Literature DB >> 35505148

New insights in craniovertebral junction MR changes leading to stenosis in children with achondroplasia.

Massimiliano Rossi1, Federico Di Rocco2,3, Sara Cabet4,1,5, Alexandru Szathmari6, Carmine Mottolese6, Patricia Franco7, Laurent Guibaud4,5.   

Abstract

PURPOSE: To characterize natural history and early changes of craniovertebral junction stenosis in achondroplasia correlating with clinical and radiological outcome.
METHODS: Retrospective measures on craniovertebral junction were performed blindly, on sagittal T2-weighted images, in 21 patients with achondroplasia referred from 2008 to 2020. Clinical and polysomnography data were retrospectively collected. Each patient was paired for age and gender with four controls. Wilcoxon means comparison or Student's t-tests were applied.
RESULTS: Twenty-one patients (11 females, from 0.1 to 39 years of age) were analyzed and paired with 84 controls. A craniovertebral junction stenosis was found in 11/21 patients (52.4%), all before the age of 2 years. Despite a significant reduction of the foramen magnum diameter (mean ± SD: patients 13.6 ± 6.2 mm, controls 28.5 ± 4.7 mm, p < .001), craniovertebral junction stenosis resulted from the narrowing of C2 dens-opisthion antero-posterior diameter (8.7 ± 3.9 mm vs 24.6 ± 5.1 mm, p < .001). Other significant changes were opisthion anterior placement (-0.4 ± 2.8 mm vs 9.4 ± 2.3 mm, p < .001), posterior tilt of C2 (46.2 ± 13.7° vs 31.6 ± 7.9°, p < .001) and of C1 (15.1 ± 4.3° vs 11.9 ± 5.0°, p = 0.01), and dens thickening (9.4 ± 2.2 mm vs 8.5 ± 2.1 mm, p = 0.03), allowing to define three distinguishable early craniovertebral junction patterns in achondroplasia. All children with C2-opisthion antero-posterior diameter of more than 6 mm had a better clinical and radiological outcome.
CONCLUSION: Craniovertebral junction in achondroplasia results from narrowing between C2 dens and opisthion related to anterior placement of opisthion, thickening of C2 dens, and posterior tilt of C1-C2. A threshold of 6 mm for dens-opisthion sagittal diameter seems to correlate with clinical and radiological outcome.
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Entities:  

Keywords:  Cervical cord; FGFR3; Skull base; Spinal cord compression

Mesh:

Year:  2022        PMID: 35505148     DOI: 10.1007/s00381-022-05514-7

Source DB:  PubMed          Journal:  Childs Nerv Syst        ISSN: 0256-7040            Impact factor:   1.532


  29 in total

1.  FGFR3 mutation causes abnormal membranous ossification in achondroplasia.

Authors:  Federico Di Rocco; Martin Biosse Duplan; Yann Heuzé; Nabil Kaci; Davide Komla-Ebri; Arnold Munnich; Emilie Mugniery; Catherine Benoist-Lasselin; Laurence Legeai-Mallet
Journal:  Hum Mol Genet       Date:  2014-01-12       Impact factor: 6.150

2.  Mortality in achondroplasia.

Authors:  J T Hecht; C A Francomano; W A Horton; J F Annegers
Journal:  Am J Hum Genet       Date:  1987-09       Impact factor: 11.025

3.  Unexpected death of children with achondroplasia after the perinatal period.

Authors:  J D Bland; J L Emery
Journal:  Dev Med Child Neurol       Date:  1982-08       Impact factor: 5.449

4.  Upper cervical myelopathy in achondroplasia.

Authors:  S S Yang; D P Corbett; A J Brough; K P Heidelberger; J Bernstein
Journal:  Am J Clin Pathol       Date:  1977-07       Impact factor: 2.493

5.  Skull growth in achondroplasic (cn) mice; a craniometric study.

Authors:  R J Jolly; W J Moore
Journal:  J Embryol Exp Morphol       Date:  1975-07

6.  Apnea and sudden unexpected death in infants with achondroplasia.

Authors:  R M Pauli; C I Scott; E R Wassman; E F Gilbert; L A Leavitt; J Ver Hoeve; J G Hall; M W Partington; K L Jones; A Sommer
Journal:  J Pediatr       Date:  1984-03       Impact factor: 4.406

7.  FGFR3 promotes synchondrosis closure and fusion of ossification centers through the MAPK pathway.

Authors:  Takehiko Matsushita; William R Wilcox; Yuk Yu Chan; Aya Kawanami; Hülya Bükülmez; Gener Balmes; Pavel Krejci; Pertchoui B Mekikian; Kazuyuki Otani; Isakichi Yamaura; Matthew L Warman; David Givol; Shunichi Murakami
Journal:  Hum Mol Genet       Date:  2008-10-15       Impact factor: 6.150

8.  Achondroplasia is defined by recurrent G380R mutations of FGFR3.

Authors:  G A Bellus; T W Hefferon; R I Ortiz de Luna; J T Hecht; W A Horton; M Machado; I Kaitila; I McIntosh; C A Francomano
Journal:  Am J Hum Genet       Date:  1995-02       Impact factor: 11.025

9.  Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia.

Authors:  R Shiang; L M Thompson; Y Z Zhu; D M Church; T J Fielder; M Bocian; S T Winokur; J J Wasmuth
Journal:  Cell       Date:  1994-07-29       Impact factor: 41.582

10.  Mutations in the gene encoding fibroblast growth factor receptor-3 in achondroplasia.

Authors:  F Rousseau; J Bonaventure; L Legeai-Mallet; A Pelet; J M Rozet; P Maroteaux; M Le Merrer; A Munnich
Journal:  Nature       Date:  1994-09-15       Impact factor: 49.962

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