Cortical cellular response in acute subarachnoid hemorrhage

1980 ◽  
Vol 52 (4) ◽  
pp. 456-462 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
David Kornhauser

✓ Acute subarachnoid hemorrhage (SAH) over the cerebral cortex causes single or multiple waves of cellular depolarization, which may occur in a self-propagating, reverberating fashion. This process is characterized by a massive K+ release and transient depression in electrocortical activity. The K+ levels in the extracellular space reach magnitudes known to substantially affect the membrane potentials of neurons and glia, and may cause a release of neurotransmitters from depolarized presynaptic terminals. The release of K+ may be the initial step in the development of cellular edema and, together with a multitude of other chemical and biochemical changes taking place at the cellular level, may underlie the loss of autoregulation. Cortical cells rather than blood vessels are the primary targets in the initial stages of SAH, and ischemia does not play a causal role in the pathogenesis of cellular dysfunction during this stage.

1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.


1982 ◽  
Vol 57 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Ram Kossowsky ◽  
Manuel Dujovny ◽  
Nir Kossovsky ◽  
Yves Keravel

✓ A 16-year-old girl died from an acute subarachnoid hemorrhage following the fracture of a blade of a Heifetz aneurysm clip. The clip was manufactured from 17-7PH steel, which on metallurgical testing was found to be highly sensitive to intergranular corrosion. The fracture mechanism was stress corrosion, brought on by the combination of a stress load, an electrolytic environment, and a susceptible steel.


2005 ◽  
Vol 103 (4) ◽  
pp. 649-655 ◽  
Author(s):  
Ichiro Yuki ◽  
Yuichi Murayama ◽  
Fernando Viñuela

Object. The authors report on a series of 29 patients presenting with acute subarachnoid hemorrhage (SAH) related to the rupture of a vertebrobasilar dissecting aneurysm. Special attention was focused on embolization techniques and immediate and midterm anatomical and clinical outcomes. Methods. Between March 1994 and January 2003, 29 patients presented with acute SAH caused by the rupture of a vertebrobasilar dissecting aneurysm. Eleven patients (37.9%) had Hunt and Hess Grade I SAH, four (13.8%) Grade II, six (20.7%) Grade III, five (17.2%) Grade IV, and three (10.3%) Grade V. Aneurysms were classified into five groups based on lesion location, and treatment courses were decided. All patients except two were treated by endovascular trapping of the aneurysm with concomitant occlusion of the involved vertebral artery (VA). No technical or clinical complication was observed in 28 patients (97%). Aneurysm perforation occurred during the procedure in one patient (3%). There was evidence of aneurysm recanalization in one patient. One patient with Hunt and Hess Grade IV SAH and two patients with Grade V SAH died. One patient died of respiratory infection 1 year after aneurysm trapping. One patient presented with a recurrent hemorrhage 1 month after treatment and died. Overall morbidity and mortality rates were 13.8 and 17.2%, respectively. Conclusions. Twenty-nine patients with acute SAH due to rupturing of vertebrobasilar dissecting aneurysms were treated using endovascular techniques. In most cases, endovascular trapping of the aneurysm and concomitant occlusion of the VA was technically and clinically successful.


1982 ◽  
Vol 56 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
David Kornhauser

✓ Local experimental subarachnoid hemorrhage (SAH) was produced over the cerebral cortex in 15 cats. The cellular response was monitored using ion-specific electrodes for extracellular potassium (K+) and calcium (Ca++) activity, DC cortical potential, and electrocorticogram. The response was characterized by a profound cellular depolarization and extracellular calcium (Ca++) depletion which accompanied extracellular potassium (K+) accumulation. The prehemorrhage baseline calcium levels measured 1.14 ± 0.11 mM, and were lowered to 0.4 to 0.7 mM/liter in different experiments. The K+ accumulation reached levels between 16 and 31 mM from a baseline of 3.17 ± 0.52 mM and were cleared to normal or nearly normal within 5 minutes. The Ca++ levels also returned to normal within 5 minutes, but remained depressed for the duration of the experiment in two animals. These results confirm that blood extravasated into the subarachnoid space has a direct effect on parenchymal elements. The combination of transient K+ elevations and calcium depression may play an important role in the development of vascular spasm by inducing or facilitating a contraction in the muscular layer in the wall of major intracranial vessels.


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.


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