Presenter:Dr.Zakeera Chairperson:Dr.K.

Krishnamurthy Date:29/2/2012

PERVASIVE DEVELOPMENTAL DISORDER: ICD-10: Qualitative abnormalities in reciprocal social interactions Patterns of communication Restricted, stereotyped, repetitive repertoire of interests and activities Includes: childhood autism, atypical autism, Retts syndrome,other childhood disintegrative disorder, over active disorder associated with mental retardation and stereotyped movements, Aspergers syndrome, other PDDs, pervasive developmental disorder unspecified

DSM-IV TR: Early onset conditions char. by delay in the development of social, communicative and other skills Includes: autistic disorder, Retts syndrome, childhood disintegrative disorder, Aspergers syndrome, Pervasive developmental disorder NOS

AUTISTIC DISORDER:
ICD-10:

Abnormal and /or impaired development Before the age of 3 years Abnormal functioning :Social interaction Communication Restricted and repetitive behavior Includes: Infantile autism Autistic disorder, Infantile psychosis, Kanners syndrome

AUTISTIC DISORDER: DSM IV TR:

The essential feature of Autistic Disorder are the presence of Markedly abnormal or impaired development in Social interaction Communication and Markedly restricted repertoire of activity and interests. Present before the age of 3 years

Also called as infantile autism, childhood autism, early infantile autism, Kanners autism

Eugen Bleuler in 1911 :Autism coined by Swiss psychiatrist ,individual with schizophrenia who lost contact with the reality (autism = within oneself) Henry Maudsley(1867):The first descriptions of this disorder

Leo Kanner 1943: published his seminal paper on autism. autistic disturbances of affective contact, Termed infantile autism

Hans asperger (1944)

1960s much confusion about the nature of autism and its etiology
By 1970s : neurobiological basis of the disorder Michael Rutter 1978 New dfinition used as basis for DSM III

In 1991:children with autism have not withdrawn from reality cuz of mental disorder rather they have failed to enter reality due to widespread serious disturbances in their development

DSM I and II :Not officially recognised viewed as continuum with schizophrenia DSM III: First recognized as condition apart from schizophrenia Termed as infantile autism Under new class of disorders called pervasive developmental disorders DSM IIIR:Provided detailed more developmentally oriented set of guidelines for diagnosis. Set of 16 very detailed criteria; grouped in the traditional three categories of social disturbance, communicative disturbance and restricted and repetitive behaviours Additional change of multi axial placement Placed in Axis II and included autistic disorder and PDD NOS

ICD-9:Infantile autism was under the category of psychosis with onset in childhood psychosis perpetuated the mistaken impression that autism was related to adult schizophrenia

ICD-10 and DSM IV : Definitions of autism in both are conceptually identical Defined on the basis of characteristic problems in three areas Present by the age of three years ICD-10 : Diagnosis of atypical autism can be made DSM IV : PDD NOS/ atypical autism Moved to Axis I

 2-5 in 10,000 in 1970s to 6-9 in 10,000 in studies conducted in 1980s

and 1 in 1000 in 1999 60/10,000 Increased prevalence: genuine increase growing awareness changing environmental factors broader definiton
Male:Female=3.5-4:1

Lower threshold for brain dysfunction than girls

GENETIC FACTORS: Concordance rates : monozygotic twins : 60-90% dizygotic twins :10% Heritability > 90% Family studies : 50-200 times increase in siblings Jorde and colleagues : Transmission pattern inconsistent with single gene inheritance Pickles and colleagues : Latent class approach to assess twin and family history data epistatic oligogenic inheritance Region on chromosome 7q, near the cystic fibrosis locus ; 2p, 4p, 19p

Chromosome 15q1113 : cytogenetically detectable duplications or deletions

Cook and colleagues : Linkage disequilibrium between GABRB3 (a marker in the gamma-aminobutyric acid receptor subunit gene)

Sutcliffe and colleagues : linkage disequilibrium in several markers in the region, including GABRB3 and UBE3A (Angleman syndrome gene)

Tuberous sclerosis(TSC1 & TSC2) chromosome 16 ,25%-50% increased rate Mutations in phosphatidyl inositol phosphate(PTEN) Fragile-X(FRAXA,FMR1): mutations of this X-linked gene(30%) Neurofibromatosis (chromosome 17) Rogers and colleagues : excluded linkage of autism to loci in HLA in genome scan Torres and colleagues : HLA-DRB1 alleles and autism

