scholarly journals Treatment of cerebral vasospasm secondary to subarachnoid hemorrhage utilizing the Comaneci device

2020 ◽  
Vol 26 (5) ◽  
pp. 582-585
Author(s):  
Clint A Badger ◽  
Brian T Jankowitz ◽  
Hamza A Shaikh

Delayed cerebral ischemia due to vasospasm following subarachnoid hemorrhage continues to have high morbidity and mortality despite current treatments. This report highlights the use of the Comaneci (Rapid Medical, Yokneam, Israel), a device FDA approved for temporary coil embolization assistance, for the treatment of symptomatic vasospasm. Ten days post subarachnoid hemorrhage, a patient developed acute left-sided hemiparesis with angiographic vasospasm. Through a Headway 17 microcatheter, a Comaneci 17 was deployed in the right ICA terminus, M1, M2, A1, and, A2 segments resulting in improvement of angiographic vasospasm and the patient’s left-sided hemiparesis. On the following day, a repeat angiogram demonstrated no recurrence of vasospasm. The patient had complete return on neurologic function by post bleed day 18 continuing to her four-week follow-up appointment. This case demonstrates the feasibility of the Comaneci device as an effective tool in the treatment of vasospasm following subarachnoid hemorrhage.

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 820
Author(s):  
Keshav Jayaraman ◽  
Meizi Liu ◽  
Gregory J. Zipfel ◽  
Umeshkumar Athiraman

Numerous studies have demonstrated the ability of isoflurane conditioning to provide multifaceted protection against aneurysmal subarachnoid hemorrhage (SAH)-associated delayed cerebral ischemia (DCI); however, preclinical studies have not yet examined whether other commonly used inhalational anesthetics in neurological patients such as sevoflurane or desflurane are also protective against SAH-induced neurovascular deficits. We therefore sought to identify the potential for sevoflurane and desflurane conditioning to protect against DCI in an endovascular perforation mouse model of SAH. Neurological function was assessed daily via neuroscore. Large artery vasospasm and microvessel thrombosis were assessed three days after SAH or sham surgery. Four groups were examined: Sham, SAH + room air, SAH + 2% Sevoflurane, and SAH + 6% Desflurane. For the SAH groups, one hour after surgery, mice received 2% sevoflurane, 6% desflurane, or room air for one hour. We found that conditioning with sevoflurane or desflurane attenuated large artery vasospasm, reduced microvessel thrombosis, and improved neurologic function. Given their frequent clinical use and strong safety profile in patients (including those with SAH), these data strongly support further studies to validate these findings in preclinical and clinical studies and to elucidate the mechanisms by which these agents might be acting.


2017 ◽  
Vol 97 ◽  
pp. 199-204 ◽  
Author(s):  
Abdulrahman Aldakkan ◽  
Alireza Mansouri ◽  
Blessing N.R. Jaja ◽  
Naif M. Alotaibi ◽  
R. Loch Macdonald ◽  
...  

2015 ◽  
Vol 122 (3) ◽  
pp. 663-670 ◽  
Author(s):  
Ali M. Elhadi ◽  
Joseph M. Zabramski ◽  
Kaith K. Almefty ◽  
George A. C. Mendes ◽  
Peter Nakaji ◽  
...  

