Advanced Imaging Modalities in the Detection of Cerebral Vasospasm

Mills, Jena; Mehta, Vivek; Russin, Jonathan; Amar, Arun Paul; Rajamohan, Anandh G.; Mack, William J.

doi:10.1155/2013/415960

Cited by 43 publications

(35 citation statements)

References 81 publications

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“…265,268,271,272,276 A mBFV > 200 cm/s in the MCA territory has high positive predictive value for angiographic vasospasm. 265,272 The progressive severity of vasospasm is indicated by an increase in mBFV, an increase in the ratio of mBFV of ipsilateral to contralateral cerebral arteries, and the reversal of diastolic blood flow during serial TCD monitoring. 265,271,275,277 TCD is better for detecting and monitoring vasospasm in the ICA and the MCA distribution than in other circulations.…”

Section: Monitoring For DCImentioning

confidence: 95%

“…[265][266][267][268][269][270][271][272][273][274][275][276][277][278] An increase in mean blood flow velocity (mBFV) >120 cm/s indicates vasospasm in the MCA. 265,268,271,272,276 A mBFV > 200 cm/s in the MCA territory has high positive predictive value for angiographic vasospasm. 265,272 The progressive severity of vasospasm is indicated by an increase in mBFV, an increase in the ratio of mBFV of ipsilateral to contralateral cerebral arteries, and the reversal of diastolic blood flow during serial TCD monitoring.…”

Section: Monitoring For DCImentioning

confidence: 99%

“…265,272 The progressive severity of vasospasm is indicated by an increase in mBFV, an increase in the ratio of mBFV of ipsilateral to contralateral cerebral arteries, and the reversal of diastolic blood flow during serial TCD monitoring. 265,271,275,277 TCD is better for detecting and monitoring vasospasm in the ICA and the MCA distribution than in other circulations. 265,271 TCD is also better in detecting proximal vasospasm than in detecting distal vasospasm.…”

Section: Monitoring For DCImentioning

confidence: 99%

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Aneurysmal Subarachnoid Hemorrhage

2011

Encyclopedia of Clinical Neuropsychology

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Aneurysmal subarachnoid hemorrhage (SAH) is a worldwide health burden with high fatality and permanent disability rates. The overall prognosis depends on the volume of the initial bleed, rebleeding, and degree of delayed cerebral ischemia (DCI). Cardiac manifestations and neurogenic pulmonary edema indicate the severity of SAH. The International Subarachnoid Aneurysm Trial (ISAT) reported a favorable neurological outcome with the endovascular coiling procedure compared with surgical clipping at the end of 1 year. The ISAT trial recruits were primarily neurologically good grade patients with smaller anterior circulation aneurysms, and therefore the results cannot be reliably extrapolated to larger aneurysms, posterior circulation aneurysms, patients presenting with complex aneurysm morphology, and poor neurological grades. The role of hypothermia is not proven to be neuroprotective according to a large randomized controlled trial, Intraoperative Hypothermia for Aneurysms Surgery Trial (IHAST II), which recruited patients with good neurological grades. Patients in this trial were subjected to slow cooling and inadequate cooling time and were rewarmed rapidly. This methodology would have reduced the beneficial effects of hypothermia. Adenosine is found to be beneficial for transient induced hypotension in 2 retrospective analyses, without increasing the risk for cardiac and neurological morbidity. The neurological benefit of pharmacological neuroprotection and neuromonitoring is not proven in patients undergoing clipping of aneurysms. DCI is an important cause of morbidity and mortality following SAH, and the pathophysiology is likely multifactorial and not yet understood. At present, oral nimodipine has an established role in the management of DCI, along with maintenance of euvolemia and induced hypertension. Following SAH, hypernatremia, although less common than hyponatremia, is a predictor of poor neurological outcome.Key Words: subarachnoid hemorrhage, intracranial aneurysm, delayed cerebral ischemia (J Neurosurg Anesthesiol 2015;27:222-240) SUBARACHNOID HEMORRHAGE (SAH) IS A WORLDWIDE HEALTH BURDEN WITH HIGH RATES OF FATALITY AND PERMANENT DISABILITYThe estimated worldwide incidence of SAH is 9/ 100,000 persons/y with regional variation. 1 One systematic review found the incidence to be lower in South and Central America (4.2/100,000 persons/y) and higher in Japan (22.7/100,000 persons/y) and Finland (19.7/100,000 persons/y). 1 Interestingly, the prevalence of intracranial aneurysm is not found to be higher in Japan or Finland, 2 but the risk for rupture is higher. 3 The incidence is also reported lower in China (2.0 //100,000 persons/y). 4 SAH accounts for only 5% of all strokes, 5 but it has high mortality and permanent disability rates. A retrospective cohort study in 2 large Norwegian populations between 1984 and 2007 reported a 30-day case fatality rate of 36%. 6 A nationwide Danish study reported a similar 30-day mortality at 38%. 7 World Health Organization Multinational Monitoring Trends...

