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From Wikipedia, the free encyclopedia

Syndromic autism (or syndromic autism spectrum disorders) denotes cases of autism spectrum disorder that are associated with a broader medical condition, generally a syndrome. Cases without such association, which account for the majority of total autism cases, are known as non-syndromic autism (or non-syndromic autism spectrum disorders).

Studying the differences and similarities (e.g. common pathways) between syndromic and non-syndromic cases can provide insights about the pathophysiology of autism and pave the way to new autism therapies. [1] [2] [3] [4]

Syndromic autism

Autism spectrum disorder (ASD) is referred to as syndromic when it is one of the many characteristics associated with a broader medical condition, generally a syndrome.

Syndromic autism represents about 25% of the total ASD cases. [4] [5] In most[ quantify] cases, its etiology is known. [2] [4]

Monogenic disorders are one of the causes of syndromic autism, which in this case are also known as monogenic autism spectrum disorders. They account for about 5% of the total ASD cases.

Certain[ which?] syndromic forms of ASD can also have different[ compared to?] phenomenology.[ clarification needed]

Non-syndromic autism

Non-syndromic autism, also called classic autism or idiopathic autism (as in most cases, the etiology is unknown), represents the majority of total autism cases.

In most[ quantify] cases, its cause is polygenic.[ citation needed]

Classification

A 2017 study[ relevant?] proposed to replace the classification "syndromic"/"non-syndromic" ASD into one based on the genetic etiology of the condition, specifying if the syndromic condition occurs in the context of a " phenotype first" clinically defined syndrome or from a " genotype first" molecularly defined syndrome. [4][ clarification needed]

Following the proposal, ASD would be divided into three genetic categories: [4]

Clinically defined

Syndromes recognized by clinicians (depending on their experience), typically confirmed by a targeted genetic testing.

Molecularly defined

Syndromes recognized by genome-wide testing, not by hypothesis-driven testing (since clinical recognition is difficult).

Currently undefined

Currently undefined.[ clarification needed]

Characteristics of syndromic ASD conditions
Condition Cause Chromosome(s) involved (if a mutation) ASD prevalence ( 95% CI) Clinically/Molecularly defined Other characteristics Ref.
Fragile X syndrome Monogenic disorder:
FMR1 (encodes FMRP)		 X  30% (20.0–31.0) [male individuals only]
 22% (15.0–30.0) [mixed sex]
14% (13–18) [female individuals only]		 Clinically defined [in some males] Long/narrow face, macroorchidism, long ears and philtrum, mild to moderate intellectual disability, hyperactivity, intellectual disability (ID), seizures [1] [3] [4] [6]
Rett syndrome Monogenic disorder:
MECP2		 X 61.0% (46.0–74.0) [female individuals only] Clinically defined Microcephaly, breathing irregularities, language deficits, repetitive/stereotyped hand movements, epilepsy, ID [1] [3] [4]
MECP2 duplication syndrome Monogenic disorder:
MECP2		 X 100% [in a single study composed by 9 male participants] Clinically defined Brachycephaly, spasticity, recurrent respiratory infections, gastrointestinal hypermotility, genitourinary abnormalities, epilepsy, ID [1] [4] [7]
Tuberous sclerosis complex Monogenic disorder:
TSC1
TSC2		 9
16		  36.0% (33.0–40.0) Clinically defined Benign tumours in multiple organs, epilepsy [1] [3] [4]
Angelman's syndrome Monogenic disorder:
UBE3A		 15  34.0% (24.0–37.0) Cheerful demeanour, microcephaly, epilepsy, speech deficits, sleep disturbance, epilepsy, ID [1] [3]
Phelan-McDermid syndrome Monogenic disorder:
SHANK3		 22  84% [in a single study composed by 32 participants] Molecularly defined [4] [8]
Timothy syndrome Monogenic disorder:
CACNA1C		 12  80% [in a single study composed by 17 participants] Clinically defined [4] [9]
Smith-Lemli-Opitz syndrome Monogenic disorder:
DHCR7		 11 55% [in a single study composed by 33 participants] [10]
Neurofibromatosis type I Monogenic disorder:
NF1		 17  18% (9.0–29.0) Clinically defined [3] [4]
PTEN hamartoma tumor syndrome Monogenic disorder:
PTEN		 10  17% (8–27) Clinically defined [4] [11]
Down syndrome Chromosomal disorder:
trisomy 21		 21 16% (8.0–24.0) Clinically defined [3] [4]
Cohen's syndrome Monogenic disorder:
VPS13B		 8  54% (44.0–64.0) Clinically defined [3] [4]
Cornelia de Lange syndrome Polygenic disorder  43% (32.0–53.0) Clinically defined [3] [4]
CHARGE syndrome Monogenic disorder:
CHD7		 8  28% (16–41) Clinically defined [4] [12] [13]
Noonan's syndrome Polygenic disorder  15% (7.0–26.0) [3]
William's syndrome Microdeletion syndrome:
7q11.23		 7  12% (6.0–20.0) [3] [14]
22q11.2 deletion syndrome Microdeletion syndrome:
22q11.2		 22 11% (5.0–19.0) Clinically defined [3] [4]
Fetal valproate spectrum disorder Teratogen:
valproate		  8–15% [in VPA exposed children] Clinically defined [4] [15] [16]

