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Spondylolisthesis

MedGen UID:
52470
Concept ID:
C0038016
Disease or Syndrome
Synonyms: Spondylistheses; Spondylisthesis; Spondylolistheses
SNOMED CT: Spondylolisthesis (274152003); SPL - Spondylolisthesis (274152003)
 
HPO: HP:0003302
Monarch Initiative: MONDO:0008475
OMIM®: 184200

Definition

Spondylolisthesis is defined as forward slipping of a vertebral body on the one below it. Spondylolysis is defined as a defect in the pars interarticularis without vertebral slipping (summary by Wiltse et al., 1975). [from OMIM]

Clinical features

From HPO
Spondylolysis
MedGen UID:
21294
Concept ID:
C0038018
Disease or Syndrome
Spondylolysis is an osseous defect of the pars interarticularis, thought to be a developmental or acquired stress fracture secondary to chronic low-grade trauma.
Spondylolisthesis at L5-S1
MedGen UID:
477430
Concept ID:
C3275799
Finding
Complete bilateral fractures of the pars interarticularis resulting in the anterior slippage of the fifth lumbar vertebral body (L5) onto the sacrum (level S1).

Conditions with this feature

Cleidocranial dysostosis
MedGen UID:
3486
Concept ID:
C0008928
Disease or Syndrome
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia that represents a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities) to mild CCD to isolated dental anomalies without the skeletal features. Most individuals come to diagnosis because they have classic features. At birth, affected individuals typically have abnormally large, wide-open fontanelles that may remain open throughout life. Clavicular hypoplasia can result in narrow, sloping shoulders that can be opposed at the midline. Moderate short stature may be observed, with most affected individuals being shorter than their unaffected sibs. Dental anomalies may include supernumerary teeth, eruption failure of the permanent teeth, and presence of the second permanent molar with the primary dentition. Individuals with CCD spectrum disorder are at increased risk of developing recurrent sinus infections, recurrent ear infections leading to conductive hearing loss, and upper-airway obstruction. Intelligence is typically normal.
Deficiency of alpha-mannosidase
MedGen UID:
7467
Concept ID:
C0024748
Disease or Syndrome
Alpha-mannosidosis encompasses a continuum of clinical findings from mild to severe. Three major clinical subtypes have been suggested: A mild form recognized after age ten years with absence of skeletal abnormalities, myopathy, and slow progression (type 1). A moderate form recognized before age ten years with presence of skeletal abnormalities, myopathy, and slow progression (type 2). A severe form manifested as prenatal loss or early death from progressive central nervous system involvement or infection (type 3). Individuals with a milder phenotype have mild-to-moderate intellectual disability, impaired hearing, characteristic coarse features, clinical or radiographic skeletal abnormalities, immunodeficiency, and primary central nervous system disease – mainly cerebellar involvement causing ataxia. Periods of psychiatric symptoms are common. Associated medical problems can include corneal opacities, hepatosplenomegaly, aseptic destructive arthritis, and metabolic myopathy. Alpha-mannosidosis is insidiously progressive; some individuals may live into the sixth decade.
Marfan syndrome
MedGen UID:
44287
Concept ID:
C0024796
Disease or Syndrome
FBN1-related Marfan syndrome (Marfan syndrome), a systemic disorder of connective tissue with a high degree of clinical variability, comprises a broad phenotypic continuum ranging from mild (features of Marfan syndrome in one or a few systems) to severe and rapidly progressive neonatal multiorgan disease. Cardinal manifestations involve the ocular, skeletal, and cardiovascular systems. Ocular findings include myopia (>50% of affected individuals); ectopia lentis (seen in approximately 60% of affected individuals); and an increased risk for retinal detachment, glaucoma, and early cataracts. Skeletal system manifestations include bone overgrowth and joint laxity; disproportionately long extremities for the size of the trunk (dolichostenomelia); overgrowth of the ribs that can push the sternum in (pectus excavatum) or out (pectus carinatum); and scoliosis that ranges from mild to severe and progressive. The major morbidity and early mortality in Marfan syndrome relate to the cardiovascular system and include dilatation of the aorta at the level of the sinuses of Valsalva (predisposing to aortic tear and rupture), mitral valve prolapse with or without regurgitation, tricuspid valve prolapse, and enlargement of the proximal pulmonary artery. Severe and prolonged regurgitation of the mitral and/or aortic valve can predispose to left ventricular dysfunction and occasionally heart failure. With proper management, the life expectancy of someone with Marfan syndrome approximates that of the general population.
