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Published on: July 5, 2021
The role of sphenoid bone in basilar invagination pathophysiology
Ítalo T Oliveira Filho1, Ricardo V Botelho2,3,4
1Health Sciences Post-Graduation Program, Instituto de Assistência Médica ao Servidor Público Estadual - IAMSPE, Av. Ibirapuera, 91. 2nd Floor, Vila Clementino, São Paulo, SP, 04029-000, Brazil.
Abstract:
Basilar invagination (BI) is characterized by rostral dislocation of the cervical spine toward the skull base. The craniometrics of the skull base have shown significant differences among craniocervical junction malformations. The sphenoid bone is the center of the skull base; however, no study has evaluated this bone in cases of BI. This was a cross-sectional study of MRI databanks from two institutions of the author's practice between 1985 and 2020. The craniometrics of the sphenoid bone were measured in BI patients and controls. Fifty-eight MRIs were selected, including 28 BI patients and 30 controls. The mean sphenoid crest-clivus length was 32.66 ± 4.7 mm in the BI group and 29.98 ± 3.0 mm in the control group (p = 0.01). The mean sphenoid planum-top of Dorsum sellae length was 28.53 ± 3.7 mm in the BI group and 26.45 ± 3.2 mm in the control group (p = 0.02). The mean tuberculum sellae-sphenoid floor height was 18.52 ± 4.4 mm in the BI group and 21.32 ± 2.9 mm in the control group (p = 0.00). The mean sella turcica-sphenoid floor height was 10.35 ± 3.8 mm in the BI group and 12.24 ± 3.5 mm in the control group (p = 0.05). The mean clivus length was 29.81 ± 6.3 mm in the BI group and 40.86 ± 4.2 mm in the control group (p = 0.00). The mean sphenoid length was 58.34 ± 7.4 mm in the BI group and 67.31 ± 6.0 mm in the control group (p = 0.00). The mean sphenoid angle was 116.33 ± 8.7° in the BI group and 112.36 ± 6.9° in the control group (p = 0.05). The BI sphenoid bone has shorter vertical dimensions and longer horizontal measures. This morphology promotes a flattening of the sphenoid angle. The sphenoid bone is significantly altered in BI, favoring the congenital hypothesis in the pathophysiology of this disease.
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