Neurodevelopmental disorder

Neurodevelopmental disorder
SpecialtyPsychiatry, neurology

Neurodevelopmental disorders are a group of mental conditions affecting the development of the nervous system, which includes the brain and spinal cord. According to the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (DSM-5) published in 2013, these conditions generally appear in early childhood, usually before children start school, and can persist into adulthood.[1] The key characteristic of all these disorders is that they negatively impact a person's functioning in one or more domains of life (personal, social, academic, occupational) depending on the disorder and deficits it has caused. All of these disorders and their levels of impairment exist on a spectrum, and affected individuals can experience varying degrees of symptoms and deficits, despite having the same diagnosis.[1][2]

The DSM-5 classifies neurodevelopmental disorders into six overarching groups: intellectual, communication, autism, attention deficit hyperactivity, motor, and specific learning disorders.[1] Often one disorder is accompanied by another.[2]

Classification

Intellectual disability

Intellectual disability, also known as general learning disability is a disorder that affects the ability to learn, retain, or process information; to think critically or abstractly, and to solve problems. Adaptive behaviour is limited, affecting daily living activities. Global developmental delay is categorized under intellectual disability and is diagnosed when several areas of intellectual functioning are affected.[3]

Communication disorders

Main article: Communication disorder

A communication disorder is any disorder that affects an individual's ability to comprehend, detect, or apply language and speech to engage in dialogue effectively with others.[4] This also encompasses deficiencies in verbal and nonverbal communication styles.[5] Examples include stuttering, sound substitution, inability to understand or use one's native language.[6]

Autism spectrum disorder

Main article: Autism

Autism, also called autism spectrum disorder (ASD) or autism spectrum condition (ASC), is a neurodevelopmental disorder characterized by symptoms of deficient reciprocal social communication and the presence of restricted, repetitive, and inflexible patterns of behavior. While its severity and specific manifestations vary widely across the spectrum, autism generally affects a person's ability to understand and connect with others, as well as their adaptability to everyday situations. Like most developmental disorders, autism exists along a dimension of symptom severity, subjective distress, and functional impairment. A consequence of this dimensionality is substantial variability in the nature and extent of support a person with ASD requires.

A formal diagnosis of ASD requires not merely the presence of ASD symptoms, but symptoms that cause significant impairment in multiple domains of functioning, in addition to being excessive or atypical enough to be developmentally and socioculturally inappropriate.[7][8]

Attention deficit hyperactivity disorder

Main article: Attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterised by executive dysfunction occasioning symptoms of inattention, hyperactivity, impulsivity and emotional dysregulation that are excessive and pervasive, impairing in multiple contexts, and developmentally-inappropriate.[3][9][10][11]

ADHD symptoms arise from executive dysfunction,[20] and emotional dysregulation is often considered a core symptom.[24] Difficulties in self-regulation such as time management, inhibition and sustained attention may cause poor professional performance, relationship difficulties and numerous health risks,[25][26] collectively predisposing to a diminished quality of life[27] and a direct average reduction in life expectancy of 13 years.[28][29] ADHD is associated with other neurodevelopmental and mental disorders as well as non-psychiatric disorders, which can cause additional impairment.[11]

Motor disorders

Motor disorders including developmental coordination disorder, stereotypic movement disorder, and tic disorders (such as Tourette's syndrome), and apraxia of speech.

Specific learning disorders

Main article: Learning disability § By function impaired

Deficits in any area of information processing can manifest in a variety of specific learning disabilities (SLD). It is possible for an individual to have more than one of these difficulties. This is referred to as comorbidity or co-occurrence of learning disabilities.[30] In the UK, the term dual diagnosis is often used to refer to co-occurrence of learning difficulties.