OBJECT Hemorrhagic origin is unidentifiable in 10%–20% of patients presenting with spontaneous subarachnoid hemorrhage (SAH). While the patients in such cases do well clinically, there is a lack of long-term angiographic followup. The authors of the present study evaluated the long-term clinical and angiographic follow-up of a patient cohort with SAH of unknown origin that had been enrolled in the Barrow Ruptured Aneurysm Trial (BRAT). METHODS The BRAT database was searched for patients with SAH of unknown origin despite having undergone two or more angiographic studies as well as MRI of the brain and cervical spine. Follow-up was available at 6 months and 1 and 3 years after treatment. Analysis included demographic details, clinical outcome (Glasgow Outcome Scale, modified Rankin Scale [mRS]), and repeat vascular imaging. RESULTS Subarachnoid hemorrhage of unknown etiology was identified in 57 (11.9%) of the 472 patients enrolled in the BRAT study between March 2003 and January 2007. The mean age for this group was 51 years, and 40 members (70%) of the group were female. Sixteen of 56 patients (28.6%) required placement of an external ventricular drain for hydrocephalus, and 4 of these subsequently required a ventriculoperitoneal shunt. Delayed cerebral ischemia occurred in 4 patients (7%), leading to stroke in one of them. There were no rebleeding events. Eleven patients were lost to followup, and one patient died of unrelated causes. At the 3-year follow-up, 4 (9.1%) of 44 patients had a poor outcome (mRS > 2), and neurovascular imaging, which was available in 33 patients, was negative. CONCLUSIONS Hydrocephalus and delayed cerebral ischemia, while infrequent, do occur in SAH of unknown origin. Long-term neurological outcomes are generally good. A thorough evaluation to rule out an etiology of hemorrhage is necessary; however, imaging beyond 6 weeks from ictus has little utility, and rebleeding is unexpected.


1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.


2011 ◽  
Vol 115 (1) ◽  
pp. 101-107 ◽  
Author(s):  
Bartosz T. Grobelny ◽  
Andrew F. Ducruet ◽  
Peter A. DeRosa ◽  
Ivan S. Kotchetkov ◽  
Brad E. Zacharia ◽  
...  

Object Cystathionine β-synthase (CBS) is an enzyme that metabolizes homocysteine to form H2S in the brain. Hydrogen sulfide functions as a vasodilator as well as a regulator of neuronal ion channels and multiple intracellular signaling pathways. Given the myriad effects of H2S, the authors hypothesized that patients possessing gain-of-function polymorphisms of the CBS gene will experience a decreased incidence of delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH). Methods Patients were enrolled in a prospective observational database of aSAH outcomes. DNA was extracted from buccal swabs and sequenced for 3 functional polymorphisms of the CBS gene (699C→T, 844ins68, and 1080C→T) by polymerase chain reaction. Serum homocysteine levels (μmol/L) were assayed. Multivariate analysis was used to determine the relationship between CBS genotype and occurrence of both angiographic vasospasm and DCI. Results There were 87 patients included in the study. None of the polymorphisms investigated were significantly associated with the incidence of angiographic vasospasm. However, after controlling for admission hypertension, patients with the gain-of-function 844 WT/ins genotypes were less likely to experience DCI relative to those with the 844 WT/WT genotype (86 patients, p = 0.050), while the decrease-in-function genotype 1080 TT was more likely to experience DCI relative to those with 1080 CC and CT genotypes (84 patients, p = 0.042). Serum homocysteine levels did not correlate with the extent of either angiographic vasospasm or DCI in this analysis. Conclusions Polymorphisms of the CBS gene that impart gain-of-function may be associated with a reduced risk of DCI after aSAH, independent of serum homocysteine. Signaling through H2S may mediate protection from DCI following aSAH through a mechanism that does not involve macrovascular vasodilation.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jimmy Young ◽  
Tarun Singh ◽  
Jennifer Fugate ◽  
Alejandro Rabinstein

Objective: To determine the effect of Selective Serotonin Reuptake Inhibitor (SSRI)/Selective Norepinephrine Reuptake Inhibitor (SNRI) use prior to or during admission for aneurysmal subarachnoid hemorrhage (aSAH) on the risk of symptomatic vasospasm and diffuse cerebral ischemia (DCI). Methods: Review of electronic records at Mayo Clinic, Rochester from Jan. 2001 to Dec. 2013 of consecutive patients with aSAH. The variables collected and analyzed were: age, sex, active smoking, transfusion, modified Fisher score, WFNS grade, and outcome at discharge. Multivariate logistic regression analysis was used to evaluate factors associated with DCI, symptomatic vasospasm, and poor outcome (modified Rankin score 3-6) within 1 year. Results: 583 [females 367 (63%)] patients with a median age of 55 (47-65) years were admitted with aSAH during the study period. WFNS at nadir was IV-V in 243 (41.6%) and modified Fisher score was 3-4 in 438 (75.2%). Eighty one (14.6%) patients were taking SSRI or SNRI prior to admission and these medications were continued in all of them. Symptomatic vasospasm was present in 154 (27.7%), radiological infarction in 172(29.5%), and DCI in 250(42.9%) patients. SSRI/SNRI use was not associated with the occurrence of DCI (p=0.458), symptomatic vasospasm (p=0.097), radiological infarction (p=0.972), or poor functional outcome (p=0.376). Conclusions: The use of SSRI/SNRI prior to admission and/or during hospitalization in patients with aSAH was not associated with symptomatic vasospasm or DCI.


