U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Generalized tonic seizure

MedGen UID:
322935
Concept ID:
C1836508
Disease or Syndrome; Finding
Synonym: Generalized tonic seizures
SNOMED CT: Generalized tonic seizure (1208969008); Generalized onset tonic epileptic seizure (1208969008); Generalized-onset tonic epileptic seizure (1208969008)
 
HPO: HP:0010818

Definition

A generalized tonic seizure is a type of generalized motor seizure characterized by bilateral limb stiffening or elevation, often with neck stiffening without a subsequent clonic phase. The tonic activity can be a sustained abnormal posture, either in extension or flexion, sometimes accompanied by tremor of the extremities. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVGeneralized tonic seizure

Conditions with this feature

Neutral 1 amino acid transport defect
MedGen UID:
6723
Concept ID:
C0018609
Disease or Syndrome
Hartnup disorder (HND) is characterized by transient manifestations of pellagra, cerebellar ataxia, and psychosis. It is caused by impaired transport of neutral amino acids across epithelial cells in renal proximal tubules and intestinal mucosa (summary by Kleta et al., 2004).
Febrile seizures, familial, 5
MedGen UID:
322934
Concept ID:
C1836507
Disease or Syndrome
Febrile seizures, familial, 6
MedGen UID:
373107
Concept ID:
C1836518
Disease or Syndrome
Febrile seizures, familial, 1
MedGen UID:
338959
Concept ID:
C1852577
Disease or Syndrome
Childhood seizures associated with febrile episodes are relatively common and represent the majority of childhood seizures. A febrile convulsion is defined as a seizure event in infancy or childhood, usually occurring between 6 months and 6 years of age, associated with fever but without any evidence of intracranial infection or defined pathologic or traumatic cause (Nabbout et al., 2002). Although the majority of patients do not develop epilepsy, the risk of developing subsequent afebrile seizures is 5 to 7 times higher in those with a history of febrile seizures compared to the general population (Annegers et al., 1987; Hedera et al., 2006). The FEB1 locus maps to chromosome 8q13-q21. Genetic Heterogeneity of Familial Febrile Seizures See FEB2 (602477), caused by mutation in the HCN2 gene (602781) on chromosome 19p13; FEB3A (604403), caused by mutation in the SCN1A gene (182389) on chromosome 2q24; FEB4 (604352), caused by mutation in the ADGRV1 gene (602851) on chromosome 5q14; FEB8 (607681), caused by mutation in the GABRG2 gene (137164) on chromosome 5q31; and FEB11 (614418), caused by mutation in the CPA6 gene (609562) on chromosome 8q13. Several loci for familial febrile seizures have been identified: see FEB3B (613863) on chromosome 2q24; FEB5 (609255) on chromosome 6q22-q24; FEB6 (609253) on chromosome 18p11; FEB7 (611515) on chromosome 21q22; FEB9 (611634) on chromosome 3p24.2-p23; and FEB10 (612637) on chromosome 3q26. A phenotype termed 'generalized epilepsy with febrile seizures plus' (GEFS+; 604233) is a clinical subset of familial febrile convulsions in which affected individuals later develop afebrile seizures. GEFS+ is associated with mutations in several genes. Deprez et al. (2009) provided a review of the genetics of epilepsy syndromes starting in the first year of life, and included a diagnostic algorithm.
Generalized epilepsy with febrile seizures plus, type 4
MedGen UID:
342858
Concept ID:
C1853345
Disease or Syndrome
Febrile seizures, familial, 4
MedGen UID:
347652
Concept ID:
C1858493
Disease or Syndrome
Any febrile seizures, familial in which the cause of the disease is a mutation in the ADGRV1 gene.
Generalized epilepsy with febrile seizures plus, type 2
MedGen UID:
388117
Concept ID:
C1858673
Disease or Syndrome
SCN1A seizure disorders encompass a spectrum that ranges from simple febrile seizures and generalized epilepsy with febrile seizures plus (GEFS+) at the mild end to Dravet syndrome and intractable childhood epilepsy with generalized tonic-clonic seizures (ICE-GTC) at the severe end. Phenotypes with intractable seizures including Dravet syndrome are often associated with cognitive decline. Less commonly observed phenotypes include myoclonic astatic epilepsy (MAE), Lennox-Gastaut syndrome, infantile spasms, epilepsy with focal seizures, and vaccine-related encephalopathy and seizures. The phenotype of SCN1A seizure disorders can vary even within the same family.
Developmental and epileptic encephalopathy, 4
MedGen UID:
436917
Concept ID:
C2677326
Disease or Syndrome