METABOLIC GENES:

Phenyl ketonuria(phenyl alanine hydroxylase) was highly associated with autism D7-Dehydrocholesterol reductaseloss or function mutation causes accumulation of dehydrocholesterolrare cause Engrailed 2(EN2):alleles of EN2 transcription factor which regulates cerebellar development SYNAPSE FORMATION AND FUNCTION: Neuroglins(NLGN2 & NLGN4):Mutations SHANK3:Rare missense mutaion in chr 22q13.3; Shank proteins are multidomain scaffold proteins of the post synaptic density that connect neurotransmitter receptors, ion channels, and other membrane proteins to the actin cytoskeleton and G-protein-coupled signaling pathways.

 ION CHANNELS:
Calcium channels:missence mutations in L-Type and T-Type channels Sodium channels(SCN1A,SCN2A):Missense mutations

HOWEVER No single gene Piven and colleagues : 38% of families of autistic individuals, both parents manifested some social and cognitive deficits Each parent could contribute one or more of requisite genes autistic disorder phenotype in their offspring

 In 1997, Skuse et al : In a study of 80 females with monosomy X

Karyotypically normal females performed better than normal males and autism and/or ASD were reported in females with 45,Xmat Turner syndrome and Xp deletions

Increased head circumference Overall brain size : 210% greater ,both in volume and weight ?due to cortical thickening

C allele in the promoter region of the MET receptor tyrosine kinase gene Turns on the cells internal signaling cascadesIncreased proliferation, motility, differentiaton, process outgrowth or survival Cerebellum: Size is reduced especially in neo cerebellar region Decreased Purkinje and granule cells Folia VI and VII of cerebellar vermis to be hypoplastic and vermal hyperplacia Amygdala --Enlargement --Decrease in total neuron number,Size --Abnormalities in the amygdala cortical loops

Postmortem studies: Decreased number of neurons and reduced dendritic arborisation in areas of the limbic system amygdala hippocampus septum anterior cingulate Suggesting prenatal dysgenesis In case of late onset autism neural density will be increased in hippocampus and other limbic area Ventricular dilation and medial temporal atrophy in few cases Lesions in the amygdala, hippocampus, or both, in monkeys features of autism Processing of social information differ in prefrontal cortical region

Frontal lobe : general hypoactivation Brain stem abnormalities and neocortical malformations Important MRI findings: 1. Head circumference : increased 2. Volume of the brain is increased 3. Volume of the intrahemispheric white matter is increased while interhemispheric is not 4. MRS-Reduced choline concentration ; decreased cellularity and density in the cortex 5. DTI - increase in pathway volume and fiber number and disruption of white matter in brain regions associated with social functioning.

fMRI Abnormalities in face recognition tasks Hypoactivation of the fusiform face area, associated with deficits in perception of people compared with objects Atypical size and location of activation on object and face recognition Abnormalities in executive functioning Lower connectivity on tasks of language, working memory, problem solving, social cognition - General problem with functional under connectivity within and between neocortical system Higher activation of Wernicke's area and lower activation of Broca's in written sentence comprehension Abnormalities in amygdala activation may be related to abnormal gaze fixation

During Imitation tasks have suggested impaired mirror neuron activity in the inferior frontal gyrus (pars opercularis) Minicolumns : --radially oriented arrays of pyramidal neurons (layers II-VI), interneurons (layers IVI), axons, and dendrites --smallest radial unit of information processing in the cortex Mini column abnormalities 1. Increased number 2. Narrow width 3. Reduced neuropil space 4. Smaller neuron bodies and nucleoli

Mirror neurons Newly detected subset of cells found in several areas of brain that seem to fire when an individual simply observes others action Inferior frontal gyrus-pars opercularis Active during observation, imitation and observation of the intentions of other's actions Mediates the emotions and internal experience of another's emotions so that feelings of others are truly felt and understood at an emotional level Children with autism showed no mirror neuron activation during observation or imitation of emotional face expressions Early mirror neuron dysfunction : core of social and emotional deficits

High functioning autism: Decreased connectivity between the spheres with intact or overdevelopment of the individual domains
Low functioning: total distortions of connections Mostly exhibited prominent patterns of ectopic striatal functional connectivity with increased functional connectivity between nearly all striatal subregions and heteromodal associative and limbic cortex Striatal functional hyper connectivity with the pons

