Intracranial Vasospasm Research Articles

A Case of Delayed Symptomatic Vasospasm after Surgical Clipping of an Unruptured Intracranial Aneurysm

Although intracranial arterial vasospasm commonly occurs after subarachnoid hemorrhage, delayed symptomatic vasospasm rarely occurs after surgical clipping of unruptured intracranial aneurysms. We report the case of a 67-year-old woman who presented with symptomatic vasospasm 10 days after surgical clipping of an unruptured middle cerebral artery aneurysm. On the 10th operative day, the patient presented mild aphasia. Angiography revealed a vasospasm at the left middle cerebral artery. We performed chemical angioplasty and observed an immediate anatomical improvement and clinical recovery. The patient was discharged without deficit.

Making Endovascular Neurosurgery Safer: Role of the Neuroanesthesiologist

AbstractThe increasing use of endovascular technique for treating neurovascular diseases underscores the need for the neuroanesthesiologist to be aware of its potentially serious perioperative complications that can directly impact the anesthetic outcome. These unique complications, including intracranial thromboembolism, hemorrhage, and vasospasm, and significant non-neurological complications that necessitate deft handling by experienced anesthesiologists. However, anesthesia for endovascular neurosurgery is generally being managed in remote hospital locations by relatively junior anesthesiologists who are likely to underestimate the importance of these closed-cranium procedures. This review reacquaints the anesthetist with the periprocedural complications of endovascular neurosurgery that would enable their anticipation, prompt diagnosis, and effective management.

Cerebral infarct with idiopathic cervical internal carotid artery vasospasm: A case report and literature review

Abstract Intracranial vasospasm that results from subarachnoid hemorrhage mostly leads to cerebral infarct. On the other hand, cervical internal carotid artery (CICA) vasospasm is caused by various factors such as cervical surgery, taking ergotamine, or is of unknown origin. We report here a rare case of cerebral infarct due to repeated idiopathic bilateral CICA vasospasm, and present a review of the literature. A 38-year-old man, who had a medical history of cerebral infarcts at the ages of 27 and 35, was admitted complaining of disturbance of consciousness and aphasia. MRI and MRA revealed cerebral infarct of the left middle cerebral artery (MCA) area due to occlusion of the left cervical internal carotid artery. Cerebral angiography at 9 days after onset, we demonstrated that the right CICA was occluded, whereas the left CICA was recanalized. On the 32nd day after onset, MRA showed the bilateral CICA to be recanalized. Idiopathic CICA vasospasm should be considered as a cause of juvenile-onset cerebral infarct. Regular follow-up is therefore needed because idiopathic CICA vasospasm is prone to recurrence.

Post-Aneurysmal Subarachnoid Hemorrhage Vasospasm, Clinical Correlation between the Aneurysm Site and Clinical Vasospasm

Background: Intracranial vasospasm is a common complication following subarachnoid hemorrhage (SAH). The radiographic vasospasm can reach up to 90% of aneurysmal SAH. Materials and Methods: 139 consecutive patients admitted to Cairo University Hospitals from June 2013 to September 2014 with SAH who had been enrolled in a retrospective controlled study were analyzed retrospectively for the occurrence of vasospasm. The data collected from the charts of Cairo University Hospitals were the patient’s demographics, clinical presentation, aneurysm location, treatment modality, and Glasgow Outcome Scale (GOS) scores. We excluded 24 patients with nonaneurysmal SAH, 3 internal carotid artery (ICA) aneurysms, 7 with multiple aneurysms and 4 patients died before treatment. Results: 72 males and 29 females were included in the study, mean age 53.5 ± 11.5 years. Twelve patients had aneurysms located in the vertebral artery group, 24 had middle cerebral artery aneurysms, 11 had pericallosal aneurysms, and 54 patients had anterior communicating artery (ACoA) complex aneurysms. Radiographic vasospasm occurred in 62.4% with the highest incidence (75.9%) at the ACoA complex group. Symptomatic vasospasm occurred in 48.5% with the highest incidence (63%) at the anterior communicating artery complex aneurysm location. The mean GOS at 6 months follow-up was 4.2. The worse GOS was found in the vertebral artery (VA) aneurysm group with a mean of 3.75. Conclusion: Aneurysms of the anterior communicating artery complex group have a greater risk of both radiographic and clinical vasospasm. Also, the worse 6 months follow-up GOS when an aneurysm was located in the VA group.