Mucopolysaccharidosis, MPS-I-S
MedGen UID:
6453
Concept ID:
C0026708
Disease or Syndrome
Mucopolysaccharidosis type I (MPS I) is a progressive multisystem disorder with features ranging over a continuum of severity. While affected individuals have traditionally been classified as having one of three MPS I syndromes (Hurler syndrome, Hurler-Scheie syndrome, or Scheie syndrome), no easily measurable biochemical differences have been identified and the clinical findings overlap. Affected individuals are best described as having either a phenotype consistent with either severe (Hurler syndrome) or attenuated MPS I, a distinction that influences therapeutic options. Severe MPS I. Infants appear normal at birth. Typical early manifestations are nonspecific (e.g., umbilical or inguinal hernia, frequent upper respiratory tract infections before age 1 year). Coarsening of the facial features may not become apparent until after age one year. Gibbus deformity of the lower spine is common and often noted within the first year. Progressive skeletal dysplasia (dysostosis multiplex) involving all bones is universal, as is progressive arthropathy involving most joints. By age three years, linear growth decreases. Intellectual disability is progressive and profound but may not be readily apparent in the first year of life. Progressive cardiorespiratory involvement, hearing loss, and corneal clouding are common. Without treatment, death (typically from cardiorespiratory failure) usually occurs within the first ten years of life. Attenuated MPS I. Clinical onset is usually between ages three and ten years. The severity and rate of disease progression range from serious life-threatening complications leading to death in the second to third decade, to a normal life span complicated by significant disability from progressive joint manifestations and cardiorespiratory disease. While some individuals have no neurologic involvement and psychomotor development may be normal in early childhood, learning disabilities and psychiatric manifestations can be present later in life. Hearing loss, cardiac valvular disease, respiratory involvement, and corneal clouding are common.
Pseudo-Hurler polydystrophy
MedGen UID:
10988
Concept ID:
C0033788
Disease or Syndrome
GNPTAB-related disorders comprise the phenotypes mucolipidosis II (ML II) and mucolipidosis IIIa/ß (ML IIIa/ß), and phenotypes intermediate between ML II and ML IIIa/ß. ML II is evident at birth and slowly progressive; death most often occurs in early childhood. Orthopedic abnormalities present at birth may include thoracic deformity, kyphosis, clubfeet, deformed long bones, and/or dislocation of the hip(s). Growth often ceases in the second year of life; contractures develop in all large joints. The skin is thickened, facial features are coarse, and gingiva are hypertrophic. All children have cardiac involvement, most commonly thickening and insufficiency of the mitral valve and, less frequently, the aortic valve. Progressive mucosal thickening narrows the airways, and gradual stiffening of the thoracic cage contributes to respiratory insufficiency, the most common cause of death. ML IIIa/ß becomes evident at about age three years with slow growth rate and short stature; joint stiffness and pain initially in the shoulders, hips, and fingers; gradual mild coarsening of facial features; and normal to mildly impaired cognitive development. Pain from osteoporosis becomes more severe during adolescence. Cardiorespiratory complications (restrictive lung disease, thickening and insufficiency of the mitral and aortic valves, left and/or right ventricular hypertrophy) are common causes of death, typically in early to middle adulthood. Phenotypes intermediate between ML II and ML IIIa/ß are characterized by physical growth in infancy that resembles that of ML II and neuromotor and speech development that resemble that of ML IIIa/ß.
Pyknodysostosis
MedGen UID:
116061
Concept ID:
C0238402
Disease or Syndrome