BMC Neurology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Christin Campe ◽  
Jens Neumann ◽  
I. Erol Sandalcioglu ◽  
Ali Rashidi ◽  
Michael Luchtmann

Abstract Background Due to improvements in both the quality and availability of intracranial imaging as well as the evolution of surgical and endovascular techniques during the last decade, the number of treatments of unruptured intracranial aneurysms (UIA) has increased steadily. However, it is not generally known that vasospasm can arise after an uneventful clipping. Case presentation We present a case of a 69-year-old woman who suffered from vasospasm and delayed cerebral ischemia that occurred after an uneventful clipping of a UIA. The aneurysm of the right middle cerebral artery was found incidentally via magnetic resonance imaging ordered after the patient complained of a short period of slight gait disturbances. To avoid a subarachnoid hemorrhage and consecutive complications like vasospasms, the patient elected microsurgical treatment. Clipping was managed by keyhole approach. Temporal clipping of the M1 was not necessary. After clip placement, appropriate flow in all distal segments was confirmed by indocyanine green video-angiography and micro-Doppler. The patient was discharged seven days after surgery without neurological deficits. After 12 days, the patient developed at home a sudden drooping on the left side of the face. Upon admission to the emergency room, the patient was alert but slightly confused. Neurological examination revealed a left-sided hemiparesis and motor speech disorder. In contrast to the preoperative transfemoral catheter angiography, the subsequent right internal carotid angiogram showed clear signs of vasospasm along the M1 and M2 segments of the right middle cerebral artery. Antithrombotic treatment with acetylsalicylic acid was begun. In accordance with guidelines for the treatment of subarachnoid hemorrhage and vasospasm, nimodipine was added. After 11 days the patient was discharged with no symptoms. Conclusion Cerebral vasospasm as a cause of ischemic stroke after uneventful surgery for a UIA seems to be a rare but possibly underestimated etiology that demands particular attention with respect to providing appropriate treatment. In future, it may be prudent to perform follow-up transcranial ultrasonography testing after the clipping of a UIA, especially considering the availability of potentially neuroprotective medications like nimodipine.


2011 ◽  
Vol 32 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Johannes Woitzik ◽  
Jens P Dreier ◽  
Nils Hecht ◽  
Ingo Fiss ◽  
Nora Sandow ◽  
...  

It has been hypothesized that vasospasm is the prime mechanism of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). Recently, it was found that clusters of spreading depolarizations (SDs) are associated with DCI. Surgical placement of nicardipine prolonged-release implants (NPRIs) was shown to strongly attenuate vasospasm. In the present study, we tested whether SDs and DCI are abolished when vasospasm is reduced or abolished by NPRIs. After aneurysm clipping, 10 NPRIs were placed next to the proximal intracranial vessels. The SDs were recorded using a subdural electrode strip. Proximal vasospasm was assessed by digital subtraction angiography (DSA). 534 SDs were recorded in 10 of 13 patients (77%). Digital subtraction angiography revealed no vasospasm in 8 of 13 patients (62%) and only mild or moderate vasospasm in the remaining. Five patients developed DCI associated with clusters of SD despite the absence of angiographic vasospasm in three of those patients. The number of SDs correlated significantly with the development of DCI. This may explain why reduction of angiographic vasospasm alone has not been sufficient to improve outcome in some clinical studies.


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