Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after subarachnoid hemorrhage

Klimo, Paul; Kestle, John R. W.; MacDonald, Joel D.; Schmidt, Richard H.

doi:10.3171/jns.2004.100.2.0215

Cited by 238 publications

(166 citation statements)

References 69 publications

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“…The initial treatment directly after SAH was proposed many years ago 20,27 and fortunately was recently rediscovered 47 . It is to remove the clot and bloody CSF thereby decreasing levels of neurotoxic oxyhemoglobin in the vicinity of conductive vessels.…”

Section: Nnos Protectionmentioning

confidence: 99%

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2008

Acta Neurochirurgica Supplement

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Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation and chemoregulation. Subarachnoid hemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space, destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase in the endogenous competitive NOS inhibitor, asymmetric dimethylarginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in cerebrospinal fluid (CSF) in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination owing to disappearance of ADMA-hydrolyzing enzyme [dimethylarginine dimethylaminohydrolase II (DDAH II)] immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of pre-clinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.

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Section: Nnos Protectionmentioning

confidence: 99%

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2008

Acta Neurochirurgica Supplement

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“…The authors demonstrated an incidence of symptomatic CVS of 28% in the clipping group and 33% in the coiling group. New therapeutic strategies which could influence the lower incidence of CVS compared to previous series might include the introduction of CSF drainage (ventricular or lumbar) in our treatment protocol [44]. TCD showed a low sensitivity to detect clinical and angiographic CVS in patients developing CVS in our series.…”

Section: Incidence Of Vasospasm and Risk Factorsmentioning

confidence: 69%

Incidence of Vasospasm, Outcome, and Quality of Life after Endovascular and Surgical Treatment of Ruptured Intracranial Aneurysms: Results of a Single-Center Prospective Study in Switzerland

Hofmann

Marbacher

Jakob

et al. 2011

ISRN Vascular Medicine

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Background. Outcome after endovascular versus surgical treatment of ruptured aneurysms is still controversial. The aim of this study was to analyze the incidence of cerebral vasospasm (CVS), outcome, and quality of life in patients undergoing endovascular or surgical treatment. Methods. This single-center prospective study included all patients undergoing aneurysm occlusion over a one-year period. All patients underwent postinterventional CT scan, TCD, and angiography on day 9 ± 2 . Outcome (Barthel Index, NIHSS, mRS, MMSE) was evaluated at 6 and 12 weeks. Quality of life (EuroQoL, SF-12) was assessed at 6 months. Results. A total of 66 patients were included. The overall mortality due to CVS was 9.9%, and higher in the surgical (14.6%) than in the endovascular group (4%). The incidence of symptomatic (29.2% versus 24%) and angiographic (70.7% versus 52%) CVS was not statistically significant different between the two groups. No differences in outcome or quality of life (SF-12) could be demonstrated. Conclusions. The outcome and quality of life of patients undergoing endovascular or surgical treatment seems not to significantly differ if demographic, radiological, and intensive care parameters are similar. A trend toward lower incidence of CVS in patients undergoing endovascular treatment was observed.

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“…Finalmente, otra estrategia que ha mostrado ser atractiva y simple es el drenaje de líquido cefalorraquídeo (LCR) de rutina por drenaje lumbar. Schmidt y col. 43 presentaron recientemente en la última Conferencia Internacional de Vasospasmo Cerebral (ICCV) celebrada en Chicago, USA, un estudio con un total de 266 pacientes. Los autores pudieron demostrar una reducción de la incidencia del VC del 27 al 7% 43 .…”

Section: Extracción Y Disolución Del Coágulo Sanguíneounclassified

Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea

et al. 2007

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ResumenEl vasospasmo cerebral sigue siendo la causa más importante de invalidez y muerte posterior a la ruptura de aneurismas saculares intracerebrales. Las estrategias terapéuticas en el vasospasmo inducido por la hemorragia subaracnoidea pueden ser agrupadas en cuatro categorías a saber: 1) terapias de prevención; 2) terapias de reversión; 3) terapias para el aumento de la perfusión cerebral; y 4) terapias de neuroprotección y rescate. Estudios experimentales recientes han permitido la realización de estudios clínicos fase II que sugieren resultados positivos con medicamentos que incluyen estatinas (simvastatina y pravastatina) y antagonistas de receptores tipo A de la endotelina-1 (clasozentan). De igual manera, evidencias experimentales y clínicas han mostrado las ventajas del drenaje de líquido cefalorraquídeo, administración intratecal de donadores de óxido nítrico, y los efectos desinhibidores de la Ca2+ Protein Kinasa C (Fasudil) y catecolaminas sobre la vascularización cerebral. Este artículo resume el estado de investigación actual de posibles agentes y estrategias terapéuticas relevantes en el tratamiento del vasospasmo cerebral. .. I would caution that vasospasm is still around, it is still alive and living in every neurosurgical unit. Hence my plea that our scientists not falter or lose interest for a final understanding and solution"C.G. Drake,1990 9

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Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after subarachnoid hemorrhage

Cited by 238 publications

References 69 publications

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Incidence of Vasospasm, Outcome, and Quality of Life after Endovascular and Surgical Treatment of Ruptured Intracranial Aneurysms: Results of a Single-Center Prospective Study in Switzerland

Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea

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