Positron Emission Tomographic Cerebral Perfusion Disturbances and Transcranial Doppler Findings among Patients with Neurological Deterioration after Subarachnoid Hemorrhage

Neurosurgery ◽  
2003 ◽  
Vol 52 (5) ◽  
pp. 1017-1024 ◽  
Author(s):  
Pawan S. Minhas ◽  
David K. Menon ◽  
Piotr Smielewski ◽  
Marek Czosnyka ◽  
Peter J. Kirkpatrick ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Cerebral Perfusion ◽  
Internal Carotid ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Positron Emission Tomographic ◽  
Positron Emission ◽  
Arterial Vasospasm ◽  
The Mean

Abstract OBJECTIVE After aneurysmal subarachnoid hemorrhage, approximately 30% of patients experience delayed neurological deficits, related in part to arterial vasospasm and dysautoregulation. Transcranial Doppler (TCD) ultrasonography is commonly used to noninvasively detect arterial vasospasm. We studied cerebral perfusion patterns and associated TCD indices for 25 patients who developed clinical signs of delayed neurological deficits. METHODS Patients were treated in a neurosurgical intensive care unit and were studied if they exhibited delayed focal or global neurological deterioration. Positron emission tomographic cerebral blood flow (CBF) studies and TCD studies measuring the mean flow velocity (FV) of the middle cerebral artery and the middle cerebral artery FV/internal carotid artery FV ratio (with the internal carotid artery FV being measured extracranially at the cranial base) were performed. Glasgow Outcome Scale scores were assessed at 6 months. RESULTS A markedly heterogeneous pattern of CBF distribution was observed, with hyperemia, normal CBF values, and reduced flow being observed among patients with delayed neurological deficits. TCD indices were not indicative of the cerebral perfusion findings. The mean CBF value was slightly lower for patients who did not survive (32.3 ml/100 g/min), compared with those who did survive (36.0 ml/100 g/min, P= 0.05). CONCLUSION Among patients who developed delayed neurological deficits after aneurysmal subarachnoid hemorrhage, a wide range of cerebral perfusion disturbances was observed, calling into question the traditional concept of large-vessel vasospasm. Commonly used TCD indices do not reflect cerebral perfusion values.

Use of the Extracranial-Intracranial Arterial Bypass in the Management of Refractory Vasospasm: A Case Report

Neurosurgery ◽  
1985 ◽  
Vol 17 (3) ◽  
pp. 474-479 ◽  
Author(s):  
Jacob Rosenstein ◽  
Hunt H. Batjer ◽  
Duke S. Samson
Keyword(s):  
Case Report ◽  
Subarachnoid Hemorrhage ◽  
Arterial Hypertension ◽  
Volume Expansion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Morbidity And Mortality ◽  
Neurological Deficits ◽  
Collateral Flow ◽  
Intravascular Volume ◽  
Arterial Vasospasm

Abstract Cerebral arterial vasospasm after aneurysmal subarachnoid hemorrhage remains one of the major causes of morbidity and mortality in patients surviving the initial hemorrhage. Once established, no known method has been shown to reverse this process in humans. Although intravascular volume expansion and induced arterial hypertension have been shown to be effective in the reversal of neurological deficits secondary to vasospasm, a large proportion of patients remain refractory to these methods. We report one such case successfully managed by the estalishment of an extracranial-intracranial anastomosis in an attempt to augment collateral flow.

Characterization of perioperative seizures and epilepsy following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 99 (6) ◽  
pp. 978-985 ◽  
Author(s):  
Chih-Lung Lin ◽  
Aaron S. Dumont ◽  
Ann-Shung Lieu ◽  
Chen-Po Yen ◽  
Shiuh-Lin Hwang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Predictive Factors ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Loss Of Consciousness ◽  
Content Type ◽  
Fisher Grade ◽  
The Mean ◽  
Fine Print

