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Restlessness

MedGen UID:
854457
Concept ID:
C3887611
Sign or Symptom
Synonyms: Feeling of Restlessness; Fidgetiness; Restiveness; Restless; Restlessness behavior
SNOMED CT: Restlessness (162221009); Restlessness behavior (162221009)
 
HPO: HP:0000711

Definition

A state of unease is characterized by diffuse motor activity or motion, which is subject to limited control, nonproductive, or disorganized behavior. [from HPO]

Conditions with this feature

Mucopolysaccharidosis, MPS-III-D
MedGen UID:
88602
Concept ID:
C0086650
Disease or Syndrome
Mucopolysaccharidosis type III (MPS III) is a multisystem lysosomal storage disease characterized by progressive central nervous system degeneration manifest as severe intellectual disability (ID), developmental regression, and other neurologic manifestations including autism spectrum disorder (ASD), behavioral problems, and sleep disturbances. Disease onset is typically before age ten years. Disease course may be rapidly or slowly progressive; some individuals with an extremely attenuated disease course present in mid-to-late adulthood with early-onset dementia with or without a history of ID. Systemic manifestations can include musculoskeletal problems (joint stiffness, contractures, scoliosis, and hip dysplasia), hearing loss, respiratory tract and sinopulmonary infections, and cardiac disease (valvular thickening, defects in the cardiac conduction system). Neurologic decline is seen in all affected individuals; however, clinical severity varies within and among the four MPS III subtypes (defined by the enzyme involved) and even among members of the same family. Death usually occurs in the second or third decade of life secondary to neurologic regression or respiratory tract infections.
Hyperglycinemia, transient neonatal
MedGen UID:
82818
Concept ID:
C0268560
Disease or Syndrome
Primrose syndrome
MedGen UID:
162911
Concept ID:
C0796121
Disease or Syndrome
Primrose syndrome is characterized by macrocephaly, hypotonia, developmental delay, intellectual disability with expressive speech delay, behavioral issues, a recognizable facial phenotype, radiographic features, and altered glucose metabolism. Additional features seen in adults: sparse body hair, distal muscle wasting, and contractures. Characteristic craniofacial features include brachycephaly, high anterior hairline, deeply set eyes, ptosis, downslanted palpebral fissures, high palate with torus palatinus, broad jaw, and large ears with small or absent lobes. Radiographic features include calcification of the external ear cartilage, multiple Wormian bones, platybasia, bathrocephaly, slender bones with exaggerated metaphyseal flaring, mild epiphyseal dysplasia, and spondylar dysplasia. Additional features include hearing impairment, ocular anomalies, cryptorchidism, and nonspecific findings on brain MRI.
X-linked intellectual disability-psychosis-macroorchidism syndrome
MedGen UID:
163232
Concept ID:
C0796222
Disease or Syndrome
The spectrum of MECP2-related phenotypes in females ranges from classic Rett syndrome to variant Rett syndrome with a broader clinical phenotype (either milder or more severe than classic Rett syndrome) to mild learning disabilities; the spectrum in males ranges from severe neonatal encephalopathy to pyramidal signs, parkinsonism, and macroorchidism (PPM-X) syndrome to severe syndromic/nonsyndromic intellectual disability. Females: Classic Rett syndrome, a progressive neurodevelopmental disorder primarily affecting girls, is characterized by apparently normal psychomotor development during the first six to 18 months of life, followed by a short period of developmental stagnation, then rapid regression in language and motor skills, followed by long-term stability. During the phase of rapid regression, repetitive, stereotypic hand movements replace purposeful hand use. Additional findings include fits of screaming and inconsolable crying, autistic features, panic-like attacks, bruxism, episodic apnea and/or hyperpnea, gait ataxia and apraxia, tremors, seizures, and acquired microcephaly. Males: Severe neonatal-onset encephalopathy, the most common phenotype in affected males, is characterized by a relentless clinical course that follows a metabolic-degenerative type of pattern, abnormal tone, involuntary movements, severe seizures, and breathing abnormalities. Death often occurs before age two years.
Intellectual disability, X-linked 30
MedGen UID:
163235
Concept ID:
C0796237
Disease or Syndrome
Any non-syndromic X-linked intellectual disability in which the cause of the disease is a mutation in the PAK3 gene.