Currently being researched

There are neurodevelopmental research projects examining potential new classifications of disorders including:

  1. Nonverbal learning disorder (NLD or NVLD), a neurodevelopmental disorder thought to be linked to white matter in the right hemisphere of the brain and generally considered to include (a) low visuospatial intelligence; (b) discrepancy between verbal and visuospatial intelligence; (c) visuoconstructive and fine-motor coordination skills; (d) visuospatial memory tasks; (e) reading better than mathematical achievement; and (f) socioemotional skills.[31][32][33] While Nonverbal learning disorder is not categorized in the ICD or DSM as a discrete classification, "the majority of researchers and clinicians agree that the profile of NLD clearly exists (but see Spreen, 2011, for an exception[34]), but they disagree on the need for a specific clinical category and on the criteria for its identification."[35]

Presentation

Consequences

The multitude of neurodevelopmental disorders spans a wide range of associated symptoms and severity, resulting in different degrees of mental, emotional, physical, and economic consequences for individuals, and in turn families, social groups, and society.[2]

Causes

The development of the nervous system is tightly regulated and timed; it is influenced by both genetic programs and the prenatal environment. Any significant deviation from the normal developmental trajectory early in life can result in missing or abnormal neuronal architecture or connectivity.[36] Because of the temporal and spatial complexity of the developmental trajectory, there are many potential causes of neurodevelopmental disorders that may affect different areas of the nervous system at different times and ages. These range from social deprivation, genetic and metabolic diseases, immune disorders, infectious diseases, nutritional factors, physical trauma, and toxic and prenatal environmental factors. Some neurodevelopmental disorders, such as autism and other pervasive developmental disorders, are considered multifactorial syndromes which have many causes that converge to a more specific neurodevelopmental manifestation.[37] Some deficits may be predicted from observed deviations in the maturation patterns of the infant gut microbiome.[38]

Social deprivation

Deprivation from social and emotional care causes severe delays in brain and cognitive development.[39] Studies with children growing up in Romanian orphanages during Nicolae Ceauşescu's regime reveal profound effects of social deprivation and language deprivation on the developing brain. These effects are time-dependent. The longer children stayed in negligent institutional care, the greater the consequences. By contrast, adoption at an early age mitigated some of the effects of earlier institutionalization.[40]

Genetic disorders

Main article: Genetic disorder
A child with Down syndrome

A prominent example of a genetically determined neurodevelopmental disorder is trisomy 21, also known as Down syndrome. This disorder usually results from an extra chromosome 21,[41] although in uncommon instances it is related to other chromosomal abnormalities such as translocation of the genetic material. It is characterized by short stature, epicanthal (eyelid) folds, abnormal fingerprints, and palm prints, heart defects, poor muscle tone (delay of neurological development), and intellectual disabilities (delay of intellectual development).[42]

Less commonly known genetically determined neurodevelopmental disorders include Fragile X syndrome. Fragile X syndrome was first described in 1943 by Martin and Bell, studying persons with family history of sex-linked "mental defects".[43] Rett syndrome, another X-linked disorder, produces severe functional limitations.[44] Williams syndrome is caused by small deletions of genetic material from chromosome 7.[45] The most common recurrent copy number variation disorder is DiGeorge syndrome (22q11.2 deletion syndrome), followed by Prader-Willi syndrome and Angelman syndrome.[46]

Immune dysfunction

Main article: Immune-mediated disease

Immune reactions during pregnancy, both maternal and of the developing child, may produce neurodevelopmental disorders. One typical immune reaction in infants and children is PANDAS,[47] or Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection.[48] Another disorder is Sydenham's chorea, which results in more abnormal movements of the body and fewer psychological sequellae. Both are immune reactions against brain tissue that follow infection by Streptococcus bacteria. Susceptibility to these immune diseases may be genetically determined,[49] so sometimes several family members may have one or both of them following an epidemic of Strep infection.[citation needed]

Infectious diseases

Systemic infections can result in neurodevelopmental consequences, when they occur in infancy and childhood of humans, but would not be called a primary neurodevelopmental disorder. For example HIV[50] Infections of the head and brain, like brain abscesses, meningitis or encephalitis have a high risk of causing neurodevelopmental problems and eventually a disorder. For example, measles can progress to subacute sclerosing panencephalitis.

