INTRODUCTION:

Autism is a developmental disorder characterized by difficulties with social interaction and communication and by restricted and repetitive behavior.^{1} It is a group of neurodevelopment disorders known as pervasive developmental disorders (PDD). These disorders are characterized by three core deficits: impaired communication, impaired reciprocal social interaction and restricted, repetitive and stereotyped patterns of behaviors or interests.

The presentation of these impairments is variable in range and severity and often changes with the acquisition of other developmental skills. In 1943, the American psychiatrist Leo Kenner used the term “early infantile autism” to describe children who lacked interest in other people.^{2} In 1944, an Austrian pediatrician, Hans Asperger, independently described another group of children with similar behaviors, but with milder severity and higher intellectual abilities. Since then, his name has become attached to a higher functioning form of autism, Asperger syndrome. It was not until the 1980s that the term pervasive developmental disorders was first used.^{3} Autism Spectrum Disorder (ASD) is typically diagnosed in childhood and has a wide range symptoms, some being more severe than others. These symptoms consist of communication, socialization, behavioral and interest impairments, as well as minimal social skills.^{4} Due to these symptoms, a child with ASD may have trouble relating to peers and forming meaningful relationships. Children diagnosed with autism communicate verbally, nonverbally or a combination of both. Due to this aspect of ASD, school curriculum and special education services may need to be of modified in accordance to their communication style. Social workers may encounter children with autism who express restricted and repetitive motor mannerisms in order to self-stimulate such as rocking, banging on objects, biting themselves and spinning.^{5} Autism is associated with a combination of genetic and environmental factors.^{6} Risk factors during pregnancy include certain infections, such as rubella, toxins including valproic acid, alcohol, cocaine, pesticides and air pollution, fetal growth restriction, and autoimmune diseases.^{{7, 8, 9}} Controversies surround other proposed environmental causes; for example, the vaccine hypothesis, which has been disproven.^{10} Autism affects information processing in the brain by altering connections and organization of nerve cells and their synapses.^{11}

Epidemiology:

ASD occurs more often in boys than girls, with a 4:1 male-to-female ratio.^{12} The reported prevalence rates of autism and its related disorders have been increasing worldwide over the past decades, from approximately 4 per 10 000 to 6 per 1000 children.^{13‑17} Globally, autism is estimated to affect 24.8 million people as of 2015.^{18} In the 2000s, the number of people affected was estimated at 1–2 per 1, 000 people worldwide.^{19} In the developed countries, about 1.5% of children are diagnosed with ASD as of 2017, ^{20}a more than doubling from 0.7% in 2000 in the United States.^{21}

Sign and symptoms:

Ø Behavior:

· Has inexplicable tantrums

· Has unusual interests or attachments

· Has unusual motor movements such as flapping hands or spinning

· Has extreme difficulty coping with change

Ø Sensory:

· Afraid of some everyday sounds

· Uses peripheral vision to look at objects

· Fascination with moving objects

· High tolerance of temperature and pain

Ø Communication:

· Not responding to his/her name by 12 months

· Not pointing or waving by 12 months

· Loss of words previously used

· Speech absent at 18 months

· No spontaneous phrases by 24 months

· Selective hearing – responding to certain sounds but ignoring the human voice

· Unusual language patterns (e.g. repetitive speech)

Ø Social skills:

· Looks away when you speak to him/her

· Does not return your smile

· Lack of interest in other children

· Often seems to be in his/her own world

· Does not seek to share interests with others

Ø Play:

· Prefers to play alone

· Very limited social play (e.g. “Peek-a-boo”)

· Play is limited to certain toys

· Plays with objects in unusual ways such as repetitive spinning or lining up

· Shows very strong interest in or attachment to a limited number of games or toys^{22}

Causes of autism:

The exact cause of ASD is unknown. The most current research demonstrates that there’s no single cause. Some of the suspected risk factors for autism include:

Ø having an immediate family member with autism

Ø genetic mutations

Ø fragile X syndrome and other genetic disorders

Ø being born to older parents

Ø low birth weight

Ø metabolic imbalances

Ø exposure to heavy metals and environmental toxins

Ø a history of viral infections

Ø fetal exposure to the medications valproic acid (Depakene) or thalidomide (Thalomid)^{{23, 24, 25}}

According to the National Institute of Neurological Disorders and Stroke (NINDS), both genetics and environment may determine whether a person develops autism.

