]
  • Minor physical anomalies are significantly increased in the autistic population. [175]
  • Preempted diagnoses. Although the DSM-IV rules out the concurrent diagnosis of many other conditions along with autism, the full criteria for Attention deficit hyperactivity disorder (ADHD), Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted. [mediese aanhaling nodig]
  • 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. [176]

A few examples of autistic symptoms and treatments were described long before autism was named. Die Tafelgesprek of Martin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic. [178] 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. [179] 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. [177]

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". [180] A Soviet child psychiatrist, Grunya Sukhareva, described a similar syndrome that was published in Russian in 1925, and in German in 1926. [181]

Clinical development and diagnoses

Die woord 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. [182] 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. [177] 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. [46] 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. [63] It is not known whether Kanner derived the term independently of Asperger. [183]

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. [184]

Terminology and distinction from schizophrenia

As late as the mid-1970s there was little evidence of a genetic role in autism while in 2007 it was believed to be one of the most heritable psychiatric conditions. [185] Although the rise of parent organizations and the destigmatization of childhood ASD have affected how ASD is viewed, [177] parents continue to feel social stigma in situations where their child's autistic behavior is perceived negatively, [186] and many primary care physicians and medical specialists express some beliefs consistent with outdated autism research. [187]

It took until 1980 for the DSM-III to differentiate autism from childhood schizophrenia. In 1987, the DSM-III-R provided a checklist for diagnosing autism. In May 2013, the DSM-5 was released, updating the classification for pervasive developmental disorders. The grouping of disorders, including PDD-NOS, autism, Asperger syndrome, Rett syndrome, and CDD, has been removed and replaced with the general term of Autism Spectrum Disorders. The two categories that exist are impaired social communication and/or interaction, and restricted and/or repetitive behaviors. [188]

The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find difficult to deal with, and has given them a way to form online communities and work remotely. [189] Societal 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. [24] [190]

An autistic culture has emerged, accompanied by the autistic rights and neurodiversity movements. [191] [192] [193] Events include World Autism Awareness Day, Autism Sunday, Autistic Pride Day, Autreat, and others. [194] [195] [196] [197] Social-science scholars study those with autism in hopes to learn more about "autism as a culture, transcultural comparisons . and research on social movements." [198] Many autistic individuals have been successful in their fields. [199] [200] [201]

Autism rights movement

The autism rights movement is a social movement within the context of disability rights that emphasizes the concept of neurodiversity, viewing the autism spectrum as a result of natural variations in the human brain rather than a disorder to be cured. [193] The autism rights movement advocates for including greater acceptance of autistic behaviors therapies that focus on coping skills rather than on imitating the behaviors of those without autism, and the recognition of the autistic community as a minority group. [202] Autism rights or neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from fringe theories that autism is caused by environmental factors such as vaccines. [193] A common criticism against autistic activists is that the majority of them are "high-functioning" or have Asperger syndrome and do not represent the views of "low-functioning" autistic people. [202]

Indiensneming

About half of autistic people are unemployed, and one third of those with graduate degrees may be unemployed. [203] Among those who find work, most are employed in sheltered settings working for wages below the national minimum. [204] While employers state hiring concerns about productivity and supervision, experienced employers of autistic people give positive reports of above average memory and detail orientation as well as a high regard for rules and procedure in autistic employees. [203] A majority of the economic burden of autism is caused by decreased earnings in the job market. [205] Some studies also find decreased earning among parents who care for autistic children. [206] [207]


Geloof

belief, faith, credence, credit mean assent to the truth of something offered for acceptance. belief may or may not imply certitude in the believer. my geloof that I had caught all the errors faith almost always implies certitude even where there is no evidence or proof. an unshakable faith in God credence suggests intellectual assent without implying anything about grounds for assent. a theory now given credence by scientists credit may imply assent on grounds other than direct proof. gave full krediet to the statement of a reputable witness

sinonieme see in addition opinion


Genetic Effects of Inbreeding

When two closely related organisms mate, their offspring have a higher level of homozygosity: in other words, an increased chance that the offspring will receive identical alleles from their mother and father. In contrast, heterozygosity occurs when the offspring receives anders allele. Dominant traits are expressed when only one copy of an allele is present, while recessive traits require two copies of an allele to be expressed.

Homozygosity increases with subsequent generations, so recessive traits that might otherwise be masked may start appearing as a result of repeated inbreeding. One negative consequence of inbreeding is that it makes the expression of undesired recessive traits more likely. However, the risk of manifesting a genetic disease, for example, isn't very high unless inbreeding continues for multiple generations.

The other negative effect of inbreeding is the reduction genetic diversity. Diversity helps organisms survive changes in the environment and adapt over time. Inbred organisms may suffer from what is called reduced biological fitness.

Scientists have also identified potential positive consequences of inbreeding. Selective breeding of animals has led to new breeds of domestic animals, genetically suited to specific tasks. It can be used to preserve certain traits that might be lost from out-crossing. The positive consequences of inbreeding are less well studied in humans, but in a study of Icelandic couples, scientists found that marriages between third cousins resulted in a greater number of children, on average than those between completely unrelated couples.


How Do You Define Family? The True Meaning (& Some Definitions) of Family

How Do You Define Family? That’s a tough question to answer.