NEUROPHYSIOLOGICAL: Deficits in: 1. Higher cortical sensory perception 2. Skilled motor abnormalities 3. Memory for complex stimuli which required organization strategy Complex information processing 4. Higher order language abilities 5. Concept formation

Do not activate the fusiform gyrus (the so-called face area) during tasks that involve perception of faces When group differences in attention to facial expressions were limited, adolescents with ASD showed greater activation in structures involved in socio-emotional processing The failure of the autism group to exhibit the normal neural signs of adaptation during learning may be attributable to impaired frontal--posterior cortical connectivity in autism Cortical underconnectivity : constrain the ability of the brain to rapidly adapt during learning

Difficulty in attributing social meaning to ambiguous visual stimuli

Eye-tracking technology : exhibit highly unusual patterns of visual search in viewing intense social situations

NEUROCOGNITIVE THEORIES: Executive dysfunction Difficulties in abstraction Inhibiting irrelevant responses Shifting attention Profiting from feed back as well as in maintaining relevant information on line is lost Weak central coherence Difficulties integrating information into meaningful wholes Leading to fragmentary and overtly concrete experience of the world Supportive data are lacking and developmental features of theory are weak This may result in semantic pragmatic deficits

Theory of mind(TOM) Childs inability to attribute mental states such as beliefs and intention to others Cuz of this child is unable to infer the thoughts and motivation of others Thus fails to predict their behavior and adjust their own action accordingly Resulting in lack of reciprocity in communication and social contact

Limitation to TOM: many children with autism do exhibit TOM skills but totally unable to utilize this capacity in their social adjustment

NEUROCHEMISTRY: Serotonin: 1/3rd increased peripheral levels of serotonin and consistent over time not specific to autism Dopamine : hyperdopaminergic functioning : over activity and stereotyped movements Raised levels of HVA which is a metabolite of dopamine seen in CSF Studies have been inconsistent Endogenous opioids: Over production Increased levels of enkephalins and endorphins in CSF Lead to social withdrawal, unusual sensitivities and behaviors Opiod may be derived from incompletely digested gluten and casein proteins(Reichelt)

ENDOCRINE FACTORS: Abnormal sex hormone levels in pregnancy, especially testosterone with its presumed effects on sexually dimorphic brain structure and behavior Maternal reproductive hormone dysregulation Intrauterine thyroid dysfunction has been linked to neurologic deficits

IMMUNE THEORIES: Maternal antibodies Directed against CNS Proteins are found in sera Targets of auto antibodies include Neuron axon filament proteins Myelin basic protein Cerebellar neurofilaments Nerve growth factors Antibodies against caudate nucleus Measles-mumps-rubella( MMR immunization)

OBSTERICS FACTORS Maternal bleeding after 1st trimester Intranatal rubella Foetal alcohol syndrome Caesarian section Meconium in amniotic fluid Respiratory distress syndrome Neonatal anemia, newborn encephalopathy Longer gestational period / post term Low birth weight Preterm delivery Low Apgar score

PSYCHOSOCIAL THEORIES: Kanner--refrigerator mother i.e mother who was not responsive to the childs emotional needs. child removed from the family generation of parents were traumatized by the experience of being blamed for their child's condition

 XENOBIOTIC EXPOSURE:

Exposed to thalidomide during the first trimester of pregnancy Valproic acid, an antiepileptic drug also used as a mood stabilizer in bipolar disorder and schizophrenia Misoprostol to induce delivery Air pollutants,most notably mercury, cadmium, and nickel found a moderate association of autism with estimated airborne metal levels at birth. OTHERS Carnitine deficiency

AGE OF ONSET: Almost always before age 3 Parents typically become concerned between the ages of 12 and 18 months as language fails to develop Child was too good, made few demands, and had little interest in social interaction 20-25% child seemed to develop some language, language either plateaued or was lost

QUALITATIVE IMPAIRMENT IN SOCIAL INTERACTION: Reciprocal social interaction Lack of social relationships, expressed in attachments and friendships Poor use of nonverbal communication e.g. eye contact, facial expressions, body postures, gestures Poor peer relationships Difficulty with social cues: The give and take of social behavior, sharing enjoyment, interests, achievement. Failure to recognize emotional cues: results in inappropriate response to distress in others which may reflect wider lack of empathy Picking context based social cues