STXBP1 encephalopathy with epilepsy is characterized by early-onset encephalopathy with epilepsy (i.e., moderate-to-severe intellectual disability, refractory seizures, and ongoing epileptiform activity). The median age of onset of seizures is six weeks (range 1 day to 13 years). Seizure types can include infantile spasms; generalized tonic-clonic, clonic, or tonic seizures; and myoclonic, focal, atonic, and absence seizures. Epilepsy syndromes can include Ohtahara syndrome, West syndrome, Lennox-Gaustaut syndrome, and Dravet syndrome (not SCN1A-related), classic Rett syndrome (not MECP2-related), and atypical Rett syndrome (not CDKL5-related). The EEG is characterized by focal epileptic activity, burst suppression, hypsarrhythmia, or generalized spike-and-slow waves. Other findings can include abnormal tone, movement disorders (especially ataxia and dystonia), and behavior disorders (including autism spectrum disorder). Feeding difficulties are common.
Autosomal recessive ataxia due to ubiquinone deficiency
MedGen UID:
436985
Concept ID:
C2677589
Disease or Syndrome
Primary coenzyme Q10 (CoQ10) deficiency is usually associated with multisystem involvement, including neurologic manifestations such as fatal neonatal encephalopathy with hypotonia; a late-onset slowly progressive multiple-system atrophy-like phenotype (neurodegeneration with autonomic failure and various combinations of parkinsonism and cerebellar ataxia, and pyramidal dysfunction); and dystonia, spasticity, seizures, and intellectual disability. Steroid-resistant nephrotic syndrome (SRNS), the hallmark renal manifestation, is often the initial manifestation either as isolated renal involvement that progresses to end-stage renal disease (ESRD), or associated with encephalopathy (seizures, stroke-like episodes, severe neurologic impairment) resulting in early death. Hypertrophic cardiomyopathy (HCM), retinopathy or optic atrophy, and sensorineural hearing loss can also be seen.
Epilepsy, idiopathic generalized, susceptibility to, 9
MedGen UID:
413424
Concept ID:
C2750887
Finding
For a general phenotypic description and a discussion of genetic heterogeneity of idiopathic generalized epilepsy, see 600669. Juvenile myoclonic epilepsy is a subtype of idiopathic generalized epilepsy; see 254770 for a general phenotypic description and a discussion of genetic heterogeneity of JME.
Developmental and epileptic encephalopathy, 14
MedGen UID:
767109
Concept ID:
C3554195
Disease or Syndrome
KCNT1-related epilepsy is most often associated with two phenotypes: epilepsy of infancy with migrating focal seizures (EIMFS) and autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). EIMFS is characterized by seizures, typically focal and asynchronous, beginning in the first six months of life with associated developmental plateau or regression. Autonomic manifestations (e.g., perioral cyanosis, flushing, apnea) are common. Seizures are intractable to multiple anticonvulsants and progress to become nearly continuous by age six to nine months. ADNFLE is characterized by clusters of nocturnal motor seizures that vary from simple arousals to hyperkinetic events with tonic or dystonic features. Individuals with KCNT1-related ADNFLE are more likely to develop seizures at a younger age, have cognitive comorbidity, and display psychiatric and behavioral problems than individuals with ADNFLE resulting from other causes. Less common seizure phenotypes in individuals with KCNT1-related epilepsy include West syndrome, Ohtahara syndrome, early myoclonic encephalopathy, leukodystrophy and/or leukoencephalopathy, focal epilepsy, and multifocal epilepsy. Additional neurologic features include hypotonia, microcephaly developing by age 12 months, strabismus, profound developmental delay, and additional movement disorders. Other systemic manifestations including pulmonary hemorrhage caused by prominent systemic-to-pulmonary collateral arteries or cardiac arrhythmia have been reported.
Developmental and epileptic encephalopathy, 17
MedGen UID:
815936
Concept ID:
C3809606
Disease or Syndrome
Developmental and epileptic encephalopathy-17 (DEE17) is a severe neurologic disorder characterized by onset of intractable seizures in the first weeks or months of life. EEG often shows a burst-suppression pattern consistent with a clinical diagnosis of Ohtahara syndrome. Affected infants have very poor psychomotor development and may have brain abnormalities, such as cerebral atrophy or thin corpus callosum. Some patients may show involuntary movements (summary by Nakamura et al., 2013). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Developmental and epileptic encephalopathy, 21