A number of infectious diseases can be transmitted congenitally (either before or at birth), and can cause serious neurodevelopmental problems, as for example the viruses HSV, CMV, rubella (congenital rubella syndrome), Zika virus, or bacteria like Treponema pallidum in congenital syphilis, which may progress to neurosyphilis if it remains untreated. Protozoa like Plasmodium[50] or Toxoplasma which can cause congenital toxoplasmosis with multiple cysts in the brain and other organs, leading to a variety of neurological deficits.

Some cases of schizophrenia may be related to congenital infections, though the majority are of unknown causes.[51]

Metabolic disorders

Metabolic disorders in either the mother or the child can cause neurodevelopmental disorders. Two examples are diabetes mellitus (a multifactorial disorder) and phenylketonuria (an inborn error of metabolism). Many such inherited diseases may directly affect the child's metabolism and neural development[52] but less commonly they can indirectly affect the child during gestation. (See also teratology).

In a child, type 1 diabetes can produce neurodevelopmental damage by the effects of excess or insufficient glucose. The problems continue and may worsen throughout childhood if the diabetes is not well controlled.[53] Type 2 diabetes may be preceded in its onset by impaired cognitive functioning.[54]

A non-diabetic fetus can also be subjected to glucose effects if its mother has undetected gestational diabetes. Maternal diabetes causes excessive birth size, making it harder for the infant to pass through the birth canal without injury or it can directly produce early neurodevelopmental deficits. Usually the neurodevelopmental symptoms will decrease in later childhood.[55]

Phenylketonuria, also known as PKU, can induce neurodevelopmental problems and children with PKU require a strict diet to prevent intellectual disability and other disorders. In the maternal form of PKU, excessive maternal phenylalanine can be absorbed by the fetus even if the fetus has not inherited the disease. This can produce intellectual disability and other disorders.[56][57]

Nutrition

Nutrition disorders and nutritional deficits may cause neurodevelopmental disorders, such as spina bifida, and the rarely occurring anencephaly, both of which are neural tube defects with malformation and dysfunction of the nervous system and its supporting structures, leading to serious physical disability and emotional sequelae. The most common nutritional cause of neural tube defects is folic acid deficiency in the mother, a B vitamin usually found in fruits, vegetables, whole grains, and milk products.[58][59] (Neural tube defects are also caused by medications and other environmental causes, many of which interfere with folate metabolism, thus they are considered to have multifactorial causes.)[60][61] Another deficiency, iodine deficiency, produces a spectrum of neurodevelopmental disorders ranging from mild emotional disturbance to severe intellectual disability. (see also congenital iodine deficiency syndrome).[62]

Excesses in both maternal and infant diets may cause disorders as well, with foods or food supplements proving toxic in large amounts. For instance in 1973 K.L. Jones and D.W. Smith of the University of Washington Medical School in Seattle found a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in children of alcoholic mothers, now called fetal alcohol syndrome, It has significant symptom overlap with several other entirely unrelated neurodevelopmental disorders.[63]

Physical trauma

Main article: Traumatic brain injury
CT scan showing epidural hematoma, a type of traumatic brain injury (upper left)

Brain trauma in the developing human is a common cause (over 400,000 injuries per year in the US alone, without clear information as to how many produce developmental sequellae)[64] of neurodevelopmental syndromes. It may be subdivided into two major categories, congenital injury (including injury resulting from otherwise uncomplicated premature birth)[65] and injury occurring in infancy or childhood. Common causes of congenital injury are asphyxia (obstruction of the trachea), hypoxia (lack of oxygen to the brain), and the mechanical trauma of the birth process itself.[66]

Placenta

Although it not clear yet as strong is the correlation between placenta and brain, a growing number of studies are linking placenta to fetal brain development.[67]

Diagnosis

Neurodevelopmental disorders are diagnosed by evaluating the presence of characteristic symptoms or behaviors in a child, typically after a parent, guardian, teacher, or other responsible adult has raised concerns to a doctor.[68]