See also

References

  1. ^ a b c d e f Benger, Matthew; Kinali, Maria; Mazarakis, Nicholas D. (December 2018). "Autism spectrum disorder: prospects for treatment using gene therapy". Molecular Autism. 9 (1): 39. doi: 10.1186/s13229-018-0222-8. PMC  6011246. PMID  29951185.
  2. ^ a b Sztainberg, Yehezkel; Zoghbi, Huda Y (November 2016). "Lessons learned from studying syndromic autism spectrum disorders". Nature Neuroscience. 19 (11): 1408–1417. doi: 10.1038/nn.4420. PMID  27786181. S2CID  3332899. Retrieved 4 June 2023.
  3. ^ a b c d e f g h i j k l Richards, Caroline; Jones, Christopher; Groves, Laura; Moss, Jo; Oliver, Chris (October 2015). "Prevalence of autism spectrum disorder phenomenology in genetic disorders: a systematic review and meta-analysis". The Lancet Psychiatry. 2 (10): 909–916. doi: 10.1016/S2215-0366(15)00376-4. PMID  26341300. Retrieved 27 May 2023.
  4. ^ a b c d e f g h i j k l m n o p q r s Fernandez, Bridget A.; Scherer, Stephen W. (31 December 2017). "Syndromic autism spectrum disorders: moving from a clinically defined to a molecularly defined approach". Dialogues in Clinical Neuroscience. 19 (4): 353–371. doi: 10.31887/DCNS.2017.19.4/sscherer. PMC  5789213. PMID  29398931.
  5. ^ Bourgeron, Thomas (September 2015). "From the genetic architecture to synaptic plasticity in autism spectrum disorder". Nature Reviews Neuroscience. 16 (9): 551–563. doi: 10.1038/nrn3992. PMID  26289574. S2CID  12742356. Retrieved 8 June 2023.
  6. ^ Marlborough, M.; Welham, A.; Jones, C.; Reckless, S.; Moss, J. (December 2021). "Autism spectrum disorder in females with fragile X syndrome: a systematic review and meta-analysis of prevalence". Journal of Neurodevelopmental Disorders. 13 (1): 28. doi: 10.1186/s11689-021-09362-5. PMC  8299695. PMID  34294028.
  7. ^ Ramocki, Melissa B.; Peters, Sarika U.; Tavyev, Y. Jane; Zhang, Feng; Carvalho, Claudia M. B.; Schaaf, Christian P.; Richman, Ronald; Fang, Ping; Glaze, Daniel G.; Lupski, James R.; Zoghbi, Huda Y. (December 2009). "Autism and other neuropsychiatric symptoms are prevalent in individuals with MeCP2 duplication syndrome". Annals of Neurology. 66 (6): 771–782. doi: 10.1002/ana.21715. PMC  2801873. PMID  20035514.
  8. ^ Soorya, Latha; Kolevzon, Alexander; Zweifach, Jessica; Lim, Teresa; Dobry, Yuriy; Schwartz, Lily; Frank, Yitzchak; Wang, A Ting; Cai, Guiqing; Parkhomenko, Elena; Halpern, Danielle; Grodberg, David; Angarita, Benjamin; Willner, Judith P; Yang, Amy; Canitano, Roberto; Chaplin, William; Betancur, Catalina; Buxbaum, Joseph D (December 2013). "Prospective investigation of autism and genotype-phenotype correlations in 22q13 deletion syndrome and SHANK3 deficiency". Molecular Autism. 4 (1): 16. doi: 10.1186/2040-2392-4-18. PMC  3707861. PMID  23758760.
  9. ^ Splawski, Igor; Timothy, Katherine W.; Sharpe, Leah M.; Decher, Niels; Kumar, Pradeep; Bloise, Raffaella; Napolitano, Carlo; Schwartz, Peter J.; Joseph, Robert M.; Condouris, Karen; Tager-Flusberg, Helen; Priori, Silvia G.; Sanguinetti, Michael C.; Keating, Mark T. (October 2004). "CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism". Cell. 119 (1): 19–31. doi: 10.1016/j.cell.2004.09.011. PMID  15454078. S2CID  15325633.