Pycnodysostosis is characterized by short-limbed short stature, typical facial appearance (convex nasal ridge and small jaw with obtuse mandibular angle), osteosclerosis with increased bone fragility, acroosteolysis of the distal phalanges, delayed closure of the cranial sutures, and dysplasia of the clavicle. In affected individuals, the facial features become more prominent with age, likely due to progressive acroosteolysis of the facial bones, but can usually be appreciated from early childhood, particularly the small jaw and convex nasal ridge. Additional features include dental and nail anomalies. Intelligence is typically normal with mild psychomotor difficulties reported in some individuals.
Aspartylglucosaminuria
MedGen UID:
78649
Concept ID:
C0268225
Disease or Syndrome
Aspartylglucosaminuria (AGU) is a severe autosomal recessive lysosomal storage disorder that involves the central nervous system and causes skeletal abnormalities as well as connective tissue lesions. The most characteristic feature is progressive mental retardation. The disorder is caused by deficient activity of the lysosomal enzyme glycosylasparaginase, which results in body fluid and tissue accumulation of a series of glycoasparagines, i.e., glycoconjugates with an aspartylglucosamine moiety at the reducing end. AGU belongs to the group of disorders commonly referred to as the Finnish disease heritage (summary by Mononen et al., 1993 and Arvio and Arvio, 2002).
Brittle cornea syndrome 1
MedGen UID:
78661
Concept ID:
C0268344
Disease or Syndrome
Brittle cornea syndrome (BCS) is characterized by blue sclerae, corneal rupture after minor trauma, keratoconus or keratoglobus, hyperelasticity of the skin, and hypermobility of the joints (Al-Hussain et al., 2004). It is classified as a form of Ehlers-Danlos syndrome (Malfait et al., 2017). Genetic Heterogeneity of Brittle Cornea Syndrome Brittle cornea syndrome-2 (BCS2; 614170) is caused by mutation in the PRDM5 gene (614161) on chromosome 4q27.
Cervical spondylosis
MedGen UID:
235174
Concept ID:
C1384641
Disease or Syndrome
Arthrosis, i.e., of degenerative joint disease, affecting the cervical vertebral column.
Koolen-de Vries syndrome
MedGen UID:
355853
Concept ID:
C1864871
Disease or Syndrome
Koolen-de Vries syndrome (KdVS) is characterized by developmental delay / intellectual disability, neonatal/childhood hypotonia, dysmorphisms, congenital malformations, and behavioral features. Psychomotor developmental delay is noted in all individuals from an early age. The majority of individuals with KdVS function in the mild-to-moderate range of intellectual disability. Other findings include speech and language delay (100%), epilepsy (~33%), congenital heart defects (25%-50%), renal and urologic anomalies (25%-50%), and cryptorchidism (71% of males). Behavior in most is described as friendly, amiable, and cooperative.
Contractures, pterygia, and spondylocarpotarsal fusion syndrome 1A
MedGen UID:
401232
Concept ID:
C1867440
Disease or Syndrome
Contractures, pterygia, and spondylocarpotarsal fusion syndrome-1A (CPSFS1) is characterized by contractures of proximal and distal joints, pterygia involving the neck, axillae, elbows, and/or knees, as well as variable vertebral, carpal, and tarsal fusions and short stature. Progression of vertebral fusions has been observed, and inter- and intrafamilial variability has been reported (Carapito et al., 2016; Zieba et al., 2017; Cameron-Christie et al., 2018). An autosomal recessive form of CPSFS (CPSFS1B; 618469) is caused by compound heterozygous mutation in the MYH3 gene.
Stickler syndrome type 1
MedGen UID:
810955
Concept ID:
C2020284
Disease or Syndrome
Stickler syndrome is a connective tissue disorder that can include ocular findings of myopia, cataract, and retinal detachment; hearing loss that is both conductive and sensorineural; midfacial underdevelopment and cleft palate (either alone or as part of the Robin sequence); and mild spondyloepiphyseal dysplasia and/or precocious arthritis. Variable phenotypic expression of Stickler syndrome occurs both within and among families; interfamilial variability is in part explained by locus and allelic heterogeneity.
Loeys-Dietz syndrome 2
MedGen UID:
382398
Concept ID:
C2674574
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Aneurysm-osteoarthritis syndrome
MedGen UID:
462437
Concept ID:
C3151087
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Loeys-Dietz syndrome 4
MedGen UID:
766676
Concept ID:
C3553762
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Rienhoff syndrome
MedGen UID:
816342
Concept ID:
C3810012
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Loeys-Dietz syndrome 1
MedGen UID:
1646567
Concept ID:
C4551955
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Short stature, facial dysmorphism, and skeletal anomalies with or without cardiac anomalies 1
MedGen UID:
1778119
Concept ID:
C5542952
Disease or Syndrome