Three clinical subtypes (based on social interaction)

The aloof: total aversion to social interaction The passive: who can be drawn into social interaction but only for as long as they are prompted The active but odd: spontaneously engage with people, but lacking the ability to develop more than a superficial relationship

QUALITATIVE IMPAIRMENT IN VERBAL AND NON VERBAL COMMUNICATION AND PLAY: 30 to 40% : never use language for communication Never speak or only echo or repeat statements -- echolalia Delays in the acquisition of language May not babble No eye contact No motivation to engage in communication or attempt to communicate via nonverbal means

Speech less flexible ; non reciprocal Pronoun reversal Jargon, idiosyncratic and unusual term can make the person incomprehensible to those who do not know them well

 Phonology (speech sounds): Impaired reception and expression in children

with the mixed receptiveexpressive syndrome and, especially, with severe verbal auditory agnosia (word deafness) in which phonologic decoding may be so compromised as to preclude speech comprehension and verbal expression Prosody (rhythm and melody of speech): In children with speech: singsong or rising intonation, high-pitched voice, or monotonous,robotic speech Syntax (grammar and word order) Impaired reception and expression in children with the mixed receptive expressive syndrome and with less severe verbal auditory agnosia

Semantics (vocabulary and meaning of language) Impaired reception and expression in children with autism e.g., impaired comprehension of questions, open-ended questions, and unable to understand nonliteral language such as irony, sarcasm, and jokes; word-retrieval problems and unusual, pedantic word choices; echolalia; difficulty formulating coherent discourse; narrow range of topics Pragmatics (communicative and conversational use of language) Impaired reception and expression in persons with autism e.g., impaired interpretation of tone of voice, body posture, and facial expression; gaze avoidance; failure to answer; speaking to no one in particular; failure to initiate, pursue, or terminate conversations; difficulty with taking turns; poor maintenance of topic;perseveration and ceaseless questioning

MARKEDLY RESTRICTED ACTIVITIES AND INTERESTS: Compulsive routines and difficulty in tolerating change or variation in routine Engage in activities in very particular ways Have interest in some part of object than its function as a whole(tyres of a truck toy) Faced with anything unexpected or changes may elicit great opposition or distress in the form of catastrophic rage Interest repetitive activity, for eg. collecting strings memorizing numbers, or repeating certain words or phrases Unusual attachments in balls or magpie series of objects results in large collection and storage problems

Attachments to objects : hard rather than soft ; class of object, rather than the particular object Preoccupied with spinning objects Last to develop Minimal until around 3 years of age

SPLINTER SKILLS: highly developed skills in specific areas that contrast with the child's overall deficits in cognitive functioning SAVANT SKILLS: high, sometimes prodigious performance on a specific skill in the presence of mild or moderate mental retardation 10% autistic individuals narrow range of capacitiesmemorizing lists or trivial information, calendar calculation, visualspatial skills such as drawing, musical skills involving a perfect pitch or playing a piece of music after hearing it only once

 SELF STIMULATORY BEHAVIORS They are repetitive body movements or movements of objects Visual:repeatative blinking, staring at lights, moving fingers infront of

light Auditory: making vocal sounds, spinning an object on a table Tactile:scratching,rubbing the skin with hands or objects Vestibular: rocking front to back and side to side Taste: placing body parts or objects in the mouth, licking objects Olfactory: smelling objects, sniffing people

MOTOR AND SENSORY ABNORMALITIES: Motor stereotypies : hand flapping, body rocking, finger twiddling , waving in front of the eyes, toe walking , assumption of odd postures, pacing, spinning, running in circles, twirling a string, tearing paper, drumming, and flipping light switches. Oral stereotypies like humming or incessant questioning. Decrease in adolescence and adulthood ; higher intellectual functioning Echopraxia:may result in tape record like play of whole scenes observed on TV or real life Over activity -- preschool years

Hyperacusis Oblivious to loud noise or people calling them Fascinated by the faint ticking of wristwatch ; sound of crumpling paper Bright lights : distressing Preference for peripheral gaze Tactile defensiveness Insensitive to pain and may not cry after a severe injury Lack of appreciation of time and space ,struggling to comprehend the passage of time Difficulty in perceiving the spatial relationship of objects ,unable to understand size and shape of their environment