Temperature variability in the day\u2013night cycle is associated with further intracranial pressure during therapeutic hypothermia

BackgroundTo assess whether circadian patterns of temperature correlate with further values of intracranial pressure (ICP) in severe brain injury treated with hypothermia.MethodsWe retrospectively analyzed temperature values in subarachnoid hemorrhage patients treated with hypothermia by endovascular cooling. The circadian patterns of temperature were correlated with the mean ICP across the following day (ICP24).ResultsWe analyzed data from 17 days of monitoring of three subarachnoid hemorrhage patients that underwent aneurysm coiling, sedation and hypothermia due to refractory intracranial hypertension and/or cerebral vasospasm. ICP24 ranged from 11.5 ± 3.1 to 24.2 ± 6.2 mmHg. The ratio between the coefficient of variation of temperature during the nocturnal period (18:00–6:00) and the preceding diurnal period (6:00–18:00) [temperature variability (TV)] ranged from 0.274 to 1.97. Regression analysis showed that TV correlated with ICP24 (Pearson correlation = −0.861, adjusted R square = 0.725, p < 0.001), and that ICP24 = 6 (4–TV) mmHg or, for 80% prediction interval, {text{ICP}}_{24} = 23.9 - 6.22,times,{text{TV }} pm 1.73,timessqrt {1.06 + (({text{TV}} - 1.1)^{2} /4.49)} mmHg. The results indicate that the occurrence of ICP24 higher than 20 mmHg is unlikely after a day with TV ≥1.0.ConclusionsTV correlates with further ICP during hypothermia regardless the strict range that temperature is maintained. Further studies with larger series could clarify whether intracranial hypertension in severe brain injury can be predicted by analysis of oscillation patterns of autonomic parameters across a period of 24 h or its harmonics.

Intracranial vasospasm associated with acute spontaneous spinal subdural hematoma

Intracranial vasospasm associated with acute spontaneous spinal subdural hematoma

Role of Genetic Polymorphisms in Predicting Delayed Cerebral Ischemia and Radiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Meta-Analysis

The pathophysiology on cerebral vasospasm and delayed cerebral ischemia (DCI) remains poorly understood. Much research has been dedicated to finding genetic loci associated with vasospasm and ischemia. We present a systematic review and meta-analysis to identify genetic polymorphisms associated with delayed ischemic neurologic deficit (DIND), radiographic infarction attributed to ischemia, and radiographic vasospasm. PubMed, the Cochrane Library, and Excerpta Medica dataBASE (EMBASE) databases were used to identify relevant studies published up to March 2015 containing the subject terms cerebral or intracranial vasospasm and DCI in combination with genetics, gene, polymorphism or marker. Meta-analyses were performed using a random-effects model to calculate summary odds ratio (ORs) and 95% confidence intervals for each respective gene. Of 269 articles initially identified, 20 studies with 1670 patients were included in our comprehensive review, including 27 polymorphisms in 11 genes. The following 6 polymorphisms in 3 genes were selected for subsequent meta-analyses: apolipoprotein E (ApoE2, E4); endothelial nitric oxide (eNOS T786C, VNTR intron 4 a/b, G894T); and haptoglobin (Hp) 1/2 phenotypes. The eNOS VNTR a allele was associated with DIND (a vs. b allele: OR 1.92 [1.31-2.81], padj = 0.008). The Hp 2-2 allele was associated with radiographic vasospasm (2-2 vs. 2-1 and 1-1: OR 3.86 [1.86-8.03], padj = 0.003) but did not reach significance for DIND. This is the first systemic review and meta-analysis to study and evaluate the associations between genetic polymorphism with DCI and radiographic vasospasm independently. In our study, eNOS VNTR and Hp polymorphisms appear to have the strongest associations with DIND and radiographic vasospasm, respectively.

Treatment of intracranial vasospasm following subarachnoid hemorrhage.

