Comparison of Symptomatic Vasospasm after Surgical Clipping and Endovascular Coiling

Vasospasm, initial neurological damage, rebleeding, and periprocedural complications are associated prognostic factors for clinical outcomes after aneurysmal subarachnoid hemorrhage (SAH). In this study, factors related to delayed ischemic neurological deficit (DIND) are evaluated using data from our institute for the last 18 years. Data from 2001 to 2018 of patients with aneurysmal SAH who underwent surgical clipping (SC) or endovascular coiling (EC) within 7 days of onset were retrospectively analyzed. Cases of mortality within 5 days after treatment were excluded. Multivariate analysis was used to identify the risk factors for DIND. In total, 840 cases of SAH were assessed; among these cases, 384 (45.7%) and 456 (54.3%) were treated with SC and EC, respectively. The frequency of DIND in the EC group was significantly less than that in the SC group (11.8% vs. 17.7%; p = 0.016). In the results of multivariate analysis, internal carotid artery (ICA) aneurysm and hemorrhagic complications were the risk factors for DIND. Cilostazol administration and EC were significant factors for vasospasm prevention after aneurysmal SAH (odds ratio of ICA aneurysm: 1.59, hemorrhagic complications: 1.76, SC: 1.51, and cilostazol administration: 0.51, respectively). Cilostazol administration was also a significant factor in patients who were treated with EC. ICA aneurysm, treatment strategy, hemorrhagic complications, and cilostazol administration were associated with DIND. Oral administration of cilostazol and avoiding hemorrhagic complications were effective in DIND prevention. If both treatments are available for ruptured aneurysms, clinicians should choose EC on the basis of its ability to prevent DIND.     

Clinical outcomes of aneurysmal subarachnoid hemorrhage patients treated with oral diltiazem and limited intensive care management

BACKGROUND: Aneurysmal subarachnoid hemorrhage (SAH) patients are frequently treated with prophylactic nimodipine and undergo invasive monitoring of blood pressure and volume status in an intensive care unit (ICU) setting to decrease the incidence of delayed ischemic neurological deficit (DIND) and improve functional outcomes. The goal of this study was to examine the incidence of DIND and poor functional outcomes in a consecutive series of SAH patients treated with a different regimen of prophylactic oral diltiazem and limited use of intensive care monitoring. METHODS: The study involved a consecutive series of 123 aneurysmal SAH patients treated by the senior author who were admitted within 72 hours of hemorrhage and who never received nimodipine or nicardipine. Functional outcomes were graded using the Glasgow Outcome Scale (GOS). RESULTS: Of the 123 patients identified, favorable outcomes (GOS 4 and 5) were achieved in 74.8%. The incidence of DIND was 19.5%. Hypertensive, hypervolemic, hemodilutional (HHH) therapy was used in 10 patients (8.1%) and no patients were treated for DIND by endovascular means. Seven patients (5.7%) had a poor functional outcome or death because of DIND and two of these were related to complications of HHH therapy. These results were compared to contemporary series of SAH patients managed with other treatment protocols. CONCLUSIONS: Functional outcomes of patients treated with a regimen of oral diltiazem, limited use of ICU monitoring and HHH therapy for DIND compare favorably with other contemporary series of SAH patients.     

The prophylactic use of transluminal balloon angioplasty in patients with Fisher Grade 3 subarachnoid hemorrhage: a pilot study.

OBJECT: Recent advances in neuroradiology have made it possible to dilate vasospastic human cerebral arteries after aneurysmal subarachnoid hemorrhage (SAH), but the time window is short and the success rate for reversal of delayed ischemic neurological deficits (DINDs) varies between 31% and 77%. In a dog model of vasospasm, transluminal balloon angioplasty (TBA) performed on Day 0 totally prevented the development of angiographically demonstrated narrowing on Day 7. Because the effect of preventive TBA in this animal model was better than any pharmacological treatment described previously for experimental vasospasm, the authors conducted a pilot trial in humans to assess the safety and efficacy of TBA performed within 3 days of SAH. METHODS: The study group consisted of 13 patients with Fisher Grade 3 SAH who had a very high probability of developing vasospasm. In all patients, regardless of the site of the ruptured aneurysm, target vessels for prophylactic TBA were as follows: the internal carotid artery, A1 segment, M1 segment, and P1 segment bilaterally; the basilar artery; and one vertebral artery. Prophylactic TBA was considered satisfactory when it could be performed in at least two of the three parts of the intracranial circulation (right and/or left carotid system and/or vertebrobasilar system), and included the aneurysm-bearing part of the circulation. Of the 13 patients, none developed a DIND or more than mild vasospasm according to transcranial Doppler ultrasonography criteria. At 3 months posttreatment eight patients had made a good recovery, two were moderately disabled, and three had died; one patient died because of a vessel rupture during TBA and two elderly individuals died of medical complications associated with poor clinical condition on admission. CONCLUSIONS: Compared with large series of patients with aneurysmal SAH reported in the literature, the results of this pilot study indicate an extremely low incidence of vasospasm and DIND after treatment with prophylactic TBA. A larger randomized study is required to determine whether prophylactic TBA is efficacious enough to justify the risks, and which vessels need to be dilated prophylactically.     

