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Neurodevelopmental disorders are a group of mental conditions negatively affecting the development of thenervous system, which includes thebrain andspinal cord. According to theAmerican Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (DSM-5) published in 2013, these conditions generally appear inearly 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]
Intellectual disability, also known asgeneral 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, affectingdaily living activities.Global developmental delay is categorized under intellectual disability and is diagnosed when several areas of intellectual functioning are affected.[3]
Autism, also calledautism spectrum disorder (ASD) orautism 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 and adapt to everyday situations. Like most developmental disorders, autism exists along a continuum of symptom severity, subjective distress, and functional impairment. A consequence of this dimensionality is substantial variability across autistic persons with respect to both the nature and the extent of required supports.
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 bedevelopmentally andsocioculturally inappropriate.[7][8]
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 andmental disorders as well as non-psychiatric disorders, which can cause additional impairment.[11]
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]
There areneurodevelopmental research projects examining potential new classifications of disorders including:
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]
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]
Thedevelopment 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 andmetabolic diseases,immune disorders,infectious diseases,nutritional factors,physical trauma, and toxic and prenatal environmental factors. Some neurodevelopmental disorders, such asautism and otherpervasive developmental disorders, are considered multifactorialsyndromes 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 gutmicrobiome.[38]
Deprivation from social and emotional care causes severe delays in brain and cognitive development.[39] Studies with children growing up in Romanian orphanages duringNicolae Ceauşescu's regime reveal profound effects ofsocial deprivation andlanguage 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 earlierinstitutionalization.[40]
Immune reactions duringpregnancy, both maternal and of the developing child, may produce neurodevelopmental disorders. One typical immune reaction in infants and children isPANDAS,[47] orPediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection.[48] Another disorder isSydenham'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 byStreptococcus bacteria. Susceptibility to these immune diseases may be genetically determined,[49] so sometimes several family members may have one or both of them following anepidemic of Strep infection.[citation needed]
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 exampleHIV[50] Infections of the head and brain, likebrain abscesses,meningitis orencephalitis have a high risk of causing neurodevelopmental problems and eventually a disorder. For example,measles can progress tosubacute sclerosing panencephalitis.
A number ofinfectious diseases can be transmitted congenitally (either before or at birth), and can cause serious neurodevelopmental problems, as for example the virusesHSV,CMV, rubella (congenital rubella syndrome),Zika virus, or bacteria likeTreponema pallidum incongenital syphilis, which may progress toneurosyphilis if it remains untreated. Protozoa likePlasmodium[50] orToxoplasma which can cause congenitaltoxoplasmosis with multiple cysts in the brain and other organs, leading to a variety of neurological deficits.
Some cases ofschizophrenia may be related to congenital infections, though the majority are of unknown causes.[51]
In a child,type 1 diabetes can produce neurodevelopmental damage by the effects of excess or insufficientglucose. 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-diabeticfetus can also be subjected to glucose effects if its mother has undetectedgestational 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 ofPKU, excessive maternalphenylalanine 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 disorders and nutritional deficits may cause neurodevelopmental disorders, such asspina bifida, and the rarely occurringanencephaly, both of which areneural tube defects with malformation and dysfunction of thenervous system and its supporting structures, leading to serious physical disability and emotional sequelae. The most common nutritional cause of neural tube defects isfolic 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] Another deficiency,iodine deficiency, produces a spectrum of neurodevelopmental disorders ranging from mild emotional disturbance to severe intellectual disability. (see alsocongenital iodine deficiency syndrome).[61]
Excesses in both maternal and infant diets may cause disorders as well, with foods orfood supplements proving toxic in large amounts. For instance in 1973 K.L. Jones and D.W. Smith of theUniversity of Washington Medical School inSeattle found a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in children ofalcoholic mothers, now calledfetal alcohol syndrome, It has significant symptom overlap with several other entirely unrelated neurodevelopmental disorders.[62]
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)[63] of neurodevelopmental syndromes. It may be subdivided into two major categories,congenital injury (including injury resulting from otherwise uncomplicated premature birth)[64] and injury occurring in infancy or childhood. Common causes of congenital injury areasphyxia (obstruction of thetrachea),hypoxia (lack of oxygen to the brain), and themechanical trauma of thebirth process itself.[65]
Although it not clear yet as strong is the correlation betweenplacenta and brain, a growing number of studies are linking placenta to fetal brain development.[66]
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.[67]
^abcDiagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Washington, D.C.: American Psychiatric Association. 2013. pp. 31–33.ISBN978-0-89042-554-1.
^abDiagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Washington, D.C.: American Psychiatric Association. 2013. pp. 58–65.ISBN978-0-89042-554-1.
^Collins, John William. "The greenwood dictionary of education". Greenwood, 2011. page 86.ISBN978-0-313-37930-7
^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.PMID15953706.
^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.PMID23247506.
^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.ISBN978-0-07-148127-4.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.
^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.ISBN978-1-4614-8106-5.
^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.PMID23082740.S2CID207221320.
^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.PMID29624671.
^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.PMID26829402.
^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.PMID30526189.S2CID54472439.
^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.PMID34585995.S2CID238218526.
^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.S2CID57620027.
^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.PMID10508514.S2CID3350350.
^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.PMID10970706.
^"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. Retrieved2008-08-02.
^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, retrieved2019-07-10