Vasospasm has been a long known source of delayed morbidity and mortality in aneurysmal subarachnoid hemorrhage patients. Delayed ischemic neurologic deficits associated with vasospasm may account for as high as 50% of the deaths in patients who survive the initial period after aneurysm rupture and its treatment. The diagnosis and treatment of vasospasm has still been met with some controversy. It is clear that subarachnoid hemorrhage is best cared for in tertiary care centers with modern resources and access to cerebral angiography. Ultimately, a high degree of suspicion for vasospasm must be kept during ICU care, and any signs or symptoms must be investigated and treated immediately to avoid permanent stroke and neurologic deficit. Treatment for vasospasm can occur through both ICU intervention and endovascular administration of intra-arterial vasodilators and balloon angioplasty. The best outcomes are often attained when these methods are used in conjunction. The following article reviews the literature on cerebral vasospasm and its treatment and provides the authors’ approach to treatment of these patients.

Brain ischemia in patients with intracranial hemorrhage: pathophysiological reasoning for aggressive diagnostic management.

Patients with intracranial hemorrhage have to be managed aggressively to avoid or minimize secondary brain damage due to ischemia, which contributes to high morbidity and mortality. The risk of brain ischemia, however, is not the same in every patient. The risk of complications associated with an aggressive prophylactic therapy in patients with a low risk of brain ischemia can outweigh the benefits of therapy. Accurate and timely identification of patients at highest risk is a diagnostic challenge. Despite the availability of many diagnostic tools, stroke is common in this population, mostly because the pathogenesis of stroke is frequently multifactorial whereas diagnosticians tend to focus on one or two risk factors. The pathophysiological mechanisms of brain ischemia in patients with intracranial hemorrhage are not yet fully elucidated and there are several important areas of ongoing research. Therefore, this review describes physiological and pathophysiological aspects associated with the development of brain ischemia such as the mechanism of oxygen and carbon dioxide effects on the cerebrovascular system, neurovascular coupling and respiratory and cardiovascular factors influencing cerebral hemodynamics. Consequently, we review investigations of cerebral blood flow disturbances relevant to various hemodynamic states associated with high intracranial pressure, cerebral embolism, and cerebral vasospasm along with current treatment options.

Toward a Stroke-Free Childhood in Sickle Cell Disease

Stroke in childhood is not common outside of congenital heart disease and a few other conditions including sickle cell disease (SCD). The background rates reported have been between 2.3 and 2.7 per 100 000 per year.1–3 Adults, on the contrary, have a background rate of ≈800 per 100 000.4 There are some special conditions that increase the risk including congenital heart disease, trauma, infections (basilar meningitis), cancer, and SCD.5 Stroke rates in SCD were estimated to be high at 500 to 1000 per 100 000.6 The Baltimore Washington Cooperative Young Stroke Study reported data from 1988 to 1991 at rate of 285 per 100 000 children for SCD.7 For children with SCD, this is a long way for a stroke-free childhood. SCD fundamental pathophysiology results from hemoglobin S forming polymer strands inside the red blood cell which causes distortion of the red blood cell, leading to microcirculatory occlusion and accelerated erythrocyte destruction with release of toxic-free hemoglobin into the vascular system.8 How SCD leads to cerebrovascular disease is only partly understood. Although there are many manifestations of vascular pathology in SCD, the one that plays the most prominent role is an intracranial cerebral large artery vasculopathy causing stenosis or occlusion. This unusual vascular disease process was confirmed 90 years ago9 as a cause of large brain infarctions in patients with SCD, typically children, and confirmed with arterial studies much later. In the mid-1980s, a confluence of factors, from disparate worlds, led to the work herein described. Aaslid et al introduced the transcranial Doppler (TCD) for detection of intracranial artery vasospasm in 1982 based on experience in Norway.10 Interest in this tool was at first manifested in neurosurgery but soon its potential as a noninvasive way to assess intracranial arteries became …

Intracranial Vasospasm Following Temporal Lobe Epilepsy Surgery Demonsrated on Conventional Angiography (P03.137)

Intracranial Vasospasm Following Temporal Lobe Epilepsy Surgery Demonsrated on Conventional Angiography (P03.137)

