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Tachypnea

MedGen UID:
66669
Concept ID:
C0231835
Finding; Finding
Synonyms: Increased respiratory rate or depth of breathing; Polypnea
SNOMED CT: Tachypneic (271823003); Tachypnea (271823003); Rapid respiration (271823003); Rapid breathing (271823003)
 
HPO: HP:0002789

Definition

Very rapid breathing. [from HPO]

Conditions with this feature

Werdnig-Hoffmann disease
MedGen UID:
21913
Concept ID:
C0043116
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adolescence or young adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. Poor weight gain with growth failure, restrictive lung disease, scoliosis, joint contractures, and sleep difficulties are common complications.
Biotinidase deficiency
MedGen UID:
66323
Concept ID:
C0220754
Disease or Syndrome
If untreated, young children with profound biotinidase deficiency usually exhibit neurologic abnormalities including seizures, hypotonia, ataxia, developmental delay, vision problems, hearing loss, and cutaneous abnormalities (e.g., alopecia, skin rash, candidiasis). Older children and adolescents with profound biotinidase deficiency often exhibit motor limb weakness, spastic paresis, and decreased visual acuity. Once vision problems, hearing loss, and developmental delay occur, they are usually irreversible, even with biotin therapy. Individuals with partial biotinidase deficiency may have hypotonia, skin rash, and hair loss, particularly during times of stress.
Autoimmune interstitial lung, joint, and kidney disease
MedGen UID:
452265
Concept ID:
C0231330
Temporal Concept
Autoimmune interstitial lung, joint, and kidney disease is an autosomal dominant systemic autoimmune disorder characterized by interstitial lung disease, inflammatory arthritis, and immune complex-mediated renal disease. Laboratory studies show high-titer autoantibodies. Symptoms appear in the first 2 decades of life, but there is incomplete penetrance (summary by Watkin et al., 2015).
Desquamative interstitial pneumonia
MedGen UID:
65962
Concept ID:
C0238378
Disease or Syndrome
Interstitial lung disease (ILD), or pneumonitis, is a heterogeneous group of disorders characterized pathologically by expansion of the interstitial compartment of the lung by inflammatory cells. Fibrosis occurs in many cases (Visscher and Myers, 2006). Desquamative interstitial pneumonitis (DIP) was originally described as a pathologic entity by Liebow et al. (1965). Lung biopsy shows diffuse and uniform filling of alveoli by clusters of cells which Liebow et al. (1965) speculated to be 'desquamated pneumocytes.' Since then, these cells have been shown primarily to be pigmented alveolar macrophages. Other features include thickened alveolar septa with an infiltrate of inflammatory cells and plump, cuboidal type II pneumocytes. Mild collagen deposition without architectural distortion or honeycombing may be present. Different forms of ILD represent pathologic classifications based on histologic patterns rather than clinical diagnoses and may occur in a variety of clinical contexts (Visscher and Myers, 2006). See also usual interstitial pneumonitis (UIP; see 178500), which is associated with pulmonary fibrosis. Although DIP occurs most often as a sporadic disorder in adults during the third to fifth decade of life and is highly associated with smoking (Carrington et al., 1978), reports of a familial form with onset in infancy and early death suggest a genetic basis (Sharief et al., 1994). Cases of DIP reported in infants are often more severe and refractory to treatment than those reported in adults (Nogee et al., 2001). With the advent of molecular genetic analysis, some cases of familial early-onset respiratory insufficiency associated with a pathologic diagnosis of DIP have been shown to result from congenital dysfunction of surfactant metabolism (see, e.g., SMDP1, 265120) due to mutations in genes involved in surfactant metabolism (Nogee et al., 2001; Whitsett and Weaver, 2002).
Propionic acidemia
MedGen UID:
75694
Concept ID:
C0268579
Disease or Syndrome