Object. The reported incidence, timing, and predictive factors of perioperative seizures and epilepsy after subarachnoid hemorrhage (SAH) have differed considerably because of a lack of uniform definitions and variable follow-up periods. In this study the authors evaluate the incidence, temporal course, and predictive factors of perioperative seizures and epilepsy during long-term follow up of patients with SAH who underwent surgical treatment. Methods. Two hundred seventeen patients who survived more than 2 years after surgery for ruptured intracranial aneurysms were enrolled and retrospectively studied. Episodes were categorized into onset seizures (≤ 12 hours of initial hemorrhage), preoperative seizures, postoperative seizures, and late epilepsy, according to their timing. The mean follow-up time was 78.7 months (range 24–157 months). Forty-six patients (21.2%) had at least one seizure post-SAH. Seventeen patients (7.8%) had onset seizures, five (2.3%) had preoperative seizures, four (1.8%) had postoperative seizures, 21 (9.7%) had at least one seizure episode after the 1st week postoperatively, and late epilepsy developed in 15 (6.9%). One (3.8%) of 26 patients with perioperative seizures (onset, preoperative, or postoperative seizure) had late epilepsy at follow up. The mean latency between the operation and the onset of late epilepsy was 8.3 months (range 0.3–19 months). Younger age (< 40 years old), loss of consciousness of more than 1 hour at ictus, and Fisher Grade 3 or greater on computerized tomography scans proved to be significantly related to onset seizures. Onset seizure was also a significant predictor of persistent neurological deficits (Glasgow Outcome Scale Scores 2–4) at follow up. Factors associated with the development of late epilepsy were loss of consciousness of more than 1 hour at ictus and persistent postoperative neurological deficit. Conclusions. Although up to one fifth of patients experienced seizure(s) after SAH, more than half had seizure(s) during the perioperative period. The frequency of late epilepsy in patients with perioperative seizures (7.8%) was not significantly higher than those without such seizures (6.8%). Perioperative seizures did not recur frequently and were not a significant predictor for late epilepsy.

Abstract 2355: 2d Perfusion Color Mapping Can Predict Hyperperfusion Syndrome After Carotid Artery Stenting

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Ryo Yoshimura ◽  
Yuko Tanaka ◽  
Kenichi Kono ◽  
Hideo Okada ◽  
Takeshi Fujimoto ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Carotid Artery Stenting ◽  
Cerebral Perfusion ◽  
Neurological Deficits ◽  
High Morbidity ◽  
Color Mapping ◽  
Hyperperfusion Syndrome ◽  
Symptomatic Vasospasm ◽  
Before And After

Background: Hyperperfusion syndrome (HPS) is one of the most important complications during carotid artery stenting (CAS), which presents headache, seizure, focal neurological deficits due to intracerebral hemorrhage. It is essential to predict HPS because of its high morbidity or mortality. 2D perfusion color mapping (2DPCoM) enables to clarify cerebral perfusion status using only digital subtraction angiography (DSA) and its workstations. We report 2DPCoM can predict HPS. Materials and Methods: 778 patients who had performed CAS have registered. All of the patients were analyzed with SPECT before and after CAS, including acetazolamide study. Transcranial doppler (TCD) have been performed before, during, and after CAS if possible. HPS was defined neurological deficits and intracerebral or subarachnoid hemorrhage with CT or MRI. DSA was performed with Allura Xper FD20/10 (Philips). 2DPCoM was analyzed with 6ml/sec contrast medium infusion from common carotid artery for 1 second. Maximum enhancement, start to peak, average wash-in rate (AWR) , Area-under-curve (AUC), mean transit time (MTT) were revealed. The data were compared with SPECT and TCD. Results: 6/778 cases have presented HPS. All of the patients manifested misery perfusion (Powers stage 2) before CAS with SPECT. Mean middle cerebral artery flow velocity markedly increased after CAS with SPECT. 2DPCoM showed remarkable hyperperfusion state after CAS, especially MTT. MTT of all HPS cases dramatically changed >25% before and after the procedure. Discussion: 2DPCoM has a lot of potential for evaluating cerebral hemodynamics with great ease compared with SPECT or TCD. It needs no more devices or drugs, needs only ‘one injection, one click, and one minute’. It might be useful for intracranial percutaneous transluminal angioplasty/stenting, symptomatic vasospasm following subarachnoid hemorrhage, and some other hemodynamic diseases. Conclusion: 2D perfusion color mapping requires only one more infusion. It needs no more devices and one-click analysis within less than 1 minute. It is very useful modality during CAS for analyzing cerebral perfusion status.