  10. ^ Thurm, Audrey; Tierney, Elaine; Farmer, Cristan; Albert, Phebe; Joseph, Lisa; Swedo, Susan; Bianconi, Simona; Bukelis, Irena; Wheeler, Courtney; Sarphare, Geeta; Lanham, Diane; Wassif, Christopher A.; Porter, Forbes D. (December 2016). "Development, behavior, and biomarker characterization of Smith-Lemli-Opitz syndrome: an update". Journal of Neurodevelopmental Disorders. 8 (1): 12. doi: 10.1186/s11689-016-9145-x. PMC  4822234. PMID  27053961.
  11. ^ Cummings, Katherine; Watkins, Alice; Jones, Chris; Dias, Renuka; Welham, Alice (December 2022). "Behavioural and psychological features of PTEN mutations: a systematic review of the literature and meta-analysis of the prevalence of autism spectrum disorder characteristics". Journal of Neurodevelopmental Disorders. 14 (1): 1. doi: 10.1186/s11689-021-09406-w. PMC  8903687. PMID  34983360.
  12. ^ Thomas, Andrea T.; Waite, Jane; Williams, Caitlin A.; Kirk, Jeremy; Oliver, Chris; Richards, Caroline (December 2022). "Phenotypic characteristics and variability in CHARGE syndrome: a PRISMA compliant systematic review and meta-analysis". Journal of Neurodevelopmental Disorders. 14 (1): 49. doi: 10.1186/s11689-022-09459-5. PMC  9429597. PMID  36045324.
  13. ^ Norina, Usman; Moushumi, Sur (2023-03-06). "CHARGE Syndrome". ncbi.nlm.nih.gov. StatPearls Publishing. PMID  32644625. Bookshelf ID: NBK559199. Archived from the original on 2023-06-06. Retrieved 2023-06-07.
  14. ^ Colleen A, Morris (2023-04-13) [9 april 1999]. "Williams Syndrome". ncbi.nlm.nih.gov. GeneReviews. PMID  20301427. Bookshelf ID: NBK1249. Archived from the original on 2023-06-06. Retrieved 2023-06-07.
  15. ^ Bromley, Rebecca; Weston, Jennifer; Adab, Naghme; Greenhalgh, Janette; Sanniti, Anna; McKay, Andrew J; Tudur Smith, Catrin; Marson, Anthony G (30 October 2014). "Treatment for epilepsy in pregnancy: neurodevelopmental outcomes in the child". Cochrane Database of Systematic Reviews. 2020 (6): CD010236. doi: 10.1002/14651858.CD010236.pub2. PMC  7390020. PMID  25354543.
  16. ^ Clayton-Smith, Jill; Bromley, Rebecca; Dean, John; Journel, Hubert; Odent, Sylvie; Wood, Amanda; Williams, Janet; Cuthbert, Verna; Hackett, Latha; Aslam, Neelo; Malm, Heli; James, Gregory; Westbom, Lena; Day, Ruth; Ladusans, Edmund; Jackson, Adam; Bruce, Iain; Walker, Robert; Sidhu, Sangeet; Dyer, Catrina; Ashworth, Jane; Hindley, Daniel; Diaz, Gemma Arca; Rawson, Myfanwy; Turnpenny, Peter (December 2019). "Diagnosis and management of individuals with Fetal Valproate Spectrum Disorder; a consensus statement from the European Reference Network for Congenital Malformations and Intellectual Disability". Orphanet Journal of Rare Diseases. 14 (1): 180. doi: 10.1186/s13023-019-1064-y. PMC  6642533. PMID  31324220.
Retrieved from " https://en.wikipedia.org/?title=Syndromic_autism&oldid=1216595415"
From Wikipedia, the free encyclopedia

Syndromic autism (or syndromic autism spectrum disorders) denotes cases of autism spectrum disorder that are associated with a broader medical condition, generally a syndrome. Cases without such association, which account for the majority of total autism cases, are known as non-syndromic autism (or non-syndromic autism spectrum disorders).

