Basilar impression and platybasia in osteogenesis imperfecta tarda

Frank, E.; Berger, Thomas; Tew, John M.

doi:10.1016/s0090-3019(82)80033-5

Cited by 38 publications

(7 citation statements)

References 9 publications

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“…It has been reasoned that in OI the weight of the cranium and its contents exceeds the load-bearing capacity of the soft bones at the skull base, deforming them gradually and leading to basilar abnormality. 7 This explanation agrees with most others favoring the idea that basilar abnormality is most prevalent in Type III and least prevalent in Type I (Table 4) and that it appears earlier in patients with severe disease. Moreover, infants with the lethal OI Type II reportedly do not show basilar abnormality, a finding related to the missing upright position and weight bearing on the upper cervical spine.…”

Section: Basilar Abnormality and The Oi Phenotypesupporting

confidence: 91%

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Skull base abnormalities in osteogenesis imperfecta: a cephalometric evaluation of 54 patients and 108 control volunteers

Kovero

Pynnönen²,

Kuurila-Svahn³

et al. 2006

JNS

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Section: Basilar Abnormality and The Oi Phenotypesupporting

confidence: 91%

“…McGregor measures such as 62 and 30 mm. 7,13 None of the patients included in this study and with a maximum McGregor measure of 35 mm has required operative management.…”

Section: Or Highmentioning

confidence: 99%

Skull base abnormalities in osteogenesis imperfecta: a cephalometric evaluation of 54 patients and 108 control volunteers

Kovero

Pynnönen²,

Kuurila-Svahn³

et al. 2006

JNS

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“…OI and BI have also been associated with hydrocephalus [8][9][10], but many of these cases were asymptomatic [1,10,11]. Thus, there are few reports of surgery for OI associated with BI and, to the knowledge, no detailed report on a patient with OI and BI associated with Chiari type-II malformation and hydrocephalus that caused neurological symptoms and required surgery.…”

Section: Discussionmentioning

confidence: 99%

Factors related to surgical outcome after posterior decompression and fusion for craniocervical junction lesions associated with osteogenesis imperfecta

et al. 2011

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Treatment for craniocervical junction lesions associated with osteogenesis imperfecta (OI) has been described, but there are divergent views on operative procedures and preoperative and postoperative therapies due to the small number of cases. It has been suggested that a major procedure such as combined anterior and posterior surgery with concomitant ventriculoperitoneal (VP) shunting is required for OI associated with basilar impression (BI). However, here we report a case with a good outcome after posterior decompression fusion only. The patient was a 29-year-old woman with OI (Sillence type-IA) who had neurological symptoms of vertigo, nausea, and shaking during walking. Diagnostic imaging revealed hydrocephalus, severe BI, and Chiari type-II malformation. Preoperative Halo traction led to improvement in symptoms, and posterior decompression fusion from the occipital bone to C6 was subsequently performed. Lateral mass screws and Nesplon cables as sublaminar wiring for reinforcement for fusion were used in the operation. The patient wore a Halo vest for 4 weeks postoperatively. She experienced no symptoms postoperatively. Bone fusion and improved hydrocephalus were clear on images at 3 years after surgery, and the postoperative course has been good. In craniocervical junction lesions associated with OI, instability with compression of the nerve and bone fragility in multiple sites can become problematic. Anterior odontoid resection and posterior fusion are required for OI with BI to give ideal decompression on images. However, the results of this case suggest that a good postoperative outcome can be achieved by performing not the combination of anterior odontoid resection and VP shunting, but only with posterior decompression fusion, especially for OI cases of Sillence type-I.

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“…The presence of basilar impression and/ or invagination is an exception since numerous such cases have been repeatedly reported and analyzed [2,4,12,13]. Apart from basilar invagination which frequently leads to brain stem compression, other neurological complications identified in patients with OI include ventricular enlargement, sulcal prominence, macrocephaly, seizures, skull fractures, long tract signs, hydrocephalus, syringohydromyelia and intracranial hypertension [2,12].…”

Section: Discussionmentioning

confidence: 99%

Intracranial meningioma in a patient with osteogenesis imperfecta

et al. 2008

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AbstractOsteogenesis imperfecta (OI) is a heritable disorder characterized mainly by connective tissue manifestations. In dinstinct cases, several neurological features have also been described. A 46-year-old male with a known family history of OI type I presented with progressive gait disturbances and diminished muscle strength. Brain MRI scans revealed an infiltrative intracranial mass occupying both frontoparietal lobes. The patient underwent surgical intervention. The histological diagnosis was an atypical (Grade II) meningioma. The bony parts demonstrated a mixture of osseous defects due to OI and infiltration by the tumor. At one-year follow up the patient′s muscle power partially returned while repeat MRI scans were negative for tumor recurrence.

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Basilar impression and platybasia in osteogenesis imperfecta tarda

Cited by 38 publications

References 9 publications

Skull base abnormalities in osteogenesis imperfecta: a cephalometric evaluation of 54 patients and 108 control volunteers

Skull base abnormalities in osteogenesis imperfecta: a cephalometric evaluation of 54 patients and 108 control volunteers

Factors related to surgical outcome after posterior decompression and fusion for craniocervical junction lesions associated with osteogenesis imperfecta

Intracranial meningioma in a patient with osteogenesis imperfecta

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