Professional guidelines

PubMed

Mohile NV, Kuczmarski AS, Lee D, Warburton C, Rakoczy K, Butler AJ
J Am Board Fam Med 2022 Dec 23;35(6):1204-1216. Epub 2022 Dec 16 doi: 10.3122/jabfm.2022.220130R1. PMID: 36526328
Katz JN, Zimmerman ZE, Mass H, Makhni MC
JAMA 2022 May 3;327(17):1688-1699. doi: 10.1001/jama.2022.5921. PMID: 35503342
Chan AK, Sharma V, Robinson LC, Mummaneni PV
Neurosurg Clin N Am 2019 Jul;30(3):353-364. doi: 10.1016/j.nec.2019.02.009. PMID: 31078236

Recent clinical studies

Etiology

Mohile NV, Kuczmarski AS, Lee D, Warburton C, Rakoczy K, Butler AJ
J Am Board Fam Med 2022 Dec 23;35(6):1204-1216. Epub 2022 Dec 16 doi: 10.3122/jabfm.2022.220130R1. PMID: 36526328
Karlsson T, Försth P, Skorpil M, Pazarlis K, Öhagen P, Michaëlsson K, Sandén B
Bone Joint J 2022 Dec;104-B(12):1343-1351. doi: 10.1302/0301-620X.104B12.BJJ-2022-0340.R1. PMID: 36453045Free PMC Article
Chung CC, Shimer AL
Clin Sports Med 2021 Jul;40(3):471-490. doi: 10.1016/j.csm.2021.03.004. PMID: 34051941
Labelle H, Mac-Thiong JM, Roussouly P
Eur Spine J 2011 Sep;20 Suppl 5(Suppl 5):641-6. Epub 2011 Aug 2 doi: 10.1007/s00586-011-1932-1. PMID: 21809015Free PMC Article
McNeely ML, Torrance G, Magee DJ
Man Ther 2003 May;8(2):80-91. doi: 10.1016/s1356-689x(02)00066-8. PMID: 12890435

Diagnosis

Mohile NV, Kuczmarski AS, Lee D, Warburton C, Rakoczy K, Butler AJ
J Am Board Fam Med 2022 Dec 23;35(6):1204-1216. Epub 2022 Dec 16 doi: 10.3122/jabfm.2022.220130R1. PMID: 36526328
Chung CC, Shimer AL
Clin Sports Med 2021 Jul;40(3):471-490. doi: 10.1016/j.csm.2021.03.004. PMID: 34051941
García-Ramos CL, Valenzuela-González J, Baeza-Álvarez VB, Rosales-Olivarez LM, Alpizar-Aguirre A, Reyes-Sánchez A
Acta Ortop Mex 2020 Sep-Oct;34(5):324-328. PMID: 33634638
Bydon M, Alvi MA, Goyal A
Neurosurg Clin N Am 2019 Jul;30(3):299-304. doi: 10.1016/j.nec.2019.02.003. PMID: 31078230
Kalichman L, Hunter DJ
Eur Spine J 2008 Mar;17(3):327-335. Epub 2007 Nov 17 doi: 10.1007/s00586-007-0543-3. PMID: 18026865Free PMC Article

Therapy

Katz JN, Zimmerman ZE, Mass H, Makhni MC
JAMA 2022 May 3;327(17):1688-1699. doi: 10.1001/jama.2022.5921. PMID: 35503342
Bussières A, Cancelliere C, Ammendolia C, Comer CM, Zoubi FA, Châtillon CE, Chernish G, Cox JM, Gliedt JA, Haskett D, Jensen RK, Marchand AA, Tomkins-Lane C, O'Shaughnessy J, Passmore S, Schneider MJ, Shipka P, Stewart G, Stuber K, Yee A, Ornelas J
J Pain 2021 Sep;22(9):1015-1039. Epub 2021 Apr 12 doi: 10.1016/j.jpain.2021.03.147. PMID: 33857615
Nava-Bringas TI, Romero-Fierro LO, Trani-Chagoya YP, Macías-Hernández SI, García-Guerrero E, Hernández-López M, Roberto CZ
Phys Ther 2021 Aug 1;101(8) doi: 10.1093/ptj/pzab108. PMID: 33792726
Försth P, Ólafsson G, Carlsson T, Frost A, Borgström F, Fritzell P, Öhagen P, Michaëlsson K, Sandén B
N Engl J Med 2016 Apr 14;374(15):1413-23. doi: 10.1056/NEJMoa1513721. PMID: 27074066
McNeely ML, Torrance G, Magee DJ
Man Ther 2003 May;8(2):80-91. doi: 10.1016/s1356-689x(02)00066-8. PMID: 12890435

