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. 2020 Sep 10;11(2):183–184. doi: 10.1177/1941874420958839

Meningitis in the Setting of Frontoethmoidal and Temporal Meningoencephaloceles

Arooshi Kumar 1,, Jugal Shah 2, Kara Melmed 1,2, Donato Pacione 2, Seth Lieberman 3, Ariane Lewis 1,2
PMCID: PMC7958690  PMID: 33791067

Abstract

This is a patient with multiple meningoencephaloceles which resulted in bacterial meningitis and subsequent status epilepticus. We identify impressive imaging findings demonstrating herniation of the meninges from nasal and bitemporal skull base defects possibly as a result of intracranial hypertension.

Keywords: meningitis, encephalocele, idiopathic intracranial hypertension, cerebrospinal fluid leak


A 70-year-old woman with BMI 43.4 kg/m2 presented with headache and fever then became unresponsive with left gaze deviation. EEG showed nonconvulsive status epilepticus that improved with antiepileptics. Lumbar puncture revealed opening pressure of 21cmH20. Cerebrospinal fluid (CSF) and blood cultures grew Streptococcus Agalactiae. MRI brain revealed a nasoethmoidal meningoencephalocele and bitemporal encephaloceles (Figure 1). Nasal discharge was positive for Beta-2 transferrin suggesting CSF leak. She was treated with six weeks of broad spectrum antibiotics. The ethmoidal encephalocele was resected, the skull base defect was repaired and a ventriculoperitoneal shunt was placed. Her mental status ultimately improved and she was discharged on hospital day 50.

Figure 1.

Figure 1.

Brain MRI A) 2019 Sagittal T1 post-contrast, ethmoidal encephalocele with diffuse pachymeningeal enhancement. B) 2019 Coronal T1 post-contrast, ethmoidal encephalocele. C) 2019 Axial T1 post-contrast, left temporal bone meningoencephalocele. D) 2019 Axial T1 post-contrast, right temporal bone meningoencephalocele. E) 2015 Sagittal, T1 non-contrast prior evidence of nasoethmoidal encephalocele. F) 2015 Axial T1 post contrast, prior evidence of L temporal encephalocele.

Frontoethmoidal encephaloceles reflect herniation of meninges and brain through congenital structural defects, iatrogenic from craniotomy or sinus surgery, or spontaneous defects in the anterior cranial fossa, sometimes due to increased intracranial pressure.1-3 Prior studies have demonstrated association of IIH with meningoencephaloceles.4-5 Any process causing long term increased intracranial pressure could lead to meningoencephaloceles.3 Given her obesity, we suspect untreated idiopathic intracranial hypertension led to the development of encephaloceles, resulting in CSF fistula and subsequent meningitis.

Footnotes

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

References

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