SLEEPING AND EATING PROBLEMS: Erratic sleep patterns Recurrent awakening at night Eating disturbances : They may sniff their food and have an intense dislike of certain tastes or textures Insistence on eating a very limited choice Refusal to try new foods Pica lead toxicity

MOOD AND AFFECTIVE DISTURBANCES: Poor affect modulation : inappropriate to social situation Sudden mood changes, laughing or crying, or giggling Intense anxiety in social situations They may also develop depression in adolescence

SELF INJURY AND AGGRESSION: Self-injurious behaviors : biting their hands or wrists , banging their heads ,Pick their skin, pull their hair, bang their chests, hit themselves,eye poking Decreased sense of danger Temper tantrums Lack of understanding or inability to communicate or sheer frustration aggressive outbursts

OTHER FEATURES Minor physical anomalies : ear malformations Embryological period in which the factors responsible for autism act Attractive Do not exhibit any forms of stigmata Diminish in adolescence and adulthood

Other pervasive developmental disorders Mental retardation (80%) 60%-IQ < 50 20% -IQ b/w 50-70 20%-IQ > 70 Seizures:10-20%,all types of seizures can occur, seen throughout the childhood ,peak in adolescents High incidence of GI disorders Language disorders Deafness Childhood onset schizophrenia Degenerative disorders

ICD-10:
Abnormal and /or impaired development

must have been prsent in the first

3 yrs or before the age of 3 years Always qualitative impairments in reciprocal Social interaction Universal qualitative impairments in communication Restricted ,repetitive and stereotyped patterns of behavior, interests and activities Can be diagnosed in any age group

A total of six or more manifestations from 1, 2, and 3 below: 1. Qualitative impairment of social interaction (at least two manifestations) a. Marked impairment in the use of multiple types of nonverbal behavior such as eyeto-eye ,gaze, facial expression, body postures, and gestures to regulate social interactions; b. Failure to develop peer relationships appropriate to developmental level; c. Lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by lack of showing, bringing, or pointing out objects of interest); and

d. Lack of social or emotional reciprocity.

Qualitative impairment of communication (at least one manifestation) a. Delay in, or lack of, development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gestures or mime); b. In individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others; c. Stereotyped and repetitive use of language or idiosyncratic language; and d. Lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level
2.

Restrictive and stereotyped patterns of behavior, interests, and activities (at least one behavioral manifestation) a. Encompassing preoccupation with one or more restricted, repetitive, and stereotyped patterns of interest that is abnormal either in intensity or focus; b. Apparently inflexible adherence to specific, nonfunctional routines or rituals; c. Stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or complex whole-body movements); and d. Persistent preoccupation with parts of objects.
3.

 Delays or abnormal functioning, with onset before the age of 3 years, in

at least one of the following areas: Social interaction; Language as used in social communication; and Symbolic or imaginative play.

Atypical autism differs : age of onset fulfill all three sets of diagnostic criteria Impaired development manifests only after three years of age Insufficient demonstrable abnormalities in one or two of the three areas of psychopathology Profoundly retarded individuals Describes a rather large and heterogeneous group of children who do not meet strict criteria for autism or other PDD but exhibit a pattern of development and behavioral dysfunction similar in autism

Differenitiated from: selective mutism, Rett's syndrome, childhood disintegrative disorder language disorder, degenerative CNS disorders Severe neglect : but other features of autism not present social deficits remit with appropriate care Childhood-onset schizophrenia : long period of normal or near-normal development before the onset of characteristic delusions, hallucinations

Seizures:10-20%,all types of seizures can occur (EEG) abnormalities --diffuse and focal spikes --paroxysmal spike-and-wave patterns --multifocal spike activity --mixed discharge Incidence of EEG abnormalities ranges from 10 to 83 percent Significantly higher in mentally retarded autistic individuals Peak period - early childhood and adolescence Lower-functioning individuals are at increased risk

ADHD : DSM IV prohibits the co-diagnosis ; significant symptoms of these two conditions commonly occur Fragile-X syndrome 20-30% meet diagnostic criteria 1-8% boys with idiopathic autism : Fragile-X mutation (FMR1 gene) Tuberous sclerosis : 0.4 to 2.8%

EARLY RECOGNITION EARLY INTENSE INTERVENTION

13-month delay before they are diagnosed 20-60 month delay from parental suspicion to diagnosis Early recognition early intervention most effective

