ساختار آموزشی (ساماندهی )کودکان اوتيستيک
مقدمه
اوتيسم سندرمی پيچيده و دارای علايم عصبی _ روانی است که در دوران ابتدائی رشد ونمو کودک ظاهر می گردد وداراي علائمي همچون اختلال و نقص درتعامل اجتماعي و روابط بين فردي، مسايل جدی در زبان وتکلم ، وجود رفتارهای تکراری والگوهای رفتاری قالبی ومحدود،اصرار بر "همانی"و عدم تغيير در محيط است كه با الگوهاي ادواري وكليشه اي رفتاري همراه مي گردد و درمجموعه اختلالات نافذ وفراگير رشدي (Pervasive .D.D ) طبقه بندي مي شود.
رشدغيرعادي مهارتهاي ارتباطي واجتماعي بعنوان ويژگيها ونشانه هاي كليدي محسوب مي گردند وافزون برآن، رشدگويش ونحوه برقراري ارتباط از عوامل مهم پيشگوئي درمورد اين افراد محسوب مي گردد.
معيارهای تشخيصی
معيارهاي مورداستفاده بعنوان مبناي تشخيص اتيسم ، قطعي ومسلم نيستندودرطي زمان دائمأ تغيير مي يابند.افزون برآن ، از زمانيكه تشخيص اختلال نافذرشد درمحيط هاي آموزشگاهي بيشترجا افتاده ومتعاقب آن كودكان بيشتر وبيشتردسته بندي مي شوند ، تشخيص وافتراق اتيسم واقعي ازسايراختلالات نافذ رشد نيز روزبه روز مشكل ومشكل تر مي شود. درمجموع چنين به نظر مي رسد كه اتيسم نتيجه ومحصول نهائي اختلالات مختلفي است كه تمامي آنها در علائمي همچون ناهنجاريهاي اجتماعي ، زباني وعصب شناختي مشترك مي باشند.
اتيسم معمولأ درمحدوده سني 2 تا 4 سالگي تشخيص داده مي شود منتها علائم ممكن است خيلي زودتر آشكار گردند. برخي از كودكان اتيستيك ممكن است درتمامي مواردوجنبه ها دچارمشكل نباشند ، در حاليكه هستنـد كــودكانـي كه فـوق العـاده آشفتــه ، پريشـان خاطر وسـردرگم انـد وحتـي احتـمال دارد كه به خودآسيب برسانند.برخـي ازآنـان مقاطع رشدي مختلف وبا اهميتي همچون صحبت كردن وراه رفتن را حتي جلوتر از زمان تعيين شده درجدول رشدكسب مي كنند. به همين دليل ، اغلب والدين با مشاهده ازدست رفتن تدريجي برخي ازاين مهارتها دركودك ، پريشان خاطر وآشفته حال مي گردند. اوتيسم واپسگرا (regressive autism ) اصطلاحي است كه به اين گروه اطلاق مي شود. دسته ديگري ازاين كودكان ازهمان ابتدا دچارتأخيرات رشدي مي شوند.
مخرب ترين ويژگيهاي اتيسم عبارتند از:
فقدان برقراري ارتباط چشمي ، رفتارهاي خودبرانگيزاننده (self-stimulatory) ، آسيب رساني به خود، الگوهاي خواب غيرمعمول ، ضايعات حسي ، خاموشي، زبان محاوره غيرمعمول، سختي وعدم انعطاف، بازي كليشه اي با اشياء كوچك، فقدان قوه تخيل، شوخي وبذله گوئي، حساسيت و واكنش نسبت به تغييرات دور وبر و همچنين ترجيحات غذائي .
البته بايداشاره كردكه اين ويژگيها ممكن است ازكودكي به كودك ديگربسيارمتفاوت باشد.
يكي ازويژگيهاي شايع اتيسم، اصرار و پافشاري آنها در عدم تغييرودست نخوردگي اوضاع وشرايط است واين كودكان اغلب بهترين عملكرد خود را بهنگام ثبات وعدم دگرگوني شرايط روزمره شان از خودنشان مي دهند.جابجايي وتغييرشرايط مانندرفتن به يك مدرسه جديد ، تعطيلات ، غذاهاي جديد وامثالهم ، بخصوص مي تواند براي اين كودكان برانگيزاننده باشد.

اين طور به نظر مي رسدكه موارد زيراحتما لأ در كودكان اتيسم بطور مشترك ديده مي شود:
 مشكلات ودرگيري مخ ومخچه
 اختلالات وضايعات مربوط به جذب موادغذايي
 اختلال درسيستم ايمني بدليل نقص سلولهاي واسطه
 نقص نوروترانسميتري وواسطه هاي شيميايي (سروتونين)

درگيري مخچه موجب بروز مشكلاتي در زمينه هاي تعادل وتوازن ، توجه ، وحس عمقي (درك ناشي از تحريك عضلات وتاندونها) مي گردد. عقيده براين است كه دوبخش آميگدال وهيپوكامپ از سيستم ليمبيك درگيرهستند. محققين اين تغييرات را «اصطلاحأ سيم پيچي معيوب مغز» تعبير كرده اندچون كودكان اتيسم نميتوانند مانند ما جهان خارج را دريافت و درك كنندبه همين خاطر است كه غالبأ وقتي نام آنها صدا زده مي شود پاسخي نمي دهند، به رفتارها وكارهاي غير معمول دل مي بندند ، به چشمهاي فرد مقابل نگاه نمي كند، و اينكه درزمينه صحبت با ديگران وبرقراري تعا ملات اجتما عي دچار مشكل هستند.
ميزان بالای بروز عقب ماندگی ذهنی وميزان بالاتر ازحد انتظار اختلالات تشنجی درکودکان اوتيسم نشان می دهد که اين اختلال پايه ای زيستی دارد. حدود 75% کودکان اوتيسم دچار عقب ماندگی ذهنی هستند. تقريباٌ يک سوم اين کودکان عقب ماندگی ذهنی خفيف تا متوسط دارند ونزديک به نيمی از آنها دچار عقب ماندگی ذهنی عميق يا شديد هستند. اختلالات همراه آن شامل عقب ماندگی ذهنی ، رفتارهای پرخاشگرانه وخودآزاری است.

رشدغيرعادي مهارتهاي ارتباطي ،اجتماعي و گويش ازجمله مواردی هستند که عدم رسيدگی به آنها می تواند کودک را کاملاٌ از عرصه تعاملات اجتماعی منفک سازد و او را به انزوای کامل رهنمون سازد.




ارزيابي

معمولاٌ ارزيابي ها شامل موارد زير مي باشند :
- ارزيابی بالينی ( آزمونهای روانشناختی ، چک ليستهای تخصصی مربوطه )
- ارزيابی فهرست مربوط به اختلالات رفتاری ABC / Aberrant Behavior Checklist))
- جدول مربوط به اوتيسم کودکی Childhood Autism Rating Scale) / CARS )
- جدول مربوط به زندگی واقعی برای اوتيسم Real life Rating Scale for Autism) / RLRSA )
- بررسی توانمندی ذهنی و ارزيابی هوشی
- استفاده از چک ليستهای مرتبط ديگر همچون سطح قابليتهای عملی ( فانکشنال ) و ...
برای شناخت محدوده توانائيها وناتوانيها

تمهيدات :

تاثيرگذارترين برنامه آموزشی زمانی شکل می گيرد که درطی آن سعی گردد کودک از انزوا و بی توجهی به دنيای اطراف خود(توجه انتخابی) خارج گردد وشرايط برای آموزش مهارتهای پايه فراهم گردد.
بنابراين بهبود روابط بين فردی واجتماعی ( interpersonal & social relatonship ) ، ارتقاء مهارتهای کلامی وشناختی ، استفاده از رويکردهای مبتنی بر تقويت وتعديل حسی (استفاده ازمداليته های حسی )، استفاده از وسائل آموزشی و سمعی- بصری ( کامپيوتر ، تلويزيون ، ضبط و ...) ، وهمچنين استفاده از مواردي همچون فعاليت درماني ، موسيقی درمانی و... ، مي توانند در درمان نقش موثري را داشته باشند.
استفاده ازفعاليتهاي موزيكال مي تواند در زمينه هاي زير مورد استفاده قرار گيرد:
 رشد مهارتهاي حركتي ظريف ودرشت
 طرح وبرنامه حركتي
 گفتار و وضوح كلامي
 مهارتهاي شنيداري
 تعامل وآگاهي از طريق موسيقي
 توجه تدريجي
 ارتقاء سطح ارتباطي ومهارتي

مشاهدات باليني وتحقيقات صورت گرفته همگي نشانگرحساسيت بالا وعلاقه وافر اين كودكان به موسيقي بوده اند.دربررسيها روشن شده است كه استفاده ازتكنيكهاي موسيقي درماني سازمان يافته مي تواند اثرات مثبتي بر شناخت ، گويش ومهارتهاي اجتماعي فرد برجاي گذارد. آسيب شناسان گفتار وزبان بر ارزش سازماندهي وتمرينات منظم موسيقي در درمان انواعي از اختلالات همچون عدم شيوائي وفصاحت كلام ، طريق وسبك اداي كلام، واختلالات ديگر زبان وگفتار تأكيد كرده اند.
موسيقي مي تواند مبنا وپايه اي باشد براي دريافت، بيان كلامي و رشد مهارتهاي زباني. نتيجـه مطالعات محققين مختـلف مؤيـد ايـن مطلب است كه كـودكان اوتيسم بدليل ضعف در ادراك، از پـژواك كلام وزبان كليشه اي به عنوان راهكارهاي اوليه براي برقراري ارتباط استفاده مي كنند . بخشهاي تكراري موجود درفعاليتهاي موزيكال وعلاقه مفرط كودكان اوتيسم به موسيقي ، موجب رشد قابليت هاي ارتباطي و تعاملي آنها مي شود.بسياري از كودكان مبتلا به طيف اختلالات اوتيستيك (ASD ) و همچنين اختلالات مرتبط ديگر، ارتباط و وابستگي زيادي به موسيقي ازخود نشان مي دهند.

نقش والدين:
اطلاعات ، بینش وطرز تلقی والدین از نحوه تمرینات وچگونگی رفتار با این کودکان بسیار تعیین کننده است و لازم است اطلاع رسانی صحيح درمورد شرايط ونيازهای اين کودکان به والدين صورت گيرد و جنبه های مختلف آموزشی و درمانی برای خانواده بيمارتشريح گردد و والدين نيز در دوره های کوتاه مدت مورد آموزش قرارگيرند تا اطلاعات کافی در زمينه نحوه آموزش و مديريت رفتاری اين کودکان را کسب نمايند.

جمع بندی:
اوتيسم اختلال لاعلاجی که فرد مبتلا را کاملاٌ از اجتماع دور سازد نيست بلکه هستند افرادی مبتلائی که هم اکنون در جامعه حضور مستقلی دارند و حتی مدارج تحصيلی را با موفقيت طی کرده اند و از کارکرد اجتماعی قابل قبولی نيز برخوردار هستند. شواهد ومدارک زيادی وجود دارد که با مداخلات زود هنگام درمانی وهمچنين پيگيريهای آموزشی، کودکان اوتيسم پيشرفت بسياری از خود نشان داده اند و توانسته اند به سطوح قابل قبولی از کارکرد اجتماعی واستقلال فردی دست يابند.