Frontotemporal dementia and/or amyotrophic lateral sclerosis 7
MedGen UID:
318833
Concept ID:
C1833296
Disease or Syndrome
CHMP2B frontotemporal dementia (CHMP2B-FTD) has been described in a single family from Denmark, in one individual with familial FTD from Belgium, and in one individual with FTD and no family history. It typically starts between ages 46 and 65 years with subtle personality changes and slowly progressive behavioral changes, dysexecutive syndrome, dyscalculia, and language disturbances. Disinhibition or loss of initiative is the most common presenting symptom. The disease progresses over a few years into profound dementia with extrapyramidal symptoms and mutism. Several individuals have developed an asymmetric akinetic rigid syndrome with arm and gait dystonia and pyramidal signs that may be related to treatment with neuroleptic drugs. Symptoms and disease course are highly variable. Disease duration may be as short as three years or longer than 20 years.
Syndromic X-linked intellectual disability Claes-Jensen type
MedGen UID:
335139
Concept ID:
C1845243
Disease or Syndrome
Claes-Jensen type of X-linked syndromic intellectual developmental disorder (MRXSCJ) is characterized by impaired intellectual development with substantial clinical heterogeneity in affected males. However, males are usually reported to have short stature, microcephaly, hyperreflexia, and aggressive behavior. In rare cases, female carriers exhibit mildly impaired intellectual development or learning difficulties (summary by Guerra et al., 2020).
Hereditary spastic paraplegia 16
MedGen UID:
375796
Concept ID:
C1846046
Disease or Syndrome
Spastic paraplegias (SPGs) are a genetically heterogeneous group of neurologic disorders characterized by progressive weakness and spasticity of the legs. Complicated SPGs are accompanied by additional neurologic symptoms such as cerebellar ataxia, sensory loss, mental retardation, nystagmus, and optic atrophy (summary by Steinmuller et al., 1997). A locus for spastic paraplegia-16 has been mapped to Xq11.2-q23 (Steinmuller et al., 1997). For a discussion of genetic heterogeneity of X-linked spastic paraplegia, see 303350.
Pontocerebellar hypoplasia type 2A
MedGen UID:
376379
Concept ID:
C1848526
Disease or Syndrome
TSEN54 pontocerebellar hypoplasia (TSEN54-PCH) comprises three PCH phenotypes (PCH2, 4, and 5) that share characteristic neuroradiologic and neurologic findings. The three PCH phenotypes (which differ mainly in life expectancy) were considered to be distinct entities before their molecular basis was known. PCH2. Children usually succumb before age ten years (those with PCH4 and 5 usually succumb as neonates). Children with PCH2 have generalized clonus, uncoordinated sucking and swallowing, impaired cognitive development, lack of voluntary motor development, cortical blindness, and an increased risk for rhabdomyolysis during severe infections. Epilepsy is present in approximately 50%. PCH4. Neonates often have seizures, multiple joint contractures ("arthrogryposis"), generalized clonus, and central respiratory impairment. PCH5 resembles PCH4 and has been described in one family.
Huntington disease-like 1
MedGen UID:
355137
Concept ID:
C1864112
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
Neuronal ceroid lipofuscinosis 8 northern epilepsy variant
MedGen UID:
355328
Concept ID:
C1864923
Disease or Syndrome
The neuronal ceroid lipofuscinoses (NCL; CLN) are a clinically and genetically heterogeneous group of neurodegenerative disorders characterized by the intracellular accumulation of autofluorescent lipopigment storage material in different patterns ultrastructurally. The lipopigment patterns observed most often in CLN8 comprise mixed combinations of 'granular,' 'curvilinear,' and 'fingerprint' profiles (Mole et al., 2005). For a general phenotypic description and a discussion of genetic heterogeneity of CLN, see CLN1 (256730).
Chromosome 2q32-q33 deletion syndrome
MedGen UID:
436765
Concept ID:
C2676739
Disease or Syndrome
SATB2-associated syndrome (SAS) is a multisystem disorder characterized by significant neurodevelopmental compromise with limited to absent speech, behavioral issues, and craniofacial anomalies. All individuals described to date have manifest developmental delay / intellectual disability, with severe speech delay. Affected individuals often have hypotonia and feeding difficulties in infancy. Behavioral issues may include autistic features, hyperactivity, and aggressiveness. Craniofacial anomalies may include palatal abnormalities (cleft palate, high-arched palate, and bifid uvula), micrognathia, and abnormal shape or size of the upper central incisors. Less common features include skeletal anomalies (osteopenia, pectus deformities, kyphosis/lordosis, and scoliosis), growth restriction, strabismus/refractive errors, congenital heart defects, genitourinary anomalies, and epilepsy. While dysmorphic features have been described in individuals with this condition, these features are not typically distinctive enough to allow for a clinical diagnosis of SAS.