RED FLAGS Absolute indications for IMMEDIATE EVALUATION No babbling, pointing or any other gesture BY 12 MONTHS age No single words BY 16 MONTHS age No 2 word spontaneous (non-echolalic) phrases BY 24 MONTHS age ANY LOSS OF ANY LANGUAGE OR SOCIAL SKILLS AT ANY AGE

Multifaceted,multidisciplanary Parent Interview Obtain thorough developmental history (attainment and/ or loss of motor, speech, self-help milestones). age of onset of each symptom, progression of the symptoms ,current status of the symptoms&level of functioning Administer semi structured interview to gather information about social and communication development, play, restricted and repetitive behaviors, and adaptive skills. Treatment history, family history Child Observation Create context in which to observe childs social communication behaviors, play, and repetitive behaviors(with both parent and examiner). Consult parents and teachers about whether behaviors observed during assessment were consistent with childs behavior in other settings

. Medical Examination Rule out sensory impairment (check hearing and vision). Conduct genetic testing if indicated based on dysmorphology or family history. Conduct neurological exam. Developmental and Language Testing Assess verbal (expressive and receptive) and nonverbal abilities. Gather information about receptive and expressive language abilities. Evaluate gross and fine motor skills.

OTHERS Mental retardation, severe neglect should be ruled out Assessment of co morbid conditions Family assessment Daily schedule of the child and the family The assets of the family Likes of the child are also obtained in the assessment Diagnoses - based on multiple observations and preferably not on single crosssectional assessments

 Childhood Autism Rating Scale (CARS)

Checklist for Autism in Toddlers (CHAT) and modified CHAT Autism spectrum screening questionnaire (ASSQ)

Social communicative questionnaire(SCQ)

Guillam autism rating scales(GARS) Autism Diagnostic Interview (ADI)

Catherine Maurice schedule

Screening tool for autism (STAT)for 2 yrs old Autism diagnostic observation schedule(ADOS)

Autism diagnostic inventory-Research(ADI-R)

Complete hemogram LFT,RFT,ECG,CSF Audiometry/auditory brainstem response/BAER Specific developmental testing - IQ test Urine screening for inborn errors of metabolism Genetic Testing(karyotyping and Molecular DNA testing) EEG Imaging (Head CT or MRI) :especially when there is abnormal head size

Multidisciplinary process Psychiatry and paediatrics, special education, psychology, occupation therapy and communication disorder specialists as well as social work and other therapists Multidisciplinary clinics

Nature of illness, clarification of misconceptions, cardinal symptoms, prognosis and reorientation from medical to developmental model, concept, nature and importance of training Appreciation of fundamental handicaps Concept of reinforcements, recording of baselines of assets and deficits, likes and dislikes Intensive work with the family and main caretakers of the children

Ideally entry into intervention should begin as soon as diagnosis is considered Begun at ages 2-4 yrs Intensive,atleast 25 hrs per week or more hours per week,12 months per year Needs to be scheduled throughout the day Systematically planned, developmentally appropriate Low child: adult ratio (1:1) Must be individualized to child and his or her family including parent training Promotion of opportunities for interaction with typically developing peers Ongoing measurement and documentation of individual child s progress

 To minimize the core features and associated deficits

To maximize functional independence and Quality of life To alleviate family distress by education and supporting the families

To facilitate development and learning

promoting socialization reducing maladaptive behaviors

What to teach? Attending skills Imitation skills Receptive language skills Expressive language skills Pre-academic skills Self help skills

SOCIALISATION Educational curricula Strategies for teaching based on autism research (STAR) Parent training, and inclusion with trained shadow Communication and language Didactic and intensive training Milieu teaching Social-skills training Social skills training and social stories Behavioral treatment Discrete trial instruction, pivotal response training, and relationship development intervention
A.

COMMUNICATION Communication intervention Pivotal response training, social pragmatics approach, and parent training Augmentative and assistive communication Picture exchange communication system, sign language, and assistive technology (eg, vocal output devices) Behavioral (eg, play, reciprocal communication) Floor time Developmental, individual differences, relationship-based approach Applied verbal behavior
B.