فرشيد خانپور
کارشناس ارشد کاردرمانی

رشد وآموزش ارتباطات و مهارتهاي اجتماعي

درميـان تمام پستانداران ،آدمـي دربدو تولد ناتـوان ترين آنهاست وبه طولاني ترين دوره رشدي نياز دارد تا بتواند به تمامي مهـارتهاي ويژه نوع خود دست يابد. كنش متقابل ودائمي بين توارث ومحيط،تعيين كننده رشدآدمي است .يعني آمادگي هاي زيستي موجود در بدو تولد ، با تجاربي كه دردوران رشدازمحيط كسب مي گردد درهم مي آميزندو مسيررشدي فرد راترسيم مي سازند.
رشدرواني- اجتماعي برخلاف انواع ديگر رشدها رونـدي است كه در تمـام طـول عمـر ادامـه مي يابـد.
رشداجتماعي ازنظر مفهوم يعني رشدتوانائي عملكرددرگروه وپذيرفتن خواستهاي فرهنگ واجتماعي كه فرد درآن زندگي مي كند.اجتماعي شدن تابع اصل يادگيري است وهيچ كودكي ذاتأ اجتماعي زاده نمي شودبلكه اين مسئله درمسير رشد ودرطي فرصتهاي فراهم شده شكل مي گيرد.
دوره اول كودكي ( ازتولد تا سه سالگي )
رفتار عاطفي نوزاد ازحدود 4 ماهگي آشكار مي شود.در 6 ماهگي ميل به تماس با ديگران درطفل شدت مي يابد و مايل است كه او را درآغوش بگيرندو نوازش كنند.در اواخر يك سالگي با شوق و لذت منتظرمادرش مي شود و به محض ديدن او شادي مي كند. درسال دوم اين علاقه مندي به سايراشياء ماننـداسبــاب بـــازي ها ، لبــاس وچيــزهاي ديگرمعطوف مي شود.
در12 ماهگي كودك اصواتي در پاسخ به گفتگوي بزرگسالان ادا مي نمايد.بين 18ماهگي تا2سالگي كنترل رفتارطفل دشوارمي گردد زيرا بواسطه توانائي كودك درحركت وكنجكاوي شديد، هرمحركي برايش جالب بوده وگاهأ اعمالش مخاطراتي براي او ايجادمي كند.چنانكه رفتارش را محدودكنند ، ناراحتي بسيارشديدي ازخودنشان مي دهد.
رابطه با همسالان
قبل از5 ماهگي كودك نمي تواند بااطفال ديگر ارتباط برقرار كند. ميان 6 تا 8 ماهگي كودك يك سوم وقت خودش را صرف توجه به محيط اطرافش نموده و توجه چنداني به هم بازي هاي ديگرخودش نشان نمي دهد. چنانچه تماس دوستانه اي برقرار شود، محدود به نگاه كردن ، و يا چنگ زدن مي گردد.
بين 9 تا13 ماهگي كودك به اسباب بازيهايش توجه بيشتري نشان مي دهدو چنانچه هم بازيهايش بخواهنداز بازيچه هاي وي استفاده نمايند ، غالباً كودك به مقابله برمي خيزدو بين آنها نزاع درمي گيرد. هرچند، بايد اذعان داشت اين نزاع جنبه عداوت وخصومت ندارد و از روي كينه توزي و دشمني نيست.
از 14 ماهگي تا 18 ماهگي بتدريج توجه كودك به سوي همبازي هايش معطوف مي گردد و تمايل به نزاع برسر بازيچه ها كاهش محسوسي مي يابد. درمحدوده 19 ماهگي تا 2 سالگي ، كودك علاقه خود به بازي با بازيـچه ها را با علاقـه به بــازي با همـسالان درهم مي آميزد و تلفيقي از اين دو پديد ميآورد بازيهايش بيشتر و طولاني ترمي شود.
شاخصه هاي رشد اجتماعي
كودك دريك سالگي هنوز فكرمي كند همه چيز، حتي وجودپدر و مادرش به او تعلق دارد. بيشترازآنچه كه مي تواند برزبان آورد ، مي فهمد. به طوركلي كودكان درخلال سالهاي اول و دوم زندگي بتدريج بازي با يكديگر را مي آموزند.همانگونه كه قبلاً اشاره شدازحدود 2 سالگي به بعد علاقه كودك براي بازي باكودكان ديگرزيادترمي شودوكودكان ازاين پس تمايل بيشتري براي بازي با همديگرازخودنشان مي دهند.اين مسئله بويژه با رشدزبان در اين دوره ابعادوسيعتري بخود مي گيرد.رعايت نوبت وكنارآمدن نسبي باخواست ديگري، ازجمله شاخصه هاي رشداجتماعي كودكان دراين دوره مي باشد.
دوره دوم كودكي ( 3 تا 7 سالگي )
در اين دوره تغييرات مهمي در روابط اجتماعي كودك رخ مي دهد.كودكان كه درآغاز افرادي خود محور و غيراجتماعي هستند، بتدريج به افرادي اجتماعي تبديل مي شوند. دراين دوره آنها مي آموزندكه چگونه با ديگران سازگار باشند، دربازيهاي گروهي شركت كنند، و بخصوص با ديگران همكاري نمايند.درخلال بازي هاي گروهي ، روح سازگاري وكنارآمدن با ديگران تقويت مي گردد.بوسيله تقليداز الگوهاي رفتاري ديگران ، مي كوشد گفتار،كردار، و هيجاناتش را مطابق باآنان شكل دهد.كودكان دراين دوره نسبت به سرزنش و يا ستايش ديگران حساسيت و دقت فراواني ازخودنشان مي دهند.
درمحدوده 2 تا 3 سالگي كودكان دائماً درحال تغيير روابط خود با سايرافراد مي باشند. در 4 سالگي كه آنرا سن ورود به مرحله هوشياري مي دانند، براي كودكان همه چيزساده ، صميمانه و داراي علت وجودي مي باشد. اگر علت چيزي را ندانند بلافاصله سؤال مي كنند.اگربه سؤال آنها قبلاً پاسخ داده شده باشد، براي ارضاء كنجكاوي درخواست اطلاعات بيشتري را مي كنند.اكنون بيشترتمايل دارندكه نوبت را رعايت نمايند و بازيهاي دسته جمعي انجام دهند.
در 5 تا 6 سالگي كودك بدنبال روند سازگاري با دنياي اطراف ، نوعي ازهم پاشيدگي را تجربه مي نمايد.كودكان 6 ساله درواقع بيش ازكودكان 5 ساله شايستگي دارند منتها درظاهرامر بالعكس به نظرمي رسد.آنچه درفاصله 5 تا 6 سالگي موجب بروز اين تغيير مي گردد، رشدآگاهي هاي اجتماعي كودك است.در اين سن معمولاً عدم توانائي آنها دربرآوردن مداوم انتظارات بزرگسالان ، حس عدم شايستگي را درآنها تقويت مي كند.كودكان به خاطردفاع ازموضع خود و از ترس قدم گذاردن به دنياي مملو ازمشكلات بزرگسالان ، ممكن است به طريقي عمل كنند كه ناپخته تر از قبل جلوه كنند.چنانچه به كودكان توجه كافي نشان داده شودو انتظار ازآنها درسطح معقولي باشد، دراين صورت آنها اين مرحله را با موفقيت سپري خواهندكرد.
رشد گويش
يكي از عوامل بسيارمهم در امر برقراري ارتباط كلام وگفتـار است .كودك از2 تا 4 سالگي بيش از هرزمان ديگردرسخنگوئي پيشرفت نشان مي دهد.جمله هاي وي پيش از 2 سالگي ازيك واژه ، اسم ، فعل ، و يا صفت تشكيل شده است منتها درآغازدوره نونهالي مي تواند جمله هاي دو واژه اي مركب از اسم ، فعل ،صفت و…را بسازد.
جمله هاي چندكلمه اي كودك در ابتدا مبهم و نارساست اما بمرور به جمله هاي واضح وگويا تبديل مي گردد.درحدود 4 سالگي كودكان از قابليت گفتگو برخوردار مي گردند. در 5 سالگي ازنظرگفتاري اختلاف فراواني دركودكان مشاهده مي گردد.دختران درقدرت سخنگوئي اندكي برپسران برتري دارند ، معلومات لغوي دختران بيشترازپسران است ، جمله هاي مكمل و طولاني بيشتري استفاده مي كنند، و به شناختن افراد ، اشياء يا آداب ورسوم اجتماعي علاقه بيشتري نشان مي دهند. اماپس از 6 سالگي اين برتري كاهش مي يابد و پس از 6 يا 7 سالگي پسران ازلحاظ گفتاري ،درك واژه ها و معني آنها پيشرفت بيشتري نشان مي دهند.
ميانگين لغاتي كه يك كودك 2 ساله مي داند 250 و درمورد كودك 3 ساله 900 تا است .اين افزايش تعداد ، نشانگر رشدمهارتهاي يادگيري زبان در اين سن است.اغلب 2 ساله ها تاحدزيادي جملات را بصورت تلگرافي بكارمي برندو همه كلمات بجزلغات اصلي را جا مي اندازند اما در 3 سالگي جملات آنها كاملتر وساختمان جملات آنها بيشتر شبيه صحبت بزرگ ترها مي گردد. از 3 تا 4 سالگي سخنان كودك شمرده و بآساني قابل درك مي شوند.
از 4 تا 5 سالگي زبان به حدي پيشرفت مي كند كه جاي عمل را مي گيرد.كودك با استفاده ازكلام مي تواند وانمود كندكه كاري را انجام داده است. مثلاً مي گويد« بياوانمودكنيم من مادرهستم و تو بچه ومن مي خواهم تورا تنبيه كنم».دراين سن كودكان بيش ازپيش از زبان بعتوان ابزاري براي آموختن درباره چيزهاي موجود دردنياي خود استفاده مي كنند. از 5 تا 6 سالگي كودكان درمورددرك و بكارگيري زبان كمترسختگير مي شوند.بطوركلي آنها دراين مرحله دراستفاده از زبان بسيارخوب عمل مي كنند و مي تواننداز زبان براي تشريح و توضيح اعمال ، بحث ، اذيت وشوخي ، و دروغ گفتن و يا باوراندن به ديگران استفاده كنند.
نقش همسالان دراجتماعي شدن كودك
همانطوركه اشاره شد روند اجتماعي شدن كودك تاحد زيادي به تعاملات او با كودكان و بزرگسالان ، و همچنين به رشدقواي ذهني او بستگي دارد.زيادشدن روابط كودك بادنياي اطراف و بويژه باكودكان ديگر، نقش بسيارمؤثري درفراينداجتماعي شدن وي ايفاء مي نمايد.اين نقش به دو صورت خودرا نشان مي دهد.
الف) به وسيله تقويت رفتار
ب) ازطريق همانندسازي والگوي تقليد
بديهي است كه دراين فرايند عوامل ديگري كه از شخصيت طفل سرچشمه مي گيرند نيزدخالت دارند.بعنوان مثال، اطفال برونگرا وآنانكه علاقه مند به ايجاد روابط عاطفي با ديگران هستند سريع ترتحت تاًثيرهمسالان خود قرارمي گيرند و در مقابل،كودكاني كه وابستگي شديدتري به افرادخانواده خود دارندكمتر تحت نفوذ گروه همسالان واقع مي شوند. سايرشرايط موقعيتي نيز مؤثرند. وجود دوستان ممكن است سبب ايجاد احساس اطمينان دركودك شودو احساس ايمني را دروي تقويت نمايد.درحاليكه وجودهمسالان نامهربان مي تواندباعث ايجاد اضطراب ، ناكامي ، ودرنهايت كناره گيري و انزواطلبي دركودك گردد.
برخي از رفتارهاي اجتماعي كه دراين دوره بروز مي كند عبارتنداز:
 منفي گري ( negativism )
به رفتاري اطلاق مي گرددكه كودك درمقابل قدرت و اراده بزرگسالان ازخودمقاومت نشان مي دهد.سرسختي كودك نخست در 18 ماهگي مشاهده مي شود و در 3 سالگي به اوج خود مي رسداما پس از 4 سالگي سرسختي آنان كاهش مي يابد.اين تغيير رويه را شايد بتوان به حساب نفوذهاي اجتماعي دركودك گذاشت و شايد هم كودك از راه تجربه آموخته باشد كه موافقت با بزرگترها و پيروي ازآنان منافع او را بيشتر تاًمين مي كند.
 رقابت ( rivalry )
ويژگي رقابت اين است كه فردحس برتري جوئي داردو مي خواهدمقامي والاترازديگران داشته باشد.رقابت ازآنجائيكه بين افراد بوجود مي آيد، نوعي رفتاراجتماعي محسوب مي شود.روان شناسان دريافته اندكه رقابت بين كودكان 2 ساله وجودندارد.در 3 سالگي نخستين آثار رقابت ظاهرمي شود.در 4 سالگي كودكان براي كسب اهميت وبرتري بايكديگر رقابت مي كنند. در 5 سالگي كه كودكان اجتماعي تر شده اند و بيشتر باهم به كار وفعاليت مي پردازند، رقابت كاملاً محسوس تراست.


