gms | German Medical Science

65th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

11 - 14 May 2014, Dresden

Late complications of spontaneous spinal subarachnoid hemorrhages

Meeting Abstract

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  • Jörg Klekamp - Zentrum Neurochirurgie, Christliches Krankenhaus Quakenbrück

Deutsche Gesellschaft für Neurochirurgie. 65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Dresden, 11.-14.05.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocMI.18.07

doi: 10.3205/14dgnc384, urn:nbn:de:0183-14dgnc3842

Published: May 13, 2014

© 2014 Klekamp.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Spinal subarachnoid hemorrhages may be caused by intracranial as well as spinal vascular malformations. If the underlying pathology is not located in the spinal canal, the initial hemorrhage may not lead to neurological deficits. However, break down products of hemoglobin cause an aseptic meningitis which leads to leptomeningeal scarring and may cause a delayed myelopathy after a variable free interval. This myelopathy is due to disturbances of spinal cord blood flow or formation of a syringomyelia.

Method: Hospital files, neuroradiological examinations, intraoperative documentations as well as outpatient examinations were analysed. The clinical course was documented for each individual symptom and rates for postoperative neurological deteriorations were calculated.

Results: Between 1980 and 2010, 345 patients with non-traumatic spinal arachnopathies were observed. Of these, 28 patients had a history of spinal subarachnoid hemorrhage. Mean age was 55±14 years (12–78 years). The arachnopathy led to new neurological deficits after an average free interval of 56±62 months. Then, another 4 years elapsed on the average before the patient presented to a neurosurgeon. The clinical history was slowly progressive in most instances and started with gait disturbances in 61% of patients. At presentation, 50% of these patients were no longer able to walk and wheelchair-dependent. For just 5 patients the arachnopathy was limited to 2 to 3 spinal segments. For the remainder, the arachnoid scarring involved most of the thoracic subarachnoid space. Of 28 patients, 7 were operated with the intent of a local cord decompression by fenestration of arachnoid pouches or cysts. In one patient, spinal cerebrospinal fluid was shunted from above the arachnopathy to the peritoneal cavity. For none of these patients could a long-term neurological stabilization be achieved. Six patients developed another neurological deterioration within one year of surgery with a mean follow-up of 34 months.

Conclusions: Spinal subarachnoid hemorrhages lead to arachnoid scarring, which may cause a delayed, slowly progressive paraplegia in an unknown proportion of patients. Disturbances of spinal cord blood flow and syringomyelia are the responsible mechanisms. No surgical therapy for the arachnopathy with a good chance of success exists for these patients. Shunting cerebrospinal fluid from the spinal canal above the arachnopathy to the peritoneal cavity with a low-pressure valve seems to offer a benefit in selected cases.