Spinal Hemorrhage Leading to Cerebral Vasospasm and Infarction

Only one case of intracranial arterial vasospasm resulting cerebral infarction was previously described in the setting of spinal hemorrhage. The speculation of such symptomatic vasospasm being caused by an intracranial extension of the spinal hemorrhage has been unproven. Here we describe two patients with extensive spinal hemorrhage demonstrated on spinal magnetic resonance imaging (MRI). During their subsequent course, both patients developed cranial signs that included encephalopathy, visual deficit and aphasia. In both cases, small amount of intracranial hemorrhage was detected on head imaging, representing an extension of the spinal hemorrhage. Multiple areas of acute ischemia were seen on brain MRI in both patients. On digital subtraction angiography, diffuse vasospasm of carotid and vertebrobasilar arteries was seen which became normalized prior to discharge. Our report suggests that in treating patients with spinal hemorrhage, physicians need to be aware of possible intracranial hemorrhagic extension and subsequent cerebral vasospasm leading to ischemia. As symptoms of intracranial origin are commonly seen in patients with spinal hemorrhage, the incidence of cerebral vasospasm in this setting could be underestimated. doi: http://dx.doi.org/10.4021/jnr119w

The “seagull cry” in a patient with a cerebral arteriovenous malformation

IntroductionThe “seagull cry” is an acoustic phenomenon heard during duplex ultrasound. It is caused by harmonic covibrations of a vessel wall in the presence of high-velocity blood flow. It has been reported in a few cases of cerebrovascular disease, such as severe intracranial stenosis, vasospasm or carotid-cavernous fistula. Material and methodsA 35-year-old man underwent transcranial color-coded sonography (TCCS) for work-up of a severe new-onset headache. ResultsDoppler spectral analysis of the right intracranial carotid bifurcation revealed multiple pairs of mirror-image parallel strings, and a high-frequency seagull cry was heard. Computed tomography-angiography and magnetic resonance imaging of the brain showed an arteriovenous malformation in the right temporal lobe. DiscussionThe seagull cry is a “musical murmur” with single or multiple frequency that sounds like a musical tone. This is the first report of this phenomenon in a cerebral arteriovenous malformation.

Spinal Hemorrhage Leading to Cerebral Vasospasm and Infarction

Only one case of intracranial arterial vasospasm resulting cerebral infarction was previously described in the setting of spinal hemorrhage. The speculation of such symptomatic vasospasm being caused by an intracranial extension of the spinal hemorrhage has been unproven. Here we describe two patients with extensive spinal hemorrhage demonstrated on spinal magnetic resonance imaging (MRI). During their subsequent course, both patients developed cranial signs that included encephalopathy, visual deficit and aphasia. In both cases, small amount of intracranial hemorrhage was detected on head imaging, representing an extension of the spinal hemorrhage. Multiple areas of acute ischemia were seen on brain MRI in both patients. On digital subtraction angiography, diffuse vasospasm of carotid and vertebrobasilar arteries was seen which became normalized prior to discharge. Our report suggests that in treating patients with spinal hemorrhage, physicians need to be aware of possible intracranial hemorrhagic extension and subsequent cerebral vasospasm leading to ischemia. As symptoms of intracranial origin are commonly seen in patients with spinal hemorrhage, the incidence of cerebral vasospasm in this setting could be underestimated. J Neurol Res. 2012;2(4):164-167 doi: https://doi.org/10.4021/jnr119w

Safety of early endovascular catheterization and intervention through extracranial-intracranial bypass grafts

