Evidence-Based Cerebral Vasospasm Surveillance

Kistka, Heather M.; Dewan, Michael C.; Mocco, J

doi:10.1155/2013/256713

Cited by 27 publications

(19 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…92 Continuous EEG has the advantage of being able to monitor broad regions of brain and to detect epileptiform discharges, which were observed in 23% of 108 patients with SAH in one series. 93 Among 32 patients with SAH, reduced rela tive (to other waves) variability in alphawave activity was 100% sensitive and 50% specific for vasospasm (defined as increased transcranial Doppler flow velocities or angio graphic arter ial narrowing).…”

Section: Eeg and Other Technologiesmentioning

confidence: 99%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

View full text Add to dashboard Cite

Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) that is mediated by effects of transient cerebral ischaemia during bleeding plus effects of the subarachnoid blood. Secondary effects of SAH include increased intracranial pressure, destruction of brain tissue by intracerebral haemorrhage, brain shift, and herniation, all of which contribute to pathology. Many patients survive these phenomena, but deteriorate days later from delayed cerebral ischaemia (DCI), which causes poor outcome or death in up to 30% of patients with SAH. DCI is thought to be caused by the combined effects of angiographic vasospasm, arteriolar constriction and thrombosis, cortical spreading ischaemia, and processes triggered by EBI. Treatment for DCI includes prophylactic administration of nimodipine, and current neurointensive care. Prompt recognition of DCI and immediate treatment by means of induced hypertension and balloon or pharmacological angioplasty are considered important by many physicians, although the evidence to support such approaches is limited. This Review summarizes the pathophysiology of DCI after SAH and discusses established treatments for this condition. Novel strategies--including drugs such as statins, sodium nitrite, albumin, dantrolene, cilostazol, and intracranial delivery of nimodipine or magnesium--are also discussed.

show abstract

Section: Eeg and Other Technologiesmentioning

confidence: 99%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

View full text Add to dashboard Cite

show abstract

“…Other groups have similarly showed a decrease in mortality and improved 6-month GOS outcomes with the addition of goal directed PbtO 2 therapy over standard ICP/CPP therapy alone [ 88 , 89 ]. In aSAH, PbtO 2 monitoring has less of a role in predicting vasospasm or outcome [ 90 ]. The utility of PbtO 2 in comatose state after cardiac arrest is not known and currently not recommended [ 61 ].…”

Section: Pbto 2 Monitoringmentioning

confidence: 99%

Brain Monitoring in Critically Neurologically Impaired Patients

Jones

Schwartzbauer

Jia

2016

IJMS

View full text Add to dashboard Cite

Assessment of neurologic injury and the evolution of severe neurologic injury is limited in comatose or critically ill patients that lack a reliable neurologic examination. For common yet severe pathologies such as the comatose state after cardiac arrest, aneurysmal subarachnoid hemorrhage (aSAH), and severe traumatic brain injury (TBI), critical medical decisions are made on the basis of the neurologic injury. Decisions regarding active intensive care management, need for neurosurgical intervention, and withdrawal of care, depend on a reliable, high-quality assessment of the true state of neurologic injury, and have traditionally relied on limited assessments such as intracranial pressure monitoring and electroencephalogram. However, even within TBI there exists a spectrum of disease that is likely not captured by such limited monitoring and thus a more directed effort towards obtaining a more robust biophysical signature of the individual patient must be undertaken. In this review, multimodal monitoring including the most promising serum markers of neuronal injury, cerebral microdialysis, brain tissue oxygenation, and pressure reactivity index to access brain microenvironment will be discussed with their utility among specific pathologies that may help determine a more complete picture of the neurologic injury state for active intensive care management and long-term outcomes. Goal-directed therapy guided by a multi-modality approach appears to be superior to standard intracranial pressure (ICP) guided therapy and should be explored further across multiple pathologies. Future directions including the application of optogenetics to evaluate brain injury and recovery and even as an adjunct monitoring modality will also be discussed.

show abstract

“…Cerebral vasospasm after subarachnoidian hemorrhage represent a challenge problem from the prevention and treatment point of view and contributes to the most devastating injury: delayed cerebral ischemia (2,5,6). When delayed cerebral ischemia occur the patient outcome is poor and this can lead even to death (6).…”

Section: Introductionmentioning

confidence: 99%

“…When delayed cerebral ischemia occur the patient outcome is poor and this can lead even to death (6).…”

Section: Introductionmentioning

confidence: 99%

Drotaverinum – a new modality of prevention and treatment in cerebral vasospasm after subarachoidian hemorrhage?

Kakucs¹,

Berce²,

Tamas-Szora³

et al. 2016

Romanian Neurosurgery

View full text Add to dashboard Cite

Aim: This study want to demonstrate the efficaciousness of drotaverinum as a replacer of papaverine in the prevention and treatment of vasospasm. Material and method: In this study were used 20 albino Wistar male rats. Rats were divided in two groups and vasospasm was induced to the both femoral artery and after that irrigation of the femoral arteries with drotaverinum was performed to demonstrate the vasodilatation that can appear (group A). In the group B after the obtaining of vasospasm irrigation of the femoral arteries with saline solution was performed and this group was used as witness. The length of the vessels was measured when was achieved the vasospasm and also before and after the administration of the solutions. Pictures were taken at every step of dissection and solutions administration to can measure the length of arteries before and after the administration of drotaverinum and the saline solution. Results: In all rats was obtained vasospasm at the femoral artery after clipping the artery and after we irrigate with adrenaline. In the group with drotaverinum we obtained the vasodilatation and in the witness group the caliber of the vessels remain the same. The statistical analysis of the data demonstrate a significant differences between the group were was used drotaverinum and the witness group were was used the saline solution (p<0,001). Conclusions: Drotaverinum has a good vasodilatative effect on arteries and he can prevent the apparition of vasospasm and it can even treat vasospasm if occur by producing local vasodilatation and a good circulation in the area where is administrated. This study showed quantitatively that drotaverinum can treat the experimental peripheral vasospasm in rats.

show abstract

Evidence-Based Cerebral Vasospasm Surveillance

Cited by 27 publications

References 49 publications

Delayed neurological deterioration after subarachnoid haemorrhage

Delayed neurological deterioration after subarachnoid haemorrhage

Brain Monitoring in Critically Neurologically Impaired Patients

Drotaverinum – a new modality of prevention and treatment in cerebral vasospasm after subarachoidian hemorrhage?

Contact Info

Product

Resources

About