Even the dictionary offers multiple definitions for the word.

A few decades ago, the word family, in most people’s eyes, referred to a mother, a father, and their children. Fast forward to present day, and beyond any personal feelings you may have, you’ll find that families come in all different forms, and the word can carry a different meaning depending on who you ask.

Apart from the pure legal definition, families today are often a mix of stepparents, half siblings, same sex parents, extended family members, etc.

Additionally (and beyond the biology), many people consider their family to be people in their lives who are not even related to them they define family based on factors such as loyalty, respect, love, and responsibility.

Indeed, perhaps a better definition of family would include a group of two or more people who share a common goal, similar values, and have a long-term commitment to one another.

To better understand the depth and dynamic behind the meaning of family, and find a better sense of how you define the word for yourself, let’s take a look below at a few of the many ways people define the word ‘family’ including Traditional Nuclear Families, Blended Families, Extended Families, Single Parent Families, Same-sex Parent Families, Childless Families, & the Family you choose.

Traditional (Nuclear) Families

The traditional make up of a family consists of a mother and father, whom are married, raising their biological children in one household. While this is the standard that many refer to when they think of the word ‘family’, the reality is this type of family dynamic is less of a norm nowadays especially as divorce rates are rising.

Blended Families

Blended families are when each parent has children from a previous relationship and both spouses’ children are now being raised in the same household. With the number of blended families in North America growing each year, more and more children are growing up with stepsiblings and stepparents making up their family.

Extended Families

Some people go beyond their household when they think of family. They think of their extended family, including aunts, uncles, grandparents, and cousins. Some children grow up very close to extended family members, some are raised by their extended family, and some families are not close with their extended family at all.

Single Parent Family

As the name suggests, this very common type of family is where either the mother or father along with the child care the key makeup of the family. While the single parent family has become increasingly more common in Western culture, it is one of the more significant changes society has seen in terms of the ‘types’ family in the last few decades. Single families are often close, as they must work together to solve problems, and these issues can be unique due to the fact that often the mother or father is the sole provider along with childcare duties.

Same Sex Parent Families

While some segments of society may struggles to accept same-sex (gay) parenting, this hasn’t stopped same-sex parents from moving forward and starting successful families. In fact, some research indicates that gay parents – in some areas – may even be more successful than straight parents. These studies went on to conclude that Children raised in gay parent households show no significant differences in their achievements, social function, or mental health. Additionally, they tend to be more open-minded, demonstrate enhanced levels of tolerance, and may even have a better understanding of equitable, healthy relationships.

Childless Family

The childless family is simply a group of people from varying backgrounds who – for whatever reason – have never had children and express no desire to have kids. Many may have wrestled with the concept of starting a family, but concluded that it simply wasn’t right for them regardless of any standard family definition. While the reasons for this vary from emotional to more practical in nature, Many childless families choose not to have children as they wish to focus on advancement in their careers, travel, or more time with their friends / spouses. Often times, childless families may opt for pets instead.

The Family You Choose

In a totally different direction, family doesn’t always have to be biological, or by marriage. Many people consider their close friends as family members, because they care for them as they care about their own family. Others may consider coworkers, community members, or other group members they are affiliated with to be an extension of their family. Family can be whomever you choose to call family, whether you are related or not.

There’s No Such Thing As “Normal”

Now more than ever before, it is important for people to understand that when it comes to what is a family, there is no such thing as normal. Every person, every child, every parent, every couple has a unique situation, and to try and define everyone in one black and white term would make no sense.

Family is not defined by biology, or marriage, or even a home. Family is the people you love and who love you back, the people you feel safe around, and the people you can count on to be there when you need them.

What is your definition of family? Share in the comments!


Ekonomiese impak

The cumulative economic and social burden of complex trauma in childhood is extremely high. Based upon data from a variety of sources, a conservative annual cost of child abuse and neglect is an estimated $103.8 billion, or $284.3 million per day (in 2007 values). This number includes both direct costs—about $70.7 billion—which include the immediate needs of maltreated children (hospitalization, mental health care, child welfare systems, and law enforcement) and also indirect costs—about $33.1 billion—which are the secondary or long-term effects of child abuse and neglect (special education, juvenile delinquency, mental health and health care, adult criminal justice system, and lost productivity to society).

A recent study examining confirmed cases of child maltreatment in the United States found the estimated total lifetime costs associated with child maltreatment over a 12-month period to be $124 billion. In the 1,740 fatal cases of child maltreatment, the estimated cost per case was $1.3 million, including medical expenses and productivity loss. For the 579,000 non-fatal cases, the estimated average lifetime cost per victim of child maltreatment was $210,012, which includes costs relating to health care throughout the lifespan, productivity losses, child welfare, criminal justice, and special education. Costs for these nonfatal cases of child maltreatment are comparable to other high-cost health conditions (i.e., $159,846 for stroke victims and $181,000 to $253,000 for those with Type 2 diabetes).

In addition to these costs are the “intangible losses” of pain, sorrow, and reduced quality of life to victims and their families. Such immeasurable losses may be the most significant cost of child maltreatment.


Kyk die video: Da li su deca na internetu bezbedna? - Nenad Dragović, Yunet (Oktober 2022).