gms | German Medical Science

63rd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Japanese Neurosurgical Society (JNS)

German Society of Neurosurgery (DGNC)

13 - 16 June 2012, Leipzig

The venous pathophysiology of chronic overdrainage syndrome

Meeting Abstract

  • M.U. Schuhmann - Klinik für Neurochirurgie, Universitätsklinikum Tübingen
  • J. Sosa - Klinik für Neurochirurgie, Universitätsklinikum Tübingen
  • F.H. Ebner - Klinik für Neurochirurgie, Universitätsklinikum Tübingen
  • M. Skardelly - Klinik für Neurochirurgie, Universitätsklinikum Tübingen
  • A. Speil - Klinik für Neurochirurgie, Universitätsklinikum Tübingen

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocP 109

DOI: 10.3205/12dgnc495, URN: urn:nbn:de:0183-12dgnc4959

Published: June 4, 2012

© 2012 Schuhmann et al.
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Outline

Text

Objective: The pathophysiology of chronic overdrainage syndrome (COS), or slit ventricle syndrome, is still not universally known or accepted. A venous pathophysiology has been proposed by Sood et al in 2004. We present an educative case-based update highlighting the intracranial dynamics of COS and supporting the venous pathophysiology.

Methods: A 27-year-old women, with years-long history of severe COS attacks (throbbing headaches, nausea/vomiting) requiring each time hospitalization, had small but non-slit ventricles, stable in size during attacks. Only “time-free-of-attacks” was during pregnancy. Patient received computerized ICP-monitoring during attack. Continuous “B-wave-storm” with peak-ICP up to 70 mmHg was recorded, high RAP and ICP-amplitudes indicated lost reserve-capacity. Episode resolved over 8–10 h with parallel stepwise normalization of ICP-parameters. Next evening ICP was -17 mmHg in upright position, taking 2 h to reach 0 mmHg when supine.

Results: Shunt at revision was patent. Patient received programmable-valve at 7 cm H2O for lying-position and programmable gravity-assisted-valve for upright-position (proSA) at 15 cm H2O. Attacks continued until proSA was stepwise raised to 32 cm H2O and never appeared thereafter.

Conclusions: High ICP, RAP and ICP-amplitudes in patient with patent shunt and non-slit ventricles, with unchanged CT and stepwise resolution of symptoms can only be explained by venous entrapment as hypothesized by Sood et. al 2004. Chronic ultra-low CSF-pressures lead to distention of capacity veins, which in turn are more collapsible. Venous collapse leads to sudden blood-entrapment and loss of reserve capacity (high RAP/amplitudes) resulting in ICP crisis. Normalization of ICP during upright-position (pregnancy, proSA) cures COS, probably by normalizing weinsize and collapsibility.