Types of ASD:

There are three different types of Autism Spectrum Disorders:

§ Autistic Disorder: (also called "classic" autism)

This is what most people think of when hearing the word "autism." People with autistic disorder usually have significant language delays, social and communication challenges, and unusual behaviors and interests. Many people with autistic disorder also have intellectual disability.

§ Asperger Syndrome:

People with Asperger syndrome usually have some milder symptoms of autistic disorder. They might have social challenges and unusual behaviors and interests. However, they typically do not have problems with language or intellectual disability.

§ Pervasive Developmental Disorder:

Not Otherwise Specified (PDD-NOS; also called "atypical autism")

People who meet some of the criteria for autistic disorder or Asperger syndrome, but not all, may be diagnosed with PDD-NOS. People with PDD-NOS usually have fewer and milder symptoms than those with autistic disorder. The symptoms might cause only social and communication challenges.^{{
26, 27, 28}}

DIAGNOSIS:

Diagnosis is based on behavior, not cause or mechanism.^{{29, 30}} Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, typically before age three, and lead to clinically significant functional impairment.^{31} Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with unusual objects. Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semi structured parent interview, and the Autism Diagnostic Observation Schedule (ADOS)^{32} uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.^{33} The Diagnostic interview for social and communication disorders (DISCO) may also be used.^[34} Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits. Girls are often diagnosed later than boys.^{35}

Pathophysiology:

Ø Autism mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.^[36] The behaviors appear to have multiple pathophysiologies.^[37]How autism occurs is not well understood.

Ø A 2015 review proposed that immune dysregulation, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction.^[38] A 2016 review concludes that enteric nervous systemabnormalities might play a role in neurological disorders such as autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain.^[39]Several lines of evidence point to synaptic dysfunction as a cause of autism. Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.^[40]

Ø All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, there is strong evidence that autism arises very early in development.^{41}

Ø Autism affects the amygdala, cerebellum, and many other parts of the brain.^{42}

Treatment of Autism spectrum disorder

There are no “cures” for autism, but therapies and other treatment considerations can help people feel better or alleviate their symptoms.

Many treatment approaches involve therapies such as:

1. Education:

Educational interventions often used include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.^{43} Early, intensive ABA therapy has demonstrated effectiveness in enhancing global functioning in preschool children.^{44}

2. Medication:

Medications may be used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.They may also be used for associated health problems, such as ADHD or anxiety.^{45}

3. Alternative treatments:

Alternative treatments for managing autism may include:

Ø high-dose vitamins

Ø chelation therapy, which involves flushing metals from the body

Ø hyperbaric oxygen therapy

Ø melatonin to address sleep issues^{{46, 47}}

4. Drugs used in the treatment of ASD:

ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.^{{48, 49}} Atypical drugs risperidone and aripiprazole are FDA-approved for treating associated aggressive and self-injurious behaviors.^{{50, 51, 52}} SSRI antidepressants, such as fluoxetine and fluvoxamine, have been shown to be effective in reducing repetitive and ritualistic behaviors.^{53}

CONCLUSIONS:

Autism is not curative but some behavioral therapies like applied behavioral analysis development models, speech language therapy, social skill therapy can help autism patients feel better or alternative their symptoms. Some allopathic drugs like Resperidone and aripiprazole is approved for curative behavioral symptoms in autism.

REFERENCE:

1. Autism Spectrum Disorder, 299.00 (F84.0). In: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Publishing; 2013.

2. Kolvin I. Studies in childhood psychoses: I. Diagnostic criteria and classification. Brit J Psychiatry.1971; 118:381–4. [PubMed]

3. Klin A. Asperger syndrome: an update. Rev Bras Psiquiatr. 2003; 25:103–9. [PubMed]

4. Weiss, J. A., & Lunsky, Y. (2011).The Brief Family Distress Scale: A measure of Ccrisis in caregivers of individuals with autism spectrum disorders. Journal of Child and Family Studies, 20(4), 521-528. doi: 10.1007/s10826-010-9419-y.