 پرخاشگري ( aggression )
پژوهشهاي روانشناختي نشان مي دهدكه اختلاف وزدوخوردكودكان خردسال براي تصاحب اسباب بازيهاي يكديگر، بيش ازهرمورد ديگراست.همچنين ثابت شده است كه كودكان 3 ساله بيش ازهمه دعوا به پا مي كنند. نكته جالب اين است كه كودكان بزرگتر بيش ازكودكان كوچكتر درمورد دعوا هراس ازخودنشان مي دهند.كودك هرچه بزرگتر شود و با اوضاع و شرايط اجتماعي سازگارتر گردد، به همان نسبت پرخاشگري و نزاع اوكاهش مي يابد.

 همكاري (cooperation )
در 2 يا 3 سالگي كودك موجودي خودمدار و پيكارجو است.بنابراين مشكل است كه او را وا داريم دربازي باكودكان ديگرهمكاري نمايد.در پايان سال سوم يا چهارم همكاري ميان كودكان افزايش مي يابد.كودك هرچه بيشتر باكودكان ديگر تماس داشته باشد و با آنان بازي كند، زودتر راه همكاري را فرا مي گيرد.رفاقت نيز تاًثيرزيادي در پديدآمدن روح همكاري دركودكان دارد.هرچه رفاقت مستحكم تر و صميمانه تر باشد ، همكاري كودك بيشتر مي گردد.

دوره سوم كودكي ( 7 سالگي تا بلوغ )
دراوائل اين دوره سني (تا 11 سالگي ) كه آنرا دوره نوباوگي ناميده اند در روابط كودكان با يكديگر، با پدر ومادران ، و بابزرگسالان ديگر دگرگوني هاي فراواني بوجود مي آيد.اين دوره از لحاظ رشداجتماعي و سازگاري كودك درآينده آنچنان داراي اهميت است كه بايدآنرا دوره اصلاح و تصحيح رفتاراجتماعي كودك ناميد.
مدرسه درمورد پيوندهاي اجتماعي همچون آزمايشگاهي به شمار مي رود و براي بسياري ازكودكان نخستين تجربه جدي گروهي و اجتماعي درخارج ازمحيط خانواده محسوب مي شود.مدرسه براي سالهاي متمادي مركزجهان خارج ازخانواده كودكان خواهدبود و بيش ازنيمي ازساعات بيداري آنها را اشغال مي نمايد.نقش مدرسه درزندگي كودك غيرقابل انكاراست زيرا نه تنها برخي ازپاسخهاي اجتماعي و ذهني قبلي اوكه والدينش به او آموخته اند را تقويت مي كند، بلكه بسياري ازپاسخهاي جديدرا نيز به او يادمي دهد. ورودبه مدرسه براي كودكان باجدائي ازمادر و محيط گرم خانوادگي همراه است. به همين خاطرمدرسه نقش مهمي دركاهش انگيزه هاي اتكائي كودك دارد.
رفتاركودكان دبستاني به ميزان زيادي بستگي به رفتارمعلمين آنها دارد.همكاري ، علاقه مندي و محبت معلم سبب ظهور ابتكار و علاقه مندي متقابل درشاگردان مي شود . اما پرخاشگري ، تهديد و بي علاقگي معلم ، مقاومت وكاهش انگيزه را دركودكان ايجاد خواهدكرد.
رابطه باگروه همسالان
پس از ورود كودك به دبستان ، همسالان نيز بتدريج در رشدو نمو شخصيت ورفتاركودك
تاًثيرات مهمي برجاي مي گذارند. گروه همسالان به كودك مي آموزند چگونــه با افـراد هم سن وسال خـودش كنــار بيايــدوچگونــه رفتــار نمايــد ،خصومت ، پرخاشگري و احساس برتري را چگونه ظاهرسازد، با رهبرگروه چه رفتاري داشته باشد يا احتمالاً چگونه نقش رهبري را ايفا نمايد.
درانتها ذكراين نكته ضروري به نظر مي رسدكه هنگام بررسي رشد در دوره هاي مختلف بايد دانست كه يك توصيف واحد از ويژگيهاي بارز يك گروه سني ، نمي تواند تمامي كودكان آن گروه را دربربگيرد. امكان داردكه تمام كودكان الگوهاي ويژه گروه سني خود را ارائه ندهند.با اين وجود، بديهي است كه رشد و تكامل هرگروه ازكودكان متاًثر از عوامل وراثتي ، اقتصادي ، اجتماعي ، و همچنين محيط فرهنگي آنها مي باشد.

تهيه وتدوين : عاطفه چلابي

The Neurodevelopment of Autism:
Recent Advances
George W. Niemann
President, Bancroft Institutes
Haddonfield, New Jersey, USA
Introduction
During the past several decades researchers have been trying to show that people with autism have definitive brain damage. However, despite the use of more sophisticated brain scanning and imaging methods that have recently become available, there is no evidence of "brain damage" per se. As Bauman (1993), who has conducted some of the most thorough and detailed neuroanatomical examination of human brains from autopsy material has stated "there is no evidence of 'brain damage' in the usual sense." Earlier Tsai (1989) had come to a similar conclusion when he reported that "results from neuropathological and brain imaging studies strongly suggest that the cerebral defect in autism is microscopic or functional, without gross neuroanatomical pathology."
Bachevalier (1994) in a very comprehensive review of numerous studies looking for cortical malformations, concluded that, " a direct role in the pathogenesis of autism seems unlikely" because no malformations confined to any specific area of the cortex could be found and they were not even present in most subjects. Yet, despite these convincing conclusions, researchers continue to look for the "holes" in the brain. Unfortunately, this kind of zealous search for neuroanatomic defects predisposes most of us to think that all people with autism must somehow be deficient because, after all, they must have damaged brains and it will only be a matter of time until technological advances produce higher resolution techniques that might find the "holes" or other anomalies in their brains.
This article argues that it is time to take a different approach and that there is much more hope for remediating the autistic brain than once thought because of recent neuroscientific findings. Fortunately, recent discoveries in the way the brain develops, from the moment of conception and during the early years, provide greater insight into the construction timetable of the human brain and the capacities and limitations imposed on behavioral and other interventions. Rather than being seen as a static event, it is important to keep in mind that the development of the brain is a dynamic process that is constantly evolving and changing in concert with the environment in which the child is placed. The limiting factors are both the biological structure of the brain as well as the environment. Limiting either one will compromise human potential. Conversely, enriching both will enhance the road to developing an individual's full potential. This paper explores the manner in which the brain develops from the point of conception, key developmental events that may be crucial to understanding the behavior of a child with autism, and the need to provide the most conducive environment to enrich brain functioning early in life and maximize the functional capacity of the individual with autism.

