scholarly journals Effect of hyperdynamic therapy by albumin infusion on patients with neurological deficits associated with cerebral vasospasm

Nosotchu ◽  
1982 ◽  
Vol 4 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Takeshi Saito ◽  
Takamaru Tanabe ◽  
Seiji Morii ◽  
Hiroshi Takagi ◽  
Kenzoh Yada
Keyword(s):  
Cerebral Vasospasm ◽  
Neurological Deficits ◽  
Albumin Infusion ◽  
Hyperdynamic Therapy

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.

Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans

1977 ◽  
Vol 46 (4) ◽  
pp. 446-453 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
John O. Eichling ◽  
Mokhtar H. Gado
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Blood Volume ◽  
Cerebral Vasospasm ◽  
Cerebral Blood Volume ◽  
Neurological Deficits ◽  
Regional Cerebral Blood ◽  
Oxygen Utilization ◽  
Ruptured Intracranial Aneurysm ◽  
Regional Cerebral Blood Volume

✓ Forty-five studies of regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), and regional cerebral oxygen utilization (rCMRO2) were performed in 30 patients undergoing diagnostic cerebral angiography for evaluation of a subarachnoid hemorrhage due to a ruptured intracranial aneurysm. Tracer methods employing radioactive oxygen-15 were used to measure rCBV, rCBF, and rCMRO2. The patient studies were divided into groups based on their neurological status and the presence or absence of cerebral vasospasm. Subarachnoid hemorrhage, with and without vasospasm, produced significant decreases in CBF and CMRO2. In general, patients with more severe neurological deficits, and patients with more severe degrees of vasospasm, had a more marked depression of CBF and CMRO2. The most striking finding was a significant (p < 0.001) increase in CBV (to 58% above normal) in patients with severe neurological deficits associated with severe cerebral vasospasm. This large increase suggests that cerebral vasospasm consists of constriction of the large, radiographically visible extraparenchymal vessels accompanied by a massive dilation of intraparenchymal vessels.

Successful treatment of severe cerebral vasospasm following hemorrhage of an arteriovenous malformation

2009 ◽  
Vol 4 (3) ◽  
pp. 266-269 ◽  
Author(s):  
Arjun V. Pendharkar ◽  
Raphael Guzman ◽  
Robert Dodd ◽  
David Cornfield ◽  
Michael S. B. Edwards
Keyword(s):  
Differential Diagnosis ◽  
Arteriovenous Malformation ◽  
Cerebral Vasospasm ◽  
Balloon Angioplasty ◽  
Cerebral Angiography ◽  
Intraventricular Hemorrhage ◽  
Mr Angiography ◽  
Neurological Deficits ◽  
Aggressive Treatment ◽  
Initial Recovery

The authors describe the case of a 13-year-old boy who presented with an intraventricular hemorrhage caused by a left trigonal arteriovenous malformation. After an initial recovery, the patient experienced complete right-sided paresis on posthemorrhage Day 6. Severe cerebral vasospasm was found on MR angiography and confirmed on conventional cerebral angiography. Intraarterial nicardipine injection and balloon angioplasty were successfully performed with improved vasospasm and subsequent neurological recovery. Cerebral vasospasm should be considered in the differential diagnosis for neurological deterioration following an arteriovenous malformation hemorrhage, and aggressive treatment can be administered to prevent ischemia and further neurological deficits.

scholarly journals Persistent Autoregulatory Disturbance after Angioplasty for Cerebral Vasospasm

2002 ◽  
Vol 8 (4) ◽  
pp. 409-415 ◽  
Author(s):  
D.K. Song ◽  
M.R. Harrigan ◽  
J.P. Deveikis ◽  
J.E. McGillicuddy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Cerebral Vasospasm ◽  
Artery Aneurysm ◽  
Response To Therapy ◽  
Large Artery ◽  
Xenon Ct ◽  
Symptomatic Vasospasm ◽  
Hyperdynamic Therapy

Hyperdynamic therapy, consisting of hypervolemia, haemodilution, and hypertension, is an established treatment for cerebral vasospasm following subarachnoid haemorrhage. Angioplasty has emerged as an additional, effective treatment for symptomatic vasospasm. Loss of autoregulation, however, can occur despite effective angioplasty, underscoring the need for treatment with hyperdynamic therapy in combination with angioplasty. A 43-year-old woman underwent endovascular coiling of a ruptured left posterior communicating artery aneurysm. The patient went on to develop symptomatic vasospasm and was treated with hyperdynamic therapy and angioplasty. Autoregulation was assessed with xenon CT cerebral blood flow (CBF) measurement. An initial CBF study was obtained when the patient received dopamine and dobutamine infusions to maintain systolic blood pressure at 160 mmHg. The vasopressor drips were then temporarily held for twenty minutes, allowing the patient's systolic blood pressure to drop to 140 mmHg, and a repeat CBF study was obtained. Several days after angioplasty, CBF decreased significantly when the patient was taken off vasopressors, indicating impaired autoregulation. Hyperdynamic therapy was continued, and another CBF study one week later showed a return of autoregulation and normalization of CBF without induced hypertension. Autoregulation is disturbed during vasospasm. Although angioplasty can improve large artery blood flow during vasospasm, hyperdynamic therapy is also needed to maintain cerebral perfusion, particularly in the face of impaired autoregulation. Quantitative CBF measurement permits the maintenance of optimal CBF and monitoring of response to therapy.

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.

Treatment of Patients with Neurological Deficits Associated with Cerebral Vasospasm by Intravascular Volume Expansion

Neurosurgery ◽  
1978 ◽  
Vol 3 (3) ◽  
pp. 364-368 ◽  
Author(s):  
Michael B. Pritz ◽  
Steven L. Giannotta ◽  
Glenn W. Kindt ◽  
John E. McGillicuddy ◽  
Richard L. Prager
Keyword(s):  
Cerebral Vasospasm ◽  
Volume Expansion ◽  
Neurological Deficits ◽  
Intravascular Volume

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.

Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage

2017 ◽  
Vol 55 (4) ◽  
pp. 2763-2779 ◽  
Author(s):  
Mohamad El Amki ◽  
Martine Dubois ◽  
Antoine Lefevre-Scelles ◽  
Nicolas Magne ◽  
Mélanie Roussel ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mouse Model ◽  
Cerebral Vasospasm ◽  
Neurological Deficits
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