Hawkinsinuria
MedGen UID:
419319
Concept ID:
C2931042
Disease or Syndrome
Hawkinsinuria (HWKS) is an autosomal dominant inborn error of metabolism. Metabolic acidosis and tyrosinemia are transient, and symptoms improve within the first year of life. Patients continue to excrete the hawkinsin metabolite in their urine throughout life (Danks et al., 1975; Tomoeda et al., 2000).
HSD10 mitochondrial disease
MedGen UID:
781653
Concept ID:
C3266731
Disease or Syndrome
HSD10 mitochondrial disease (HSD10MD) most commonly presents as an X-linked neurodegenerative disorder with highly variable severity and age at onset ranging from the neonatal period to early childhood. The features are usually multisystemic, consistent with mitochondrial dysfunction. Some affected males have a severe infantile form associated with cardiomyopathy that may result in death in early childhood, whereas other rare patients may have juvenile onset or even atypical presentations with normal neurologic development. More severely affected males show developmental regression in infancy or early childhood, often associated with early-onset intractable seizures, progressive choreoathetosis and spastic tetraplegia, optic atrophy or retinal degeneration resulting in visual loss, and mental retardation. Heterozygous females may show non-progressive developmental delay and intellectual disability, but may also be clinically normal. Although the diagnosis can be aided by the observation of increased urinary levels of metabolites of isoleucine breakdown (2-methyl-3 hydroxybutyrate and tiglylglycine), there is not a correlation between these laboratory features and the phenotype. In addition, patients do not develop severe metabolic crises in the neonatal period as observed in other organic acidurias, but may show persistent lactic acidosis, most likely reflecting mitochondrial dysfunction (summary by Rauschenberger et al., 2010; Zschocke, 2012). In a review of this disorder, Zschocke (2012) noted that although it was originally thought to be an inborn error of branched-chain fatty acid and isoleucine metabolism resulting from decreased HSD17B10 dehydrogenase activity (HSD17B10 'deficiency'), subsequent studies have shown that the HSD17B10 gene product has additional functions and also acts as a component of the mitochondrial RNase P holoenzyme, which is involved in mitochondrial tRNA processing and maturation and ultimately mitochondrial protein synthesis. The multisystemic features of HSD10MD most likely result from the adverse effect of HSD17B10 mutations on mitochondrial function, rather than from the effects on the dehydrogenase activity (see PATHOGENESIS).
Encephalopathy, lethal, due to defective mitochondrial peroxisomal fission 1
MedGen UID:
482290
Concept ID:
C3280660
Disease or Syndrome
Encephalopathy due to defective mitochondrial and peroxisomal fission-1 (EMPF1) is characterized by delayed psychomotor development and hypotonia that may lead to death in childhood. Many patients develop refractory seizures, consistent with an epileptic encephalopathy, and thereafter show neurologic decline. The age at onset, features, and severity are variable, and some patients may not have clinical evidence of mitochondrial or peroxisomal dysfunction (summary by Sheffer et al., 2016; Fahrner et al., 2016). Genetic Heterogeneity of Encephalopathy Due to Defective Mitochondrial And Peroxisomal Fission See also EMPF2 (617086), caused by mutation in the MFF gene (614785) on chromosome 2q36.
Severe intellectual disability-progressive spastic diplegia syndrome
MedGen UID:
767363
Concept ID:
C3554449
Disease or Syndrome
CTNNB1 neurodevelopmental disorder (CTNNB1-NDD) is characterized in all individuals by mild-to-profound cognitive impairment and in up to 39% of reported individuals by exudative vitreoretinopathy, an ophthalmologic finding consistent with familial exudative vitreoretinopathy (FEVR). Other common findings include truncal hypotonia, peripheral spasticity, dystonia, behavior problems, microcephaly, and refractive errors and strabismus. Less common features include intrauterine growth restriction, feeding difficulties, and scoliosis.
