Article
Development of intracranial hypertension after treatment of temporal arachnoid cysts: possible pathophysiology and 2 case reports
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Authors
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Dieter Class
- Otto-von-Guericke-Universität, Universitätsklinik für Neurochirurgie, Magdeburg, Deutschland
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Osamah Melhem
- Otto-von-Guericke-Universität, Universitätsklinik für Neurochirurgie, Magdeburg, Deutschland
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Jana Kohl
- Otto-von-Guericke-Universität, Universitätsklinik für Neurochirurgie, Magdeburg, Deutschland
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Raimund Firsching
- Otto-von-Guericke-Universität, Universitätsklinik für Neurochirurgie, Magdeburg, Deutschland
| Published: | June 9, 2017 |
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Outline
Text
Objective: Temporal arachnoid cysts are well known intracranial space occupying lesions. They are rarely associated with increase in intracranial pressure (ICP). We report 2 patients with cysto-peritoneal shunts presenting with significant clinical worsening 18 and 6 years after primary shunt placement. At the same time progressive enlargement of the CSF spaces in CT and MRI studies was not noticed in both patients despite severe clinical symptoms. This clinical and radiological phenomenon appears comparable to similar findings in patients with hydrocephalus treated by shunt placement but the underlying pathophysiological mechanisms remain unclear.
Methods: Clinical and radiological data of 2 patients now in care of our department were reviewed as far as available as primary operations were performed in other clinics with both patients. Follow up is complete as both patients were operated for shunt malfunction only this year in our department.
Results: One 3 year old boy was treated because of a large temporal arachnoid cyst by a cysto-peritoneal shunt system in 1998. 2 shunt revisions were necessary and now in 2016 signs of progressive intracranial hypertension with papilledema and increasing epileptic seizures were noted. Shunt revision was performed at the age of 21 years. The other 9 year old boy was treated similarly with a cysto-peritoneal shunt device. No shunt revision was necessary until operation for shunt malfunction in 2016 at the age of 15 years. Clinical symptoms showed rapid improvement in both boys but radiological findings before and after the last operation were found unchanged.
Conclusion: Arachnoid cysts are classified according to size, location and free passage of CSF from the cyst to subarachnoid spaces which can be studied by cisternography or phase contrast MRI. In patients with a longer follow up after primary shunt placement who are now presenting with clinical signs of increasing intracranial pressure the situation is often unclear. Cysto-peritoneal shunts may be related to complex disturbances of CSF circulation. Radiological findings may be of little help in this situation. So even in the absence of radiological signs early shunt revisions are to be recommended in doubtful cases as in patients with hydrocephalus treated by a shunt system where real dilatation of the ventricular system is not seen.