5. Mays, N. M, Beal-Alvarez, J., & Jolivette, K. (2011).Using movement-based sensory interventions to address self-stimulatory behaviors in students with autism. Teaching Exceptional Children, 43(6), 46-52. Retrieved from EBSCO Mega FILE database.

6. Chaste P, Leboyer M (2012). "Autism risk factors: genes, environment, and gene-environment interactions". Dialogues in Clinical Neuroscience. 14 (3): 281– PMC 3513682. PMID 23226953.

7. Ornoy A, Weinstein-Fudim L, Ergaz Z (2015). "Prenatal factors associated with autism spectrum disorder (ASD)". Reproductive Toxicology. 56: 155–. PMID 26021712.

8. Vohr BR, Poggi Davis E, Wanke CA, Krebs NF (2017). "Neurodevelopment: The Impact of Nutrition and Inflammation During Preconception and Pregnancy in Low-Resource Settings". Pediatrics (Review). 139 (Suppl1):S38–S49. doi:10.1542/peds.2016- PMID 28562247.

9. Samsam M, Ahangari R, Naser SA (2014). "Pathophysiology of autism spectrum disorders: revisiting gastrointestinal involvement and immune imbalance". WorldJ Gastroenterol (Review). 20 (29):9942–. PMC 4123375. PMID 25110424.

10. Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". ActaPaediatr. 94 (1):2–15. doi:10.1111/j.1651-227.2005.tb01779.x. PMID 15858952.

11. Levy SE, Mandell DS, Schultz RT (2009). "Autism". Lancet. 374 (9701):1627–38. doi:10.1016/S0140-6736(09)61376-3. PMC 2863325. PMID 19819542.

12. Fombonne E, Zakarian R, Bennett A, Meng L, McLean-Heywood D. Pervasive evelopmental disorders in Montreal, Quebec, Canada: prevalence and links with immunizations. Pediatrics. 2006; 118:e139–50. Available from: http://pediatrics.aappublications.org/cgi/reprint/118/1/e139 [lastcited on 2009 Jun 19] [PubMed}.

13. Chakrabarti S, Fombonne E. Pervasive developmental disorders in preschool children. JAMA.2001; 285:3093–9. [PubMed]

14. Chakrabarti S, Fombonne E. Pervasive developmental disorders in preschool children: confirmationof high prevalence. Am J Psychiatry. 2005; 162:1133–41. [PubMed]

15. Centers for Disease Control and Prevention. Mental health in the United States: parental report of diagnosed autism in children aged 4-17 years, United States, 2003-2004. MMWR Morb Mortal WklyRep. 2006; 55:481–6. [PubMed]

16. Bertrand J, Mars A, Boyle C, Bove F, Yeargin-Allsop M, DeCoufle P. Prevalence of autism in a United States population: the Brick Township, New Jersey, investigation. Pediatr. 2001; 108:1155–61.[PubMed]

17. Yeargin-Allsopp M, Rice C, Karapurkar T, Doernberg N, Boyle C, Murphy C. Prevalence of autismin a US metropolitan area. JAMA. 2003; 289:49–55. [PubMed]

18. GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.

19. Newschaffer CJ, Croen LA, Daniels J, Giarelli E, Grether JK, Levy SE, Mandell DS, Miller LA, Pinto-Martin J, Reaven J, Reynolds AM, Rice CE, Schendel D, Windham GC (2007). "The epidemiology of autism spectrum disorders". Annual Review of Public Health. 28: 235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.

20. Lyall K, Croen L, Daniels J, Fallin MD, Ladd-Acosta C, Lee BK, Park BY, Snyder NW, Schendel D, Volk H, Windham GC, Newschaffer C (March 2017). "The Changing Epidemiology of Autism Spectrum Disorders". Annual Review of Public Health. 38: 81–102. doi:10.1146/annurev-publhealth-031816-044318. PMID 28068486.