Studying the differences and similarities (e.g. common pathways) between syndromic and non-syndromic cases can provide insights about the pathophysiology of autism and pave the way to new autism therapies. [1] [2] [3] [4]

Syndromic autism

Autism spectrum disorder (ASD) is referred to as syndromic when it is one of the many characteristics associated with a broader medical condition, generally a syndrome.

Syndromic autism represents about 25% of the total ASD cases. [4] [5] In most[ quantify] cases, its etiology is known. [2] [4]

Monogenic disorders are one of the causes of syndromic autism, which in this case are also known as monogenic autism spectrum disorders. They account for about 5% of the total ASD cases.

Certain[ which?] syndromic forms of ASD can also have different[ compared to?] phenomenology.[ clarification needed]

Non-syndromic autism

Non-syndromic autism, also called classic autism or idiopathic autism (as in most cases, the etiology is unknown), represents the majority of total autism cases.

In most[ quantify] cases, its cause is polygenic.[ citation needed]

Classification

A 2017 study[ relevant?] proposed to replace the classification "syndromic"/"non-syndromic" ASD into one based on the genetic etiology of the condition, specifying if the syndromic condition occurs in the context of a " phenotype first" clinically defined syndrome or from a " genotype first" molecularly defined syndrome. [4][ clarification needed]

Following the proposal, ASD would be divided into three genetic categories: [4]

Clinically defined

Syndromes recognized by clinicians (depending on their experience), typically confirmed by a targeted genetic testing.

Molecularly defined

Syndromes recognized by genome-wide testing, not by hypothesis-driven testing (since clinical recognition is difficult).

Currently undefined

Currently undefined.[ clarification needed]

Characteristics of syndromic ASD conditions
Condition Cause Chromosome(s) involved (if a mutation) ASD prevalence ( 95% CI) Clinically/Molecularly defined Other characteristics Ref.
Fragile X syndrome Monogenic disorder:
FMR1 (encodes FMRP)		 X  30% (20.0–31.0) [male individuals only]
 22% (15.0–30.0) [mixed sex]
14% (13–18) [female individuals only]		 Clinically defined [in some males] Long/narrow face, macroorchidism, long ears and philtrum, mild to moderate intellectual disability, hyperactivity, intellectual disability (ID), seizures [1] [3] [4] [6]
Rett syndrome Monogenic disorder:
MECP2		 X 61.0% (46.0–74.0) [female individuals only] Clinically defined Microcephaly, breathing irregularities, language deficits, repetitive/stereotyped hand movements, epilepsy, ID [1] [3] [4]
MECP2 duplication syndrome Monogenic disorder:
MECP2		 X 100% [in a single study composed by 9 male participants] Clinically defined Brachycephaly, spasticity, recurrent respiratory infections, gastrointestinal hypermotility, genitourinary abnormalities, epilepsy, ID [1] [4] [7]
Tuberous sclerosis complex Monogenic disorder:
TSC1
TSC2		 9
16		  36.0% (33.0–40.0) Clinically defined Benign tumours in multiple organs, epilepsy [1] [3] [4]
Angelman's syndrome Monogenic disorder:
UBE3A		 15  34.0% (24.0–37.0) Cheerful demeanour, microcephaly, epilepsy, speech deficits, sleep disturbance, epilepsy, ID [1] [3]
Phelan-McDermid syndrome Monogenic disorder:
SHANK3		 22  84% [in a single study composed by 32 participants] Molecularly defined [4] [8]
Timothy syndrome Monogenic disorder:
CACNA1C		 12  80% [in a single study composed by 17 participants] Clinically defined [4] [9]
Smith-Lemli-Opitz syndrome Monogenic disorder:
DHCR7		 11 55% [in a single study composed by 33 participants] [10]
Neurofibromatosis type I Monogenic disorder:
NF1		 17  18% (9.0–29.0) Clinically defined [3] [4]
PTEN hamartoma tumor syndrome Monogenic disorder:
PTEN		 10  17% (8–27) Clinically defined [4] [11]
Down syndrome Chromosomal disorder:
trisomy 21		 21 16% (8.0–24.0) Clinically defined [3] [4]
Cohen's syndrome Monogenic disorder:
VPS13B		 8  54% (44.0–64.0) Clinically defined [3] [4]
Cornelia de Lange syndrome Polygenic disorder  43% (32.0–53.0) Clinically defined [3] [4]
CHARGE syndrome Monogenic disorder:
CHD7		 8  28% (16–41) Clinically defined [4] [12] [13]
Noonan's syndrome Polygenic disorder  15% (7.0–26.0) [3]
William's syndrome Microdeletion syndrome:
7q11.23		 7  12% (6.0–20.0) [3] [14]
22q11.2 deletion syndrome Microdeletion syndrome:
22q11.2		 22 11% (5.0–19.0) Clinically defined [3] [4]
Fetal valproate spectrum disorder Teratogen:
valproate		  8–15% [in VPA exposed children] Clinically defined [4] [15] [16]