Mitochondrial complex III deficiency nuclear type 4
MedGen UID:
767521
Concept ID:
C3554607
Disease or Syndrome
Most people with mitochondrial complex III deficiency have a buildup of a chemical called lactic acid in the body (lactic acidosis). Some affected individuals also have buildup of molecules called ketones (ketoacidosis) or high blood glucose levels (hyperglycemia). Abnormally high levels of these chemicals in the body can be life-threatening.\n\nThe severity of mitochondrial complex III deficiency varies widely among affected individuals. People who are mildly affected tend to have muscle weakness (myopathy) and extreme tiredness (fatigue), particularly during exercise (exercise intolerance). More severely affected individuals have problems with multiple body systems, such as liver disease that can lead to liver failure, kidney abnormalities (tubulopathy), and brain dysfunction (encephalopathy). Encephalopathy can cause delayed development of mental and motor skills (psychomotor delay), movement problems, weak muscle tone (hypotonia), and difficulty with communication. Some affected individuals have a form of heart disease called cardiomyopathy, which can lead to heart failure. \n\nMitochondrial complex III deficiency can be fatal in childhood, although individuals with mild signs and symptoms can survive into adolescence or adulthood.\n\nMitochondrial complex III deficiency is a genetic condition that can affect several parts of the body, including the brain, kidneys, liver, heart, and the muscles used for movement (skeletal muscles). Signs and symptoms of mitochondrial complex III deficiency usually begin in infancy but can appear later.
Encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy, 1
MedGen UID:
934642
Concept ID:
C4310675
Disease or Syndrome
Early-onset progressive encephalopathy with brain edema and/or leukoencephalopathy-1 (PEBEL1) is an autosomal recessive severe neurometabolic disorder characterized by rapidly progressive neurologic deterioration that is usually associated with a febrile illness. Affected infants tend to show normal early development followed by acute psychomotor regression with ataxia, hypotonia, respiratory insufficiency, and seizures, resulting in coma and death in the first years of life. Brain imaging shows multiple abnormalities, including brain edema and signal abnormalities in the cortical and subcortical regions (summary by Kremer et al., 2016). Genetic Heterogeneity of PEBEL See also PEBEL2 (618321), caused by mutation in the NAXD gene (615910) on chromosome 13q34.
Developmental and epileptic encephalopathy, 73
MedGen UID:
1681654
Concept ID:
C5193065
Disease or Syndrome
Developmental and epileptic encephalopathy-73 (DEE73) is a neurologic disorder characterized by the onset of refractory seizures in the first months of life. Affected individuals meet almost no developmental milestones: they have hypotonia and are unable to walk, speak, or feed properly. They have poor overall growth with small head circumference and dysmorphic facial features. Additional manifestations include cortical visual impairment with roving eye movements and variable hearing loss (summary by Edvardson et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Neurodevelopmental disorder with seizures and brain abnormalities
MedGen UID:
1794189
Concept ID:
C5561979
Disease or Syndrome
Neurodevelopmental disorder with seizures and brain abnormalities (NEDSBA) is an autosomal recessive neurologic disorder characterized by global developmental delay and onset of seizures in the first months of life associated with structural brain defects on brain imaging. Additional features may include pigmentary retinopathy with poor visual fixation and spasticity (summary by Duncan et al., 2021).
Congenital disorder of deglycosylation 1
MedGen UID:
989503
Concept ID:
CN306977
Disease or Syndrome
Individuals with NGLY1-related congenital disorder of deglycosylation (NGLY1-CDDG) typically display a clinical tetrad of developmental delay / intellectual disability in the mild to profound range, hypo- or alacrima, elevated liver transaminases that may spontaneously resolve in childhood, and a complex hyperkinetic movement disorder that can include choreiform, athetoid, dystonic, myoclonic, action tremor, and dysmetric movements. About half of affected individuals will develop clinical seizures. Other findings may include obstructive and/or central sleep apnea, oral motor defects that affect feeding ability, auditory neuropathy, constipation, scoliosis, and peripheral neuropathy.