21. ASD Data and Statistics". CDC.gov. Archived from the original on 18 April 2014. Retrieved 11 July 2016.

22. Landa RJ (2008). "Diagnosis of autism spectrum disorders in the first 3 years of life". Nat Clin Pract Neurol. 4 (3): 138–47. doi:10.1038/ncpneuro0731. PMID 18253102.

23. Abrahams BS, Geschwind DH (May 2008). "Advances in autism genetics: on the threshold of a new neurobiology". Nature Reviews. Genetics. 9 (5): 341– PMC 2756414. PMID 18414403.

24. Buxbaum JD (2009). "Multiple rare variants in the etiology of autism spectrum disorders". Dialogues in Clinical Neuroscience. 11 (1): 35–43. PMC 3181906. PMID 19432386.

25. Lyall K, Schmidt RJ, Hertz-Picciotto I (April 2014). "Maternal lifestyle and environmental risk factors for autism spectrum disorders". Int J Epidemiol. 43 (2): 443–PMC 3997376. PMID 24518932.

26. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed.Arlington, VA: American Psychiatric Publishing, Inc; 2000. pp. 69–84.

27. World Health Organization. International Statistical Classification of Diseases and Related HealthProblems, 10th Revision. World Health Organization; 2007 Available from:http://www.who.int/classifications/apps/icd/icd10°nline/ [last cited on 2009 Mar 19]

28. Mattila ML, Kielinen M, Jussila K, Linna SL, Bloigu R, Ebeling H, Moilanen I. An epidemiologicaland diagnostic study of Asperger syndrome according to four sets of diagnostic criteria. J Am Acad Child Adolesc Psychiatry. 2007; 46:636–46. [PubMed]

29. London E (2007). "The role of the neurobiologist in redefining the diagnosis of autism". Brain Pathol. 17 (4): 408–11. doi:10.1111/j.1750-3639.2007.00103.x. PMID 17919126.

30. Baird G, Cass H, Slonims V (2003). "Diagnosis of autism". BMJ. 327 (7413): 488–93. doi:10.1136/bmj.327.7413.488. PMC 188387. PMID 12946972.

31. Autism Spectrum Disorder, 299.00 (F84.0). In: American Psychiatric ssociation. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Publishing; 2013.

32. Gotham K, Risi S, Dawson G, Tager-Flusberg H, Joseph R, Carter A, Hepburn S, McMahon W, Rodier P, Hyman SL, Sigman M, Rogers S, Landa R, Spence MA, Osann K, Flodman P, Volkmar F, Hollander E, Buxbaum J, Pickles A, Lord C (June 2008). "A replication of the Autism Diagnostic Observation Schedule (ADOS) revised algorithms". Journal of the American Academy of Child and Adolescent Psychiatry. 47 (6): 642–. PMC 3057666. PMID 18434924.

33. Volkmar FR, Paul R, Pelphrey KA, Rogers SJ, eds. (2014). Handbook of Autism and Pervasive Developmental Disorders: Volume Two: Assessment, Interventions, and Policy. 2 (4th ed.). Hoboken, New Jersey: John Wiley & Sons. p. 301. ISBN 978-1-118-28220-5. LCCN 2013034363. OCLC 946133861. Retrieved 1 March 2019 – via Google Books.

34. Kan CC, Buitelaar JK, van der Gaag RJ (June 2008). "[Autism spectrum disorders in adults]". Nederlands Tijdschrift voor Geneeskunde. 152 (24): 1365–9. PMID 18664213.

35. Why Many Autistic Girls are Overlooked (Report). Child Mind Institute. Retrieved 13 February 2018.

36. Penn HE (2006). "Neurobiological correlates of autism: a review of recent research". Child Neuropsychol. 12 (1): 57–79. doi:10.1080/09297040500253546. PMID 16484102.