MedGen UID:
862867
Concept ID:
C4014430
Disease or Syndrome
Developmental and epileptic encephalopathy-21 (DEE21) is an autosomal recessive neurologic disorder characterized by the onset of intractable seizures in the first months of life. Affected individuals have severely impaired psychomotor development with poor head control and inability to fix and follow visually. Other features may include axial hypotonia, peripheral hypertonia, and cerebral atrophy or delayed myelination on brain imaging (summary by Alazami et al., 2014 and Alsahli et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Intellectual disability, autosomal dominant 38
MedGen UID:
895359
Concept ID:
C4225343
Mental or Behavioral Dysfunction
Any autosomal dominant non-syndromic intellectual disability in which the cause of the disease is a mutation in the EEF1A2 gene.
Lissencephaly due to TUBA1A mutation
MedGen UID:
930822
Concept ID:
C4305153
Congenital Abnormality
A congenital cortical development anomaly due to abnormal neuronal migration involving neocortical and hippocampal lamination, corpus callosum, cerebellum and brainstem. A large clinical spectrum can be observed, from children with severe epilepsy and intellectual and motor deficit to cases with severe cerebral dysgenesis in the antenatal period leading to pregnancy termination due to the severity of the prognosis.
Early-onset progressive diffuse brain atrophy-microcephaly-muscle weakness-optic atrophy syndrome
MedGen UID:
934638
Concept ID:
C4310671
Disease or Syndrome
PEBAT is an autosomal recessive neurodevelopmental disorder characterized by severely delayed psychomotor development apparent soon after birth or in infancy, profound intellectual disability, poor or absent speech, and seizures. Most patients are never able to walk due to hypotonia or spasticity. Brain imaging shows cerebral and cerebellar atrophy, thin corpus callosum, and secondary hypomyelination. The disorder shows progressive features, including microcephaly, consistent with a neurodegenerative process (summary by Miyake et al., 2016; Flex et al., 2016).
Developmental and epileptic encephalopathy, 41
MedGen UID:
934684
Concept ID:
C4310717
Disease or Syndrome
Developmental and epileptic encephalopathy-41 (DEE41) is a neurologic disorder characterized by the onset of seizures in the first days or weeks of life. Affected infants show severely impaired psychomotor development with hypotonia, spasticity, lack of speech, poor visual fixation, feeding difficulties sometimes necessitating tube feeding, poor overall growth and microcephaly, and contractures. Brain imaging may show delayed myelination, thin corpus callosum, and cerebral atrophy (summary by the EPI4K Consortium, 2016). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Intellectual disability, autosomal dominant 42
MedGen UID:
934741
Concept ID:
C4310774
Mental or Behavioral Dysfunction
GNB1 encephalopathy (GNB1-E) is characterized by moderate-to-severe developmental delay / intellectual disability, structural brain abnormalities, and often infantile hypotonia and seizures. Other less common findings include dystonia, reduced vision, behavior issues, growth delay, gastrointestinal (GI) problems, genitourinary (GU) abnormalities in males, and cutaneous mastocytosis.
Developmental and epileptic encephalopathy, 51
MedGen UID:
1372686
Concept ID:
C4479208
Disease or Syndrome
Developmental and epileptic encephalopathy-51 (DEE51) is an autosomal recessive severe neurodevelopmental disorder characterized by onset of intractable seizures and hypotonia in the first days or weeks of life. Affected individuals have severely delayed psychomotor development and may show abnormal movements. Brain imaging shows nonspecific abnormalities, such as cerebral atrophy, cerebellar atrophy, and delayed myelination. Laboratory studies showed increased lactate, suggesting mitochondrial dysfunction (summary by Ait-El-Mkadem et al., 2017). For a discussion of genetic heterogeneity of DEE, see 308350.
Congenital disorder of glycosylation, type IIq
MedGen UID:
1390458
Concept ID:
C4479353
Disease or Syndrome
A rare congenital disorder of glycosylation caused by mutations in the COG2 gene and with characteristics of normal presentation at birth, followed by progressive deterioration with postnatal microcephaly, developmental delay, intellectual disability, seizures, spastic quadriplegia, liver dysfunction, hypocupremia and hypoceruloplasminemia in the first year of life. Diffuse cerebral atrophy and thin corpus callosum may be observed on brain MRI.