Professional guidelines

PubMed

Schindler EAD, Burish MJ
BMJ 2022 Mar 16;376:e059577. doi: 10.1136/bmj-2020-059577. PMID: 35296510
Hoffmann J, May A
Lancet Neurol 2018 Jan;17(1):75-83. Epub 2017 Nov 23 doi: 10.1016/S1474-4422(17)30405-2. PMID: 29174963
Rami Reddy SR, Cappell MS
Curr Gastroenterol Rep 2017 Jun;19(6):28. doi: 10.1007/s11894-017-0566-9. PMID: 28439845

Recent clinical studies

Etiology

Vlăduțu D, Popescu SM, Mercuț R, Ionescu M, Scrieciu M, Glodeanu AD, Stănuși A, Rîcă AM, Mercuț V
Int J Environ Res Public Health 2022 Apr 29;19(9) doi: 10.3390/ijerph19095415. PMID: 35564810Free PMC Article
Malu OO, Bailey J, Hawks MK
Am Fam Physician 2022 Jan 1;105(1):24-32. PMID: 35029932
Peri A
Front Horm Res 2019;52:36-48. Epub 2019 Jan 15 doi: 10.1159/000493235. PMID: 32097927
DeMartini J, Patel G, Fancher TL
Ann Intern Med 2019 Apr 2;170(7):ITC49-ITC64. doi: 10.7326/AITC201904020. PMID: 30934083
Pary R, Sarai SK, Micchelli A, Lippmann S
Prim Care Companion CNS Disord 2019 Jan 31;21(1) doi: 10.4088/PCC.18nr02335. PMID: 30806999

Diagnosis

Al-Khazali HM, Christensen RH, Lambru G, Dodick DW, Ashina H
Curr Pain Headache Rep 2023 Oct;27(10):543-550. Epub 2023 Aug 11 doi: 10.1007/s11916-023-01156-9. PMID: 37566220
Santifort KM, Mandigers PJJ
J Vet Intern Med 2022 Nov;36(6):1872-1881. Epub 2022 Sep 10 doi: 10.1111/jvim.16532. PMID: 36086931Free PMC Article
Silva EAD Junior, Medeiros WMB, Torro N, Sousa JMM, Almeida IBCM, Costa FBD, Pontes KM, Nunes ELG, Rosa MDD, Albuquerque KLGD
Trends Psychiatry Psychother 2022 Jun 13;44:e20200149. doi: 10.47626/2237-6089-2020-0149. PMID: 34043900Free PMC Article
DeMartini J, Patel G, Fancher TL
Ann Intern Med 2019 Apr 2;170(7):ITC49-ITC64. doi: 10.7326/AITC201904020. PMID: 30934083
Hoffmann J, May A
Lancet Neurol 2018 Jan;17(1):75-83. Epub 2017 Nov 23 doi: 10.1016/S1474-4422(17)30405-2. PMID: 29174963

Therapy

Xu LL, Wang C, Deng CM, Dai SB, Zhou Q, Peng YB, Shou HY, Han YQ, Yu J, Liu CH, Xia F, Zhang SQ, Wang DX, Chen XZ
JAMA Netw Open 2023 Apr 3;6(4):e239321. doi: 10.1001/jamanetworkopen.2023.9321. PMID: 37083664Free PMC Article
Strawn JR, Mills JA, Poweleit EA, Ramsey LB, Croarkin PE
Pharmacotherapy 2023 Jul;43(7):675-690. Epub 2023 Jan 27 doi: 10.1002/phar.2767. PMID: 36651686Free PMC Article
Silva EAD Junior, Medeiros WMB, Torro N, Sousa JMM, Almeida IBCM, Costa FBD, Pontes KM, Nunes ELG, Rosa MDD, Albuquerque KLGD
Trends Psychiatry Psychother 2022 Jun 13;44:e20200149. doi: 10.47626/2237-6089-2020-0149. PMID: 34043900Free PMC Article
Brannan SK, Sawchak S, Miller AC, Lieberman JA, Paul SM, Breier A
N Engl J Med 2021 Feb 25;384(8):717-726. doi: 10.1056/NEJMoa2017015. PMID: 33626254Free PMC Article
DeMartini J, Patel G, Fancher TL
Ann Intern Med 2019 Apr 2;170(7):ITC49-ITC64. doi: 10.7326/AITC201904020. PMID: 30934083

