Predicting Delayed Ischemic Deficits after Aneurysmal Subarachnoid Hemorrhage Using a Transient Hyperemic Response Test of Cerebral Autoregulation

Neurosurgery ◽  
2000 ◽  
Vol 47 (4) ◽  
pp. 819-826 ◽  
Author(s):  
Joseph M. K. Lam ◽  
Peter Smielewski ◽  
Marek Czosnyka ◽  
John D. Pickard ◽  
Peter J. Kirkpatrick
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Neurological Deficits ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Response Test ◽  
Baseline Values ◽  
Hyperemic Response

Abstract OBJECTIVE To assess whether the development of delayed ischemic deficits (DIDs) after aneurysmal subarachnoid hemorrhage can be predicted using transcranial Doppler ultrasonography and the transient hyperemic response test (THRT). METHODS An increase in the middle cerebral artery peak flow velocity (FV) of more than 9% of baseline values after 5 to 9 seconds of carotid artery compression was defined as a normal THRT result, indicating good autoregulatory reserve. The transcranial Doppler criteria for vasospasm were a FV of more than 120 cm/s and a Lindegaard ratio of more than 3. Twenty patients with no immediate postoperative neurological deficits were studied. The FVs at all of the major cerebral arteries were measured daily after surgery, and the THRT results were assessed bilaterally. RESULTS Five of six patients with abnormal THRT results in the first examination after surgery (primary THRT impairment) developed DIDs; none of the remaining patients developed DIDs (Fisher exact test, P = 0.0004). All five patients with DIDs initially exhibited low FVs but all subsequently developed increases in FVs to values of more than 150 cm/s and four exhibited FVs of more than 200 cm/s. The time of onset of DIDs corresponded to the time of onset of moderate vasospasm (FV > 150 cm/s). None of the patients with initially normal THRT results developed DIDs, although four patients did exhibit late (secondary) THRT impairment, which was associated with FVs of more than 120 cm/s. CONCLUSION When the effects of primarily impaired (after surgery) autoregulation are magnified by vasospasm, the risk of DIDs seems to be very high. Vasospasm alone does not seem to cause DIDs. The development of DIDs could therefore be predicted using the THRT for patients after aneurysm clipping.

Detection of Microemboli by Transcranial Doppler Ultrasonography in Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2002 ◽  
Vol 50 (5) ◽  
pp. 1026-1031 ◽  
Author(s):  
Jose G. Romano ◽  
Alejandro M. Forteza ◽  
Mauricio Concha ◽  
Sebastian Koch ◽  
Roberto C. Heros ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Doppler Ultrasonography ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Statistical Significance ◽  
Cerebral Arteries ◽  
Transcranial Doppler Ultrasonography ◽  
Control Subjects

Abstract OBJECTIVE: To determine the frequency and characteristics of microembolic signals (MES) in subarachnoid hemorrhage (SAH). METHODS: Twenty-three patients with aneurysmal SAH were monitored with transcranial Doppler ultrasonography for the presence of MES and vasospasm. Each middle cerebral artery was monitored for 30 minutes three times each week. Patients were excluded if they had traumatic SAH or cardiac or arterial sources of emboli. Monitoring was initiated 6.3 days (1–16 d) after SAH and lasted 6.6 days (1–13 d). Eleven individuals without SAH or other cerebrovascular diseases who were treated in the same unit served as control subjects. Each patient underwent monitoring of both middle cerebral arteries a mean of three times; therefore, 46 vessels were studied (a total of 138 observations). Control subjects underwent assessment of each middle cerebral artery once, for a total of 22 control vessels. RESULTS: MES were detected for 16 of 23 patients (70%) and 44 of 138 patient vessels (32%) monitored, compared with 2 of 11 control subjects (18%) and 2 of 22 control vessels (9%) (P < 0.05). MES were observed for 83% of patients with clinical vasospasm and 54% of those without clinical vasospasm. Ultrasonographic vasospasm was observed for 71 of 138 vessels monitored; MES were observed for 28% of vessels with vasospasm and 36% of those without vasospasm. Aneurysms proximal to the monitored artery were identified in 38 of 138 vessels, of which 34% exhibited MES, which is similar to the frequency for vessels without proximal aneurysms (31%). Coiled, clipped, and unsecured aneurysms exhibited similar frequencies of MES. CONCLUSION: MES were common in SAH, occurring in 70% of cases of SAH and one-third of all vessels monitored. Although MES were more frequent among patients with clinical vasospasm, this difference did not reach statistical significance. We were unable to demonstrate a relationship between ultrasonographic vasospasm and MES, and the presence of a proximal secured or unsecured aneurysm did not alter the chance of detection of MES. Further studies are required to determine the origin and clinical relevance of MES in SAH.