The spectrum of propionic acidemia (PA) ranges from neonatal-onset to late-onset disease. Neonatal-onset PA, the most common form, is characterized by a healthy newborn with poor feeding and decreased arousal in the first few days of life, followed by progressive encephalopathy of unexplained origin. Without prompt diagnosis and management, this is followed by progressive encephalopathy manifesting as lethargy, seizures, or coma that can result in death. It is frequently accompanied by metabolic acidosis with anion gap, lactic acidosis, ketonuria, hypoglycemia, hyperammonemia, and cytopenias. Individuals with late-onset PA may remain asymptomatic and suffer a metabolic crisis under catabolic stress (e.g., illness, surgery, fasting) or may experience a more insidious onset with the development of multiorgan complications including vomiting, protein intolerance, failure to thrive, hypotonia, developmental delays or regression, movement disorders, or cardiomyopathy. Isolated cardiomyopathy can be observed on rare occasion in the absence of clinical metabolic decompensation or neurocognitive deficits. Manifestations of neonatal and late-onset PA over time can include growth impairment, intellectual disability, seizures, basal ganglia lesions, pancreatitis, and cardiomyopathy. Other rarely reported complications include optic atrophy, hearing loss, premature ovarian insufficiency, and chronic renal failure.
Holocarboxylase synthetase deficiency
MedGen UID:
120653
Concept ID:
C0268581
Disease or Syndrome
Holocarboxylase synthetase deficiency, a biotin-responsive multiple carboxylase deficiency (MCD), is characterized by metabolic acidosis, lethargy, hypotonia, convulsions, and dermatitis. Most patients present in the newborn or early infantile period, but some become symptomatic in the later infantile period (summary by Suzuki et al., 2005). Also see biotinidase deficiency (253260), another form of MCD with a later onset. Care must be taken to differentiate the inherited multiple carboxylase deficiencies from acquired biotin deficiencies, such as those that develop after excessive dietary intake of avidin, an egg-white glycoprotein that binds specifically and essentially irreversibly to biotin (Sweetman et al., 1981) or prolonged parenteral alimentation without supplemental biotin (Mock et al., 1981).
Familial methionine malabsorption
MedGen UID:
78693
Concept ID:
C0268622
Disease or Syndrome
Very long chain acyl-CoA dehydrogenase deficiency
MedGen UID:
87459
Concept ID:
C0342784
Disease or Syndrome
Deficiency of very long-chain acyl-CoA dehydrogenase (VLCAD), which catalyzes the initial step of mitochondrial ß-oxidation of long-chain fatty acids with a chain length of 14 to 20 carbons, is associated with three phenotypes. The severe early-onset cardiac and multi-organ failure form typically presents in the first months of life with hypertrophic or dilated cardiomyopathy, pericardial effusion, and arrhythmias, as well as hypotonia, hepatomegaly, and intermittent hypoglycemia. The hepatic or hypoketotic hypoglycemic form typically presents during early childhood with hypoketotic hypoglycemia and hepatomegaly, but without cardiomyopathy. The later-onset episodic myopathic form presents with intermittent rhabdomyolysis, muscle cramps and/or pain, and/or exercise intolerance. Hypoglycemia typically is not present at the time of symptoms.
Succinyl-CoA acetoacetate transferase deficiency
MedGen UID:
137979
Concept ID:
C0342792
Disease or Syndrome
Ketone bodies are major vectors of energy transfer from the liver to extrahepatic tissues and are the main source of lipid-derived energy for the brain. Mitchell et al. (1995) reviewed medical aspects of ketone body metabolism, including the differential diagnosis of abnormalities. As the first step of ketone body utilization, succinyl-CoA:3-oxoacid CoA transferase (SCOT, or OXCT1; EC 2.8.3.5) catalyzes the reversible transfer of CoA from succinyl-CoA to acetoacetate.
Cholesterol pneumonia
MedGen UID:
154291
Concept ID:
C0549472
Disease or Syndrome
Neonatal severe hyperparathyroidism
MedGen UID:
331326
Concept ID:
C1832615
Gene or Genome
Neonatal severe hyperparathyroidism usually manifests in the first 6 months of life with severe hypercalcemia, bone demineralization, and failure to thrive. Early diagnosis is critical because untreated NSHPT can be a devastating neurodevelopmental disorder, which in some cases is lethal without parathyroidectomy. Some infants have milder hyperparathyroidism and a substantially milder clinical presentation and natural history (summary by Egbuna and Brown, 2008).
Arima syndrome
MedGen UID:
340930
Concept ID:
C1855675
Disease or Syndrome