MILIEU TEACHING: Naturalistic method Targeting social communication and social skills Teaching in the context of every day activities both at home and in school ,following the childs lead and providing natural consequences for the communication Procedures involved are: Modeling [ Demonstrating an action ] Mand modeling[Demonstrating saying a word with goal of having the child repeat that same word to request something]

MILIEU TEACHING CONT.. Time delay: presenting an item and allowing a period of time to pass for the child to respond spontaneously before providing any guidance Environmental arrangements:in such a way that it will create an opportunity for the child to engage in communication Ex:giving the child materials that require assistance in order for them to be used Giving small pices of snacks so that child is motivated to ask more Giving wrong object,removing necessary piece of toy so that child is motivated to ask for it

PIVOTAL RESPONSE TRAINING[PRT]

Highly efficient evidence based approach Addresses core `pivotal areas appears to be essential to vast areas of functioning Can be implemented in school,home or community contexts throughout the day Approx 90% nonverbal children with PRT intervention before 3 yrs are able to learn verbal communication

PIVOTAL RESPONSE TRAINING CONT..

Areas of PRT includes Pivotal area of motivation: targets child's apparent lack of motivation to learn and engage in social communication/interaction with others Ex:establishing attention,providing clear prompts and reinforce attempts Pivotal area of attention to multiple cues: targeted to respond to multiple cues and thus broadening their abilities in this area Pivotal area of self initiation: taught to make intiating social communicative interactions

Discrete trial method: teaching verbal behavior

Incidental teaching: Is initiated by the child and focusses on childs interest Natural reinforcing the child to follow what the child is trying to communicate Sign language and picture communication to jump start the speech system and boost the cognitive and social underpinnings

BEHAVIOR Behavioral intervention Discrete trial instruction comprehensive programmers using applied behavior analysis Psychopharmacology Selective serotonin reuptake inhibitors anticonvulsants atypical antipsychotics -2 agonists
C.

BEHAVIOR MANAGEMENT Classical and operant conditioning methods Providing clear warnings Taking care not to reward unknowingly behaviors that are undesirable Teaching alternative, reinforcable behaviors to a child in order to eliminate an undesirable behavior Structuring of activities

OTHER INTERVENTIONS: Sensory Integration therapy: Repeated exposure to vestibular, proprioceptive, and tactile activities To Organize sensory input and reduce anxiety associated with hypersensitivity to sensations Auditory Integration Therapy: Headphones to listen to filtered sound frequencies to Reduce sensitivity to sounds, Thereby increasing social interaction and attentiveness Vision therapy :Use of tinted eyeglasses, prism lenses, or eye exercises to Improve eye contact and diminish repetitive behaviors that involve visual stimuli such as spinning objects

Much controversy Medications control specific target behavioral symptoms Aggression Self-injurious behavior Hyperactivity Stereotypies and stimming Erratic sleep and appetite (circadian rhythm disorders) Temper tantrums-if severe and unmanageable by behavior management Help in rehabilitation process by making the child amenable for training

Risperidone: USFDA approved (2006) for the symptomatic treatment of irritability ; <20kg : 0.5-1.5mg >20kg: 1.5-2.5mg Olanzapine , aripiprazole : used as off label for treatment of aggression SSRIs : fluoxetine mood symptoms and RRBIs ;starting dose 2.5mg up to 10mg Methylphenidate: inattention and hyperactivity Seizure disorder: carbamazepine, lamotrigine, topiramate, valproic acid Clonidine Naltrexone Melatonin in sleep disturbances

FAMILY IN TREATMENT Parents must be co-therapists An effective therapist is one who involves the parents/care-givers in therapy instead of keeping them out of the therapy room Individual needs of parents and siblings must NOT be neglected family should be given a daily training schedule which includes leisure activities for the child as well as the family Parent Networks and NGOs run by parents of children with autism are important resources for families

BIOLOGICAL

Supplements

Mega vitamin therapy B6 18mg/kg/day Folate Magnesium 8mg/kg/day Dimethyl glycine, and cod-liver oil Tetra hydro biopterin Immunoglobulins Food additiveseg, secretin Chelation medications Gastrointestinal medications Elimination or special dietseg, gluten free or casein free Hyperbaric oxygen administration

NON BIOLOGICAL

Auditory integration training Music therapy Exercise therapy Chiropractic therapy Facilitated communication Massage therapy Interactive metronome Reiki Yoga