Neurodevelopmental Process
The earlier analysis of data typically divided gestation somewhat arbitrarily into three periods or trimesters, with little consideration of brain development. Schull and colleagues (Schull and Otake, 1986; Otake, Schull and Yoshimaru, 1991), have shown that, based on what happens from a neurodevelopmental perspective, it makes far greater sense to divide the gestational period into four "critical" periods. It can be seen from Table 1 that the four critical periods correspond to major events of brain neuronal development.
Trimester Timetable Neurodevelopmental Timetable
0 - 12 weeks Neuronal Proliferation
0 - 7 weeks
Migration of Neurons
8 - 15 weeks
13 - 25 weeks Differentiation of Neurons
16 - 25 weeks
25 - 39 weeks Continued Differentiation
26 - 39 weeks
Table 1: A comparison of the trimester periods of gestation and a timetable formulated on the basis of major neuronal stages of growth and development.
During the first few weeks of gestation neural cells begin to proliferate at an exponential rate, peaking at a rate of approximately two hundred and fifty thousand per minute. At around the eighth week, neurons begin to migrate from the deepest layer of the brain out towards the periphery or cortex. Each neuron has a specific address and it has to reach that final destination if it is to perform the functions for which it was designed. As Schull (Schull and Otake, 1986) has pointed out, cells have to be in the right place to perform their correct functions. They cannot perform correct functions if they are not in the proper place at the right time. In this regard, brain functioning (and consequently early behavior) is critically dependent upon the position of neurons in the brain or the structural composition of neuronal networks (brain matter). Therefore, if the normal sequence of development is disrupted in any way, the consequences can be far-reaching. This is especially the case when neural migration is disrupted. Schull and others (Clarren, 1990; Streissguth, Barr and Martin, 1984) have shown that radiation or alcohol ingestion during the eighth to sixteenth week of gestation produces mental retardation in over eighty per cent of cases. This is, therefore, a critical period of development that will have lifelong consequences on behavior that are irreversible.
After about the fifteenth week of gestation, when most of the neural brain matter is already laid down, the neural cells begin to differentiate or branch out. At around thirty weeks the neurons in the cerebellum begin to connect with other areas. The cerebellum is critically important for coordinating many aspects of brain processing. It is a veritable relay station, connecting with all other important brain regions. Thirty weeks is a crucial period for the all important Purkinje cells to complete their intricate connections with other neural fibers. Purkinje cells in the cerebellum are very large neurons that form extensive parallel networks with other neurons from many regions of the brain, thereby allowing coordination of functions vital to the survival of the newborn. Although developing later in the gestational timetable, the cerebellum is normally fully formed at birth, even though not yet entirely mature. Basically, the neurons begin to connect with others through further development and maturation. This period of differentiation continues as the process of myelinization (insulation of nerve fibers) begins and continues until birth and well after, into the early childhood years.
From the point of conception until birth, neural brain cells migrate and develop at different times, move to different sites, and do so at varying but quite rapid rates. It is important to keep in mind that many processes are underway during gestation -- neural cells proliferate and migrate, then differentiate, dendrites (the end branches of neural cells) and axons (the stem of neural cells) grow at varying rates, synapses (the gaps between neural cells which contain transmitter substances) form and some are lost, and myelin (a white fatty tissue) insulates axons and speeds transmission of signals. After birth the process continues, although at a relatively slower pace during the first two years of life, and then slows down in pace in the years to come and finally reaches a plateau around fifteen years.. Any invasive event that disrupts this course of development will have more profound effects if it occurs earlier in the developmental timetable, because obviously more neural tissue will be involved in such a case and the consequences on behavior will be more profound.
Neurodevelopmental Course of Autism
Most recent neurobiological data suggests that autism is caused by late disruption of the Central Nervous System (CNS) just prior to birth, perinatally, or postnatally (Bachevalier, 1994; Kemper and Baumann, 1993). When viewed from a neurodevelopmental perspective, this is very encouraging because it means that most all of the neurons have already been established and therefore very little neural tissue would be damaged or affected. It follows from what was said previously about the timing of a disruptive event that later disruption will produce less neural tissue involvement, if any at all. This certainly corroborates the findings by Tsai (1989) and Kemper and Bauman (1993) that there is no gross neuranatomic involvement in autism. It may also offer much greater hope for reversing the behavioral disturbances that occur with the syndrome of autism.
Most interestingly, data from some of the most carefully conducted studies (Kemper and Baumann,1993; Coleman, Romano, Lapham and Simon, 1985) suggest that the cortex or outer layer of the brain in autism is intact and has no structural abnormalities. Their investigations suggest that any disruption in the developing brain of someone with autism occurs before the thirty week period of gestation and specifically disrupts connections in the midbrain and brainstem areas. This is a period of time when neurons are primarily differentiating and making connections with each other from one area of the brain to another. Such interconnections are vital to the successful integration of information that accompanies typical brain information processing and adaptive behavior. Kemper and Bauman's (1993) studies indicate that the primary areas of abnormality in autism occur in two areas, the limbic system and the cerebellum and its circuits.
The limbic system plays a significant role in various aspects of emotion, memory and learning, and motivation. It includes multiple areas of the brain - the hippocampus, amygdala, mammalary bodies, anterior cingulate gyrus and nuclei of the septum. Kemper and Bauman's (1993) studies indicate that the neural cells of the limbic system in autism are small in size and more densely packed per unit volume as compared with age and sex-matched controls. Such a picture is consistent with a chronologically younger brain where the limbic system is curtailed in its development. The fact that the brain cells are so tightly packed and small suggests that the normal atrophy of some of the cells was disrupted. In any event, the consequence is abnormal information processing at this level of brain functioning.
The second major area of abnormality found by Kemper and Bauman was in the cerebellum and its many circuits and interconnections. Basically what they found was a substantial loss of Purkinje cells throughout the cerebellum, especially in the posterior regions. The loss of Purkinje cells helps establish the timing of the abnormalities. During gestation, climbing fibers start out from the olivary nucleus, located in the brainstem, and migrate to connect posteriorly with Purkinje cells. Research studies in humans suggest that these connections occur at thirty weeks of gestation. Also, once the connections are made, the system becomes one single unit (olivary nucleus, climbing fibers and Purkinje cells). Should anything happen to the Purkinje cells after the connections have been made, the entire system degenerates and atrophies. However, in the brains of people with autism Kemper and Bauman found that, even though there was a major loss of Purkinje cells, the olivary nuclei were preserved. This suggests that whatever happened to the Purkinje cells had to have happened just prior to thirty weeks of gestation. Furthermore, they also found that many of the neurons concentrated in the deep nuclei of the cerebellum, those responsible for input and output of information and communication with other portions of the brain, were abnormal. In the younger cases, the neurons appeared normal but were abnormally large ("hypertrophied") whereas in their older cases the same neurons were reduced in size in every case and there was evidence of cell loss. They hypothesized that, because of the loss of Purkinje cells, the normal circuit (i.e. olivary nucleus, connecting fibers and Purkinje cells) was not established and the autistic person had to rely on to the more primitive circuit as the dominant means of neuronal communication. Furthermore, they postulate that because the more primitive fetal circuit was not designed for adult life, they become enlarged (hypertrophied) in response to extended demand and may eventually "burn out" and die. This would especially be the case if there was no attempt to modulate the stimuli reaching the young autistic brain and cause it to become overtaxed and unable to handle external demands. On the other hand, a program designed to deliver stimuli or information in a carefully modulated manner would give the autistic brain a better opportunity to process the information more adaptively without the overload. It would give the developing brain an opportunity to establish more normal circuitry through the brain structure - brain function inter-relationship. It is well known that brain structure initiates brain function, but that structures only develop appropriately if they are in turn stimulated by external environmental events (Hudspeth and Pribram, 1992). The structure and function cycle is crucial for the growth and maturation of the brain and, consequently, adaptive behavior. Obviously any program designed to enhance the more normal growth and development of the brain increases the probability for more normative brain-behavior functioning. How much can be done to establish normal brain development and functioning in someone with autism, from a purely neuroscientific viewpoint, still remains to be seen. More research is obviously needed in this area to definitvely answer this question. Nevertheless, the findings reviewed in this paper suggest that much can be gained if the appropriate program is used with autistic children, starting at a very early age and applying the correct technique intensively for a duration of several years.
Subclassification of Autism
A review of the most carefully controlled neuroscientific studies (Bachevalier, 1994) using various methods such as autopsy material, brain scanning and imaging (MRI, CAT, PET, SPECT, rCBF) suggest that it may be helpful to divide autism into two distinct subclasses: Type1, where there are distinct neurologic signs and varying ranges of mental retardation (encompassing approximately 60-70% of the autistic population); Type 2, where the CNS is anatomically intact and there is no mental retardation (encompassing approximately 30-40% of the autistic population). Obviously a continuum from severe functioning deficits to very minor exists in the autism population. DeLong (DeLong and Nohria, 1994) has appropriately described this phenomenon as the "spectrum" of disorders in autism. The two sub-types should be seen as fitting into such a spectrum or continuum.
It makes greater sense to subclassify autism in the above manner when the neurodevelopmental evidence is taken into consideration. For example, we know from the earlier discussion about critical periods, particularly during 8-16 weeks of gestation, that mental retardation is most likely to occur if any event interferes with the process of neuronal migration. This earlier onset disruption of the developing fetus, regardless of the cause, would produce more severe consequences. This type of disruption would affect many brain areas and have definite abnormalities such as those seen by Kemper and Bauman (1993). Cells in the limbic system (amygdala, hippocampus, cingulate, septum) would most likely be affected. The development of the Purkinje cells and deep cerebellar nuclei would also undoubtedly be affected. In this case, many neural circuits would not be properly formed and brain functioning would therefore be compromised later in life. The blend with mental retardation would make it difficult to reverse the brain functioning difficulties found with such people. Level of improvement would obviously be influenced to a very large extent by the degree of brain impairment.
In the second type of autism proposed, any disruptive event would have to occur later in the gestational timetable and would, therefore, hardly disrupt brain development at all. In this case there would be no anatomical abnormalities as the neural structures would be fully formed. Therefore, we would expect to find very subtle anatomical signs, if any, as has been reported by Kemper and Bauman (1993) and Tsai (1983). Most likely the major problem related to brain functioning would be dysfunction of the neurotransmitter system where the chemical substances responsible for conducting nerve impulses across synapses would be affected. Such a situation is much easier to reverse or correct, either through pharmacological therapy, by activating the correct pathways in the young brain that produce normative brain development, or both.
Predicting Successful Outcomes
The neurodevelopmental findings discussed previously, when combined with the growing clinical and experimental evidence on the memory systems necessary for learning, can help us understand the most effective ways to teach youngsters with autism and produce more successful outcomes. For example, the work of Mishkin and others (Mishkin and Appenzeller, 1987; Zola-Morgan and Squire, 1993; Bachevalier, 1990) has shown that there are basically two types of memory systems which underlie successful learning. The first has been referred to as "habit, rote, or procedural" memory. This system develops early and becomes functional during the first months of life in humans. It is the kind of memory we use for skill learning and is acquired by repeated presentation of the same stimulus until the task is correctly stored and accessed in memory and thereby learned. The striatum and neocortex of the cerebral hemispheres are the areas which mediate this kind of memory. It will be recalled that both of these brain structures have been found to be anatomically intact and normal in the brains of children with autism.
The second type of memory evident from the work of Mishkin and his colleagues has been termed the "representational, associative, or cognitive" system, which is anatomically distinct from the "habit or procedural" type mentioned previously. Most importantly though, Mishkin states that the "representational" system coordinates all of the sensory modalities, including the processing of experiences and events, and the generalization of such information which leads to higher-order cognition and learning. This "representational" system depends on the integrity of the lmbic system, especially the amygdala and hippocampus and areas connected to them. Any disruption to these connections or limbic areas would interfere with the acquisition and meaning of information obtained from the continual presentation of novel stimuli typical in the daily life of a developing infant and child. There is little doubt that disturbances in the CNS which would disrupt the "representational" system would lead to disorganized cognition, problems with modulation of sensory events, inapproprite social interaction and abnormal language development. These are the features so typical of autism.
From what has beeen discussed so far in this paper, conclusions can be drawn as follows: a). Children with autism, particularly those that fall into the Type 2 classification (probably also a large number of the Type 1) have intact brain cortices and, therefore, their habit, rote, or procedural memory systems should be intact. They should be fully capable of acquiring skills through repeated presentation of stimuli until tasks are properly learned. They will appear to be quite normal during their first few years of life and then show difficulty acquiring language and social skills because of disorders in their limbic system and cerebellum disrupting "representational" memory functions. However, due to the nature of the late onset of disturbances in brain development, they should be prime candidates for recovery if given the appropriate treatment early in life (certainly starting at around two years of age or soon thereafter) so that their limbic and cerebellar circuits can be activated and they can utilize their associative or representational learning systems. This would allow them to form basic cause-effect relationhips, associations and generalizations so crucial to adaptive behavior functioning. b). Children with autism falling into the Type 1 class who most likely had earlier onset disruption of a critical period of brain development (most likely starting early in gestation during the 8-16 week period) and therefore different levels of mental retardation complicating their autism, would have less probability for full recovery. However, if their cortical brain areas are intact, they too would be quite normal in their first two years of development and they would have normal rote or habit learning. They should, therefore, acquire early rote learning skills easily, provided they are placed in an environment ideally suited to maximize such learning through repeated presentations of stimuli. Once they acquired the necessary rote learning, which is a prerequisite to the higher-order or associative learning sytem, they could then be taught to use the latter, depending on the integrity of their limbic circuits. The best way to determine how much these children would be constrained in their learning would be by screening them comprehensively with neurodiagnostic techniques. Those children discovered to be neuroanatomically "intact" would undoubtedly experience the most success following intensive teaching and training. Those with neurological involvement would learn skills to a lesser extent, yet still profit greatly from intensive early intervention.
What follows, therefore, from the above discussion is the critical need to carefully screen children suspected of having autism, at the earliest possible moment in life, using thorough neurodiagnostic methods. This will assist in predicting learning potential and recovery to a great extent. Also, just as important, is the need for early intervention or therapy which will allow the youngster with autism to maximize rote learning capabilities and then move on to higher-order, associative, learning. Since the ability to transfer skills from the rote to the associative stages is critically dependent upon the interaction of brain maturation and stimulation from the outside environment, it is crucial that the correct teaching strategies be started early, that they be presented consistently and repeatedly over most of the time the child is awake and functioning, and for several years in duration. We know from neuroscientific evidence that neuronal networks develop and mature very slowly over time in humans. Any lasting changes to such a slow developing system takes many years (Hudspeth and Pribram, 1992). Given what we know of brain development and what has been discussed in this paper, it is hard to conceive of any techniques of teaching or remediation that will be effective with the autistic child unless they meet these conditions. This kind of knowledge ertainly argues very strongly against any short, or brief, therapies being capable of establishing long-lasting changes in brain functioing and behavior.
Fortunately, several recent studies (Lovaas, 1987; Perry, Cohen and DeCarlo, 1995; Wetherby, Koegel and Mendel, 1981; Luce, Niemann, Wright, and Dyer, 1995) support the notion that early, intensive therapy of several years duration are most effective in treating autism. These methods not only meet the criteria of early intervention and intensity over time but also start out by teaching rote learning skills in an ideal format of repeated presentation, at the correct pace, along with numerous contingencies of optimal reinforcement. Following the acquisition of basic rote skills, such programs then move on to the higher-order associative skills which allow generalization and the development of more adaptive behaviors necessary for independent daily functioning. These studies, in effect, follow the ideal course of brain development and employ the best principles of brain maturation and development. Little wonder, then, that they can achieve such good outcomes and report various levels of recovery from earlier autistic behaviors.
From what has been presented in this paper, it can be argued that autism should be reversible, possibly in at least 40 to 50% of cases, provided they are properly identified, carefully screened neurologically, and provided early intervention that is intensive on a daily basis and lasts several years. This is the encouraging news. However, it also raises a dilemma because we know from brain development that there is a narrow window of opportunity to achieve optimal results. Waiting until the child is five or six years old may be too late because the brain may already have passed the stage of plasticity which would allow it to benefit from any remedial technique, no matter how intensive. Any child with autism who is not given early intervention of an intensive nature may, therefore, be deprived of an opportunity to change later in life. This may lead to permanent disabilities that will continue to exact more costly emotional and economic costs on the individual, his family, and society. It also raises the issue of neglect for those cases that never get appropriate therapy. Such issues will undoubtedly keep debate alive in this area for years to come. Nevertheless, it is hoped that the recent findings in the neurosciences that have been reviewed in this paper and offer so much hope for improvement, will lead to more urgently needed research and to a greater understanding of autism and how best to maximize functioning for people born with this syndrome.
References
Bachevalier, J. (1994). Medial temporal lobe structures and autism: A review of clinical and experimental findings. Neuropsychologia, 32, 627-648.
Bachevalier, J. (1990). Ontogenetic development of habit and memory formation in primates. In Development and Neural Bases of Higher Cognitive functions. A Diamond (Ed.), New York Academy of Science, New York, pp.457-484.
Bauman, M.L. (1993). Understanding autism through neuropathologic studies. Keynote address; Annual Conference of the New Jersey Center for Outreach & Community Services, Princeton, NJ,
Clarren, S.K. (1990). Fetal alcohol syndrome: diagnosis, treatment and mechanisms of teratogenesis. In Transplacental disorders: Perinatal Detection, Treatment and Management. Alan R. Liss, Inc., pp. 37-55.
Coleman, P.D., Romano, J., Lapham, L., & Simon, W. (1985). Cell counts in cerebral cortex in an autistic patient. Journal of Autism and Developmental disorders, 15, 245-246.
DeLong, G. R., and Nohria, C. (1994). Psychiatric family history and neurologic disease in autistic spectrum disorders. Developmental Medicine and Child Neurology, 36, 441-448.
Hudspeth, W.J., and Pribram, K.H. (1992). Psychophysiological indices of cerebral maturation. International Journal of Psychophysiology, 12, 19-29.
Kemper, T.L., and Bauman, M.L. (1993). The contribution of neuropathologic studies to the understanding of autism. Behavioral Neurology, 11, 175-187.
Luce, S.C., Niemann, G.W., Wright, S., and Dyer, K. (1995). A comparison of two delivery models of early and intensive intervention with young autistic children; preliminary data. World Congress of Behavioral & Cognitive Therapy, Copenhagen, Denmark.
Lovaas, O. I. (1987). Behavioral treatment and normal educational and intellectual functioning in young autistic children. Journal of Consulting and Clinical Psychology, 55, 3-9.
Mishkin, M., and Appenzeller, T. (1987). The anatomy of memory. Scientific American, 256, 80-89.
Otake, M., Schull, W.J., and Yoshimaru, H. (1991). brain damage among the prenatally exposed. Journal of Radiation Research, Supplement, 249-264.
Perry, R., Cohen, I, and DeCarlo, R. (1995). Case Study: Deterioration, autism and recovery in two siblings. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 232-237.
Schull, W.J., and Otake, M. (1986). Effects of radiation on the developing nervous system. In Radiation risks to the developing nervous system, K. Krieger et. al., (Eds.) Gustav Fischer Verlag, Stuttgart, pp. 399-419.
Streissguth, A.P., Barr, H.M., and Martin, D.C. (1984). Alcohol exposure in utero and deficits in children during the first four years of life. In R. Porter, M. O'Conner, and J. Whelan (Eds.), Mechanisms of alcohol damage in utero. Pitman Publisihing, London, pp.176-196.
Tsai, L.Y. (1989). Recent neurobiological findings in autism. Paper presented at the State-of-the-Art Conference on Diagnosis & Treatment of Infantile Autism. Gothenberg, Sweden.
Wetherby, A.M., Koegel, R.L., and Mendel, M. (1981). Central auditory nervous system dysfunction in echolalic autistic individuals. Journal of Speech and Hearing, 24, 420-429.
Zola-Morgan, S., and Squire, L.R. (1993). The neuroanatomy of memory. Annual Review of Neurosciences, 16, 547-563.
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Occupational Therapy
and the
Child with Down Syndrome
by Maryanne Bruni, BSc OT(C)