Classic Joubert syndrome is characterized by three primary findings: A distinctive cerebellar and brain stem malformation called the molar tooth sign (MTS). Hypotonia. Developmental delays. Often these findings are accompanied by episodic tachypnea or apnea and/or atypical eye movements. In general, the breathing abnormalities improve with age, truncal ataxia develops over time, and acquisition of gross motor milestones is delayed. Cognitive abilities are variable, ranging from severe intellectual disability to normal. The designation Joubert syndrome and related disorders (JSRD) is used to describe individuals with JS who have additional findings including retinal dystrophy, renal disease, ocular colobomas, occipital encephalocele, hepatic fibrosis, polydactyly, oral hamartomas, and endocrine abnormalities. Both intra- and interfamilial variation are seen.
Leigh syndrome, French Canadian type
MedGen UID:
387801
Concept ID:
C1857355
Disease or Syndrome
The French Canadian type of Leigh syndrome is an autosomal recessive severe neurologic disorder with onset in infancy. Features include delayed psychomotor development, mental retardation, mild dysmorphic facial features, hypotonia, ataxia, and the development of lesions in the brainstem and basal ganglia. Affected individuals tend to have episodic metabolic and/or neurologic crises in early childhood, which often lead to early death (summary by Debray et al., 2011). For a phenotypic description and a discussion of genetic heterogeneity of Leigh syndrome, see 256000.
Spinal muscular atrophy, distal, autosomal recessive, 1
MedGen UID:
388083
Concept ID:
C1858517
Disease or Syndrome
Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is an inherited condition that causes muscle weakness and respiratory failure typically beginning in infancy. Early features of this condition are difficult and noisy breathing, especially when inhaling; a weak cry; problems feeding; and recurrent episodes of pneumonia. Typically between the ages of 6 weeks and 6 months, infants with this condition will experience a sudden inability to breathe due to paralysis of the muscle that separates the abdomen from the chest cavity (the diaphragm). Normally, the diaphragm contracts and moves downward during inhalation to allow the lungs to expand. With diaphragm paralysis, affected individuals require life-long support with a machine to help them breathe (mechanical ventilation). Rarely, children with SMARD1 develop signs or symptoms of the disorder later in childhood.Soon after respiratory failure occurs, individuals with SMARD1 develop muscle weakness in their distal muscles. These are the muscles farther from the center of the body, such as muscles in the hands and feet. The weakness soon spreads to all muscles; however, within 2 years, the muscle weakness typically stops getting worse. Some individuals may retain a low level of muscle function, while others lose all ability to move their muscles. Muscle weakness severely impairs motor development, such as sitting, standing, and walking. Some affected children develop an abnormal side-to-side and back-to-front curvature of the spine (scoliosis and kyphosis, often called kyphoscoliosis when they occur together). After approximately the first year of life, individuals with SMARD1 may lose their deep tendon reflexes, such as the reflex being tested when a doctor taps the knee with a hammer.Other features of SMARD1 can include reduced pain sensitivity, excessive sweating (hyperhidrosis), loss of bladder and bowel control, and an irregular heartbeat (arrhythmia).
Respiratory distress syndrome in premature infants
MedGen UID:
368840
Concept ID:
C1968593
Disease or Syndrome
The main cause of respiratory distress syndrome (RDS) in premature infants is a developmental deficiency of pulmonary surfactant. The frequency of RDS is inversely proportional to gestational age. However, not all infants born prematurely develop RDS, suggesting that there may be susceptibility factors. Because multiple factors can contribute to the pathogenesis of RDS specifically in premature infants, the etiology is considered to be multifactorial (summaries by Ramet et al., 2000; Clark and Clark, 2005). Pathogenic germline mutations in several genes involved in surfactant metabolism, including SFTPB (178640) and SFTPC (178620), can cause clinical features of respiratory distress syndrome in term neonates, children, and adults, disorders referred to as 'surfactant metabolism dysfunction' (see, e.g., SMDP1, 265120). Susceptibility to the development of RDS in premature infants may be associated with polymorphisms in surfactant genes, such as surfactant protein A1 (SFTPA1; 178630), SFTPB, and SFTPC (see MOLECULAR GENETICS).