The goal of this study was to demonstrate feasibility and evaluate technical aspects of early endovascular access through extracranial-intracranial (EC-IC) bypass grafts. Patients undergoing endovascular interventions through the graft in the acute postoperative period following EC-IC bypass are presented. Results, complications, and technical nuances are reviewed. Fourteen endovascular procedures were performed in 5 patients after EC-IC bypass for ruptured aneurysms in 4 patients and posterior circulation ischemia in 1 patient. In 2 patients, a saphenous vein graft (SVG) was used to bypass the common carotid artery (CCA) to the middle cerebral artery (MCA). One patient underwent a superficial temporal artery (STA)-MCA bypass, and in 2 other patients the STA stump was connected to the intracranial circulation via an interposition SVG. The interval from surgery to endovascular intervention spanned 2-18 days; the indication was intracranial vasospasm in all patients. One case involved angioplasty of the proximal anastomosis on postoperative Day 14. All other interventions entailed proximal access through the bypass conduit for intraarterial infusion of vasodilators. Significant vasospasm of the STA itself was encountered in 2 patients during endovascular manipulation, and it was treated with intraarterial nitroglycerin. There were no cases of anastomotic disruption. Endovascular catheterization and intervention involving a recent EC-IC bypass is feasible. The main limitation in this series was catheter-induced vasospasm involving the STA. A vein graft may be the more appropriate option in patients with subarachnoid hemorrhage who may require subsequent endovascular intervention for vasospasm.

Ischemic stroke following intracranial hemorrhage from moyamoya disease

Sir, We read with great interest the article entitled “Ischaemic stroke after acute intracranial hemorrhage in patients with moyamoya disease: six new cases and a short literature review” by Kim et al. [4]. The authors reported six cases of ischemic stroke after intracranial hemorrhage (ICH) from moyamoya disease (MMD), and reviewed the literature. Their review showed that the vast majority of patients (94%) had intraventricular hemorrhages (IVH) without subarachnoid hemorrhage, and revealed that most cerebral infarcts (CI) after ICH from MMD were multiple, large, and cortically involved. The authors suggested that thromboembolism or vasospasm might play a role in the pathogenesis of CI after ICH from MMD. We completely agree with the authors’ findings and wish to provide further comment. We also believe that vasospasm is one of the contributing factors to CI after ICH from MMD. Preventive measures to reduce the risks of CI after ICH from MMD are important, because the optimal treatment strategy remains unclear. Su et al. [6] reported a case of CI after IVH from MMD, and suggested that early perfusion computed tomography (CT) scanning was a powerful tool for identifying patients at high risk of CI. Additionally, Ko et al. [5] reported that IVH volume was a prognostic factor for cerebral vasospasm. We suggest that perfusion CT scanning may be especially useful for predicting cerebral vasospasm in patients with massive IVH from MMD. There is no evidence for the optimal treatment for IVH from MMD; however, dehydration and hypotension should be avoided to prevent CI, regardless of the mechanisms involved [2]. Some authors have reported a relationship between increased intracranial pressure and cerebral vasospasm [3], and surgical interventions, such as ventricular drainage and/or endoscopic removal of the hematoma, may thus be indicated if increased intracranial pressure is suspected. Nimodipine or nicardipine may also be effective for preventing or treating cerebral vasospasm after ICH from MMD [1]. Further investigations into the optimal methods of predicting, preventing, and treating CI after ICH from MMD are required.

Multidetector-Row CT Angiography of Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Comparison of Bone Subtraction and Standard CT Angiography with Digital Subtraction Angiography

Copyrights © 2011 The Korean Society of Radiology Purpose: To evaluate the usefulness of multidetector-row CT angiography (MDCTA) for the diagnosis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) by comparison of digital subtraction angiography (DSA) and to compare the bone subtraction CT angiography (BS-CTA) and standard CT angiography (S-CTA). Materials and Methods: Thirty-three patients who were treated with intraarterial nimodipine infusion for the cerebral vasospasm after aneurysmal SAH were evaluated with MDCTA and DSA. BS-CTA images were reconstructed from the S-CTA and unenhanced CT source images. A total of 207 vascular segments were evaluated. A fourstep scale for the degree of stenosis was applied for each segment. With DSA as the standard images, BS-CTA and S-CTA images were comparied. Results: On DSA, 56 segments (27%) presented vasospasm. Concordance between the DSA and S-CTA and between DSA and BS-CTA were 94.7% and 82.1%, respectively. Overestimation for the degree of stenosis was shown in 37 segments on BS-CTA and in 8 segments on S-CTA, but underestimated segments were only shown on SCTA (n = 4). Conclusion: MDCTA with standard technique seems to be a useful imaging tool for the evaluation of the cerebral vasospasm after aneurysmal SAH. However, BS-CTA is not needed because of additional radiation and overestimation of the degree of stenosis. Index terms Intracranial Aneurysm Subarachnoid Hemorrhage Vasospasm, Intracranial Cerebral Angiography Tomography, X-Ray Computed Multidetector-Row CT Angiography of Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Comparison of Bone Subtraction and Standard CT Angiography with Digital Subtraction Angiography 동맥류성 거미막밑출혈 후 발생한 뇌혈관 연축의 다중검출기 CT 혈관조영술: 골감산 및 표준기법의 CT 혈관조영술과 디지털감산혈관조영술의 비교