Cerebral blood flow following induced subarachnoid hemorrhage in the monkey

1972 ◽  
Vol 37 (3) ◽  
pp. 316-324 ◽  
Author(s):  
K. C. Petruk ◽  
G. R. West ◽  
M. R. Marriott ◽  
J. W. McIntyre ◽  
T. R. Overtone ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Content Type ◽  
Arterial Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Angiographic Demonstration

✓ The acute effects of experimental subarachnoid hemorrhage on cerebral blood flow were investigated in 14 adult rhesus monkeys injected with fresh autogenous blood through a needle positioned within the subfrontal subarachnoid space. Cerebral blood flow was measured by the xenon133 tissue clearance method before hemorrhage, and afterward at 30-minute intervals for a 3-hour period. Post-anesthetic neurological status was graded according to Botterell's classification. Twelve monkeys showed a significant decrease in cerebral perfusion, eight displayed focal neurological deficits, and four were moribund. There was a correlation between the degree of impaired circulation and the severity of neurological deficit. Four additional monkeys subjected to subarachnoid acidic saline injection showed no reduction in cerebral blood flow. In three animals cerebral perfusion was increased during the first hour after injection. It is suggested that measurement of cerebral blood flow may be a more valuable prognostic indication of cerebral function and survival than the angiographic demonstration of arterial vasospasm.

scholarly journals Rationale for graft selection in patients with complex internal carotid artery aneurysms treated with extracranial to intracranial high-flow bypass and therapeutic internal carotid artery occlusion

2018 ◽  
Vol 128 (6) ◽  
pp. 1753-1761 ◽  
Author(s):  
Hidetoshi Matsukawa ◽  
Shiro Miyata ◽  
Toshiyuki Tsuboi ◽  
Kosumo Noda ◽  
Nakao Ota ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Internal Carotid ◽  
Pressure Ratio ◽  
Low Flow ◽  
Neurological Deficits ◽  
External Carotid ◽  
Graft Size ◽  
Ischemic Complications ◽  
The Mean

OBJECTIVEAfter internal carotid artery (ICA) sacrifice without revascularization for complex aneurysms, ischemic complications can occur. In addition, hemodynamic alterations in the circle of Willis create conditions conducive to the formation of de novo aneurysms or the enlargement of existing untreated aneurysms. Therefore, the revascularization technique remains indispensable. Because vessel sizes and the development of collateral circulation are different in each patient, the ideal graft size to prevent low flow–related ischemic complications (LRICs) in external carotid artery (ECA)–middle cerebral artery (MCA) bypass with therapeutic ICA occlusion (ICAO) has not been well established. Authors of this study hypothesized that the adequate graft size could be calculated from the size of the sacrificed ICA and the values of MCA pressure (MCAP) and undertook an investigation in patients with complex ICA aneurysms treated with ECA-graft-MCA bypass and therapeutic ICAO.METHODSIn the period between July 2006 and January 2016, 80 patients with complex ICA aneurysms were treated with ECA-MCA bypass and therapeutic ICAO. Preoperative balloon test occlusion (BTO) was performed, and the BTO pressure ratio was defined as the mean stump pressure/mean preocclusion pressure. Low flow–related ischemic complications were defined as new postoperative neurological deficits and ipsilateral cerebral blood flow reduction. Initial MCAP (iMCAP), MCAP after clamping the ICA (cMCAP), and MCAP after releasing the graft (gMCAP) were intraoperatively monitored. The MCAP ratio was defined as gMCAP/iMCAP. Based on the Hagen-Poiseuille law, the expected MCAP ratio ([expected gMCAP]/iMCAP) was hypothesized as follows: (1 – cMCAP/iMCAP)(graft radius/ICA radius)2 + (cMCAP/iMCAP). Correlations between the BTO pressure ratio and cMCAP/iMCAP, and between the actual and expected MCAP ratios, were evaluated. Risk factors for LRICs were also evaluated.RESULTSThe mean BTO pressure ratio was significantly correlated with the mean cMCAP/iMCAP (r = 0.68, p < 0.0001). The actual MCAP ratio correlated with the expected MCAP ratio (r = 0.43, p < 0.0001). If the expected MCAP ratio was set up using the BTO pressure ratio instead of cMCAP/iMCAP (BTO-expected MCAP ratio), the mean BTO-expected MCAP ratio significantly correlated with the expected MCAP ratio (r = 0.95, p < 0.0001). During a median follow-up period of 26.1 months, LRICs were observed in 9 patients (11%). An actual MCAP ratio < 0.80 (p = 0.003), expected MCAP ratio < 0.80 (p = 0.001), and (M2 radius/graft radius)2 < 0.49 (p = 0.002) were related to LRICs according to the Cox proportional-hazards model.CONCLUSIONSData in the present study indicated that it was important to use an adequate graft to achieve a sufficient MCAP ratio in order to avoid LRICs and that the adequate graft size could be evaluated based on a formula in patients with complex ICA aneurysms treated with ICAO.