Surfactant metabolism dysfunction, pulmonary, 1
MedGen UID:
368844
Concept ID:
C1968602
Disease or Syndrome
Inborn errors of pulmonary surfactant metabolism are genetically heterogeneous disorders resulting in severe respiratory insufficiency or failure in full-term neonates or infants. These disorders are associated with various pathologic entities, including pulmonary alveolar proteinosis (PAP), desquamative interstitial pneumonitis (DIP), or cellular nonspecific interstitial pneumonitis (NSIP) (Clark and Clark, 2005). A clinically similar disorder characterized by respiratory distress (267450) can affect preterm infants, who show developmental deficiency of surfactant. Acquired PAP (610910) is an autoimmune disorder characterized by the presence of autoantobodies to CSF2 (138960). Genetic Heterogeneity of Pulmonary Surfactant Metabolism Dysfunction See also SMDP2 (610913), caused by mutation in the SPTPC gene (178620) on 8p21; SMDP3 (610921), caused by mutation in the ABCA3 gene (601615) on 16p13; SMDP4 (300770), caused by mutation in the CSF2RA gene (306250) on Xp; and SMDP5 (614370), caused by mutation in the CSF2RB gene (138981) on 22q12.
Surfactant metabolism dysfunction, pulmonary, 3
MedGen UID:
410074
Concept ID:
C1970456
Disease or Syndrome
For a general phenotypic description and a discussion of genetic heterogeneity of pulmonary surfactant metabolism dysfunction, see SMDP1 (265120).
Surfactant metabolism dysfunction, pulmonary, 2
MedGen UID:
410078
Concept ID:
C1970470
Disease or Syndrome
Surfactant protein C (SPC) deficiency is a rare autosomal dominant disease associated with progressive respiratory insufficiency and lung disease with a variable clinical course. The pathophysiology of the disorder is postulated to involve intracellular accumulation of a structurally defective SPC protein (Thomas et al., 2002). For a general phenotypic description and a discussion of genetic heterogeneity of pulmonary surfactant metabolism dysfunction, see SMDP1 (265120).
Surfactant metabolism dysfunction, pulmonary, 4
MedGen UID:
393858
Concept ID:
C2677877
Disease or Syndrome
Pulmonary alveolar proteinosis (PAP) is a rare lung disorder in which surfactant-derived lipoproteins accumulate excessively within pulmonary alveoli, causing severe respiratory distress. Three forms of PAP have been described: hereditary (usually congenital), secondary, and acquired. Hereditary PAP is associated with mutations in the CSF2RA gene or in genes encoding surfactant proteins. Secondary PAP develops in conditions in which there are reduced numbers or functional impairment of alveolar macrophages and is associated with inhalation of inorganic dust (silica) or toxic fumes, hematologic malignancies, pharmacologic immunosuppression, infections, and impaired CSF2RB (138960) expression. Acquired PAP (610910), the most common form, usually occurs in adults and is caused by neutralizing autoantibodies to CSF2 (138960) (Martinez-Moczygemba et al., 2008). For a general phenotypic description and a discussion of genetic heterogeneity of congenital pulmonary surfactant metabolism dysfunction, see SMDP1 (265120).
Spondylometaphyseal dysplasia, megarbane-dagher-melki type
MedGen UID:
413221
Concept ID:
C2750075
Disease or Syndrome
Multisystemic smooth muscle dysfunction syndrome
MedGen UID:
462551
Concept ID:
C3151201
Disease or Syndrome
METHYLMALONIC ACIDURIA AND HOMOCYSTINURIA, cblJ TYPE
MedGen UID:
766829
Concept ID:
C3553915
Disease or Syndrome
Combined methylmalonic aciduria (MMA) and homocystinuria is a genetically heterogeneous metabolic disorder of cobalamin (cbl; vitamin B12) metabolism, which is essential for hematologic and neurologic function. Biochemically, the defect causes decreased levels of the coenzymes adenosylcobalamin (AdoCbl) and methylcobalamin (MeCbl), which results in decreased activity of the respective enzymes methylmalonyl-CoA mutase (MUT; 609058) and methyltetrahydrofolate:homocysteine methyltransferase, also known as methionine synthase (MTR; 156570). CblJ is phenotypically and biochemically similar to cblF (277380) (summary by Coelho et al., 2012).
JOUBERT SYNDROME 23
MedGen UID:
900119
Concept ID:
C4084822
Disease or Syndrome