Copyright 2001, All rights reserved


If you are a parent reading this web site, you likely have a child with Down syndrome, as I do. My intent with this article is to provide you with some information about how an occupational therapist (OT) may be able to help you and your child. Occupational therapists who work with children have education and training in child development, neurology, medical conditions, psychosocial development, and therapeutic techniques. Occupational therapists focus on the child's ability to master skills for independence. This can include:
• self care skills (feeding, dressing, grooming etc.)
• fine and gross motor skills
• skills related to school performance (eg: printing, cutting etc.)
• play and leisure skills
When your child is an infant, your immediate concerns relate to his health and growth, development of the basic motor milestones, social interaction with you and others, interest in things going on around him, and early speech sounds and responses. At this stage an OT may become involved to:
• assist with oral-motor feeding problems (this can also be addressed by Speech Pathologists). Due to hypotonia and weakness of the muscles of the cheeks, tongue and lips, feeding is difficult for some infants with Down syndrome. OTs suggest positioning and feeding techniques, and can be involved in doing feeding studies, if necessary.
• help facilitate motor milestones, particularly for fine motor skills. Occupational therapists and Physical therapists work closely together to help the young child develop gross motor milestones (eg: sitting, crawling, standing, walking).OTs work with the child at this stage to promote arm and hand movements that lay the foundation for later developing fine motor skills. The low muscle tone and loose ligaments at the joints associated with Down syndrome are real challenges to early motor development and occupational therapy can help your child meet those challenges.
When your child is a toddler and preschooler, she will likely have some independent mobility and will be busy exploring her environment. To assist her development you will want to provide her with many opportunities for learning, you will want to encourage the beginning steps in learning to feed and dress herself, you will want her to learn how to play appropriately with toys and interact with other children, you will be encouraging speech and language skills, and you will continue to provide opportunities for refinement of gross motor skills. At this stage an OT may become involved to:
• facilitate the development of fine motor skills. This is an important stage in the development of fine motor skills for children with Down syndrome. Now they will be developing the movements in their hands that will allow them to do many things as they get older, but many children need some therapy input to ensure that these movements do develop. Children do this through play; they open and close things, pick up and release toys of varying sizes and shapes, stack and build, manipulate knobs and buttons, experiment with crayons etc. Your child may face more challenges learning fine motor skills because of low muscle tone, decreased strength and joint ligament laxity.
• help you promote the beginning steps of self help skills. An OT can help parents break down the skills so expectations are appropriate, and can suggest positioning or adaptations that might help the child be more independent. For example, a child may have more success feeding herself with a particular type of spoon and dish.
Then your child enters the school system and the focus of your energies changes somewhat again! You help your child adjust to new routines, you attend school meetings to plan your child's educational program, you focus on speech and communication, you help your child practise fine motor skills for school (such as learning to print), you expect your child to develop more independence in self help activities, and you search out extracurricular activities that will expose your child to a variety of social, physical and learning experiences. At this stage an OT may become involved to:
• facilitate fine motor skill development in the classroom. Many OTs work in the school system and provide programs to help children with Down syndrome learn printing, handwriting, keyboarding, cutting etc. They will also look at physical positioning for optimal performance (eg: desk size etc.) and assist with program adaptations based on the child's physical abilities.
• facilitate self help skills at home and at school. As with all children, our kids with Down syndrome vary in personality, temperament, and motivation to be independent. Some children with Down syndrome have a desire to do things themselves, such as dress and feed themselves. These children may learn these skills by watching others and participating from a young age. Other children may be happy to let others do things for them, and may resist attempts to help them learn these skills. In these cases an OT may be able to help a parent work out these challenges, while helping the child develop better motor skills to be successful in self help skills.
• address any sensory needs your child may have. Sometimes a parent has a concern about things their child does that may relate to the child's sensory development. For example, a child may excessively put toys in her mouth, she may have poor awareness of her body in space, she may squeeze everything too hard or drop things a lot, or she may not tolerate very well some routines like washing and brushing hair. An OT can offer suggestions to help the child and parents deal with these issues.
As parents we must be concerned with the well-being of our child in all respects. We have so many things to think about and keep track of: medical and dental needs, motor and communication needs, educational needs, advocacy, social and behavioral needs : the list seems to go on and on! We need the help of trained professionals to guide us and to work with our children to help them achieve their potential in life. An occupational therapist is one member of the team that we can rely on to provide professional assistance throughout the growth and development of our children. In Canada, occupational therapy services for children with Down syndrome can be accessed through hospitals, home care programs, infant development programs, specialty nursery schools, public schools, and through private therapy services.
(Editor's note: In the US, OT services can be obtained through Early Childhood Intervention programs, public and private schools, and from private therapists.)
Further information about fine motor development can be found in my book "Fine Motor Skills in Children with Down Syndrome", published by Woodbine House (800-843-7323) in 1998.



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Looking At Metabolism

by Joan E. Medlen, R.D., L.D.

