Cerebral Vasospasm After Transsphenoidal Resection of Pituitary Macroadenomas

2012 ◽  
Vol 71 (suppl_1) ◽  
pp. ons173-ons181 ◽  
Author(s):  
Ajit S. Puri ◽  
Gabriel Zada ◽  
Hekmat Zarzour ◽  
Edward Laws ◽  
Kai Frerichs
Keyword(s):  
Cerebral Vasospasm ◽  
De Novo ◽  
Early Recognition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Significant Risk ◽  
Neurological Deficits ◽  
Delayed Cerebral Vasospasm ◽  
Neurological Morbidity ◽  
Pituitary Macroadenomas ◽  
Transsphenoidal Resection

Abstract BACKGROUND: Delayed ischemic events due to vasospasm are a well-known complication of aneurysmal subarachnoid hemorrhage (SAH). Severe vasospasm in other neurosurgical settings is not as well recognized. Delay in diagnosis and treatment of vasospasm in such settings may be associated with significant neurological morbidity. OBJECTIVE: To present three cases of symptomatic delayed cerebral vasospasm after transsphenoidal resection of pituitary macroadenomas. METHODS: Transsphenoidal resection in all cases was complicated by peritumoral hemorrhage with extension into the subarachnoid space. Two of the 3 patients required re-operation to evacuate the hematoma in the tumor bed because of progressive worsening neurological deficits. RESULTS: All 3 patients developed vasospasm of the intracranial vessels, starting as early as postoperative day 5 and appearing as late as postoperative day 10. Comparisons to the non-vascular pre-operative magnetic resonance imaging studies confirmed the “de-novo” nature of the vasospasm based on the caliber of the flow voids. CONCLUSION: Transsphenoidal surgery complicated by peritumoral hemorrhage is associated with a significant risk of neurological morbidity because of delayed cerebral vasospasm. Early recognition and management according to guidelines used for postaneurysmal SAH may help to improve outcomes in these patients.

scholarly journals Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

2009 ◽  
Vol 26 (3) ◽  
pp. E6 ◽  
Author(s):  
Christopher S. Eddleman ◽  
Michael C. Hurley ◽  
Andrew M. Naidech ◽  
H. Hunt Batjer ◽  
Bernard R. Bendok
Keyword(s):  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Mortality Rates ◽  
Neurological Deficits ◽  
Acute Management ◽  
Treatment Algorithms ◽  
Angiographic Evidence ◽  
Intraarterial Therapy ◽  
Clinical Changes

The second leading cause of death and disability in patients with aneurysmal subarachnoid hemorrhage (SAH) is delayed cerebral ischemia due to vasospasm. Although up to 70% of patients have been shown to have angiographic evidence of vasospasm, only 20–30% will present with clinical changes, including mental status changes and neurological deficits that necessitate acute management. Endovascular capabilities have progressed to become viable options in the treatment of cerebral vasospasm. The rationale for intraarterial therapy includes the fact that morbidity and mortality rates have not changed in recent years despite optimized noninvasive medical care. In this report, the authors discuss the most common endovascular options—namely intraarterial vasodilators and transluminal balloon angioplasty—from the standpoint of mechanism, efficacy, limitations, and complications as well as the treatment algorithms for cerebral vasospasm used at our institution.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

scholarly journals Matrix Metalloproteinases in Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Vivek Mehta ◽  
Jonathan Russin ◽  
Alexandra Spirtos ◽  
Shuhan He ◽  
Peter Adamczyk ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Matrix Metalloproteinases ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Critical Role ◽  
Morbidity And Mortality ◽  
Cellular Mechanisms ◽  
Delayed Cerebral Vasospasm ◽  
Membrane Bound ◽  
Existing Data

Delayed cerebral vasospasm is a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). While the cellular mechanisms underlying vasospasm remain unclear, it is believed that inflammation may play a critical role in vasospasm. Matrix metalloproteinasees (MMPs) are a family of extracellular and membrane-bound proteases capable of degrading the blood-rain barrier (BBB). As such, MMP upregulation following SAH may result in a proinflammatory extravascular environment capable of inciting delayed cerebral vasospasm. This paper presents an overview of MMPs and describes existing data pertinent to delayed cerebral vasospasm.

scholarly journals The natural history of cerebral cavernous malformations in children

2016 ◽  
Vol 17 (2) ◽  
pp. 123-128 ◽  
Author(s):  
Bradley A. Gross ◽  
Rose Du ◽  
Darren B. Orbach ◽  
R. Michael Scott ◽  
Edward R. Smith
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Natural History ◽  
Significant Risk ◽  
Neurological Deficits ◽  
Cerebral Cavernous Malformations ◽  
Similar Data ◽  
Cavernous Malformations ◽  
Neurological Morbidity ◽  
History Of