Developmental and epileptic encephalopathy, 63
MedGen UID:
1646846
Concept ID:
C4693810
Disease or Syndrome
Developmental and epileptic encephalopathy-63 (DEE63) is an autosomal recessive neurologic disorder characterized by early-onset refractory infantile spasms and myoclonic seizures in the first months to years of life. Affected individuals have severe to profound developmental delay, often with hypotonia and inability to sit or speak (summary by Redler et al., 2017). For a discussion of genetic heterogeneity of DEE, see 308350.
Developmental and epileptic encephalopathy, 66
MedGen UID:
1648486
Concept ID:
C4748070
Disease or Syndrome
Developmental and epileptic encephalopathy-66 (DEE66) is a neurologic disorder characterized by the onset of various types of seizures in the first days or weeks of life. Most seizures have focal origins; secondary generalization is common. Seizure control is difficult at first, but may become easier with time. Affected individuals show global developmental delay with hypotonia, behavioral abnormalities, and dysmorphic features or ophthalmologic defects. Brain imaging often shows cerebellar dysgenesis. A subset of patients have extraneurologic manifestations, including hematologic and distal limb abnormalities (summary by Olson et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Leukoencephalopathy, progressive, infantile-onset, with or without deafness
MedGen UID:
1779519
Concept ID:
C5542996
Disease or Syndrome
Infantile-onset progressive leukoencephalopathy with or without deafness (LEPID) is an autosomal recessive complex neurodegenerative disorder with onset of symptoms in infancy or early childhood. Most patients present with sensorineural deafness or hypoacousia and global developmental delay. Affected individuals show episodic regression with progressive motor deterioration resulting in spastic tetraplegia and loss of ambulation, as well as impaired intellectual development with poor or absent speech. Additional more variable features may include poor overall growth with microcephaly, seizures, visual loss, microcytic anemia, and hepatic enlargement or abnormal liver enzymes. Brain imaging shows deep white matter abnormalities consistent with a progressive leukoencephalopathy. The brain and spinal cord are usually both involved; calcifications of these regions are often observed. Laboratory studies show increased serum lactate and deficiencies of mitochondrial respiratory chain complexes, consistent with global mitochondrial dysfunction. Early death often occurs (summary by Itoh et al., 2019).
Kohlschutter-Tonz syndrome-like
MedGen UID:
1781649
Concept ID:
C5543202
Disease or Syndrome
Den Hoed-de Boer-Voisin syndrome (DHDBV) is characterized by global developmental delay with moderately to severely impaired intellectual development, poor or absent speech, and delayed motor skills. Although the severity of the disorder varies, many patients are nonverbal and have hypotonia with inability to sit or walk. Early-onset epilepsy is common and may be refractory to treatment, leading to epileptic encephalopathy and further interruption of developmental progress. Most patients have feeding difficulties with poor overall growth and dysmorphic facial features, as well as significant dental anomalies resembling amelogenesis imperfecta. The phenotype is reminiscent of Kohlschutter-Tonz syndrome (KTZS; 226750). More variable features of DHDBV include visual defects, behavioral abnormalities, and nonspecific involvement of other organ systems (summary by den Hoed et al., 2021).
Epilepsy, idiopathic generalized, susceptibility to, 17
MedGen UID:
1794141
Concept ID:
C5561931
Finding
Neurodevelopmental disorder with microcephaly, seizures, and neonatal cholestasis
MedGen UID:
1794262
Concept ID:
C5562052
Disease or Syndrome
Neurodevelopmental disorder with microcephaly, seizures, and neonatal cholestasis (NEDMSC) is an autosomal recessive disorder characterized by severely impaired global development apparent from infancy, progressive microcephaly, and neonatal cholestasis manifest as jaundice and elevated liver enzymes. The liver disease resolves, but affected individuals show feeding difficulties, failure to thrive, hypotonia, seizures, hyperkinetic movements, irritability, and poor eye contact or vision, and achieve almost no motor or cognitive developmental milestones. Brain imaging demonstrates agenesis or hypoplasia of the corpus callosum. Death in early childhood may occur (summary by Schneeberger et al., 2021).