Neurodevelopmental disorders may also be confirmed by genetic testing. Traditionally, disease related genetic and genomic factors are detected by karyotype analysis, which detects clinically significant genetic abnormalities for 5% of children with a diagnosed disorder. As of 2017, chromosomal microarray analysis (CMA) was proposed to replace karyotyping because of its ability to detect smaller chromosome abnormalities and copy-number variants, leading to greater diagnostic yield in about 20% of cases.[46] The American College of Medical Genetics and Genomics and the American Academy of Pediatrics recommend CMA as standard of care in the US.[46]

Management

See also

References

  1. ^ a b c Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Washington, D.C.: American Psychiatric Association. 2013. pp. 31–33. ISBN 978-0-89042-554-1.
  2. ^ a b c Morris-Rosendahl DJ, Crocq MA (March 2020). "Neurodevelopmental disorders-the history and future of a diagnostic concept". Dialogues in Clinical Neuroscience. 22 (1): 65–72. doi:10.31887/DCNS.2020.22.1/macrocq. PMC 7365295. PMID 32699506.
  3. ^ a b Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Washington, D.C.: American Psychiatric Association. 2013. pp. 58–65. ISBN 978-0-89042-554-1.
  4. ^ Collins, John William. "The greenwood dictionary of education". Greenwood, 2011. page 86. ISBN 978-0-313-37930-7
  5. ^ "Definitions of Communication Disorders and Variations". American Speech-Language-Hearing Association. 1993. Retrieved 2023-11-07.
  6. ^ Gleason, Jean Berko (2001). The development of language. Boston: Allyn and Bacon. ISBN 978-0-205-31636-6. OCLC 43694441.
  7. ^ "Autism spectrum disorder". Retrieved 8 September 2024.
  8. ^ "IACC Subcommittee Diagnostic Criteria - DSM-5 Planning Group | IACC". iacc.hhs.gov. Retrieved 2024-08-01.
  9. ^ Diagnostic and Statistical Manual of Mental Disorders (Fifth, Text Revision (DSM-5-TR) ed.). Washington, D.C.: American Psychiatric Publishing. February 2022. ISBN 978-0-89042-575-6. OCLC 1288423302.
  10. ^ Foreman DM (February 2006). "Attention deficit hyperactivity disorder: legal and ethical aspects". Archives of Disease in Childhood. 91 (2): 192–194. doi:10.1136/adc.2004.064576. PMC 2082674. PMID 16428370.
  11. ^ a b Faraone SV, Banaschewski T, Coghill D, Zheng Y, Biederman J, Bellgrove MA, et al. (September 2021). "The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder". Neuroscience and Biobehavioral Reviews. 128. Elsevier BV: 789–818. doi:10.1016/j.neubiorev.2021.01.022. ISSN 0149-7634. PMC 8328933. PMID 33549739.
  12. ^ Pievsky MA, McGrath RE (March 2018). "The Neurocognitive Profile of Attention-Deficit/Hyperactivity Disorder: A Review of Meta-Analyses". Archives of Clinical Neuropsychology. 33 (2): 143–157. doi:10.1093/arclin/acx055. PMID 29106438.
  13. ^ Schoechlin C, Engel RR (August 2005). "Neuropsychological performance in adult attention-deficit hyperactivity disorder: meta-analysis of empirical data". Archives of Clinical Neuropsychology. 20 (6): 727–744. doi:10.1016/j.acn.2005.04.005. PMID 15953706.
  14. ^ Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K (February 2013). "Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects". JAMA Psychiatry. 70 (2): 185–198. doi:10.1001/jamapsychiatry.2013.277. PMID 23247506.