Joan E. Medlen, R.D., L.D., is the mother of two boys, one of whom has Down syndrome.
She is a registered, licensed dietitian in private practice in Oregon and frequent speaker
at Down syndrome symposiums. This article was originally published in the journal
Disability Solutions, Volume 1, Issue 3, Sept/Oct 1996. Reprinted here with permission.
© 1996

In the first weeks after our son with Down syndrome was born, my thoughts strayed to his health throughout his life. My impression was that all adults with Down syndrome were very obese. As a dietitian, most of my work had been in the weight management area. I had seen first-hand the effects long-term obesity had on a person's life. I remember emphatically explaining to my husband that we needed to be an aerobically active family. I asked him to consider cross-country skiing instead of downhill skiing, and to plan for activities like family biking trips.
Now, seven years later, Andy is a slender, tall boy, like his brother. He eats well, but not perfectly. He appears "active," but it's not very aerobic. And, when I look at other children with Down syndrome at conferences and in my community, there seems to be a mix of body types: some are slight and petite, some are thick and stocky, and some are overweight. Where did that early image of obese adults come from? Had I fallen for a myth? Could it be that this younger generation of persons with Down syndrome will not have as many obese adults? Has the increase in community inclusion changed the incidence of obesity?
Probably not. Research suggests children with Down syndrome are as active as their peers, yet use fewer calories overall. They appear to have a lowered Basal Metabolic Rate, which is the rate a person burns calories for fuel when completely at rest - or sleeping. This means that children with Down syndrome use less energy when they are resting or sleeping.
Taking that information one step further, it means that they use fewer calories throughout the day to accomplish the same activities as their normal peers. When Andy hangs out with his friend, and eats the same amount and kind of foods, does the same activities with the same intensity for the same amount of time, he will burn up to 15% fewer calories than his buddy. Since he ate the same amount of food as his buddy, but needs less to do the job, he has calories left over. These extra calories - even as few as 50 calories a day - can lead to an increase in weight. For example, 50 calories is equal to a half of a large Red Delicious Apple. The calories from half an apple left over at the end of the day for one year will lead to about 5 pounds of increased weight. If that continues for 5 years, it becomes a troublesome 25 pounds. With this in mind, it is easy to see how slender children and adolescents with Down syndrome can change into overweight young adults.
There are three ways to adapt for this difference in metabolism:
• Increase activity
• Limit calories
• Increase activity and limit calories.
Focusing on Calories alone is one option. However, unless there are other medical reasons, it is risky to limit calories for children under 18 years of age without direct medical supervision. Children have great vitamin, mineral, protein, carbohydrate and energy needs while they are growing. Limiting calories may cause children to get too few of what they need to grow and develop well. For adults, a sole focus on calories becomes a battle of will-power, and feels like a punishment.
As with everything else, focusing on positives and abilities has a far greater effect. Beginning with a focus on physical activity has many more positives. A person can choose from a variety of aerobic activities that are enjoyable. Additionally, regular aerobic activity has many health benefits: increased muscle tone, decreased resting heart rate, decreased blood pressure, a sense of well-being , better sleep, and an increase in metabolism.
Being physically active, and focusing on aerobic activity doesn't mean you need to be an Olympian athlete. For the average person, with or without Down syndrome, adding small amounts of aerobic activity on a regular basis makes a difference. Even small changes in daily activities can be beneficial.
Ideas for adding aerobic activity:
For parents, adults, and children:
• Park farther away from where you are going
• Take the stairs instead of the elevator. My son and I are often seen taking the stairs up and the elevator down -- many times.
• Walk or bike to activities that are in your community.
• When you go to the park, play "tag" for 10 minutes with the kids. Don't catch them, just chase them around. Parents think of swinging and climbing the play structure as being active. It's not aerobic activity, except when running between structures.
For teenagers and adults:
• Use a push mower to mow the lawn.
• Go on a long walk, hike, or bike with a friend once a week.
• Join a local recreation facility.
• Join a walking club.
• Create some rules: for every one hour of TV watched, go for a walk around the block. (Be prepared to live by the same rules.)
Coming up with ideas to increase activity is the easy part. The hard part is choosing activities that are motivating. It is important that the person with Down syndrome make the choice of activity and be involved in setting the goals. The important part is to keep moving and have fun!
Working together as a team in the plans for activity will help. Sit down and make plans together. Write them down in a special place. Create a list of 3 small, but specific activities to add in a week. Begin with things that are 99% achievable. Talk about when these activities will be done and who they will be done with, if appropriate. Write them on the calendar. Then, create a way to keep track visually as those goals are met with a chart or check list. Remember to leave room for doing more than the goals you write down - a chance to over achieve!
For Andy, we hope to build habits that will last a lifetime, and be fun. Habits that will increase his activity overall, and hopefully, reduce the risk that he will have to fight the battles that extra weight can bring. And ours too.
Reference: Luke, A., Rozien, N.J., Sutton, M., Schoeller, D.A. Energy Expenditure in children with Down Syndrome: Correcting Metabolic Rate for Movement. Journal of Pediatrics, Vol. 125, 1994.



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Last Updated:
Sep 20, 2000 Mosaic Down Syndrome

by Dr. Len Leshin, MD, FAAP
Copyright 1997, 2000, All rights reserved



Before reading this essay on the mosaic form of Down syndrome, you should be familiar with how typical Down syndrome occurs. If you aren't, take the time to read through my essay on the origin of Down syndrome.



What is Mosaicism?
Every cell in the human body comes from one initial cell: the fertilized egg, which is also called the zygote. After fertilization, the zygote then proceeds to divide. As new cells form, the chromosomes duplicate themselves so that the resulting cells have the same number of chromosomes as the original cell. However, mistakes sometimes happen and one cell ends up with a different number of chromosomes. From then on, all cells originating from that cell will have the different chromosomal number, unless another mistake happens. (All like cells originating from a single type of cell is called a cell line; for example, the skin cell line, the blood cell line, the brain cell line, etc.)
When a person has more than one type of chromosomal makeup, that is called mosaicism, like the mosaic style of art in which a picture is made up of different colors of tiles. In Down syndrome, mosaicism means that some cells of the body have trisomy 21, and some have the typical number of chromosomes.

How is Mosaicism Diagnosed?
The usual way in which mosaic Down syndrome is discovered is through genetic testing of the baby's blood. Typically, 20 to 25 cells are examined. If some of the cells have trisomy 21 and some don't, then the diagnosis of mosaicism is made. However, this blood test can only determine the level of mosaicism in the blood cell line.
While mosaicism can occur in just one cell line (some blood cells have trisomy 21 and the rest don't), it can also occur across cell lines (skin cells may have trisomy 21 while other cell lines don't). In the latter case, it may be more difficult to diagnose mosaicism. When mosaicism is suspected but not confirmed through the blood test, other cell types may be tested: skin and bone marrow are most commonly the next cells checked. Because skin cells and brain cells arise from the same type of cell at the beginning of fetal development (ectoderm), many doctors believe that skin cell tests reflect the chromosomal makeup of the brain cells as well.

How Does Mosaicism Happen in Down Syndrome?
There are two different ways mosaicism can occur:
• The initial zygote had three 21st chromosomes, which normally would result in simple trisomy 21, but during the course of cell division one or more cell lines lost one of the 21st chromosomes.
Here's a diagram of this method.
• The initial zygote had two 21st chromosomes, but during the course of cell division one of the 21st chromosomes were duplicated.
Here's a diagram of this method.
It's possible to determine the origin of mosaicism in individual cases using special DNA markers, but this isn't done on a regular basis.
What Does Mosaicism Mean for my Child?
At the present time, there is not much research on the similarities and differences between simple trisomy 21 and mosaic trisomy 21. One report published in 1991 on mental development in Down syndrome mosaicism compared 30 children with mosaic Down syndrome with 30 children with typical Down syndrome. IQ testing showed that the mean IQ of the mosaic group was 12 points higher than the mean of the non-mosaic group. However, some children with typical Down syndrome did score higher on the IQ tests than some of the children with mosaic Down syndrome.
The Department of Human Genetics at the Medical College of Virginia has had an ongoing study project of children with mosaic DS. In a survey of 45 children with mosaicism, they found that these children did show delayed development compared to their siblings. When 28 of these children with mosaicism were matched up with 28 children with typical Down syndrome for age and gender, the children with mosaicism reached certain motor milestones earlier than children with typical DS, such as crawling and walking alone. However, the speech development was equally delayed in both groups.

Resources
The Department of Human Genetics at the Medical College of Virginia/Virginia Commonwealth University has a very nice booklet on this topic that is available free of charge. Contact Dr. Colleen Jackson-Cook or Lauren Vanner at:
Dept of Human Genetics
Virginia Commonwealth University
P.O.Box 980033
Richmond, VA 23298-0033

The National Mosaic Down Syndrome Association is a new organization devoted to support and research of this form of Down syndrome.
References
1. Understanding the mechanism(s) of mosaic trisomy 21, by using DNA polymorphism analysis. Pangalos C et al. Am. J. Hum. Genet. 54:473-481, 1994.
2. Mental Development in Down Syndrome Mosaicism. Fishler K and Koch R. Am. J. Mental Retardation 96(3):345-351, 1991.
3. Medical Care in Down Syndrome, Rogers PT and Coleman M, Marcel Dekker, NY, 1992; p14-16.