Professional guidelines

PubMed

Zuberi SM, Wirrell E, Yozawitz E, Wilmshurst JM, Specchio N, Riney K, Pressler R, Auvin S, Samia P, Hirsch E, Galicchio S, Triki C, Snead OC, Wiebe S, Cross JH, Tinuper P, Scheffer IE, Perucca E, Moshé SL, Nabbout R
Epilepsia 2022 Jun;63(6):1349-1397. Epub 2022 May 3 doi: 10.1111/epi.17239. PMID: 35503712
Migdady I, Rosenthal ES, Cock HR
Anaesthesia 2022 Jan;77 Suppl 1:78-91. doi: 10.1111/anae.15606. PMID: 35001380
Abboud H, Probasco JC, Irani S, Ances B, Benavides DR, Bradshaw M, Christo PP, Dale RC, Fernandez-Fournier M, Flanagan EP, Gadoth A, George P, Grebenciucova E, Jammoul A, Lee ST, Li Y, Matiello M, Morse AM, Rae-Grant A, Rojas G, Rossman I, Schmitt S, Venkatesan A, Vernino S, Pittock SJ, Titulaer MJ; Autoimmune Encephalitis Alliance Clinicians Network
J Neurol Neurosurg Psychiatry 2021 Jul;92(7):757-768. Epub 2021 Mar 1 doi: 10.1136/jnnp-2020-325300. PMID: 33649022Free PMC Article

Recent clinical studies

Etiology

Negishi Y, Aoki Y, Itomi K, Yasuda K, Taniguchi H, Ishida A, Arakawa T, Miyamoto S, Nakashima M, Saitsu H, Saitoh S
Brain Dev 2021 Aug;43(7):804-808. Epub 2021 Apr 4 doi: 10.1016/j.braindev.2021.03.004. PMID: 33827760
Trivisano M, Pavia GC, Ferretti A, Fusco L, Vigevano F, Specchio N
Epilepsy Behav 2019 Jul;96:219-223. Epub 2019 Jun 4 doi: 10.1016/j.yebeh.2019.03.043. PMID: 31174070
Kim HJ, Kim SH, Kim HD, Lee JS, Lee YM, Koo KY, Lee JS, Kang HC
Yonsei Med J 2012 May;53(3):495-500. doi: 10.3349/ymj.2012.53.3.495. PMID: 22476991Free PMC Article
Kim H, Lee JH, Ryu HW, Lim BC, Chae JH, Choi J, Kim KJ, Hwang YS, Hwang H
Epilepsy Res 2012 Aug;101(1-2):70-5. Epub 2012 Mar 28 doi: 10.1016/j.eplepsyres.2012.03.003. PMID: 22459640
Kim H, Jeoung JY, Ham SY, Kim SR
J Korean Med Sci 1999 Jun;14(3):342-4. doi: 10.3346/jkms.1999.14.3.342. PMID: 10402182Free PMC Article

Diagnosis

Trivisano M, Pavia GC, Ferretti A, Fusco L, Vigevano F, Specchio N
Epilepsy Behav 2019 Jul;96:219-223. Epub 2019 Jun 4 doi: 10.1016/j.yebeh.2019.03.043. PMID: 31174070
Lv Y, Zheng X, Zhang X, Zhao D, Cui L
J Nerv Ment Dis 2019 Mar;207(3):188-191. doi: 10.1097/NMD.0000000000000946. PMID: 30741775
Kim HJ, Kim SH, Kim HD, Lee JS, Lee YM, Koo KY, Lee JS, Kang HC
Yonsei Med J 2012 May;53(3):495-500. doi: 10.3349/ymj.2012.53.3.495. PMID: 22476991Free PMC Article
Kim H, Lee JH, Ryu HW, Lim BC, Chae JH, Choi J, Kim KJ, Hwang YS, Hwang H
Epilepsy Res 2012 Aug;101(1-2):70-5. Epub 2012 Mar 28 doi: 10.1016/j.eplepsyres.2012.03.003. PMID: 22459640
Labate A, Barone R, Gambardella A, Civitelli D, Fiumara A, Annesi G, Zappia M, Pavone L, Quattrone A
Brain Dev 2004 Mar;26(2):130-3. doi: 10.1016/S0387-7604(03)00069-X. PMID: 15036433

