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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 other skeletal features. Individuals with classic CCD spectrum disorder typically have abnormally large, wide-open fontanelles at birth 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 delayed eruption of secondary dentition, failure to shed the primary teeth, and supernumerary teeth. 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
The clinical phenotype of alpha-mannosidosis varies considerably, with a wide spectrum of clinical findings and broad variability in individual presentation. At least three clinical types have been suggested in untreated individuals: mild (clinically recognized after age ten years, with myopathy, slow progression, and absence of skeletal abnormalities); moderate (clinically recognized before age ten years, with myopathy, slow progression, and presence of skeletal abnormalities); and severe (obvious progression leading to early death from primary central nervous system involvement or infection). Core features of untreated individuals generally include early childhood-onset non-progressive hearing loss, frequent infections due to immunodeficiency, rheumatologic symptoms (especially systemic lupus erythematosus), developmental delay / intellectual disability, low tone, ataxia, spastic paraplegia, psychiatric findings, bone disease (ranging from asymptomatic osteopenia to focal lytic or sclerotic lesions and osteonecrosis), gastrointestinal dysfunction (including diarrhea, swallowing issues / aspiration, and enlarged liver and spleen), poor growth, eye issues (including tapetoretinal degeneration and optic nerve atrophy), cardiac complications in adults, and pulmonary issues (including parenchymal lung disease). However, with the advent of enzyme replacement therapy, the natural history of this condition may change. Long-term velmanase alfa (VA) treatment outcomes are still being elucidated, but may include improvement in hearing, immunologic profile, and quality of life (improved clinical outcomes for muscle strength). Similarly, affected individuals who underwent hematopoietic stem cell transplantation (HSCT) experienced improvement in development (with preservation of previously learned skills), ability to participate in activities of daily living, stabilization or improvement in skeletal abnormalities, and improvement in hearing ability, although expressive speech and hearing deficiencies remained the most significant clinical problems after HSCT.
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 is a lysosomal storage disorder characterized by developmental delay, intellectual disability, behavioral manifestations (hyperactivity in young children, anxiety and restlessness in adolescence, and apathy in adulthood), recurrent infections, musculoskeletal features, and characteristic craniofacial features (prominent supraorbital ridges, hypertelorism, periorbital fullness, short nose with broad nasal bridge, thick vermilion of the upper and lower lips, and macroglossia) that become more prominent with age. Additional neurologic manifestations can include seizures, poor balance and coordination, and progressive cerebral atrophy in adulthood. Macrocephaly is common. Musculoskeletal features include lordosis, scoliosis, and arthritis in adolescents and young adults; vertebral dysplasia and/or rib cage abnormalities; and progressive muscle wasting, joint contractures, bursitis, and osteoporosis in adulthood. Skin manifestations (facial seborrhea, rosacea, and angiofibromas), gastrointestinal manifestations, neutropenia, and thrombocytopenia occur in some individuals. The clinical manifestations of aspartylglucosaminuria worsen with age, and adults have progressive psychomotor decline.
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 congenital malformations, developmental delay / intellectual disability, neonatal/childhood hypotonia, epilepsy, dysmorphisms, 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. 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 Pierre Robin sequence); and early-onset degenerative joint disease. 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, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, 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, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, 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, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, 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, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, 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, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, 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
Intellectual developmental disorder, x-linked, syndromic 37
MedGen UID:
1854940
Concept ID:
C5935567
Disease or Syndrome
X-linked syndromic intellectual developmental disorder-37 (MRXS37) is a developmental disorder showing phenotypic variability and variable severity. Male mutation carriers tend to be more severely affected than female mutation carriers, some of whom may even be asymptomatic. In general, the disorder is characterized by global developmental delay with delayed walking, speech delay, impaired intellectual development that ranges from borderline low to moderate, and behavioral abnormalities, such as autism and sleeping difficulties. Many patients are able to attend mainstream schools with assistance and work under supervision. Additional more variable features include sensorineural hearing loss, ocular anomalies, feeding difficulties, dysmorphic facial features, inguinal and umbilical hernia, genitourinary defects, congenital heart defects, musculoskeletal anomalies, and endocrine dysfunction, such as hypogonadism or hyperparathyroidism (Shepherdson et al., 2024).

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
Chung CC, Shimer AL
Clin Sports Med 2021 Jul;40(3):471-490. doi: 10.1016/j.csm.2021.03.004. PMID: 34051941
Jones TR, Rao RD
J Am Acad Orthop Surg 2009 Oct;17(10):609-17. doi: 10.5435/00124635-200910000-00003. PMID: 19794218
McNeely ML, Torrance G, Magee DJ
Man Ther 2003 May;8(2):80-91. doi: 10.1016/s1356-689x(02)00066-8. PMID: 12890435
Saraste H
Acta Orthop Scand Suppl 1993;251:84-6. doi: 10.3109/17453679309160129. PMID: 8451998

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
Daniels JM, Arguelles C, Gleason C, Dixon WH
Prim Care 2020 Mar;47(1):147-164. Epub 2019 Oct 17 doi: 10.1016/j.pop.2019.10.008. PMID: 32014131
Koreckij TD, Fischgrund JS
J Spinal Disord Tech 2015 Aug;28(7):236-41. doi: 10.1097/BSD.0000000000000298. PMID: 26172828

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
Resnick DK, Schmidt BT
Neurol Clin 2022 May;40(2):261-268. Epub 2022 Mar 31 doi: 10.1016/j.ncl.2021.11.005. PMID: 35465873
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
Cohen SP, Raja SN
Anesthesiology 2007 Mar;106(3):591-614. doi: 10.1097/00000542-200703000-00024. PMID: 17325518
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
Cassas KJ, Cassettari-Wayhs A
Am Fam Physician 2006 Mar 15;73(6):1014-22. PMID: 16570735
Ganju A
Neurosurg Focus 2002 Jul 15;13(1):E1. doi: 10.3171/foc.2002.13.1.2. PMID: 15916408
Starr JK, Eismont FJ
Spine (Phila Pa 1976) 1993 Oct 15;18(14):1954-7. doi: 10.1097/00007632-199310001-00005. PMID: 8272942
Martinelli TA, Wiesel SW
Instr Course Lect 1992;41:179-81. PMID: 1588062

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
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
Weinstein JN, Lurie JD, Tosteson TD, Hanscom B, Tosteson AN, Blood EA, Birkmeyer NJ, Hilibrand AS, Herkowitz H, Cammisa FP, Albert TJ, Emery SE, Lenke LG, Abdu WA, Longley M, Errico TJ, Hu SS
N Engl J Med 2007 May 31;356(22):2257-70. doi: 10.1056/NEJMoa070302. PMID: 17538085Free PMC Article

Recent systematic reviews

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
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
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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