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Is Asperger’s syndrome/High-Functioning Autism necessarily a disability?
Simon Baron-Cohen
Departments of Experimental Psychology and Psychiatry,
University of Cambridge
Invited submission for Special Millennium Issue of Developmental and Psychopathology Draft: 5th January 2000
Acknowledgements: I am grateful to Bridget Lindley, David Andrews, Liane Holliday-Willey, Chris Wilson, Temple Grandin and Therese Jolliffe, for discussion of these ideas. David Andrews can be credited for having introduced this topic at an early point, whilst Uta Frith and Franky Happe can be credited for their influential notion of 'cognitive style'. Finally, Dante Cicchetti and Alan Sroufe provided excellent editorial advice.
Abstract
This article considers whether Asperger Syndrome (AS) or high-functioning autism (HFA) necessarily lead to disability or whether AS/HFA simply lead to 'difference'. It concludes that the term 'difference' in relation to AS/HFA is a more neutral, value-free, and fairer description than terms such as 'impairment', 'deficiency' or 'disability'; that the term 'disability' only applies to the lower functioning cases of autism; but that the term 'disability' may need to be retained for AS/HFA as long as the legal framework only provides financial and other support for individuals with a disability. Two models are summarized which attempt to define in what way individuals with AS/HFA are 'different': the central coherence model, and the folk psychology-folk physics model. The challenge for research is to test the value of such models and to precisely characterise the differences in cognitive style.
We have grown familiar with the idea that autism is a 'psychiatric condition', a 'disorder', a 'disability' or a 'handicap'. Ever since Kanner's description of the 'aloneness' of these children , psychiatry has labelled and categorised them as abnormal, ill, and deficient. Through the changing definitions of autism enshrined in successive editions of both DSM (Diagnostic and Statistical Manual, published by the American Psychiatric Association) or ICD (International Classification of Diseases, published by the World Health Organisation), we have had a single view of autism thrust upon us: an essentially negative view in which children or adults with autism are characterised as "impaired" .
This article challenges the received view through a subtle but important shift of emphasis. Rather than conceiving of autism as a deficiency, it instead considers if autism might be better characterised as a different cognitive style. This important idea can be traced to Uta Frith's book , and has been recently discussed in relation to 'central coherence' theory , but deserves a fuller discussion because of the massive implications of this shift of emphasis. Using the term "different" rather than "deficient" may seem unimportant (after all, both words begin with 'd', end in 't' and have 7 letters in between). But this small shift could mean the difference between whether the diagnosis of autism is received as a family tragedy, akin to being told that the child has some other severe, life-long illness like diabetes or haemophilia, or whether the diagnosis of autism is received as interesting information, akin to being told that the child is right or left-handed. In this millennium special issue of Development and Psychopathology, the intention is to highlight this as an issue for the agenda.
Asperger's syndrome (AS) and High-Functioning Autism (HFA)
Autism is diagnosed on the basis of abnormalities in the areas of social development, communicative development, and imagination, together with marked repetitive or obsessional behaviour or unusual, narrow interests . Individuals with autism may have an IQ at any level. By convention, if an individual with autism has an IQ in the normal range (or above), they are said to have 'high-functioning autism' (HFA). If an individual meets all of the criteria for HFA except communicative abnormality/history of language delay, they are said to have Asperger's syndrome (AS). In this paper, we focus on AS and HFA since we accept that an individual who is lower-functioning necessarily has a disability in the form of retardation. What is not clear, and therefore the subject of the debate presented next, is whether individuals with AS/HFA necessarily have a disability. For the present purposes, we consider the arguments in relation to AS and HFA, without attempting to draw any distinction between these.
The arguments for viewing AS/HFA as a difference rather than a disability
1. The child spends more time involved with objects and physical systems than with people (Swettenham et al., 1998);
2. The child communicates less than other children do;
3. The child tends to follow their own desires and beliefs rather than paying attention to, or being easily influenced by, others’ desires and beliefs (Baron- Cohen, Leslie & Frith, 1985);
4. The child shows relatively little interest in what the social group is doing, or being a part of it (Bowler, 1992; Lord, 1984);
5. The child has strong, persistent[2] interests;
6. The child is very accurate at perceiving the details of information (Plaisted, O'Riordan & Baron-Cohen, 1998a; Plaisted, O'Riordan & Baron-Cohen, 1998b)
7. The child notices and recalls things other people may not (Frith, 1989);
8. The child’s view of what is relevant and important in a situation may not coincide with others (Frith, 1989);
9. (dates, . The child may be fascinated by patterned material, be it visual (shapes), numeric timetables), alphanumeric (number plates), or lists (of cars, songs, etc.);
10. The child may be fascinated by systems, be they simple (light switches, water taps), a little more complex (weather fronts), or abstract (mathematics);
11. The child may have a strong drive to collect categories of objects (e.g., bottletops, train maps), or categories of information (types of lizard, types of rock, types of fabric, etc.); and
12. The child has a strong preference for experiences that are controllable rather than unpredictable.
The list could be expanded but these 12 behavioural features are sufficient to illustrate that children with AS/HFA are different in ways that can be described in value-free terms: none imply any necessary disability. Rather, most of the above facts show the child as immersed in the world of things rather than people. This might be a basic way of defining the difference between a person with an autism spectrum condition and one without it .
Being more object-focused than people-focused is clearly only a disability in an environment that expects everyone to be social. But a moment's reflection highlights the injustice of this expectation. Thus, people who show the opposite pattern (of being more people-focused than object-focused) are not necessarily considered disabled. On this view, people with AS/HFA would cease to be disabled as soon as society's expectations change. For example, a child with AS/HFA who prefers to stay in the classroom poring over encyclopaedias and rock collections during break-time, when other children are outside playing together, could simply be seen as different, not disabled. It is not clear why the child with AS/HFA is seen as doing something less valuable than the other children or why their behaviour should be seen as an index of impairment.
Equally, a child with AS/HFA who has strong narrow interests of an unusual nature (learning the names of every kind of bird) may be different to a typical child who has only been interested to learn the names of common animals. But surely the narrow deep knowledge is no less valuable than the broad, shallower variety, and certainly not a necessary index of deficit? A final example should help drive this point home. Just because a child with AS/HFA notices the unique numbers on lamp-posts which the rest of us are unaware of, does this make him impaired? We could say it is simply different. The same argument can be applied to all of the other facts listed above.
II. The neurobiology of AS/HFA is not better or worse than in typical development.
AS/HFA involves a range of neural differences. A full review of these is beyond the scope of this article, but the reader can consult other excellent summaries . In some regions of the brain increased cell density has been found , - for example, in the limbic system - whilst in other regions of the brain structures are reported to be smaller. For example, the cerebellar vermis lobule 7 and the posterior section of the corpus callosum have both been reported to be reduced in size in autism. However, whilst these neural abnormalities signal differences between brains of people with and without AS/HFA, they cannot be taken as evidence that one type of brain is better or worse than the other.
Similarly, AS/HFA appears to be strongly familial, implying a genetic aetiology, and the first report from an international molecular genetic consortium study reported a linkage on Chromosome 7 in affected individuals . The molecular genetic basis of AS/HFA remains to be worked out in detail, but again such findings are at best evidence of difference and in no way implies that the genotype of AS/HFA is deficient.
III. 'Difference' avoids value-laden judgements
Many features of AS/HFA may be redescribed in ways that are more neutral, in terms of AS/HFA comprising a different 'cognitive style', with no implication that this is better or worse than a non-autistic cognitive style . For example, the AS/HFA cognitive style may be described as being more object-oriented, and more focused on detail. Another change in terminology is that the term 'autistic spectrum disorders' is being replaced by the term 'autistic spectrum conditions'. Like the term 'cognitive style', this avoids the possibly pejorative associations of the term 'disorder', though it may be questioned whether even using the term 'condition' is an appropriate medicalizing of an individual's cognitive style. But the spirit of such changes in terminology is clear. It is possible to describe AS/HFA in value-free ways.
IV. The difference view is more compatible with the 'continuum' concept
A further argument for favouring the difference view over the disability view is that it is easier to accommodate within the now widely accepted notion that autism appears on a continuum . The notion of a continuum assumes that there is an underlying dimension or set of dimensions along which all people vary. There is still debate over precisely what constitutes the underlying dimension. Later in the paper we consider two models which aim to characterise the autistic spectrum.
Arguments for viewing AS/HFA as a disability rather than a difference
1. Differences are caused by cognitive deficits
The obvious first rejoinder to the difference argument is that children with AS/HFA show differences precisely because they are disabled, impaired, suffer cognitive deficits, etc. Thus, one might argue that they are less influenced by others because they do not spontaneously stop to consider other people's points of view, feelings and thoughts (the theory of mind deficit) ; they may communicate less and may be less socially focused for the same reason; their unusual perception may arise because of their "weak" central coherence ; whilst their strong interests may reflect a "failure" to switch attention flexibly, possibly as a sign of their "executive disorder" . For all these reasons, the rejoinder goes, we should retain the notion of AS/HFA as a disability.
This could be regarded as unfair because there may be a chicken-and-egg problem in the logic. We cannot yet prove that their difference is due to a disability and not the other way around. For example, is their "mindblindness" the cause of them being less socially-focused/more object-focused, or a consequence of it? The development of a mind-reading skill may require months of social input so a lack of early social interest could contribute to mindblindness. One could make a similar case in relation to their weak central coherence: Is this a cause of their relatively greater interest in detail , or simply a consequence of it?
2. Lack of social interest reflects disability
Here is a second argument for seeing AS/HFA as a disability: the absence of a behaviour may itself reflect a disability in that area. In this case, the lack of normal sociability or communication is seen as a sign of disability. But this can be seen as unfair: it calls attention to what someone does not do (so well, or so much) in the case of AS/HFA, when we do not do this in the case of people without AS/HFA. For example, I do not spend much, if any, time thinking about mathematics problems, but I spend quite a lot of time thinking about people. In contrast, the person in the next door office spends a lot of time thinking about mathematics problems, and hardly any thinking about people. Yet I do not describe myself as having a disability in mathematics. I would instead say that I simply prefer to spend time thinking about people: they are more interesting to me. To call what a person does little of a disability could be seen as unreasonable. It might be a little like saying that the basketball player Michael Jordan has a deficit in fine motor coordination on the grounds that he is not known for spending much (if any) time engaged in needlework. This may be true of him, but to highlight this aspect of his skills, whilst ignoring his obvious assets in hand-eye coordination, physical speed, strength, agility, etc., is to put things back to front, and would be an unfair description of him.
3. AS/HFA is a disability when viewed from the family or peer perspective
One might argue that AS/HFA is a disability when viewed from the perspective and needs of their family and the wider social groups, (e.g. school, peers, etc.). Parents may be at their wits end over the extreme behaviours their child shows. For example, the child may insist that the living room light should be on whilst the hallway light should be off, that the plug switches should all be in the 'up' position, and just certain taps should be on, etc. . Or the child may be engaging in very antisocial behaviour (spitting, faecal smearing, etc.). Quite reasonably, parents, teachers, peers and others should not have to put up with such a tyrannical, strong will on the part of their child, or with antisocial behaviour, since they as parents, teachers, or peers also have needs.
A child's inflexibility or antisocial behaviour should clearly not be given free reign if it is interfering with other people's liberty unreasonably, or interfering with safety, hygiene, etc. Help with parenting may be needed, to facilitate the child accommodating to others, and vice-versa. But this is still not a clear justification for calling AS/HFA a disability - it is no more justified than a woman saying her husband is disabled simply because his hobby is dominating her life unreasonably, or saying that your neighbour is disabled simply because his behaviour interferes with your privacy. Individuals clearly need to accommodate to each other, since there may be a clash of interests or styles, but is one disabled? Not necessarily.
4. AS/HFA is a disability because of its associated medical conditions
Another argument may be that AS/HFA should be viewed as a disability because it carries with it an increased risk of medical conditions, such as epilepsy or mental retardation. For example, in classic autism, epilepsy occurs in one third of cases and mental retardation (IQ below the average range) occurs in about three quarters of cases . However, such associated medical conditions are clearly not specific to AS/HFA, and it is AS/HFA-specific features that are under discussion. Epilepsy or mental retardation may be justifiably seen as disabilities. These will require separate examination. But is AS/HFA (which by definition involves no retardation) necessarily a disability?
One might argue that some associated conditions are clearly disabilities. An example is language impairment. Many young children with HFA have little language. In some cases this applies to both their expression and comprehension. The combination of an autistic lack of social interest, together with little or no language, can be seen as a major disadvantage in a world of other people. Even if we down-play the importance of sociability, the child can still be regarded as disabled in being delayed in developing the ability to make his or her needs known. But whilst the notion of a disability may reasonably apply to extreme cases, the earlier point remains valid: that individuals with HFA need not necessarily be viewed as disabled as most of them will develop enough language even after a delay.