Prognosis

Karlsson T, Försth P, Skorpil M, Pazarlis K, Öhagen P, Michaëlsson K, Sandén B
Bone Joint J 2022 Dec;104-B(12):1343-1351. doi: 10.1302/0301-620X.104B12.BJJ-2022-0340.R1. PMID: 36453045Free PMC Article
Yamada K, Suzuki A, Takahashi S, Inui K, Koike T, Okano T, Yabu A, Hori Y, Toyoda H, Nakamura H
J Bone Miner Metab 2022 Jan;40(1):120-131. Epub 2021 Aug 23 doi: 10.1007/s00774-021-01261-y. PMID: 34424413
Ghogawala Z, Dziura J, Butler WE, Dai F, Terrin N, Magge SN, Coumans JV, Harrington JF, Amin-Hanjani S, Schwartz JS, Sonntag VK, Barker FG 2nd, Benzel EC
N Engl J Med 2016 Apr 14;374(15):1424-34. doi: 10.1056/NEJMoa1508788. PMID: 27074067
Herman MJ, Pizzutillo PD
Clin Orthop Relat Res 2005 May;(434):46-54. doi: 10.1097/01.blo.0000162992.25677.7b. PMID: 15864031
Ganju A
Neurosurg Focus 2002 Jul 15;13(1):E1. doi: 10.3171/foc.2002.13.1.2. PMID: 15916408

Clinical prediction guides

Rathbone J, Rackham M, Nielsen D, Lee SM, Hing W, Riar S, Scott-Young M
Eur Spine J 2023 Jun;32(6):1911-1926. Epub 2023 Apr 18 doi: 10.1007/s00586-023-07567-x. PMID: 37071155
Katz JN, Zimmerman ZE, Mass H, Makhni MC
JAMA 2022 May 3;327(17):1688-1699. doi: 10.1001/jama.2022.5921. PMID: 35503342
Austevoll IM, Hermansen E, Fagerland MW, Storheim K, Brox JI, Solberg T, Rekeland F, Franssen E, Weber C, Brisby H, Grundnes O, Algaard KRH, Böker T, Banitalebi H, Indrekvam K, Hellum C; NORDSTEN-DS Investigators
N Engl J Med 2021 Aug 5;385(6):526-538. doi: 10.1056/NEJMoa2100990. PMID: 34347953
de Kunder SL, van Kuijk SMJ, Rijkers K, Caelers IJMH, van Hemert WLW, de Bie RA, van Santbrink H
Spine J 2017 Nov;17(11):1712-1721. Epub 2017 Jun 21 doi: 10.1016/j.spinee.2017.06.018. PMID: 28647584
Försth P, Ólafsson G, Carlsson T, Frost A, Borgström F, Fritzell P, Öhagen P, Michaëlsson K, Sandén B
N Engl J Med 2016 Apr 14;374(15):1413-23. doi: 10.1056/NEJMoa1513721. PMID: 27074066

Recent systematic reviews

Petersen T, Laslett M, Juhl C
BMC Musculoskelet Disord 2017 May 12;18(1):188. doi: 10.1186/s12891-017-1549-6. PMID: 28499364Free PMC Article
Lurie J, Tomkins-Lane C
BMJ 2016 Jan 4;352:h6234. doi: 10.1136/bmj.h6234. PMID: 26727925Free PMC Article
Brinjikji W, Diehn FE, Jarvik JG, Carr CM, Kallmes DF, Murad MH, Luetmer PH
AJNR Am J Neuroradiol 2015 Dec;36(12):2394-9. Epub 2015 Sep 10 doi: 10.3174/ajnr.A4498. PMID: 26359154Free PMC Article
Chiu CC, Chuang TY, Chang KH, Wu CH, Lin PW, Hsu WY
Clin Rehabil 2015 Feb;29(2):184-95. Epub 2014 Jul 9 doi: 10.1177/0269215514540919. PMID: 25009200
McNeely ML, Torrance G, Magee DJ
Man Ther 2003 May;8(2):80-91. doi: 10.1016/s1356-689x(02)00066-8. PMID: 12890435

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