Intracranial vasospasm with delayed ischaemic deficit following epidermoid cyst resection

Intracranial vasospasm following surgical removal of intracranial tumours is rare. To our knowledge there have been no previously reported cases of delayed vasospasm occurring post debulking of epidermoid cysts. We report a case in which vasospasm led to established cerebral infarction 2 weeks postoperatively. MRI and serial magnetic resonance angiography (MRA) reliably show initial multiple stenoses in the vertebral and internal carotid arteries followed by their spontaneous normalisation. MRA imaging is now of sufficient quality to enable it to be a safe and effective means of both looking for vasospasm and monitoring its resolution.

Time-critical neurological emergencies: the unfulfilled role for point-of-care testing

BackgroundNeurological emergencies are common and frequently devastating. Every year, millions of Americans suffer an acute stroke, severe traumatic brain injury, subarachnoid hemorrhage, status epilepticus, or spinal cord injury severe enough to require medical intervention.AimsFull evaluation of the diseases in the acute setting often requires advanced diagnostics, and treatment frequently necessitates transfer to specialized centers. Delays in diagnosis and/or treatment may result in worsened outcomes; therefore, optimization of diagnostics is critical.MethodsPoint-of-care (POC) testing brings advanced diagnostics to the patient’s bedside in an effort to assist medical providers with real-time decisions based on real-time information. POC testing is usually associated with blood tests (blood glucose, troponin, etc.), but can involve imaging, medical devices, or adapting existing technologies for use outside of the hospital. Noticeably missing from the list of current point-of-care technologies are real-time bedside capabilities that address neurological emergencies.ResultsUnfortunately, the lack of these technologies may result in delayed identification of patients of these devastating conditions and contribute to less aggressive therapies than is seen with other disease processes. Development of time-dependent technologies appropriate for use with the neurologically ill patient are needed to improve therapies and outcomes.ConclusionPOC-CENT is designed to support the development of novel ideas focused on improving diagnostic or prognostic capabilities for acute neurological emergencies. Eligible examples include biomarkers of traumatic brain injury, non-invasive measurements of intracranial pressure or cerebral vasospasm, and improved detection of pathological bacteria in suspected meningitis.

Intracranial vasospasm with subsequent stroke after traumatic subarachnoid hemorrhage in a 22-month-old child

Clinical and radiographic evidence of subarachnoid hemorrhage (SAH)-related vasospasm is rare in children and has not been reported in infants. In this report the authors present the case of a 22-month-old child who developed clinically symptomatic, radiographically identifiable vasospasm after traumatic SAH. To the authors' knowledge, this is the first report of vasospasm associated with SAH in a child this young. This 22-month-old boy fell and had a dense SAH. He had a history of surgically corrected craniosynostosis and nonsymptomatic ventriculomegaly. The boy was evaluated for occult vascular lesions using imaging; none were found and normal vessel caliber was noted. Ten days later, the child developed left-sided weakness and a right middle cerebral artery infarct was identified. Evaluation disclosed significant intracranial vasospasm. This diagnosis was supported by findings on CT angiography, transcranial Doppler ultrasonography, MR imaging, and conventional angiography. The child was treated using intraarterial verapamil with a good result, as well as with conventional intensive care measures to reduce vasospasm. This report documents the first known case of intracranial vasospasm with stroke after SAH in a patient under the age of 2 years. This finding is important because it demonstrates that the entity of SAH-associated vasospasm can affect the very young, widening the spectrum of ages susceptible to this condition. This case is also important because it demonstrates that even very young children can respond to conventional therapeutic interventions such as intraarterial verapamil. Thus, clinicians need to be alert to the possibility of vasospasm as a potential diagnosis when evaluating young children with SAH.