Earlier intervention improves long-term outcome for many individuals 15 to 20 percent able to achieve independence and self-sufficiency in adulthood 20 to 30 percent of individuals able to function with occasional support Improvement in social relatedness, communication, and self-help skills with age Ritualistic and repetitive behaviors may not improve over time Presence of some communicative speech by the age of 5 or 6 and higher nonverbal intellectual level have good outcome During adolescence, some autistic children may exhibit behavioral deterioration Few adults with autism achieve complete independence Language and social skills : seizure disorder

Depressive and anxiety : higher-functioning adolescents, who become painfully aware of their inability to form friendships despite a desire to do so and begin to experience the cumulative effect of years of failed contact with others and teasing by peers Able to work successfully in mainstream jobs ; communication and social problems often cause difficulties in many areas of life Encouragement and moral support in their struggle for an independent life Capable of employment in sheltered workshops under the supervision of managers trained in working with persons with disabilities

Living arrangements for persons with autistic disorder: Independent living Living at home Foster homes and skill development homes Supervised group living Institutions

By adult age three groups can be identified

Autistic (50-60%) Friendly but exhibit symptoms under stress (25-30%)

occasional support
Active but odd (10-15%) independent

 Much progress has been made with diagnosis and management of

autism spectrum disorder.

Hopefully, early detection and diagnosis of infants and children at risk

will enable treatments to be designed and implemented to alter the course of early behaviour and brain development.

Through neuroimaging approaches such as diffusion tensor imaging, functional MRI, and magnetoencephalography, abnormal findings have been identified in neuronal patterning, cortical connectivity, synaptic organisation,and electrophysiology.

Improved early identification with phenotypic characteristics and possible biological markers should allow for increasingly individualised and effective treatment.

Promotion of early identification, improved understanding of brain

mechanisms, development of effective treatments, and strategies to moderate the effect of autism spectrum disorder on families is needed

Lovaas O I Teaching Developmentally Disabled Children: The Me Book, 1981, PRO-ED, Autin, Texas Maurice C .Let Me Hear Your Voice:- A Familys Triumph Over Autism. NY, Fawcett Columbine Books, 11993 Maurice C, Green G, and Foxx MR (Eds) Making a Difference: Behavioral Intervention for Autism,Austin,Texas,Pro-ed,2001 Maurice C, Green G and Luce SE; Behavioral Intervention for Young Children With Autism: A Manual for Parents and Professionals, Austin, Texas, Pro Ed

INDIA Action For Autism (AFA) The National Centre for Autism Jasola Vihar New Delhi-110025 Tel: 011- 65347422, 40540991/92 e-mail: actionforautism@gmail.com Karnataka:Autism Society of India ,bangalore Email: autismsociety@gmail.com India Autism Forum,bangalore Email: Info@ashaforautism.com Autism research institute, San Diego, USA Autism society of America Autism society of UK

Persistent deficits in social communication and social interaction across contexts, not accounted for by general developmental delays, and manifest by all 3 of the following: 1. Deficits in social-emotional reciprocity; ranging from abnormal social approach and failure of normal back and forth conversation through reduced sharing of interests, emotions, and affect and response to total lack of initiation of social interaction, 2. Deficits in nonverbal communicative behaviors used for social interaction; ranging from poorly integrated- verbal and nonverbal communication, through abnormalities in eye contact and body-language, or deficits in understanding and use of nonverbal communication, to total lack of facial expression or gestures. 3. Deficits in developing and maintaining relationships, appropriate to developmental level (beyond those with caregivers); ranging from difficulties adjusting behavior to suit different social contexts through difficulties in sharing imaginative play and in making friends to an apparent absence of interest in people

B. Restricted, repetitive patterns of behavior, interests, or activities as manifested by at least two of the following: 1. Stereotyped or repetitive speech, motor movements, or use of objects; (such as simple motor stereotypies, echolalia, repetitive use of objects, or idiosyncratic phrases). 2. Excessive adherence to routines, ritualized patterns of verbal or nonverbal behavior, or excessive resistance to change; (such as motoric rituals, insistence on same route or food, repetitive questioning or extreme distress at small changes). 3. Highly restricted, fixated interests that are abnormal in intensity or focus; (such as strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests). 4. Hyper-or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment; (such as apparent indifference to pain/heat/cold, adverse response to specific sounds or textures, excessive smelling or touching of objects, fascination with lights or spinning objects). C. Symptoms must be present in early childhood (but may not become fully manifest until social demands exceed limited capacities) D. Symptoms together limit and impair everyday functioning. American Psychiatric Association