  15. ^ Hoogman M, Muetzel R, Guimaraes JP, Shumskaya E, Mennes M, Zwiers MP, et al. (July 2019). "Brain Imaging of the Cortex in ADHD: A Coordinated Analysis of Large-Scale Clinical and Population-Based Samples". The American Journal of Psychiatry. 176 (7): 531–542. doi:10.1176/appi.ajp.2019.18091033. PMC 6879185. PMID 31014101.
  16. ^ Brown TE (October 2008). "ADD/ADHD and Impaired Executive Function in Clinical Practice". Current Psychiatry Reports. 10 (5): 407–411. doi:10.1007/s11920-008-0065-7. PMID 18803914. S2CID 146463279.
  17. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapters 10 and 13". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 266, 315, 318–323. ISBN 978-0-07-148127-4. Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.
  18. ^ Diamond A (2013). "Executive functions". Annual Review of Psychology. 64: 135–168. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641. EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not.
  19. ^ Antshel KM, Hier BO, Barkley RA (2014). "Executive Functioning Theory and ADHD". In Goldstein S, Naglieri JA (eds.). Handbook of Executive Functioning. New York, NY: Springer. pp. 107–120. doi:10.1007/978-1-4614-8106-5_7. ISBN 978-1-4614-8106-5.
  20. ^ [12][13][14][15][16][17][18][19]
  21. ^ Retz W, Stieglitz RD, Corbisiero S, Retz-Junginger P, Rösler M (October 2012). "Emotional dysregulation in adult ADHD: What is the empirical evidence?". Expert Review of Neurotherapeutics. 12 (10): 1241–1251. doi:10.1586/ern.12.109. PMID 23082740. S2CID 207221320.
  22. ^ Faraone SV, Rostain AL, Blader J, Busch B, Childress AC, Connor DF, et al. (February 2019). "Practitioner Review: Emotional dysregulation in attention-deficit/hyperactivity disorder - implications for clinical recognition and intervention". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 60 (2): 133–150. doi:10.1111/jcpp.12899. PMID 29624671.
  23. ^ Shaw P, Stringaris A, Nigg J, Leibenluft E (March 2014). "Emotion dysregulation in attention deficit hyperactivity disorder". The American Journal of Psychiatry. 171 (3): 276–293. doi:10.1176/appi.ajp.2013.13070966. PMC 4282137. PMID 24480998.
  24. ^ [21][22][23]
  25. ^ Barkley RA, Murphy KR (2011-06-01). "The Nature of Executive Function (EF) Deficits in Daily Life Activities in Adults with ADHD and Their Relationship to Performance on EF Tests". Journal of Psychopathology and Behavioral Assessment. 33 (2): 137–158. doi:10.1007/s10862-011-9217-x. ISSN 1573-3505.
  26. ^ Fleming M, Fitton CA, Steiner MF, McLay JS, Clark D, King A, et al. (July 2017). "Educational and Health Outcomes of Children Treated for Attention-Deficit/Hyperactivity Disorder". JAMA Pediatrics. 171 (7): e170691. doi:10.1001/jamapediatrics.2017.0691. PMC 6583483. PMID 28459927.
  27. ^ Lee YC, Yang HJ, Chen VC, Lee WT, Teng MJ, Lin CH, et al. (2016-04-01). "Meta-analysis of quality of life in children and adolescents with ADHD: By both parent proxy-report and child self-report using PedsQL™". Research in Developmental Disabilities. 51–52: 160–172. doi:10.1016/j.ridd.2015.11.009. PMID 26829402.
  28. ^ Barkley RA, Fischer M (July 2019). "Hyperactive Child Syndrome and Estimated Life Expectancy at Young Adult Follow-Up: The Role of ADHD Persistence and Other Potential Predictors". Journal of Attention Disorders. 23 (9): 907–923. doi:10.1177/1087054718816164. PMID 30526189. S2CID 54472439.