Abstract P350: Early Transcranial Doppler Velocity Changes as a Predictor for Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Matthew Triano ◽  
Maite J Corbin ◽  
Sameer Desale ◽  
Ai-Hsi Liu ◽  
Daniel R Felbaum ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Delayed Cerebral Ischemia ◽  
Multivariate Logistic Regression Analysis ◽  
Absolute Velocity ◽  
Doppler Velocity ◽  
Velocity Change

Introduction: Although transcranial Doppler (TCD) evaluation for vasospasm remains an important study in aneurysmal subarachnoid hemorrhage (aSAH) management, its precise role in predicting delayed cerebral ischemia (DCI) remains unclear. Hypothesis: We evaluated optimal measures for evaluating TCD velocities and hypothesized that TCD velocity change would be the best predictor for DCI in patients with aSAH. Methods: Patients with aSAH over a two-year period were retrospectively analyzed. Baseline characteristics, outcomes, and TCD velocities in bilateral middle cerebral arteries (MCA) for hospital days 2 to14 were recorded. TCD variables, including absolute velocity and change in velocity, were obtained by creating a smoothing curve. A variable representing change in TCD velocity was then created through a linear regression model that confirmed greatest change in velocity associated with DCI occurred at days 2-7. Multivariate logistic regression analysis using DCI as outcome was then completed. Results: 95 patients with aSAH were evaluated. Increased TCD velocity at days 2-7 proved to be a better predictor for DCI than absolute velocity with an optimal cutoff of 8.9 cm/sec/day ( p = 0.019) and AUC 0.651. Multivariate logistic analysis using DCI as the outcome showed that poor admission Hunt-Hess scores (OR 5.02, 95%CI 1.22-22.67, p = 0.028) and increase in TCD velocity during days 2-7 (OR 5.32, 95%CI 1.41-23.33, p = 0.018) were independently associated with DCI. Conclusions: We found that relative increases in TCD velocities in the MCAs during the first 7 days (threshold increase of 8.9 cm/sec/day or 53.4 cm/sec from days 2-7) after aSAH were independently associated with DCI. Our findings suggest that vasospasm should be confirmed and treated aggressively when detected via increased TCD velocities during the first seven days in order to minimize DCI. This association requires independent confirmation.

scholarly journals Concentrations of estradiol, progesterone and testosterone in sefrum and cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage correlate weakly with transcranial Doppler flow velocities

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jan Martin ◽  
Eva Plank ◽  
Bernhard Ulm ◽  
Jens Gempt ◽  
Maria Wostrack ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Blood Flow Velocities ◽  
Flow Velocities

Abstract Background The implication of the steroids estradiol, progesterone and testosterone in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) has not been comprehensively assessed. In rodents, studies suggested beneficial effects of steroids on cerebral vasospasm after experimental SAH. Studies in humans are warranted, however, a general dilemma of human studies on neuroactive substances is that the brain is not directly accessible and that concentrations in the periphery may not adequately parallel concentrations in the central compartments. In the present study, concentrations of estradiol, progesterone and testosterone in serum and cerebrospinal fluid (CSF) of patients with aSAH were determined. Blood flow velocities in cerebral arteries were measured by transcranial Doppler sonography (TCD). The aim of this study was to evaluate the correlations between the cerebral blood flow velocities and levels of estradiol, progesterone and testosterone in CSF and serum. Results Samples of serum and CSF of 42 patients with aSAH were collected concomitantly daily or every other day via the arterial line and the external ventricular drainage for two weeks after the hemorrhage. Blood flow velocities in the cerebral arteries were determined by TCD. Total estradiol, progesterone and testosterone concentrations were measured by electro-chemiluminescence immunoassay. The strength of correlation was assessed by Spearman’s rank correlation coefficient. The correlation analysis revealed very weak correlations between cerebral blood flow velocities and concentrations of estradiol, progesterone and testosterone levels in both compartments with correlation coefficients below 0.2. Conclusions In humans with aSAH, merely very weak correlations between flow velocities in cerebral arteries and concentrations of estradiol, progesterone and testosterone in serum and CSF were demonstrated. These results suggest a limited influence of the respective steroids on cerebral vascular tone although vasodilatory effects were described in rodent studies. Thus, the implication of steroids in processes of neurological deterioration warrants further clarification.