Effect of transluminal angioplasty on cerebral blood flow in the management of symptomatic vasospasm following aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 86 (5) ◽  
pp. 830-839 ◽  
Author(s):  
Andrew D. Firlik ◽  
Anthony M. Kaufmann ◽  
Charles A. Jungreis ◽  
Howard Yonas
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Transluminal Angioplasty ◽  
T Test ◽  
Neurological Deficits ◽  
Symptomatic Vasospasm ◽  
The Mean

✓ In this study the authors have examined the effects of transluminal angioplasty on cerebral blood flow (CBF) in the management of intractable vasospasm following aneurysmal subarachnoid hemorrhage (SAH). Fourteen consecutively enrolled patients underwent attempted angioplasty with or without intraarterial infusion of papaverine. Twelve patients underwent pre- and postangioplasty xenon-enhanced computerized tomography (Xe-CT) scanning to measure regional CBF in 55 to 65 regions of interest (ROIs) per patient. Angioplasty was possible in 13 (93%) of 14 patients, with angiographically demonstrated improvement in all 13. Twelve (92%) of the 13 patients were neurologically improved following angioplasty; seven (58%) of the 12 patients who improved had a complete reversal of all delayed ischemic deficits. Angioplasty significantly decreased the mean number of ROIs at risk (11.4 ROIs pre- and 0.9 ROIs postangioplasty) (p < 0.00005, t-test). All patients had a reduction in the number of ROIs at risk after angioplasty; six (50%) of 12 no longer had any ROIs remaining at risk after angioplasty. Angioplasty significantly increased the mean CBF within at-risk ROIs (13 ml/100 g/minute pre- and 44 ml/100 g/minute postangioplasty) (p < 0.00005, t-test). All patients experienced an improvement in mean CBF in at-risk ROIs after angioplasty, with the mean CBF improving to above 20 ml/100 g/minute in all cases. No differences in the degree of improvement were found in patients who received intraarterial papaverine compared with those who did not. In the majority of patients with refractory vasospasm following SAH, angioplasty effectively dilated spastic arteries, reversed delayed neurological deficits, and significantly improved CBF in areas of brain at risk of infarction.

Alpha-II spectrin breakdown products in aneurysmal subarachnoid hemorrhage: a novel biomarker of proteolytic injury

2007 ◽  
Vol 107 (4) ◽  
pp. 792-796 ◽  
Author(s):  
Stephen B. Lewis ◽  
Gregory J. Velat ◽  
Lynn Miralia ◽  
Linda Papa ◽  
Jada M. Aikman ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Acute Onset ◽  
Neurological Deficits ◽  
Focal Neurological Deficit ◽  
Fisher Grade ◽  
Arterial Vasospasm ◽  
Grade 3

Object Aneurysmal subarachnoid hemorrhage (ASAH) is a serious event with grave consequences. Delayed ischemic neurological deficits caused by cerebral arterial vasospasm contribute significantly to death and disability. Biomarkers may reflect brain injury and provide an early warning of impending neurological decline and stroke from ASAH-induced vasospasm. Alpha-II spectrin is a cytoskeletal protein whose breakdown products are candidate surrogate markers of injury magnitude, treatment efficacy, and outcome. In addition, αII spectrin breakdown products (SBDPs) can provide information on the proteolytic mechanisms of injury. Methods Twenty patients who received a diagnosis of Fisher Grade 3 ASAH were enrolled in this study to examine the clinical utility of SBDPs in the detection of cerebral vasospasm in patients with ASAH. All patients underwent placement of a ventriculostomy for continual cerebrospinal fluid drainage within 72 hours of ASAH onset. Cerebrospinal fluid samples were collected every 6 hours and analyzed using Western Blotting for SBDPs. Onset of vasospasm was defined as an acute onset of a focal neurological deficit or a change in Glasgow Coma Scale score of two or more points. All suspected cases of vasospasm were confirmed on imaging studies. Results Both calpain- and caspase-mediated SBDP levels are significantly increased in patients suffering ASAH. The concentration of SBDPs was found to increase significantly over baseline level up to 12 hours before the onset of cerebral arterial vasospasm. Conclusions Differential expression of SBDPs suggests oncotic necrotic proteolysis may be predominant in acute brain injury after ASAH and cerebral arterial vasospasm.

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