Recent clinical studies

Etiology

Moresco L, Calevo MG, Baldi F, Cohen A, Bruschettini M
Cochrane Database Syst Rev 2016 May 23;(5):CD011877. doi: 10.1002/14651858.CD011877.pub2. PMID: 27211231
Moresco L, Bruschettini M, Cohen A, Gaiero A, Calevo MG
Cochrane Database Syst Rev 2016 May 23;(5):CD011878. doi: 10.1002/14651858.CD011878.pub2. PMID: 27210618
Kim BB, Chung SH, Yoon HS, Hahn WH, Bae CW, Choi YS
Pediatr Neonatol 2016 Jun;57(3):195-200. Epub 2015 Oct 3 doi: 10.1016/j.pedneo.2015.08.006. PMID: 26879216
Rauch D, Wetzke M, Reu S, Wesselak W, Schams A, Hengst M, Kammer B, Ley-Zaporozhan J, Kappler M, Proesmans M, Lange J, Escribano A, Kerem E, Ahrens F, Brasch F, Schwerk N, Griese M; PTI (Persistent Tachypnea of Infancy) Study Group of the Kids Lung Register.
Am J Respir Crit Care Med 2016 Feb 15;193(4):438-47. doi: 10.1164/rccm.201508-1655OC. PMID: 26474448
Costa S, Rocha G, Leitão A, Guimarães H
J Matern Fetal Neonatal Med 2012 Jul;25(7):992-4. Epub 2011 Oct 1 doi: 10.3109/14767058.2011.604366. PMID: 21745094

Diagnosis

Rauch D, Wetzke M, Reu S, Wesselak W, Schams A, Hengst M, Kammer B, Ley-Zaporozhan J, Kappler M, Proesmans M, Lange J, Escribano A, Kerem E, Ahrens F, Brasch F, Schwerk N, Griese M; PTI (Persistent Tachypnea of Infancy) Study Group of the Kids Lung Register.
Am J Respir Crit Care Med 2016 Feb 15;193(4):438-47. doi: 10.1164/rccm.201508-1655OC. PMID: 26474448
Fuchs J, Pathak S, Lee C, Schmidt HJ
Pediatr Rev 2015 Feb;36(2):74-5. doi: 10.1542/pir.36-2-74. PMID: 25646311
Chiang J, Raiman J, Cutz E, Solomon M, Dell S
Pediatrics 2014 Sep;134(3):e884-8. Epub 2014 Aug 11 doi: 10.1542/peds.2013-2765. PMID: 25113300
Bianchi W, Dugas AF, Hsieh YH, Saheed M, Hill P, Lindauer C, Terzis A, Rothman RE
Ann Emerg Med 2013 Jan;61(1):37-43. Epub 2012 Jun 26 doi: 10.1016/j.annemergmed.2012.05.030. PMID: 22738682
Costa S, Rocha G, Leitão A, Guimarães H
J Matern Fetal Neonatal Med 2012 Jul;25(7):992-4. Epub 2011 Oct 1 doi: 10.3109/14767058.2011.604366. PMID: 21745094

Therapy

Seo MH, Choa M, You JS, Lee HS, Hong JH, Park YS, Chung SP, Park I
Yonsei Med J 2016 Nov;57(6):1361-9. doi: 10.3349/ymj.2016.57.6.1361. PMID: 27593863Free PMC Article
Moresco L, Calevo MG, Baldi F, Cohen A, Bruschettini M
Cochrane Database Syst Rev 2016 May 23;(5):CD011877. doi: 10.1002/14651858.CD011877.pub2. PMID: 27211231
Moresco L, Bruschettini M, Cohen A, Gaiero A, Calevo MG
Cochrane Database Syst Rev 2016 May 23;(5):CD011878. doi: 10.1002/14651858.CD011878.pub2. PMID: 27210618
Perez M, Kumar TK, Figueroa M, Johnson J, Absi MA
Pediatr Rev 2015 Jan;36(1):33-5. doi: 10.1542/pir.36-1-33. PMID: 25554110
Bianchi W, Dugas AF, Hsieh YH, Saheed M, Hill P, Lindauer C, Terzis A, Rothman RE
Ann Emerg Med 2013 Jan;61(1):37-43. Epub 2012 Jun 26 doi: 10.1016/j.annemergmed.2012.05.030. PMID: 22738682