Intravenous Magnesium versus Nimodipine in the Treatment of Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized Study

Neurosurgery ◽  
2006 ◽  
Vol 58 (6) ◽  
pp. 1054-1065 ◽  
Author(s):  
Robert Schmid-Elsaesser ◽  
Matthias Kunz ◽  
Stefan Zausinger ◽  
Stefan Prueckner ◽  
Josef Briegel ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Randomized Study ◽  
Fatal Outcome ◽  
Neuron Specific Enolase ◽  
Neurological Deficits ◽  
Secondary Outcome ◽  
Neuronal Markers ◽  
Angiographic Vasospasm

Abstract OBJECTIVE: The prophylactic use of nimodipine in patients with aneurysmal subarachnoid hemorrhage reduces the risk of ischemic brain damage. However, its efficacy seems to be rather moderate. The question arises whether other types of calcium antagonists offer better protection. Magnesium, nature's physiological calcium antagonist, is neuroprotective in animal models, promotes dilatation of cerebral arteries, and has an established safety profile. The aim of the current pilot study is to evaluate the efficacy of magnesium versus nimodipine to prevent delayed ischemic deficits after aneurysmal subarachnoid hemorrhage. METHODS: One hundred and thirteen patients with aneurysmal subarachnoid hemorrhage were enrolled in the study and were randomized to receive either magnesium sulfate (loading 10 mg/kg followed by 30 mg/kg daily) or nimodipine (48 mg/d) intravenously until at least postoperative Day 7. Primary outcome parameters were incidence of clinical vasospasm and infarction. Secondary outcome measures were the incidence of transcranial Doppler/angiographic vasospasm, the neuronal markers (neuron-specific enolase, S-100), and the patients' Glasgow Outcome Scale scores at discharge and after 1 year. RESULTS: One hundred and four patients met the study requirements. In the magnesium group (n = 53), eight patients (15%) experienced clinical vasospasm and 20 (38%) experienced transcranial Doppler/angiographic vasospasm compared with 14 (27%) and 17 (33%) patients in the nimodipine group (n = 51). If clinical vasospasm occurred, 75% of the magnesium-treated versus 50% of the nimodipine-treated patients experienced cerebral infarction resulting in fatal outcome in 37 and 14%, respectively. Overall, the rate of infarction attributable to vasospasm was virtually the same (19 versus 22%). There was no difference in outcome between groups. CONCLUSION: The efficacy of magnesium in preventing delayed ischemic neurological deficits in patients with aneurysmal subarachnoid hemorrhage seems to be comparable with that of nimodipine. The difference in their pharmacological properties makes studies on the combined administration of magnesium and nimodipine seem promising.

Lower Incidence of Transcranial Doppler and Symptomatic Vasospasm After Aneurysmal Subarachnoid Hemorrhage and Aneurysm Clipping in the Elderly Patient?

Neurosurgery ◽  
2011 ◽  
Vol 69 (2) ◽  
pp. 261-267 ◽  
Author(s):  
Dorothee Wachter ◽  
Franz Hans ◽  
Ilonka Kreitschmann-Andermahr ◽  
Veit Rohde
Keyword(s):  
Elderly Patient ◽  
Subarachnoid Hemorrhage ◽  
Transcranial Doppler ◽  
Lower Incidence ◽  
Older Patients ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
The Elderly ◽  
Neurological Deficits ◽  
Medical Complications ◽  
Symptomatic Vasospasm

Abstract BACKGROUND: Vasospasm is the major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage. It is well known that the vasoreactivity decreases with advancing age, but it is not well investigated in a large patient cohort whether, as a consequence, the incidence of vasospasm is lower in elderly patients. OBJECTIVE: To investigate whether transcranial Doppler vasospasm, delayed ischemic neurological deficits, and vasospasm-associated ischemic lesions are less frequent in older patients. METHODS: Seven hundred fifty-eight patients who suffered from subarachnoid hemorrhage were included in this study. Clinical presentation, Hunt and Hess score, Fisher grade, incidence of vasospasm, neurological deficits and ischemic lesions on radiographic imaging, transcranial Doppler blood flow velocities, medical complications, and outcome were registered. RESULTS: Four hundred seventy-eight patients < 60 years of age and 280 patients ≥ 60 years of age were identified; 55.2% of the younger and 25.7% of the older age group developed post-hemorrhagic vasospasm (P < .001). Older patients developed less vasospasm (P = .00), fewer neurological deficits (P < .001), and fewer ischemic lesions on computed tomography imaging (P = .06). On the other hand, older patients had significantly worse outcomes than younger patients (P = .01) and more frequently died of medical complications (P = .01). CONCLUSION: Vasospasm, delayed ischemic neurological deficits, and vasospasm-associated ischemic lesions are more likely to occur in patients < 60 years of age than in older patients. The lower incidence of vasospasm and vasospasm-related ischemia in the elderly patient does not translate into better outcome because of the higher rate of fatal medical complications in patients ≥ 60 years of age.

Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial

2013 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Nobuo Senbokuya ◽  
Hiroyuki Kinouchi ◽  
Kazuya Kanemaru ◽  
Yasuhiro Ohashi ◽  
Akira Fukamachi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Symptomatic Vasospasm ◽  
Angiographic Vasospasm ◽  
Significant Difference ◽  
Length Of Hospitalization

Object Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of subsequent morbidity and mortality. Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm. Methods Patients admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH onset were enrolled at 7 neurosurgical sites in Japan. These patients were assigned to one of 2 groups: the usual therapy group (control group) or the add-on 100 mg cilostazol twice daily group (cilostazol group). The group assignments were done by a computer-generated randomization sequence. The primary study end point was the onset of symptomatic vasospasm. Secondary end points were the onset of angiographic vasospasm and new cerebral infarctions related to cerebral vasospasm, clinical outcome as assessed by the modified Rankin scale, and length of hospitalization. All end points were assessed for the intention-to-treat population. Results Between November 2009 and December 2010, 114 patients with SAH were treated by clipping within 72 hours from the onset of SAH and were screened. Five patients were excluded because no consent was given. Thus, 109 patients were randomly assigned to the cilostazol group (n = 54) or the control group (n = 55). Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021, Fisher exact test). The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055, Fisher exact test). Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm. The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304, Fisher exact test). Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period. Conclusions Oral administration of cilostazol is effective in preventing cerebral vasospasm with a low risk of severe adverse events. Clinical trial registration no. UMIN000004347, University Hospital Medical Information Network Clinical Trials Registry.

Early focal brain injury after subarachnoid hemorrhage correlates with spreading depolarizations

Neurology ◽  
2018 ◽  
Vol 92 (4) ◽  
pp. e326-e341 ◽  
Author(s):  
Nina Eriksen ◽  
Egill Rostrup ◽  
Martin Fabricius ◽  
Michael Scheel ◽  
Sebastian Major ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Predictive Value ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rank Order ◽  
Time Windows ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Focal Brain Injury

ObjectiveTo investigate whether spreading depolarization (SD)-related variables at 2 different time windows (days 1–4 and 5–8) after aneurysmal subarachnoid hemorrhage (aSAH) correlate with the stereologically determined volume of early focal brain injury on the preinterventional CT scan.MethodsIn this observational multicenter study of 54 patients, volumes of unaffected brain tissue, ventricles, cerebellum, aSAH, intracerebral hemorrhage, and focal parenchymal hypodensity were stereologically estimated. Patients were electrocorticographically monitored using subdural electrodes for 81.8 hours (median) (interquartile range: 70.6–90.5) during days 1–4 (n = 54) and for 75.9 (59.5–88.7) hours during days 5–8 (n = 51). Peak total SD-induced depression duration of a recording day (PTDDD) and peak numbers of (1) SDs, (2) isoelectric SDs, and (3) spreading depressions of a recording day were determined following the recommendations of the Co-Operative Studies on Brain Injury Depolarizations.ResultsThirty-three of 37 patients with early focal brain injury (intracerebral hemorrhage and/or hypodensity) in contrast to 7 of 17 without displayed SDs during days 1–4 (sensitivity: 89% [95% confidence interval, CI: 75%–97%], specificity: 59% [CI: 33%–82%], positive predictive value: 83% [CI: 67%–93%], negative predictive value: 71% [CI: 42%–92%], Fisher exact test, p < 0.001). All 4 SD-related variables during days 1–4 significantly correlated with the volume of early focal brain injury (Spearman rank order correlations). A multiple ordinal regression analysis identified the PTDDD as the most important predictor.ConclusionsOur findings suggest that early focal brain injury after aSAH is associated with early SDs and further support the notion that SDs are a biomarker of focal brain lesions.

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