See also

References

  1. ^ a b c d e f Benger, Matthew; Kinali, Maria; Mazarakis, Nicholas D. (December 2018). "Autism spectrum disorder: prospects for treatment using gene therapy". Molecular Autism. 9 (1): 39. doi: 10.1186/s13229-018-0222-8. PMC  6011246. PMID  29951185.
  2. ^ a b Sztainberg, Yehezkel; Zoghbi, Huda Y (November 2016). "Lessons learned from studying syndromic autism spectrum disorders". Nature Neuroscience. 19 (11): 1408–1417. doi: 10.1038/nn.4420. PMID  27786181. S2CID  3332899. Retrieved 4 June 2023.
  3. ^ a b c d e f g h i j k l Richards, Caroline; Jones, Christopher; Groves, Laura; Moss, Jo; Oliver, Chris (October 2015). "Prevalence of autism spectrum disorder phenomenology in genetic disorders: a systematic review and meta-analysis". The Lancet Psychiatry. 2 (10): 909–916. doi: 10.1016/S2215-0366(15)00376-4. PMID  26341300. Retrieved 27 May 2023.
  4. ^ a b c d e f g h i j k l m n o p q r s Fernandez, Bridget A.; Scherer, Stephen W. (31 December 2017). "Syndromic autism spectrum disorders: moving from a clinically defined to a molecularly defined approach". Dialogues in Clinical Neuroscience. 19 (4): 353–371. doi: 10.31887/DCNS.2017.19.4/sscherer. PMC  5789213. PMID  29398931.
  5. ^ Bourgeron, Thomas (September 2015). "From the genetic architecture to synaptic plasticity in autism spectrum disorder". Nature Reviews Neuroscience. 16 (9): 551–563. doi: 10.1038/nrn3992. PMID  26289574. S2CID  12742356. Retrieved 8 June 2023.
  6. ^ Marlborough, M.; Welham, A.; Jones, C.; Reckless, S.; Moss, J. (December 2021). "Autism spectrum disorder in females with fragile X syndrome: a systematic review and meta-analysis of prevalence". Journal of Neurodevelopmental Disorders. 13 (1): 28. doi: 10.1186/s11689-021-09362-5. PMC  8299695. PMID  34294028.
  7. ^ Ramocki, Melissa B.; Peters, Sarika U.; Tavyev, Y. Jane; Zhang, Feng; Carvalho, Claudia M. B.; Schaaf, Christian P.; Richman, Ronald; Fang, Ping; Glaze, Daniel G.; Lupski, James R.; Zoghbi, Huda Y. (December 2009). "Autism and other neuropsychiatric symptoms are prevalent in individuals with MeCP2 duplication syndrome". Annals of Neurology. 66 (6): 771–782. doi: 10.1002/ana.21715. PMC  2801873. PMID  20035514.
  8. ^ Soorya, Latha; Kolevzon, Alexander; Zweifach, Jessica; Lim, Teresa; Dobry, Yuriy; Schwartz, Lily; Frank, Yitzchak; Wang, A Ting; Cai, Guiqing; Parkhomenko, Elena; Halpern, Danielle; Grodberg, David; Angarita, Benjamin; Willner, Judith P; Yang, Amy; Canitano, Roberto; Chaplin, William; Betancur, Catalina; Buxbaum, Joseph D (December 2013). "Prospective investigation of autism and genotype-phenotype correlations in 22q13 deletion syndrome and SHANK3 deficiency". Molecular Autism. 4 (1): 16. doi: 10.1186/2040-2392-4-18. PMC  3707861. PMID  23758760.
  9. ^ Splawski, Igor; Timothy, Katherine W.; Sharpe, Leah M.; Decher, Niels; Kumar, Pradeep; Bloise, Raffaella; Napolitano, Carlo; Schwartz, Peter J.; Joseph, Robert M.; Condouris, Karen; Tager-Flusberg, Helen; Priori, Silvia G.; Sanguinetti, Michael C.; Keating, Mark T. (October 2004). "CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism". Cell. 119 (1): 19–31. doi: 10.1016/j.cell.2004.09.011. PMID  15454078. S2CID  15325633.