Prognosis

Seo MH, Choa M, You JS, Lee HS, Hong JH, Park YS, Chung SP, Park I
Yonsei Med J 2016 Nov;57(6):1361-9. doi: 10.3349/ymj.2016.57.6.1361. PMID: 27593863Free PMC Article
Kim BB, Chung SH, Yoon HS, Hahn WH, Bae CW, Choi YS
Pediatr Neonatol 2016 Jun;57(3):195-200. Epub 2015 Oct 3 doi: 10.1016/j.pedneo.2015.08.006. PMID: 26879216
Rauch D, Wetzke M, Reu S, Wesselak W, Schams A, Hengst M, Kammer B, Ley-Zaporozhan J, Kappler M, Proesmans M, Lange J, Escribano A, Kerem E, Ahrens F, Brasch F, Schwerk N, Griese M; PTI (Persistent Tachypnea of Infancy) Study Group of the Kids Lung Register.
Am J Respir Crit Care Med 2016 Feb 15;193(4):438-47. doi: 10.1164/rccm.201508-1655OC. PMID: 26474448
Cooper CB, Calligaro GL, Quinn MM, Eshaghian P, Coskun F, Abrazado M, Bateman ED, Raine RI
Respir Physiol Neurobiol 2014 Jan 1;190:76-80. Epub 2013 Aug 27 doi: 10.1016/j.resp.2013.08.002. PMID: 23994176
Lahaije AJ, Willems LM, van Hees HW, Dekhuijzen PN, van Helvoort HA, Heijdra YF
Clin Physiol Funct Imaging 2013 Jan;33(1):62-9. Epub 2012 Sep 2 doi: 10.1111/j.1475-097X.2012.01164.x. PMID: 23216767

Clinical prediction guides

Seo MH, Choa M, You JS, Lee HS, Hong JH, Park YS, Chung SP, Park I
Yonsei Med J 2016 Nov;57(6):1361-9. doi: 10.3349/ymj.2016.57.6.1361. PMID: 27593863Free PMC Article
Cooper CB, Calligaro GL, Quinn MM, Eshaghian P, Coskun F, Abrazado M, Bateman ED, Raine RI
Respir Physiol Neurobiol 2014 Jan 1;190:76-80. Epub 2013 Aug 27 doi: 10.1016/j.resp.2013.08.002. PMID: 23994176
Lahaije AJ, Willems LM, van Hees HW, Dekhuijzen PN, van Helvoort HA, Heijdra YF
Clin Physiol Funct Imaging 2013 Jan;33(1):62-9. Epub 2012 Sep 2 doi: 10.1111/j.1475-097X.2012.01164.x. PMID: 23216767
Bianchi W, Dugas AF, Hsieh YH, Saheed M, Hill P, Lindauer C, Terzis A, Rothman RE
Ann Emerg Med 2013 Jan;61(1):37-43. Epub 2012 Jun 26 doi: 10.1016/j.annemergmed.2012.05.030. PMID: 22738682
Costa S, Rocha G, Leitão A, Guimarães H
J Matern Fetal Neonatal Med 2012 Jul;25(7):992-4. Epub 2011 Oct 1 doi: 10.3109/14767058.2011.604366. PMID: 21745094

Recent systematic reviews

Moresco L, Calevo MG, Baldi F, Cohen A, Bruschettini M
Cochrane Database Syst Rev 2016 May 23;(5):CD011877. doi: 10.1002/14651858.CD011877.pub2. PMID: 27211231
Moresco L, Bruschettini M, Cohen A, Gaiero A, Calevo MG
Cochrane Database Syst Rev 2016 May 23;(5):CD011878. doi: 10.1002/14651858.CD011878.pub2. PMID: 27210618
Gurrera RJ, Caroff SN, Cohen A, Carroll BT, DeRoos F, Francis A, Frucht S, Gupta S, Levenson JL, Mahmood A, Mann SC, Policastro MA, Rosebush PI, Rosenberg H, Sachdev PS, Trollor JN, Velamoor VR, Watson CB, Wilkinson JR
J Clin Psychiatry 2011 Sep;72(9):1222-8. Epub 2011 Jun 28 doi: 10.4088/JCP.10m06438. PMID: 21733489
Simbalista R, Araújo M, Nascimento-Carvalho CM
Clinics (Sao Paulo) 2011;66(1):95-100. PMID: 21437443Free PMC Article
Lewis V, Whitelaw A
Cochrane Database Syst Rev 2002;(1):CD003064. doi: 10.1002/14651858.CD003064. PMID: 11869651

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