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Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 532--533

Migrating pseudomeningocele: A rare complication of posterior fossa surgery

Manoj K Kapanigowda, Anita Nagadi, Sriram Patwari, Vineetha Raghu, Harsha Chadaga 
 Department of Radiology, Columbia Asia Referral Hospital, Bangalore, Karnataka, India

Correspondence Address:
Dr. Sriram Patwari
Department of Radiology, Columbia Asia Referral Hospital, Bangalore - 560 055, Karnataka
India




How to cite this article:
Kapanigowda MK, Nagadi A, Patwari S, Raghu V, Chadaga H. Migrating pseudomeningocele: A rare complication of posterior fossa surgery.Neurol India 2019;67:532-533


How to cite this URL:
Kapanigowda MK, Nagadi A, Patwari S, Raghu V, Chadaga H. Migrating pseudomeningocele: A rare complication of posterior fossa surgery. Neurol India [serial online] 2019 [cited 2020 Jul 8 ];67:532-533
Available from: http://www.neurologyindia.com/text.asp?2019/67/2/532/258050


Full Text



Sir,

Pseudomeningocele is an extradural accumulation of cerebrospinal fluid (CSF) because of the defect in the overlying dura.[1] It is a relatively common complication of posterior fossa surgery with its incidence varying from 4.5% to as high as 28%.[2] The proposed causes for pseudomeningocele formation are insufficient dural closure (most common), hydrocephalus, and arachnoidal scarring due to aseptic meningitis.[3],[4]

The pseudomeningoceles are often asymptomatic but on occasion can cause a cosmetic deformity, headaches, chronic meningitis, and rarely pressure effect on the underlying neural tissue leading to neurologic deficits. Most are managed conservatively;[5] however, in the presence of hydrocephalus, CSF diversion is considered. We report a case of spontaneous intracerebellar migration of a sub-occipital pseudomeningocele with the formation of a cerebellar cyst, a rare complication following midline posterior fossa surgery.

A 24–year old gentleman with a previous history of surgical excision of posterior fossa hemangioblastoma presented with complaints of progressive headache and vomiting. A clinical suspicion of tumor recurrence led to magnetic resonance imaging (MRI). A review of a previous 3-year follow-up magnetic resonance imaging (MRI) scan showed a moderate sized sub-occipital extradural fluid collection, having the CSF signal intensity on all the MRI sequences, confirming with the diagnosis of a pseudomeningocele. The cerebellum was normal with no evidence of recurrence/residual tumor [Figure 1]a,[Figure 1]b,[Figure 1]c.{Figure 1}

The current MRI demonstrated a new large cystic lesion in the left cerebellar lobe causing partial effacement of the 4th ventricle and mild compression of the brain stem [Figure 2]. There was no abnormal enhancement or mural nodule seen. There was a mild reduction in size of the sub-occipital pseudomeningocele in comparison with the previous MRI [Figure 1]d,[Figure 1]e,[Figure 1]f. On careful evaluation of the 3D CISS (three-dimensional constructive interference steady state images), a dural defect with communication of the subarachnoid space with the pseudomeningocele, and another dural defect with the pseudomeningocele communicating with cerebellar cystic lesion were clearly seen. The features were suggestive of migration of pseudomeningocele into the left cerebellar lobe [Figure 3].{Figure 2}{Figure 3}

Pseudomeningocele is formed secondary to leakage of CSF from the subarachnoid space into the surrounding tissue. It collects in a potential space not covered by an epithelial wall and is, therefore, termed a pseudomeningocele. Most cases are asymptomatic and resolve spontaneously or are managed conservatively with pressure dressing/bed rest. The pressure dressing augments the CSF absorption and also reduces the potential space available for CSF collection. Bed rest helps in reduction of the CSF pressure. In non-resolved or symptomatic cases, particularly with hydrocephalus, CSF diversion is considered.[1]

The highest rate of pseudomeningocele formation is from midline posterior fossa surgeries (16.5%), and the lowest rate is following the adoption of the retrosigmoid approach (11.9%). Literature states that lumbar puncture is about 90% efficacious in the management of a pseudomeningocele.[6] Sometimes, a lumbar drainage, in an attempt to resolve a pseudomeningocele, can result in an acute posterior fossa syndrome because of rapid movement of CSF from the pseudomeningocele into the cerebellum at the site of the weak dura.[2] The time span between surgery and pseudomeningocele formation has been described in the literature as 5–115 days, with an average duration of 18 days.[1] In our case, there was no prior lumbar drainage of the CSF to treat the post-surgical pseudomeningocele. The proposed mechanism of intra-cerebellar migration of the pseudomeningocele in our case was the slow progressive movement of CSF into the pseudomeningocele leading to increased pressure within. This increased pressure may have, in turn, led to the dissection of the pseudomeningocele into the cerebellum through the defective dura/arachnoid. The slow progressive movement of the CSF may have been because of the unidirectional valve mechanism under the influence of CSF pulsations.[7] Multiple treatment options have been discussed for pseudomeningocele management in the literature including both conservative and surgical managements. Initially, conservative treatments such as head elevation and wrapping of the head with a compression bandage can be tried. In failed or complicated cases such as a large migrating pseudomeningocele, the non-resolving (as a few migrating pseudomeningoceles may resolve with conservative management) cases require a direct dural defect repair or a lumboperitoneal shunt.[8]

The radiological findings and the comparison with prior imaging were the key to an accurate diagnosis. The lack of peripheral enhancement or a mural nodule excluded tumor recurrence. The 3D CISS sequences also aided in the diagnosis by demonstrating the areas of dural defects. Knowledge of this rare entity is important for management and also to avoid unnecessary investigations.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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