Prognosis

Strawn JR, Mills JA, Poweleit EA, Ramsey LB, Croarkin PE
Pharmacotherapy 2023 Jul;43(7):675-690. Epub 2023 Jan 27 doi: 10.1002/phar.2767. PMID: 36651686Free PMC Article
Yang Y, Sun H, Luo X, Li W, Yang F, Xu W, Ding K, Zhou J, Liu W, Garg S, Jackson T, Chen Y, Xiang YT
J Affect Disord 2022 Jul 15;309:358-367. Epub 2022 Apr 25 doi: 10.1016/j.jad.2022.04.119. PMID: 35472477
Thippaiah SM, Fargason RE, Birur B
Psychopharmacol Bull 2021 Jun 1;51(3):72-78. PMID: 34421146Free PMC Article
Vieta E, Garriga M, Cardete L, Bernardo M, Lombraña M, Blanch J, Catalán R, Vázquez M, Soler V, Ortuño N, Martínez-Arán A
BMC Psychiatry 2017 Sep 8;17(1):328. doi: 10.1186/s12888-017-1490-0. PMID: 28886752Free PMC Article
Tyrer P, Baldwin D
Lancet 2006 Dec 16;368(9553):2156-66. doi: 10.1016/S0140-6736(06)69865-6. PMID: 17174708

Clinical prediction guides

Schultz W
Proc Natl Acad Sci U S A 2024 May 14;121(20):e2316658121. Epub 2024 May 8 doi: 10.1073/pnas.2316658121. PMID: 38717856Free PMC Article
Ferré S, Winkelman JW, García-Borreguero D, Belcher AM, Chang JH, Earley CJ
Sleep 2024 Mar 11;47(3) doi: 10.1093/sleep/zsad273. PMID: 37864837Free PMC Article
Thompson AE, Thompson PD
Handb Clin Neurol 2023;196:443-455. doi: 10.1016/B978-0-323-98817-9.00008-9. PMID: 37620084
Xu LL, Wang C, Deng CM, Dai SB, Zhou Q, Peng YB, Shou HY, Han YQ, Yu J, Liu CH, Xia F, Zhang SQ, Wang DX, Chen XZ
JAMA Netw Open 2023 Apr 3;6(4):e239321. doi: 10.1001/jamanetworkopen.2023.9321. PMID: 37083664Free PMC Article
Brannan SK, Sawchak S, Miller AC, Lieberman JA, Paul SM, Breier A
N Engl J Med 2021 Feb 25;384(8):717-726. doi: 10.1056/NEJMoa2017015. PMID: 33626254Free PMC Article

Recent systematic reviews

Silva EAD Junior, Medeiros WMB, Torro N, Sousa JMM, Almeida IBCM, Costa FBD, Pontes KM, Nunes ELG, Rosa MDD, Albuquerque KLGD
Trends Psychiatry Psychother 2022 Jun 13;44:e20200149. doi: 10.47626/2237-6089-2020-0149. PMID: 34043900Free PMC Article
Nadeem IM, Shanmugaraj A, Sakha S, Horner NS, Ayeni OR, Khan M
Sports Health 2021 May-Jun;13(3):265-277. Epub 2020 Nov 19 doi: 10.1177/1941738120949181. PMID: 33211984Free PMC Article
Monahan K, Cuzens-Sutton J, Siskind D, Kisely S
Aust N Z J Psychiatry 2021 Aug;55(8):772-783. Epub 2020 Oct 16 doi: 10.1177/0004867420965693. PMID: 33059460
Rami Reddy SR, Cappell MS
Curr Gastroenterol Rep 2017 Jun;19(6):28. doi: 10.1007/s11894-017-0566-9. PMID: 28439845
Beller EM, van Driel ML, McGregor L, Truong S, Mitchell G
Cochrane Database Syst Rev 2015 Jan 2;1(1):CD010206. doi: 10.1002/14651858.CD010206.pub2. PMID: 25879099Free PMC Article

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