  29. ^ Cattoi B, Alpern I, Katz JS, Keepnews D, Solanto MV (April 2022). "The Adverse Health Outcomes, Economic Burden, and Public Health Implications of Unmanaged Attention Deficit Hyperactivity Disorder (ADHD): A Call to Action Resulting from CHADD Summit, Washington, DC, October 17, 2019". Journal of Attention Disorders. 26 (6): 807–808. doi:10.1177/10870547211036754. PMID 34585995. S2CID 238218526.
  30. ^ Kirby A (2011-10-26). Dyslexia, Dyspraxia & Overlapping Learning Difficulties. Retrieved 2024-11-29 – via YouTube.
  31. ^ Mammarella IC, Cornoldi C (2020). "Nonverbal learning disability (developmental visuospatial disorder)". Neurocognitive Development: Disorders and Disabilities. Handbook of Clinical Neurology. Vol. 174. pp. 83–91. doi:10.1016/B978-0-444-64148-9.00007-7. ISBN 9780444641489. PMID 32977898. S2CID 221939377.
  32. ^ Incháustegui MV (2019-06-18). "Nonverbal Learning Disabilities (Nld) – Clinical Description about Neurodevelopmental Disabilities". Archives in Neurology & Neuroscience. 4 (1). doi:10.33552/ANN.2019.04.000579.
  33. ^ Mammarella IC, Cornoldi C (2020). "Nonverbal learning disability (developmental visuospatial disorder)". Neurocognitive Development: Disorders and Disabilities. Handbook of Clinical Neurology. Vol. 174. Elsevier. pp. 83–91. doi:10.1016/b978-0-444-64148-9.00007-7. ISBN 978-0-444-64148-9. PMID 32977898. S2CID 221939377.
  34. ^ Spreen O (September 2011). "Nonverbal learning disabilities: a critical review". Child Neuropsychology. 17 (5): 418–443. doi:10.1080/09297049.2010.546778. PMID 21462003. S2CID 31974898. Archived from the original on 2021-07-20. Retrieved 2021-04-29.
  35. ^ Mammarella IC, Cornoldi C (2014-05-04). "An analysis of the criteria used to diagnose children with Nonverbal Learning Disability (NLD)". Child Neuropsychology. 20 (3): 255–280. doi:10.1080/09297049.2013.796920. hdl:11577/2668053. PMID 23705673. S2CID 34107811.
  36. ^ Pletikos M, Sousa AM, Sedmak G, Meyer KA, Zhu Y, Cheng F, et al. (January 2014). "Temporal specification and bilaterality of human neocortical topographic gene expression". Neuron. 81 (2): 321–332. doi:10.1016/j.neuron.2013.11.018. PMC 3931000. PMID 24373884.{{cite journal}}: CS1 maint: overridden setting (link)
  37. ^ Samaco RC, Hogart A, LaSalle JM (February 2005). "Epigenetic overlap in autism-spectrum neurodevelopmental disorders: MECP2 deficiency causes reduced expression of UBE3A and GABRB3". Human Molecular Genetics. 14 (4): 483–492. doi:10.1093/hmg/ddi045. PMC 1224722. PMID 15615769.
  38. ^ Sizemore N, Oliphant K, Zheng R, Martin CR, Claud EC, Chattopadhyay I (2024-04-12). "A digital twin of the infant microbiome to predict neurodevelopmental deficits". Science Advances. 10 (15): eadj0400. Bibcode:2024SciA...10J.400S. doi:10.1126/sciadv.adj0400. ISSN 2375-2548. PMC 11006218. PMID 38598636.
  39. ^ van IJzendoorn MH, Palacios J, Sonuga-Barke EJ, Gunnar MR, Vorria P, McCall RB, et al. (December 2011). "Children in Institutional Care: Delayed Development and Resilience". Monographs of the Society for Research in Child Development. 76 (4): 8–30. doi:10.1111/j.1540-5834.2011.00626.x. PMC 4130248. PMID 25125707.{{cite journal}}: CS1 maint: overridden setting (link)