37. London E (2007). "The role of the neurobiologist in redefining the diagnosis of autism". Brain Pathol. 17 (4): 408–11. doi:10.1111/j.1750-3639.2007.00103.x. PMID 17919126.

38. Wasilewska J, Klukowski M (2015). "Gastrointestinal symptoms and autism spectrum disorder: links and risks - a possible new overlap syndrome". Pediatric Health Med Ther(Review). 6: 153–166. doi:10.2147/PHMT.S85717. PMC 5683266. PMID 29388597

39. Rao M, Gershon MD (September 2016). "The bowel and beyond: the enteric nervous system in neurological disorders". Nat Rev Gastroenterol Hepatol (Review). 13 (9): 517–28. doi:10.1038/nrgastro.2016.107. PMC 5005185. PMID 27435372.

40. Betancur C, Sakurai T, Buxbaum JD (2009). "The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders". Trends Neurosci. 32 (7): 402–12. doi:10.1016/j.tins.2009.04.003. PMID 19541375.

41. Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci. 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245.

42. Amaral DG, Schumann CM, Nordahl CW (2008). "Neuroanatomy of autism". Trends Neurosci. 31 (3): 137–45. doi:10.1016/j.tins.2007.12.005. PMID 18258309

43. Myers SM, Johnson CP (November 2007). "Management of children with autism spectrum disorders". Pediatrics. 120 (5): 1162–82. doi:10.1542/peds.2007-2362. PMID 17967921.

44. Eikeseth S (2009). "Outcome of comprehensive psycho-educational interventions for young childrenwithautism". ResDevisabil. 30 (1):158–:10.1016/j.ridd.2008.02.003. PMID 18385012.

45. Sanchack, KE; Thomas, CA (15 December 2016). "Autism Spectrum Disorder: Primary Care Principles". American Family Physician. 94 (12): 972–79. PMID 28075089

46. Tye C, Runicles AK, Whitehouse AJ, Alvares GA (2018). "Characterizing the Interplay Between Autism Spectrum Disorder and Comorbid Medical Conditions: An Integrative Review". FrontPsychiatry (Review). 9::10.3389/fpsyt.2018.00751. PMC 6354568. PMID 30733689.

47. James S, Stevenson SW, Silove N, Williams K (2015). "Chelation for autism spectrum disorder(ASD)". (Review):10.1002/14651858.CD010766. PMID 26106752.

48. Oswald DP, Sonenklar NA (June 2007). "Medication use among children with autism spectrum disorders". Journal of Child and Adolescent Psychopharmacology. 17 (3): 348–55. doi:10.1089/cap.2006.17303. PMID 17630868.

49. Doyle CA, McDougle CJ (September 2012). "Pharmacologic treatments for the behavioral symptoms associated with autism spectrum disorders across the lifespan". Dialogues in Clinical Neuroscience. 14 (3): 263–79. PMC 3513681. PMID 23226952.

50. i N, Findling RL (March 2015). "An update on pharmacotherapy for autism spectrum disorder in children and adolescents". Current Opinion in Psychiatry. 28 (2): 91–101. doi:10.1097/YCO.0000000000000132. PMID 25602248.

51. Rapin I, Tuchman RF (October 2008). "Autism: definition, neurobiology, screening, diagnosis". Pediatric Clinics of North America. 55 (5): 1129–46, . PMID 18929056.

52. 52 . Leskovec TJ, Rowles BM, Findling RL (2008). "Pharmacological treatment options for autism spectrum disorders in children and adolescents". Harvard Review of Psychiatry. 16(2): 97–112. Doi:10.1080/10673220802075852. PMID 18415882.

53. Myers SM, Johnson CP (November 2007). "Management of children with autism spectrum disorders". Pediatrics. 120 (5): 1162–82. doi:10.1542/peds.2007-2362. PMID 17967921.

Received on 03.04.2019 Modified on 11.04.2019

Res. J. Pharmacology and Pharmacodynamics.2019; 11(2):76-80 .

DOI: 10.5958/2321-5836.2019.00013.2