Therapy

Hatanaka K, Kamijo Y, Kitamoto T, Hanazawa T, Yoshizawa T, Ochiai H, Haga Y
Clin Toxicol (Phila) 2022 Mar;60(3):379-381. Epub 2021 Aug 18 doi: 10.1080/15563650.2021.1953518. PMID: 34405740
Kim H, Lee JH, Ryu HW, Lim BC, Chae JH, Choi J, Kim KJ, Hwang YS, Hwang H
Epilepsy Res 2012 Aug;101(1-2):70-5. Epub 2012 Mar 28 doi: 10.1016/j.eplepsyres.2012.03.003. PMID: 22459640
Nishiyama T, Komatsu K
Minerva Anestesiol 2010 Dec;76(12):1088-90. PMID: 21178915
Labate A, Barone R, Gambardella A, Civitelli D, Fiumara A, Annesi G, Zappia M, Pavone L, Quattrone A
Brain Dev 2004 Mar;26(2):130-3. doi: 10.1016/S0387-7604(03)00069-X. PMID: 15036433
Wakai S, Kotagal P
Pediatr Int 2001 Feb;43(1):61-5. doi: 10.1046/j.1442-200x.2001.01326.x. PMID: 11208002

Prognosis

Yao Q, Fu M, Ren L, Lin C, Cao L
BMC Neurol 2022 Jan 28;22(1):42. doi: 10.1186/s12883-022-02555-y. PMID: 35090404Free PMC Article
Trivisano M, Pavia GC, Ferretti A, Fusco L, Vigevano F, Specchio N
Epilepsy Behav 2019 Jul;96:219-223. Epub 2019 Jun 4 doi: 10.1016/j.yebeh.2019.03.043. PMID: 31174070
Mueller LP, Theurich S, Christopeit M, Grothe W, Muetherig A, Weber T, Guenther S, Behre G
Eur J Haematol 2007 Jun;78(6):527-31. doi: 10.1111/j.1600-0609.2007.00851.x. PMID: 17509106
Fukuhara S, Migita K, Iida K, Okabayashi K, Inoue T, Iwasaki Y, Wada S, Yamanoue T, Ohtani M
Hiroshima J Med Sci 2001 Mar;50(1):37-40. PMID: 11314857
Kim H, Jeoung JY, Ham SY, Kim SR
J Korean Med Sci 1999 Jun;14(3):342-4. doi: 10.3346/jkms.1999.14.3.342. PMID: 10402182Free PMC Article

Clinical prediction guides

Yao Q, Fu M, Ren L, Lin C, Cao L
BMC Neurol 2022 Jan 28;22(1):42. doi: 10.1186/s12883-022-02555-y. PMID: 35090404Free PMC Article
Negishi Y, Aoki Y, Itomi K, Yasuda K, Taniguchi H, Ishida A, Arakawa T, Miyamoto S, Nakashima M, Saitsu H, Saitoh S
Brain Dev 2021 Aug;43(7):804-808. Epub 2021 Apr 4 doi: 10.1016/j.braindev.2021.03.004. PMID: 33827760
Mueller LP, Theurich S, Christopeit M, Grothe W, Muetherig A, Weber T, Guenther S, Behre G
Eur J Haematol 2007 Jun;78(6):527-31. doi: 10.1111/j.1600-0609.2007.00851.x. PMID: 17509106
Kimizuka T, Ozaki Y, Sumi Y
Ann Nucl Med 2002 Jul;16(5):351-4. doi: 10.1007/BF02988620. PMID: 12230095
Wakai S, Kotagal P
Pediatr Int 2001 Feb;43(1):61-5. doi: 10.1046/j.1442-200x.2001.01326.x. PMID: 11208002

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...