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Section: Monitoring For DCImentioning

confidence: 95%

Section: Monitoring For DCImentioning

confidence: 99%

Section: Monitoring For DCImentioning

confidence: 99%

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Aneurysmal Subarachnoid Hemorrhage

2011

Encyclopedia of Clinical Neuropsychology

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“…As for other perfusion studies (see CTP), the assessment of contrast medium concentration in an artery and tissue yields quantitative measures of CBF and CBV. Comparison of DWI and PWI can reveal a mismatch and can differentiate between ischemic penumbra and infracted core [100]. MRI has further interesting applications in SAH patients such as BOLD MRI for assessment of oxygen consumption, determination of CVR as with the CO 2 challenge test [30] and finally blood flow quantitation.…”

Section: Magnetic Resonancementioning

confidence: 99%

Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools

et al. 2015

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In the first weeks following aneurysmal subarachnoid haemorrhage, cerebrovascular alterations may impact the outcome significantly. Diagnosis of cerebral vasospasm and detection of alterations at risk of delayed cerebral ischemia are key targets to be monitored in the post-acute phase. Available tools include clinical monitoring, as well as studies that can detect possible arterial narrowing, alterations of perfusion, metabolism and neurophysiology. Each technique is able to investigate possible vascular impairment and has different advantages and limits. All available techniques have been described. Among these, the most practical have been selected and compared for their peculiar characteristics. Based on this analysis, a flowchart to monitor these patients is finally proposed.

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“…3,12,17,18,21,28,29 The ideal diagnostic tool should be noninvasive, easy, fast, and repeatable, and should allow not only the identification of patients with vasospasm but also of patients at risk for DIND and DCI. Digital subtraction angiography (DSA) is considered the gold standard for the diagnosis of cerebral vasospasm, but its invasiveness precludes its use for monitoring purposes.…”

mentioning

confidence: 99%

Early whole-brain CT perfusion for detection of patients at risk for delayed cerebral ischemia after subarachnoid hemorrhage

Malinova¹,

Dolatowski

Schramm

et al. 2016

JNS

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C erebral infarction with permanent vasospasminduced delayed ischemic neurological deficits (DIND) after aneurysmal subarachnoid hemorrhage (aSAH) is a feared and unfortunately frequent complication, responsible for poor functional and overall outcome. 2 The pathophysiology of DIND and vasospasminduced delayed cerebral infarction (DCI) after aSAH is multifactorial and still not fully understood. It is well accepted that vasospasm is a major contributor to DIND and DCI, but it is also assumed that processes already initiated shortly after aSAH render some brain areas more vulnerable for vasospasm than others. 20,27,33 In up to 15% of patients, cerebral infarction and a fixed neurological deficit (including death) are irreversible end points of a dynamic process starting with tissue predisposition and asymptomatic vasospasm, followed by symptomatic vasospasm and transient DIND. For the successful prevention of infarction by antivasospastic therapy, timely recognition of abbreviatioNs aSAH = aneurysmal subarachnoid hemorrhage; BFV = blood flow velocity; CBF = cerebral blood flow; CBV = cerebral blood volume; CTA = CT angiography; CTP = CT perfusion; DCI = delayed cerebral infarction; DIND = delayed ischemic neurological deficits; DSA = digital subtraction angiography; MIP = maximum-intensity projection; MTT = mean transit time; NPV = negative predictive value; PPV = positive predictive value; ROI = region of interest; TCD = transcranial Doppler sonography; TTP = time to peak; TTS = time to start. obJective This prospective study investigated the role of whole-brain CT perfusion (CTP) studies in the identification of patients at risk for delayed ischemic neurological deficits (DIND) and of tissue at risk for delayed cerebral infarction (DCI). methods Forty-three patients with aneurysmal subarachnoid hemorrhage (aSAH) were included in this study. A CTP study was routinely performed in the early phase (Day 3). The CTP study was repeated in cases of transcranial Doppler sonography (TCD)-measured blood flow velocity (BFV) increase of > 50 cm/sec within 24 hours and/or on Day 7 in patients who were intubated/sedated. results Early CTP studies revealed perfusion deficits in 14 patients, of whom 10 patients (72%) developed DIND, and 6 of these 10 patients (60%) had DCI. Three of the 14 patients (21%) with early perfusion deficits developed DCI without having had DIND, and the remaining patient (7%) had neither DIND nor DCI. There was a statistically significant correlation between early perfusion deficits and occurrence of DIND and DCI (p < 0.0001). A repeated CTP was performed in 8 patients with a TCD-measured BFV increase > 50 cm/sec within 24 hours, revealing a perfusion deficit in 3 of them (38%). Two of the 3 patients (67%) developed DCI without preceding DIND and 1 patient (33%) had DIND without DCI. In 4 of the 7 patients (57%) who were sedated and/or comatose, additional CTP studies on Day 7 showed perfusion deficits. All 4 patients developed DCI. coNclusioNs Whole-brain CTP on Day 3 after aSAH allows early and rel...

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Advanced Imaging Modalities in the Detection of Cerebral Vasospasm

Cited by 43 publications

References 81 publications

Aneurysmal Subarachnoid Hemorrhage

Aneurysmal Subarachnoid Hemorrhage

Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools

Early whole-brain CT perfusion for detection of patients at risk for delayed cerebral ischemia after subarachnoid hemorrhage

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