OBJECT Cerebral cavernous malformations (CMs) are a source of neurological morbidity from seizures and focal neurological deficits due to mass effect and hemorrhage. Although several natural history reports exist for adults with CMs, similar data for pediatric patients are limited. METHODS The authors reviewed hospital databases to identify children with CMs who had not been treated surgically and who had clinical and radiological follow-up. Annual hemorrhage rates were calculated in lesion-years, and risk factors were assessed using the Cox proportional hazards model. RESULTS In a cohort of 167 patients with 222 CMs, the mean patient age at the time of diagnosis was 10.1 years old (SD 6.0). Ninety patients (54%) were male. One hundred four patients (62%) presented with hemorrhage from at least 1 CM, 58 (35%) with seizures with or without CM hemorrhage, and 43 (26%) with incidental lesions. Twenty-five patients (15%) had multiple CMs, 17 (10%) had a family history of CMs, and 33 (20%) had radiologically apparent developmental venous anomalies (DVAs). The overall annual hemorrhage rate was 3.3%. Permanent neurological morbidity was 29% per hemorrhage, increasing to 45% for brainstem, thalamic, or basal ganglia CM and decreasing to 15% for supratentorial lobar or cerebellar lesions. The annual hemorrhage rate for incidental CMs was 0.5%; for hemorrhagic CMs, it was 11.3%, increasing to 18.2% within the first 3 years. Hemorrhage clustering within 3 years was statistically significant (HR 6.1, 95% CI 1.72–21.7, p = 0.005). On multivariate analysis, hemorrhagic presentation (HR 4.63, 95% CI 1.53–14.1, p = 0.007), brainstem location (HR 4.42, 95% CI 1.57–12.4, p = 0.005), and an associated radiologically apparent DVA (HR 2.91, 95% CI 1.04–8.09, p = 0.04) emerged as significant risk factors for hemorrhage, whereas age, sex, CM multiplicity, and CM family history did not. CONCLUSIONS Prior hemorrhage, brainstem location, and associated DVAs are significant risk factors for symptomatic hemorrhage in children with CMs. Hemorrhage clustering within the first 3 years of a bleed can occur, a potentially important factor in patient management and counseling.

scholarly journals Long-acting statin for aneurysmal subarachnoid hemorrhage: A randomized, double-blind, placebo-controlled trial

2017 ◽  
Vol 38 (7) ◽  
pp. 1190-1198 ◽  
Author(s):  
Masato Naraoka ◽  
Naoya Matsuda ◽  
Norihito Shimamura ◽  
Kenichiro Asano ◽  
Kenichi Akasaka ◽  
...  
Keyword(s):  
Placebo Group ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Controlled Trial ◽  
Delayed Cerebral Ischemia ◽  
Pleiotropic Effects ◽  
Neurological Deficits ◽  
Double Blind ◽  
Long Acting

Statins have pleiotropic effects that are considered beneficial in preventing cerebral vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (aSAH). Many studies using statins have been performed but failed to show remarkable effects. We hypothesized that a long-acting statin would be more effective, due to a longer half-life and stronger pleiotropic effects. Patients with aSAH were randomly assigned to a pitavastatin group (4 mg daily; n = 54) and a placebo group ( n = 54) after repair of a ruptured aneurysm. The primary efficacy end point was vasospasm-related delayed ischemic neurological deficits (DIND), and the secondary end points were cerebral vasospasm evaluated by digital subtraction angiography (DSA), vasospasm-related new cerebral infarctions, and outcome at three months. Severe cerebral vasospasms on DSA were statistically fewer in the pitavastatin group than in the placebo group (14.8% vs. 33.3%; odds ratio, 0.32; 95% confidence interval, 0.11–0.87, p = 0.042); however, the occurrence of DIND and new infarctions and outcome showed no statistically significant differences between the groups. The present study is the first to prove the definite, statin-induced amelioration of cerebral vasospasm on DSA. However, administration of any type of statin at the acute phase of aSAH is not recommended.

Individual variations in response of human cerebral arterioles to vasoactive substances, human plasma, and CSF from patients with aneurysmal SAH

1981 ◽  
Vol 55 (3) ◽  
pp. 431-437 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt
Keyword(s):  
Human Plasma ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Vessel ◽  
Content Type ◽  
Vasoactive Substances ◽  
Delayed Cerebral Vasospasm ◽  
Prostaglandin F ◽  
Cerebral Arterioles

✓ The capricious appearance of delayed cerebral vasospasm in some but not all patients with an aneurysmal subarachnoid hemorrhage (SAH) was the stimulus for studying the reactivity of human cerebral arterioles in vitro to various vasoactive agents (prostaglandin F2a, noradrenaline, serotonin, human plasma, and cerebrospinal fluid from patients with aneurysmal SAH). There was a marked variability in response between arterioles from different individuals. The finding of a markedly individual profile in terms of reactivity toward vasoactive substances emphasizes the importance of a human cerebral vessel wall factor in the pathogenesis of cerebral vasospasm.

Effects of ML-9 on experimental delayed cerebral vasospasm

1989 ◽  
Vol 71 (6) ◽  
pp. 916-922 ◽  
Author(s):  
Kiyokazu Kokubu ◽  
Eiichi Tani ◽  
Masaru Nakano ◽  
Nobutaka Minami ◽  
Hideki Shindo
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Canine Model ◽  
Neurological Deficits ◽  
Content Type ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Blood ◽  
Complete Reversal ◽  
The Mean ◽  
Dose Dependent

✓ Experimental delayed cerebral vasospasm was produced in a two-hemorrhage canine model. The spastic basilar artery was exposed via the transclival route under a surgical microscope, and was dilated by the topical application of 1-(5-chloronaphthalenesulfonyl)-1H-hexa-hydro-1,4-diazepine(ML-9), a selective antagonist of myosin light chain kinase. Dilation was dose-dependent, with a median effective dose (± standard deviation) of 51.4 ± 6.9 µM. In addition, 50 µM of ML-9 was injected into the cisterna magna until the intracranial pressure (ICP) reached 200 mm H2O for 30 minutes, including a complete reversal of angiographic delayed vasospasm in three of seven dogs; in contrast, 150 µM of ML-9 was infused at 1.52 ml/min into the vertebral artery for 30 minutes, producing little dilation of the spastic basilar artery. In another study, the intracisternal perfusion of 50 µM of ML-9 at 1.48 ml/min for 30 minutes in dogs with an ICP of less than 200 mm H2O produced no serious electroencephalographic abnormalities, and the mean arterial blood pressure and pulse rate remained normal; no neurological deficits or significant histological abnormalities ascribable to the intracisternal ML-9 were found.

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