Acoustic neurinoma presenting as subarachnoid hemorrhage

1978 ◽  
Vol 49 (4) ◽  
pp. 602-604 ◽  
Author(s):  
Robert K. Gleeson ◽  
John F. Butzer ◽  
Oliver D. Grin

✓ A case of an acoustic neurinoma presenting as a subarachnoid hemorrhage is described. This is the second such case in the literature.

1974 ◽  
Vol 41 (3) ◽  
pp. 391-393 ◽  
Author(s):  
Kevin McCoyd ◽  
Kevin D. Barron ◽  
Robert J. Cassidy

✓An acute subarachnoid hemorrhage arising from a neurinoma of the eighth cranial nerve is reported.


1972 ◽  
Vol 36 (5) ◽  
pp. 548-551 ◽  
Author(s):  
Iftikhar A. Raja

✓ Forty-two patients with aneurysm-induced third nerve palsy are described. After carotid ligation, 58% showed satisfactory and 42% unsatisfactory functional recovery. In some patients the deficit continued to increase even after carotid ligation. Early ligation provided a better chance of recovery of third nerve function. Patients in whom third nerve palsy began after subarachnoid hemorrhage had a poor prognosis. No relationship was noted between the size of the aneurysm and the recovery of third nerve function.


1975 ◽  
Vol 42 (4) ◽  
pp. 457-461 ◽  
Author(s):  
Charles J. Hodge ◽  
Robert B. King

✓ The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports.


1984 ◽  
Vol 61 (6) ◽  
pp. 1009-1028 ◽  
Author(s):  
Lindsay Symon ◽  
Janos Vajda

✓ A series of 35 patients with 36 giant aneurysms is presented. Thirteen patients presented following subarachnoid hemorrhage (SAH) and 22 with evidence of a space-occupying lesion without recent SAH. The preferred technique of temporary trapping of the aneurysm, evacuation of the contained thrombus, and occlusion of the neck by a suitable clip is described. The danger of attempted ligation in atheromatous vessels is stressed. Intraoperatively, blood pressure was adjusted to keep the general brain circulation within autoregulatory limits. Direct occlusion of the aneurysm was possible in over 80% of the cases. The mortality rate was 8% in 36 operations. Six percent of patients had a poor result. Considerable improvement in visual loss was evident in six of seven patients in whom this was a presenting feature, and in four of seven with disturbed eye movements.


2000 ◽  
Vol 93 (5) ◽  
pp. 808-814 ◽  
Author(s):  
Mette K. Schulz ◽  
Lars Peter Wang ◽  
Mogens Tange ◽  
Per Bjerre

Object. The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.Methods. By using low-flow intracerebral microdialysis monitoring, central nervous system extracellular fluid concentrations of glucose, pyruvate, lactate, glutamate, and glycerol were determined in 46 patients suffering from poor-grade SAH. The results in two subgroups were analyzed: those patients with no clinical or radiological signs of cerebral ischemia (14 patients) and those who succumbed to brain death (five patients).Significantly lower levels of energy substrates and significantly higher levels of lactate and neuronal injury markers were observed in patients with severe and complete ischemia when compared with patients without symptoms of ischemia (glucose 0 compared with 2.12 ± 0.15 mmol/L; pyruvate 0 compared with 151 ± 11.5 µmol; lactate 6.57 ± 1.07 compared with 3.06 ± 0.32 mmol/L; glycerol 639 ± 91 compared with 81.6 ± 12.4 µmol; and glutamate 339 ± 53.4 compared with 14 ± 3.33 µmol). Immediately after catheter placement, glutamate concentrations declined over the first 4 to 6 hours to reach stable values. The remaining parameters exhibited stable values after 1 to 2 hours.Conclusions. The results confirm that intracerebral microdialysis monitoring of patients with SAH can be used to detect patterns of cerebral ischemia. The wide range from normal to severe ischemic values calls for additional studies to characterize further incomplete and possible subclinical levels of ischemia.


2004 ◽  
Vol 101 (2) ◽  
pp. 255-261 ◽  
Author(s):  
Christopher Reilly ◽  
Chris Amidei ◽  
Jocelyn Tolentino ◽  
Babak S. Jahromi ◽  
R. Loch Macdonald

Object. This study was conducted for two purposes. The first was to determine whether a combination of measurements of subarachnoid clot volume, clearance rate, and density could improve prediction of which patients experience vasospasm. The second was to determine if each of these three measures could be used independently to predict vasospasm. Methods. Digital files of the cranial computerized tomography (CT) scans obtained in 75 consecutive patients admitted within 24 hours of subarachnoid hemorrhage (SAH) were analyzed in a blinded fashion by an observer who used quantitative imaging software to measure the volume of SAH and its density. Clot clearance rates were measured by quantifying SAH volume on subsequent CT scans. Vasospasm was defined as new onset of a focal neurological deficit or altered consciousness 5 to 12 days after SAH in the absence of other causes of deterioration, diagnosed with the aid of or exclusively by confirmatory transcranial Doppler ultrasonography and/or cerebral angiography. Univariate analysis showed that vasospasm was significantly associated with the SAH grade as classified on the Fisher scale, the initial clot volume, initial clot density, and percentage of clot cleared per day (p < 0.05). In multivariate analysis, initial clot volume and percentage of clot cleared per day were significant predictors of vasospasm (p < 0.05), whereas Fisher grade and initial clot density were not. Conclusions. Quantitative analysis of subarachnoid clot shows that vasospasm is best predicted by initial subarachnoid clot volume and the percentage of clot cleared per day.