  40. ^ Nelson CA, Zeanah CH, Fox NA, Marshall PJ, Smyke AT, Guthrie D (December 2007). "Cognitive recovery in socially deprived young children: the Bucharest Early Intervention Project". Science. 318 (5858): 1937–1940. Bibcode:2007Sci...318.1937N. doi:10.1126/science.1143921. PMID 18096809. S2CID 1460630.[permanent dead link‍]
  41. ^ Diamandopoulos K, Green J (October 2018). "Down syndrome: An integrative review". Journal of Neonatal Nursing. 24 (5): 235–241. doi:10.1016/j.jnn.2018.01.001. S2CID 57620027.
  42. ^ "Facts about down syndrome". National Association of Down Syndrome. Archived from the original on 2012-04-03.
  43. ^ Martin JP, Bell J (July 1943). "A Pedigree of Mental Defect Showing Sex-Linkage". Journal of Neurology and Psychiatry. 6 (3–4): 154–157. doi:10.1136/jnnp.6.3-4.154. PMC 1090429. PMID 21611430.
  44. ^ Amir RE, Van den Veyver IB, Wan M, Tran CQ, Francke U, Zoghbi HY (October 1999). "Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2". Nature Genetics. 23 (2): 185–188. doi:10.1038/13810. PMID 10508514. S2CID 3350350.
  45. ^ Merla G, Howald C, Henrichsen CN, Lyle R, Wyss C, Zabot MT, et al. (August 2006). "Submicroscopic deletion in patients with Williams-Beuren syndrome influences expression levels of the nonhemizygous flanking genes". American Journal of Human Genetics. 79 (2): 332–341. doi:10.1086/506371. PMC 1559497. PMID 16826523.{{cite journal}}: CS1 maint: overridden setting (link)
  46. ^ a b c Martin CL, Ledbetter DH (June 2017). "Chromosomal Microarray Testing for Children With Unexplained Neurodevelopmental Disorders". JAMA. 317 (24): 2545–2546. doi:10.1001/jama.2017.7272. PMC 7058144. PMID 28654998.
  47. ^ Pavone P, Bianchini R, Parano E, Incorpora G, Rizzo R, Mazzone L, et al. (February 2004). "Anti-brain antibodies in PANDAS versus uncomplicated streptococcal infection". Pediatric Neurology. 30 (2): 107–110. doi:10.1016/S0887-8994(03)00413-2. hdl:2108/194065. PMID 14984902.
  48. ^ Dale RC, Heyman I, Giovannoni G, Church AW (October 2005). "Incidence of anti-brain antibodies in children with obsessive-compulsive disorder". The British Journal of Psychiatry. 187 (4): 314–319. doi:10.1192/bjp.187.4.314. PMID 16199788.
  49. ^ Swedo SE (December 2001). "Genetics of childhood disorders: XXXIII. Autoimmunity, part 6: poststreptococcal autoimmunity". Journal of the American Academy of Child and Adolescent Psychiatry. 40 (12): 1479–1482. doi:10.1097/00004583-200112000-00021. PMID 11765296. Archived from the original on 2021-07-20. Retrieved 2008-08-17.
  50. ^ a b Boivin MJ, Kakooza AM, Warf BC, Davidson LL, Grigorenko EL (November 2015). "Reducing neurodevelopmental disorders and disability through research and interventions". Nature. 527 (7578): S155–S160. Bibcode:2015Natur.527S.155B. doi:10.1038/nature16029. PMID 26580321.
  51. ^ Brown AS (April 2006). "Prenatal infection as a risk factor for schizophrenia". Schizophrenia Bulletin. 32 (2): 200–202. doi:10.1093/schbul/sbj052. PMC 2632220. PMID 16469941.
  52. ^ Richardson AJ, Ross MA (July 2000). "Fatty acid metabolism in neurodevelopmental disorder: a new perspective on associations between attention-deficit/hyperactivity disorder, dyslexia, dyspraxia and the autistic spectrum". Prostaglandins, Leukotrienes, and Essential Fatty Acids. 63 (1–2): 1–9. doi:10.1054/plef.2000.0184. PMID 10970706.
