Tag: Cerebral vasospasm

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Vitamin D—A New Perspective in Treatment of Cerebral Vasospasm

Neurosurgery 88 (3) 2021: 674–685

Cerebral vasospasm (CVS) is a frequent complication after subarachnoid hemorrhage (SAH), with no sufficient therapy and a complex pathophysiology.

OBJECTIVE: To explore the vitamin D system as a potential treatment for CVS.

METHODS: 25-vitamin D3 levels tested between 2007 and 2015 and data of SAH patients admitted during themonthswith a peak vs nadir of VitD3 valueswere analyzed, retrospectively. We prospectively correlated VitD3 and vasospasm/outcome data in SAH patients admitted in 2017. An experimental mice SAH model and cell culture model were used to investigate the effect of 1,25-dihydroxyvitamin D3 (1,25-VitD3). Additionally, the mediators acting in the VitD mechanism were researched and detected.

RESULTS: Based on the retrospective analysis demonstrating an increased frequency of vasospasm in SAH patients during the low vitamin D period in winter, we started basic research experiments. Active 1,25-VitD3 hormone attenuated CVS, neurological deficit, and inflammation after intrathecal blood injection inmice. Deletion of the vitaminDreceptor in the endothelium or in myeloid cells decreased the protective 1,25-VitD3 effect. Co-culture experiments ofmyeloid and endothelial cells with blood confirmed the anti-inflammatory 1,25-VitD3 effect but also revealed an induction of stroma-cell-derived factor 1α (SDF1α), vascular endothelial growth factor, and endothelial nitric oxide synthase by 1,25-VitD3. In mice, SDF1α mimicked the protective effect of 1,25-VitD3 against CVS. From bench to bedside, CVS severity was inversely correlated with vitamin D plasma level, prospectively. Patients with more severe CVS exhibited attenuated expression of SDF1α and 1,25-VitD3- responsive genes on circulating myeloid cells.

CONCLUSION: 1,25-VitD3 attenuates CVS after SAH by inducing SDF1α. However, VitD administration should be tested as optional treatment to prevent CVS.

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The use of nicardipine prolonged release implants (NPRI) in microsurgical clipping after aneurysmal subarachnoid haemorrhage: comparison with endovascular treatment

Acta Neurochir (2011) 153:2119–2125. DOI 10.1007/s00701-011-1129-8

Nicardipine prolonged release implants (NPRI) have been shown to decrease the incidence of cerebral vasospasm and infarcts significantly in patients after aneurysmal subarachnoid haemorrhage (SAH) follow- ing microsurgical clipping. Yet, the comparison with results after endovascular coiling is lacking. This study was conducted to determine the differences in the incidence of cerebral vasospasm and infarctions between those two treatment modalities

Methods The design of this investigation reflects a case- control study; 27 patients suffering from acute SAH were treated by microsurgical clipping and received an intracisternal implantation of NPRI. Twenty-seven matching consecutive patients after microsurgical treatment without implantation of NPRI or endovascular treatment, respectively, served as controls. The incidence of angiographic vasospasm and cerebral infarctions were documented.

Results All groups were comparable concerning demographics and severity of SAH. Twenty-four of 81 patients developed angiographic vasospasm (>33% constriction). The incidence of vasospasm was 48%, 44% and 11% for patients after endovascular treatment, microsurgical clipping without NPRI and microsurgical clipping with NPRI, respectively. New cerebral infarctions occurred in 28%, 22% and 7% of the treated patients, respectively. A good clinical recovery 1 year after the initial bleeding (modified Rankin scale 0–2) was seen in 48%, 50% and 77% of the treated patients, respectively.

Conclusion The use of NPRI during microsurgical clipping was confirmed to be safe and effective. Patients who received intracisternally implanted NPRI during clipping after aneurysmal SAH yielded significantly lower vasospasm and infarction rates, and showed a better clinical outcome when compared with clipping without NPRI and also when compared with endovascular coiling.

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Prediction of early secondary complications in patients with spontaneous subarachnoid hemorrhage based on accelerated sympathovagal ratios

Acta Neurochir (2009) 151:1631–1637 DOI 10.1007/s00701-009-0517-9

Purpose The development of secondary complications following spontaneous subarachnoid hemorrhage (SAH) largely depends on sympathetic overexcitation. The roles of vagal activities, however, are poorly defined. Because both components of the autonomic nervous system can be explored in the frequency domain of heart rate variability (HRV), the present study aimed to determine the dynamic evolution of autonomic activities and to identify patients at high risk for complications following hemorrhage. Methods Thirty patients with SAH were enrolled in our study. Those who suffered from symptomatic vasospasm, cerebral infarction, neurogenic pulmonary edema, or early mortality within 1 week of ictus were categorized into the complication group. Spectral analysis of HRV explored three important indices of sympathetic and vagal modu- lations: low-frequency (LF), high-frequency (HF), and LF/HF ratios. Patterns of HRV dynamics within the first 3 days were compared between complication and non complication groups. The group trends, estimated by the slopes of HRV changes, were determined for further univariate and multivariate analysis. Results Our study showed that daily HRV in the complica- tion group exhibited an approximately 2.7-fold increase of sympathovagal ratio (denoted by LF/HF). This resulted from reciprocal changes of sympathoexcitation (LF) and vagal withdrawal (HF). Multivariate analysis revealed that LF/HF slope, an indicator of the trend of sympathovagal change, was an independent variable significantly associat- ed with the development of complications.

Conclusions This study confirmed that during early SAH period, patients with and without complications presented different patterns of sympathovagal changes. LF/HF slope during the first 3 days was a significant predictor of secondary complications after SAH.

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