1983 ◽  
Vol 59 (6) ◽  
pp. 917-924 ◽  
Author(s):  
Ken Kamiya ◽  
Hideyuki Kuyama ◽  
Lindsay Symon

✓ A baboon model of subarachnoid hemorrhage (SAH) has been developed to study the changes in cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral edema associated with the acute stage of SAH. In this model, hemorrhage was caused by avulsion of the posterior communicating artery via a periorbital approach, with the orbit sealed and ICP restored to normal before SAH was produced. Local CBF was measured in six sites in the two hemispheres, and ICP monitored by an implanted extradural transducer. Following sacrifice of the animal, the effect of the induced SAH on ICP, CBF, autoregulation, and CO2 reactivity in the two hemispheres was assessed. Brain water measurements were also made in areas of gray and white matter corresponding to areas of blood flow measurements, and also in the deep nuclei. Two principal patterns of ICP change were found following SAH; one group of animals showed a return to baseline ICP quite quickly and the other maintained high ICP for over an hour. The CBF was reduced after SAH to nearly 20% of control values in all areas, and all areas showed impaired autoregulation. Variable changes in CO2 reactivity were evident, but on the side of the hemorrhage CO2 reactivity was predominantly reduced. Differential increase in pressure lasting for over 7 minutes was evident soon after SAH on the side of the ruptured vessel. There was a significant increase of water in all areas, and in cortex and deep nuclei as compared to control animals.


1994 ◽  
Vol 80 (3) ◽  
pp. 476-483 ◽  
Author(s):  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Hirofumi Oyama ◽  
Toshihiko Tanazawa ◽  
Masakazu Takayasu ◽  
...  

✓ To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 µmol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.


1996 ◽  
Vol 85 (3) ◽  
pp. 410-418 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Neal F. Kassell ◽  
Teresa P. Germanson ◽  
Gail L. Kongable ◽  
Laura L. Truskowski ◽  
...  

✓ Advanced age is a recognized prognostic indicator of poor outcome after subarachnoid hemorrhage (SAH). The relationship of age to other prognostic factors and outcome was evaluated using data from the multicenter randomized trial of nicardipine in SAH conducted in 21 neurosurgical centers in North America. Among the 906 patients who were studied, five different age groups were considered: 40 years or less, 41 to 50, 51 to 60, 61 to 70, and more than 71 years. Twenty-three percent of the individuals enrolled were older than 60 years of age. Women outnumbered men in all age groups. Level of consciousness (p = 0.0002) and World Federation of Neurological Surgeons grade (p = 0.0001) at admission worsened with advancing age. Age was also related to the presence of a thick subarachnoid clot (p = 0.0001), intraventricular hemorrhage (p = 0.0003), and hydrocephalus (p = 0.0001) on an admission computerized tomography scan. The rebleeding rate increased from 4.5% in the youngest age group to 16.4% in patients more than 70 years of age (p = 0.002). As expected, preexisting medical conditions, such as diabetes (p = 0.028), hypertension (p = 0.0001), and pulmonary (p = 0.0084), myocardial (p = 0.0001), and cerebrovascular diseases (p = 0.0001), were positively associated with age. There were no age-related differences in the day of admission following SAH, timing of the surgery and/or location, and size (small vs. large) of the ruptured aneurysm. During the treatment period, the incidence of severe complications (that is, those complications considered life threatening by the reporting investigator) increased with advancing age, occurring in 28%, 33%, 36%, 40%, and 46% of the patients in each advancing age group, respectively (p = 0.0002). No differences were observed in the reported frequency of surgical complications. No age-related differences were found in the overall incidence of angiographic vasospasm; however, symptomatic vasospasm was more frequently reported in the older age groups (p = 0.01). Overall outcome, assessed using the Glasgow Outcome Scale at 3 months post-SAH, was poorer with advancing age (p < 0.001). Multivariate analysis of overall outcome, adjusting for the different prognostic factors, did not remove the age effect, which suggests that the aging brain has a less optimal response to the initial bleeding. Age as a risk factor is a continuum; however, there seems to be a significant increased risk of poor outcome after the age of 60 years.


1993 ◽  
Vol 78 (4) ◽  
pp. 548-553 ◽  
Author(s):  
E. Clarke Haley ◽  
Neal F. Kassell ◽  
James C. Torner ◽  
_ _

✓ Calcium antagonist drugs were proposed for use in patients with recent aneurysmal subarachnoid hemorrhage (SAH) because of their ability to block the effects of a wide variety of vasoconstrictor substances on cerebral arteries in vitro. It was suggested that these agents might, therefore, be useful in ameliorating cerebral vasospasm and its ischemic consequences which frequently complicate SAH. This hypothesis was tested in an arm of a randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine in patients with recently ruptured aneurysms. Participating investigators were required to send selected copies of all admission and follow-up angiograms obtained between Days 7 and 11 following hemorrhage (the peak period of risk for vasospasm) to the Central Registry of the Cooperative Aneurysm Study for blinded interpretation and review for the presence and severity of angiographic vasospasm. In centers with transcranial Doppler ultrasound (TCD) capabilities, middle cerebral artery (MCA) mean flow velocities were measured and recorded. Angiograms obtained between Days 7 and 11 were available for 103 (23%) of 449 patients receiving nicardipine and 121 (26%) of 457 receiving placebo. There was a balance of prognostic factors for vasospasm between the groups. Fifty-one percent of placebo-treated patients had moderate or severe vasospasm on “Day 7–11 angiograms” compared to 33% of nicardipine-treated patients. This difference is statistically significant (p < 0.01). Sixty-seven (49%) of 137 placebo-treated patients examined with TCD between Days 7 and 11 had mean MCA flow velocities exceeding 120 cm/sec compared to 26 (23%) of 112 nicardipine-treated patients (significant difference, p < 0.001). These data suggest that high-dose intravenous nicardipine reduces the incidence and severity of delayed cerebral arterial narrowing in patients following aneurysmal SAH.


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