  53. ^ Northam EA, Anderson PJ, Jacobs R, Hughes M, Warne GL, Werther GA (September 2001). "Neuropsychological profiles of children with type 1 diabetes 6 years after disease onset". Diabetes Care. 24 (9): 1541–1546. doi:10.2337/diacare.24.9.1541. PMID 11522696.
  54. ^ Olsson GM, Hulting AL, Montgomery SM (March 2008). "Cognitive function in children and subsequent type 2 diabetes". Diabetes Care. 31 (3): 514–516. doi:10.2337/dc07-1399. PMC 2453642. PMID 18083794.[permanent dead link‍]
  55. ^ Ornoy A, Wolf A, Ratzon N, Greenbaum C, Dulitzky M (July 1999). "Neurodevelopmental outcome at early school age of children born to mothers with gestational diabetes". Archives of Disease in Childhood. Fetal and Neonatal Edition. 81 (1): F10–F14. doi:10.1136/fn.81.1.F10. PMC 1720965. PMID 10375355.
  56. ^ Lee PJ, Ridout D, Walter JH, Cockburn F (February 2005). "Maternal phenylketonuria: report from the United Kingdom Registry 1978-97". Archives of Disease in Childhood. 90 (2): 143–146. doi:10.1136/adc.2003.037762. PMC 1720245. PMID 15665165.
  57. ^ Rouse B, Azen C, Koch R, Matalon R, Hanley W, de la Cruz F, et al. (March 1997). "Maternal Phenylketonuria Collaborative Study (MPKUCS) offspring: facial anomalies, malformations, and early neurological sequelae". American Journal of Medical Genetics. 69 (1): 89–95. doi:10.1002/(SICI)1096-8628(19970303)69:1<89::AID-AJMG17>3.0.CO;2-K. PMID 9066890.{{cite journal}}: CS1 maint: overridden setting (link)
  58. ^ "Folic Acid". March of Dimes. Archived from the original on 2021-08-26. Retrieved 2014-11-10.
  59. ^ "Folate (Folacin, Folic Acid)". Ohio State University Extension. Archived from the original on 2021-08-26. Retrieved 2008-08-06.
  60. ^ "Folic scid: topic home". Centers for Disease Control and Prevention. U.S. Department of Health and Human Services. Archived from the original on 2021-08-26. Retrieved 2008-08-02.
  61. ^ "The basics about spina bifida". Centers for Disease Control and Prevention. U.S. Department of Health and Human Services. Archived from the original on 2021-08-26. Retrieved 2008-08-02.
  62. ^ Skeaff SA (February 2011). "Iodine deficiency in pregnancy: the effect on neurodevelopment in the child". Nutrients. 3 (2): 265–273. doi:10.3390/nu3020265. PMC 3257674. PMID 22254096.
  63. ^ Fetal alcohol syndrome: guidelines for referral and diagnosis (PDF). Archived 2009-04-23 at the Wayback Machine CDC (July 2004). Retrieved on 2007-04-11
  64. ^ "Facts About TBI" (PDF). U.S. Centers for Disease Control and Prevention. Archived from the original on 2021-08-26. Retrieved 2008-08-06.
  65. ^ Murray RM, Lewis SW (September 1987). "Is schizophrenia a neurodevelopmental disorder?". British Medical Journal. 295 (6600): 681–682. doi:10.1136/bmj.295.6600.681. PMC 1247717. PMID 3117295.
  66. ^ Collins KA, Popek E (December 2018). "Birth Injury: Birth Asphyxia and Birth Trauma". Academic Forensic Pathology. 8 (4): 788–864. doi:10.1177/1925362118821468. PMC 6491540. PMID 31240076.
  67. ^ Kratimenos P, Penn AA (August 2019). "Placental programming of neuropsychiatric disease". Pediatric Research. 86 (2): 157–164. doi:10.1038/s41390-019-0405-9. PMID 31003234. S2CID 124094051.
  68. ^ Neurodevelopmental Disorders (PDF), America's Children and the Environment (3 ed.), EPA, August 2017, p. 12, archived (PDF) from the original on 2021-07-20, retrieved 2019-07-10

Further reading