Giant syringobulbia in childhood

Sengar, R. L. S.; Prasad, V. S. S. V.; Prasad, B. C. M.; Reddy, D. Raja

doi:10.1007/bf00335179

Cited by 6 publications

(2 citation statements)

References 5 publications

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“…10,13,17,23,27 Giant SB in childhood and fatal hemorrhage have been reported. 31,34,35 Intractable hiccups 4,33 have been observed in SB and SM, and in 1 case the hiccups resolved after posterior fossa surgery. 33 Another consistent observation we report relates to SB location: SB in the medulla was present in all of our 13 cases.…”

Section: Discussionmentioning

confidence: 99%

Syringobulbia in pediatric patients with Chiari malformation type I

Menezes

Greenlee

Dlouhy

2018

Journal of Neurosurgery: Pediatrics

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OBJECTIVESyringobulbia (SB) is a rare entity, with few cases associated with Chiari malformation type I (CM-I) in the pediatric population. The authors reviewed all pediatric cases of CM-I–associated SB managed at their institution in order to better understand the presentation, treatment, and surgical outcomes of this condition.METHODSA prospectively maintained institutional database of craniovertebral junction abnormalities was analyzed to identify all cases of CM-I and SB from the MRI era (i.e., after 1984). The authors recorded presenting symptoms, physical examination findings, radiological findings, surgical treatment strategy, intraoperative findings, and outcomes. SB cases associated with tumors, infections, or type II Chiari malformations were excluded.RESULTSThe authors identified 326 pediatric patients with CM-I who were surgically treated. SB was identified in 13 (4%) of these 326 patients. Headache and neck pain were noted in all 13 cases. Cranial nerve abnormalities were common: vagus and glossopharyngeal nerve dysfunction was the most frequent observation. Other cranial nerves affected included the trigeminal, abducens, and hypoglossal nerves. Several patients exhibited multiple cranial nerve palsies at presentation. Central sleep apnea was present in 6 patients.Syringomyelia (SM) was present in all 13 patients. SB involved the medulla in all cases, and extended rostrally into the pons and midbrain in 2 patients; in 1 of these 2 cases the cavity extended further rostrally to the cerebrum (syringocephaly). SB communicated with the fourth ventricle in 7 of the 13 cases.All 13 patients were treated with posterior fossa decompression with intradural exploration to ensure CSF egress out of the fourth ventricle and through the foramen magnum. The foramen of Magendie was found to be occluded by an arachnoid veil in 9 cases. Follow-up evaluation revealed that SB improved before SM. Cranial nerve palsies regressed in 11 of the 13 patients, and SB improved in all 13.CONCLUSIONSThe incidence of SB in our surgical series of pediatric patients with CM-I was 4%, and all of these patients had accompanying SM. The SB cavity involved the medulla in all cases and was found to communicate with the fourth ventricle in 54% of cases. Posterior fossa decompression with intradural exploration and duraplasty is an effective treatment for these patients.

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Section: Discussionmentioning

confidence: 99%

Syringobulbia in pediatric patients with Chiari malformation type I

Menezes

Greenlee

Dlouhy

2018

Journal of Neurosurgery: Pediatrics

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“…8 Samples et al also reported on syringomesencephalia in the pre-MRI era. 25 There have been several publications since, 2,9,13,23,27 and a review of the literature was performed by Afifi and Menezes 1 in 1997 and subsequently by Greenlee et al in 2005. 7 Valentini and colleagues detailed an evaluation of 75 patients with syringomyelia, 8 of whom had a syringobulbic extension.…”

Section: Discussionmentioning

confidence: 99%

Syringohydromyelia in association with syringobulbia and syringocephaly: case report

Menezes¹,

Greenlee²,

Longmuir

et al. 2015

PED

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The authors present the case of a 14-year-old boy with holocord syringohydromyelia extending into the brainstem, cerebral peduncle, internal capsule, and cerebral cortex. At the posterior fossa exploration, an opaque thickened arachnoid with occlusion of the foramen of Magendie was encountered. Careful documentation of postoperative regression of the syringocephaly, syringobulbia, and syringohydromyelia was made. The pathophysiology is discussed.

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