  10. ^ Thurm, Audrey; Tierney, Elaine; Farmer, Cristan; Albert, Phebe; Joseph, Lisa; Swedo, Susan; Bianconi, Simona; Bukelis, Irena; Wheeler, Courtney; Sarphare, Geeta; Lanham, Diane; Wassif, Christopher A.; Porter, Forbes D. (December 2016). "Development, behavior, and biomarker characterization of Smith-Lemli-Opitz syndrome: an update". Journal of Neurodevelopmental Disorders. 8 (1): 12. doi: 10.1186/s11689-016-9145-x. PMC  4822234. PMID  27053961.
  11. ^ Cummings, Katherine; Watkins, Alice; Jones, Chris; Dias, Renuka; Welham, Alice (December 2022). "Behavioural and psychological features of PTEN mutations: a systematic review of the literature and meta-analysis of the prevalence of autism spectrum disorder characteristics". Journal of Neurodevelopmental Disorders. 14 (1): 1. doi: 10.1186/s11689-021-09406-w. PMC  8903687. PMID  34983360.
  12. ^ Thomas, Andrea T.; Waite, Jane; Williams, Caitlin A.; Kirk, Jeremy; Oliver, Chris; Richards, Caroline (December 2022). "Phenotypic characteristics and variability in CHARGE syndrome: a PRISMA compliant systematic review and meta-analysis". Journal of Neurodevelopmental Disorders. 14 (1): 49. doi: 10.1186/s11689-022-09459-5. PMC  9429597. PMID  36045324.
  13. ^ Norina, Usman; Moushumi, Sur (2023-03-06). "CHARGE Syndrome". ncbi.nlm.nih.gov. StatPearls Publishing. PMID  32644625. Bookshelf ID: NBK559199. Archived from the original on 2023-06-06. Retrieved 2023-06-07.
  14. ^ Colleen A, Morris (2023-04-13) [9 april 1999]. "Williams Syndrome". ncbi.nlm.nih.gov. GeneReviews. PMID  20301427. Bookshelf ID: NBK1249. Archived from the original on 2023-06-06. Retrieved 2023-06-07.
  15. ^ Bromley, Rebecca; Weston, Jennifer; Adab, Naghme; Greenhalgh, Janette; Sanniti, Anna; McKay, Andrew J; Tudur Smith, Catrin; Marson, Anthony G (30 October 2014). "Treatment for epilepsy in pregnancy: neurodevelopmental outcomes in the child". Cochrane Database of Systematic Reviews. 2020 (6): CD010236. doi: 10.1002/14651858.CD010236.pub2. PMC  7390020. PMID  25354543.
  16. ^ Clayton-Smith, Jill; Bromley, Rebecca; Dean, John; Journel, Hubert; Odent, Sylvie; Wood, Amanda; Williams, Janet; Cuthbert, Verna; Hackett, Latha; Aslam, Neelo; Malm, Heli; James, Gregory; Westbom, Lena; Day, Ruth; Ladusans, Edmund; Jackson, Adam; Bruce, Iain; Walker, Robert; Sidhu, Sangeet; Dyer, Catrina; Ashworth, Jane; Hindley, Daniel; Diaz, Gemma Arca; Rawson, Myfanwy; Turnpenny, Peter (December 2019). "Diagnosis and management of individuals with Fetal Valproate Spectrum Disorder; a consensus statement from the European Reference Network for Congenital Malformations and Intellectual Disability". Orphanet Journal of Rare Diseases. 14 (1): 180. doi: 10.1186/s13023-019-1064-y. PMC  6642533. PMID  31324220.
Retrieved from " https://en.wikipedia.org/?title=Syndromic_autism&oldid=1216595415"

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