5. AS/HFA is a disability because it involves special needs and extra support
Perhaps the most compelling reason for viewing AS/HFA as a disability is that such individuals clearly have special needs (they need to be recognised as different, may require different kinds of teaching methods or schooling, or specific kinds of treatment) and access to such support in the present legal framework only flows to the child and their family if the case can be made that autism is a disability. Special funding does not automatically flow simply because one regards the child as 'different'. Given this economic reality, one should not remove the term 'disability' from the description of AS/HFA without ensuring that extra provision would still be available even if the term 'difference' was more appropriate. This is really an issue relating to social policy, health and education economics, and the legal system.
Characterising the underlying difference in AS/HFA
We turn next to consider two different models which attempt to characterise the dimension(s) along which AS/HFA differs from normality.
1. The Folk Psychology-Folk Physics Model
The first model suggests that the two relevant dimensions along which to characterise individuals with AS/HFA might be 'folk psychology' and 'folk physics'. Folk psychology involves understanding how people work. Folk physics involves understanding how inanimate things work. The model assumes that all individuals on the autistic continuum show degrees of folk psychology impairment, whilst their folk physics may be intact or even superior, relative to their mental age . This model is shown in Figure 1.
insert Figure 1 here
Folk Psychology
There is plenty of evidence that people with autism spectrum conditions have degrees of difficulty in mind-reading, or folk psychology. There have been more than 30 experimental tests, the vast majority revealing profound impairments in the development of their folk psychological understanding. These are reviewed elsewhere but include deficits in: joint attention ; use of mental state terms in language ; production and comprehension of pretence ; understanding that "seeing-leads-to-knowing" ; distinguishing mental from physical entities ; making the appearance-reality distinction ; understanding false belief ; understanding beliefs about beliefs ; and understanding complex emotions . Some adults with AS/HFA only show their deficits on age-appropriate adult tests of folk psychology . This deficit in their folk psychology is thought to underlie the difficulties such children have in social and communicative development , and the development of imagination .
Folk Physics
Other evidence suggests that children with AS/HFA may not only be intact but also superior in their folk physics. First, clinical and parental descriptions of children with AS/HFA frequently refer to their fascination with machines [the paragon of non-intentional systems] . Indeed, it is hard to find a clinical account of autism spectrum conditions that does not involve the child being obsessed by some machine or another. Examples include extreme fascinations with electricity pylons, burglar alarms, vacuum cleaners, washing machines, video players, calculators, computers, trains, planes, and clocks. Sometimes the machine that is the object of the child's obsession is quite simple (e.g., the workings of drain-pipes, or the design of windows, etc.). A systematic survey of obsessions in such children has confirmed such clinical descriptions .
Of course, a fascination with machines need not necessarily imply that the child understands the machine, but in fact most of these anecdotes also reveal that children with autism have a precocious understanding, too. The child (with enough language, such as is seen in children with AS/HFA may be described as holding forth, like a "little professor", on their favourite subject or area of expertise, often failing to detect that their listener may have long since become bored of hearing more on the subject. The apparently precocious mechanical understanding, whilst being relatively oblivious to their listener's level of interest, suggests that their folk physics might be outstripping their folk psychology in development. The anecdotal evidence includes not just an obsession with machines, but with other kinds of physical systems. Examples include obsessions with the weather (meteorology), the formation of mountains (geography), motion of the planets (astronomy), and the classification of lizards (taxonomy).
Leaving clinical/anecdotal evidence to one side, experimental studies converge on the same conclusion, that children with AS/HFA not only have an intact folk physics, they have accelerated or superior development in this domain (relative to their folk psychology and relative to their mental age, both verbal and nonverbal). First, using a picture sequencing paradigm, we found that children with autism performed significantly better than mental-age matched controls in sequencing physical-causal stories . The children with autism also produced more physical-causal justifications in their verbal accounts of the picture sequences they made, compared to intentional accounts. This study however did not involve a chronological age (CA) matched control group, so the apparent superiority in folk physics in autism may simply have reflected their higher CA.
Second, two studies have found that children with autism showed good understanding of a camera . In these studies, children with autism could accurately infer what would be depicted in a photograph, even though the photograph was at odds with the current visual scene. This contrasted with their poor performance on False Belief tests. The pattern of results by the children with autism on these two tests was interpreted as showing that whilst their understanding of mental representations was impaired, their understanding of physical representations was not. This pattern has been found in other domains . But the False Photo Test is also evidence of their folk physics outstripping their folk psychology and being superior to mental age (MA) matched controls.
Family studies add to this picture. Parents of children with AS also show mild but significant deficits on an adult folk psychology task, mirroring the deficit in folk psychology seen in patients with AS/HFA . This is assumed to reflect genetic factors, since AS/HFA appear to have a strong heritable component . On the basis of this model, one should also expect that parents of children with autism or AS to be over-represented in occupations in which possession of superior folk physics is an advantage, whilst a deficit in folk psychology would not necessarily be a disadvantage. The paradigm occupation for such a cognitive profile is engineering.
A recent study of 1000 families found that fathers and grandfathers (patri- and matrilineal) of children with autism or AS were more than twice as likely to work in the field of engineering, compared to control groups . Indeed, 28.4% of children with autism or AS had at least one relative (father and/or grandfather) who was an engineer. Related evidence comes from a survey of students at Cambridge University, studying either sciences (physics, engineering, or maths) or humanities (English or French literature). When asked about family history of a range of psychiatric conditions (schizophrenia, anorexia, autism, Down Syndrome, language delay, or manic depression), the students in the science group showed a six-fold increase in the rate of autism in their families, and this was specific to autism .
Finally, children with AS have been found to perform at a superior level on a test of folk physics , and some adults with AS have reached the highest levels in physics and mathematics, despite their deficits in folk psychology .
2. The central coherence model
The Folk Psychology-Folk Physics Model is not the only attempt to capture the relevant dimensions underlying the autistic spectrum. A second model suggests the relevant dimension may be from weak to strong central coherence. Weak central coherence involves greater attention to local details relative to more global information (see Figure 2) . Central coherence is a slippery notion to define. The essence of it is the normal drive to integrate information into context, gist, gestalt, and meaning. Frith argues that the autistic person's superior ability on the Embedded Figures Test and on an unsegmented version of the Block Design subtest in the Wechsler Intelligence Scale for Children (WISC) and Wechsler Adult Intelligence Scale (WAIS) arises because of a relative immunity to context effects in autism . Happe also reports a failure, by people with autism, to use context in reading, such that homophones are mispronounced [e.g., "There was a tear in her eye" might be misread so as sound like "There was a tear in her dress"] . A recent study has shown that children with autism are equally good at judging the identity of familiar faces in photographs, whether they are given the whole face or just part of the face. Non-autistic controls show a "global advantage" on such a test, performing significantly better when given the whole face, not just the parts of the face . The central coherence account of autism is attractive in having the potential to explain the nonholistic, piecemeal, perceptual style characteristic of autism, and the unusual cognitive profile seen in this condition (including the islets of ability). Recently, work in visual search has shown that individuals with autism spectrum conditions may be superior in their ability to make fine discriminations of targets from distractors . Such work may help take forward the concept of weak central coherence.
insert Figure 2 here
Note that these two models (Folk Psychology-Folk Physics; and Central Coherence) are not necessarily incompatible, since it is possible to imagine how weak central coherence could cause superior folk physics, as well as difficulties in folk psychology. Jarrold reports that in normal individuals, folk psychology and central coherence are indeed inversely correlated .
Whatever the relevant model, the dimensional approach is useful in reminding us that AS/HFA may simply be part of quantitative variation and individual differences in cognitive profiles, or styles of information processing. This approach could be re-cast to avoid the implication that one style is better (stronger) or worse (weaker), or that one is intact and another deficient. For example, the terms 'weak' and 'strong' central coherence are sometimes replaced by the more neutral terms, 'local' vs 'global' processing (referring to whether one spends more time processing at one level than another). See Figure 3.
insert Figure 3 here
The advantage of both of these models is that individuals with AS/HFA are understood in terms of an underlying dimension, and that this dimension blends seamlessly with normality, so that we are all situated somewhere on the same continuum. Most importantly, to reiterate, one's position on the continuum is said to reflect a different cognitive style . Dimensional models also do not require a line to be drawn between ability and disability. Finally, they avoid the notion that individuals with AS/HFA are in some sense qualitatively different from those without AS/HFA. Such a notion is increasingly hard to defend in the light of intermediate cases. These are easier to accommodate in terms of quantitative variation.
Implications for understanding the apparent increase in prevalence of AS/HFA
There are some reports that AS/HFA is increasing in prevalence . It is unclear if this simply reflects better detection or if there is a genuine increase. However, if there is a genuine increase, this presents something of a paradox for the disability view: disabilities with a genetic basis which affect social skill and thus potentially reduce mating opportunities should be subject to negative selective pressures. Such disabilities should therefore be expected to reduce in prevalence with time. In order to be on the increase, such genes would have to be being positively selected. Increased prevalence presents no difficulties for the difference view however, since a cognitive style can at different times or under different conditions confer advantages to the individual. For example, the computer revolution in the 20th Century has created unprecedented opportunities for employment and economic prosperity for individuals with superior folk physics. This may have had positive effects on the reproductive fitness of such individuals, leading to an increase in the genes for AS/HFA in the gene pool. Such a speculation is testable: for example, one would predict higher rates of AS/HFA in the children of couples living in environments which function as a niche for individuals with superior folk-physics abilities (e.g.'Silicon Valley', MIT, Caltech) compared to environments where no such niche exists. Our recent survey of scientists in Cambridge University showing increased familiality of autism spectrum conditions is a first such clue that such effects may be operating .
Summary
In a world where individuals are all expected to be social, people with AS/HFA are seen as disabled. The implication is that if environmental expectations change, or in a different environment, they may not necessarily be seen as disabled. As we have known in relation to other conditions, concepts of disability and handicap are relative to particular environments, both cultural and biological . It may be time to extend this way of thinking to the field of AS/HFA. We could imagine, for example, people with AS/HFA might not necessarily be disabled in an environment in which they can exert greater control of events. The social world is very hard to control, whilst the technological world of machines is in principle highly controllable. Equally, people with AS/HFA might not necessarily be disabled in an environment in which an exact mind, attracted to detecting small details, is an advantage. In the social world there is no great benefit to such a precise eye for detail, but in the world of maths, computing, cataloguing, music, linguistics, craft, engineering or science, such an eye for detail can lead to success rather than disability. In the world of business, for example, a mathematical bent for estimating risk and profit, together with a relative lack of concern for the emotional states of one's employees or rivals, can mean unbounded opportunities.
It is hoped that this article, at the dawn of the new millennium, will open the debate towards identifying if there are any arguments for necessarily viewing AS/HFA as disabilities. In this article, none are found to apply persuasively to AS/HFA, even if they may apply to the 'lower-functioning' cases. In contrast, the arguments in favour of viewing AS/HFA as a 'difference' are more compatible with the 'continuum' notion, and may be morally more defensible. The sole reason for retaining the term disability in relation to AS/HFA may be to ensure access to provision; it may be the legal system that needs revision, so that a child whose autistic 'difference' leads them to have special needs, will still receive special support.
Figure Legends
Figure 1: This first model shows the relationship between Folk Physics (or understanding how things work) and Folk Psychology (or understanding how people work). For shorthand, folk psychology is referred to as 'empathy', and folk physics is referred to as 'scientist'. Note that this is not the same as the ordinary usage of the word 'scientist', as folk physics includes everyday understanding of objects that is not necessarily the result of formal teaching. Individuals with AS/HFA are conceptualized as comprising types A-J.
Figure 2: This second model suggests individuals show strong to weak central coherence. Individuals with AS/HFA may be at the extreme left of this distribution .
Figure 3: This third model redescribes the second model in less value-laden terminology. Individuals are seen as showing local to global information processing styles. Again, individuals with AS/HFA may be at the extreme left of this distribution, spending relatively more time processing detail rather than processing in a broad-brush approach .
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