Delayed neurological deficits detected by an ischemic pattern in the extracellular cerebral metabolites in patients with aneurysmal subarachnoid hemorrhage

OBJECT: In the treatment of patients with aneurysmal subarachnoid hemorrhage (SAH), early occlusion of the aneurysm is necessary as well as monitoring and treatment of complications following the primary bleeding episode. Monitoring with microdialysis has been studied for its ability to indicate and predict the occurrence of delayed ischemic neurological deficits (DINDs) in patients with SAH. METHODS: In 42 patients with aneurysmal SAH microdialysis monitoring of metabolites was performed using a 0.3-microl/minute perfusion flow over several days, and the results were correlated to clinical events and to brain infarction observed on computerized tomography scans. The microdialysis probe was inserted into the territory of the parent artery of the aneurysm. The authors defined an ischemic pattern as increases in the lactate/glucose (L/G) and lactate/pyruvate (L/P) ratios that were greater than 20% followed by a 20% increase in glycerol concentration. This ischemic pattern was found in 17 of 18 patients who experienced a DIND and in three of 24 patients who did not experience a delayed clinical deterioration. The ischemic pattern preceded the occurrence of a DIND by a mean interval of 11 hours. Maximum L/G and L/P ratios did not correlate with the presence of DIND or outcome, and there was no association between the glycerol level and subsequent brain infarction. CONCLUSIONS: Microdialysis monitoring of the cerebral metabolism in patients with SAH may predict with high sensitivity and specificity the occurrence of a DIND. Whether an earlier diagnosis results in better treatment of DINDs and, therefore, in overall better outcomes remains to be proven, as it is linked to an efficacious treatment of cerebral vasospasm.     

No effect of enoxaparin on outcome of aneurysmal subarachnoid hemorrhage: a randomized, double-blind, placebo-controlled clinical trial

OBJECT: From the moment an intracranial aneurysm ruptures, cerebral blood flow is impaired, and this impairment mainly determines the outcome in patients who survive after the initial bleeding. The exact mechanism of impairment is unknown, but activation of coagulation and fibrinolysis correlate with clinical condition and outcome after aneurysmal subarachnoid hemorrhage (SAH). The purpose of this study was to determine whether enoxaparin, a low-molecular-weight heparin, which is a well-known anticoagulating agent, has any effect on the outcome of aneurysmal SAH postoperatively. METHODS: In this randomized, double-blind, single-center clinical trial, 170 patients (85 per group) with aneurysmal SAH were randomly assigned to receive either enoxaparin (40 mg subcutaneously once daily) or a placebo, starting within 24 hours after occlusion of the aneurysm and continuing for 10 days. Analysis was done on an intention-to-treat basis. Outcome was assessed at 3 months on both the Glasgow Outcome and modified Rankin Scales. Patients were eligible for the study if surgery was performed within 48 hours post-SAH, and no intracerebral hemorrhage was larger than 20 mm in diameter on the first postoperative computerized tomography scan. At 3 months, there were no significant differences in outcome by treatment group. Of the 170 patients, 11 (6%) died, and only 95 (56%) had a good outcome. Principal causes of unfavorable outcome were poor initial condition, delayed cerebral ischemia, and surgical complications. There were four patients with additional intracranial bleeding in the group receiving enoxaparin. The bleeding was not necessarily associated with the treatment itself, nor did it require treatment, and there were no such patients in the placebo group. CONCLUSIONS: Enoxaparin seemed to have no effect on the outcome of aneurysmal SAH in patients who had already received routine nimodipine and who had received triple-H therapy when needed. Routine use of low-molecular-weight heparin should be avoided during the early postoperative period in patients with SAH, because this agent seems to increase intracranial bleeding complications slightly, with no beneficial effect on neurological outcome.     

Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage: a novel method to predict symptomatic vasospasm on admission computerized tomography scans

OBJECT: Predicting which patients with aneurysmal subarachnoid hemorrhage (SAH) will develop delayed ischemic neurological deficit (DIND) due to vasospasm remains subjective and unreliable. The authors analyzed the utility of a novel software-based technique to quantify hemorrhage volume in patients with Fisher Grade 3 aneurysmal SAH. METHODS: Patients with aneurysmal SAH in whom a computerized tomography (CT) scan was performed within 72 hours of ictus and demonstrated Fisher Grade 3 SAH were analyzed. Severe DIND was defined as new onset complete focal deficit or coma. Moderate DIND was defined as new onset partial focal deficit or impaired consciousness without coma. Fifteen consecutive patients with severe DIND, 13 consecutive patients with moderate DIND, and 12 consecutive patients without DIND were analyzed. Software-based volumetric quantification was performed on digitized admission CT scans by a single examiner blinded to clinical information. There was no significant difference in age, sex, admission Hunt and Hess grade, or time to admission CT scan among the three groups (none, moderate, or severe DIND). Patients with severe DIND had a significantly higher cisternal volume of hemorrhage (median 30.5 cm3) than patients with moderate DIND (median 12.4 cm3) and patients without DIND (median 10.3 cm3; p < 0.001). Intraparenchymal hemorrhage and intraventricular hemorrhage were not associated with DIND. All 13 patients with cisternal volumes greater than 20 cm3 developed DIND, compared with 15 of 27 patients with volumes less than 20 cm3 (p = 0.004). CONCLUSIONS: The authors developed a simple and potentially widely applicable method to quantify SAH on CT scans. A greater volume of cisternal hemorrhage on an admission CT scan in patients with Fisher Grade 3 aneurysmal SAH is highly associated with DIND. A threshold of cisternal hemorrhage volume (> 20 cm3) may exist above which patients are very likely to develop DIND. Prospective application of software-based volumetric quantification of cisternal SAH may predict which patients will develop DIND.     

HLA-type of cerebral vasospasm patients after aneurysmal subarachnoid hemorrhage

We studied human lymphocyte antigen (HLA) types in a group of 45 patients who had aneurysmal subarachnoid hemorrhage (SAH). A significantly increased frequency of HLA antigen A31 and a significantly decreased frequency of HLA antigen B40 were found. In patients with delayed ischemic neurological deficit (DIND) following aneurysmal SAH and HLA typing, HLA-Bw60 antigen showed significant increases; in patients who did not develop HLA-Aw33 and-Cw4 antigens showed significant. Among the patients with Fisher's Group 3 on CT, in particular, these antigens significantly increased when compared with controls from the same geographic area. These results suggest that HLA-Bw60 antigen plays a role as a predisposing factor of DIND resulting from vasospasm following aneurysmal SAH, and that HLA-Aw33 and-Cw4 exert protective influence against DIND.     

Severe subarachnoid hemorrhage with pulmonary edema successfully treated by intra-aneurysmal embolization using Guglielmi detachable coils--Two case reports

A 48-year-old male and a 39-year-old female presented with subarachnoid hemorrhage (SAH) due to ruptured anterior communicating artery aneurysms. Both patients were comatose on admission. Chest radiography disclosed pulmonary edema. They were conservatively treated under controlled ventilation, but cardiopulmonary dysfunction persisted over 2 days. The patients were then treated by intra-aneurysmal embolization with Guglielmi detachable coils (GDCs) 2 days after the onset. The postoperative courses were uneventful, and the patients showed full recovery from pulmonary edema and were discharged without neurological deficits. Neurogenic pulmonary edema is one of the serious complications of SAH, and is a leading cause of poor clinical outcome. The favorable outcomes of the present cases suggest that intra-aneurysmal embolization with GDCs is an excellent choice for the patients with severe aneurysmal SAH complicated with pulmonary edema, in whom conventional surgical treatment under general anesthesia is difficult to perform in the acute stage.     

Pulmonary complications of aneurysmal subarachnoid hemorrhage

OBJECTIVE: Pulmonary complications challenge the medical management of patients who have sustained aneurysmal subarachnoid hemorrhage (SAH). We assessed the frequency and types of pulmonary complications after aneurysmal SAH and analyzed the impact of pulmonary complications on patient outcome. METHODS: We reviewed the records of all patients with acute SAH treated at our institution between 1990 and 1997. Three hundred five consecutive patients with an aneurysmal hemorrhage source documented by angiography and treated within 7 days of ictus were analyzed. Outcomes at longest follow-up (mean, 16 mo) were measured by use of the Glasgow Outcome Scale. RESULTS: Pulmonary complications were documented in 66 patients (22%). The pulmonary complications were nosocomial pneumonia in 26 patients (9%), congestive heart failure in 23 (8%), aspiration pneumonia in 17 (6%), neurogenic pulmonary edema in 5 (2%), pulmonary embolus in 2 (<1%), and other pulmonary disorders in 4 (1%); 11 patients had two pulmonary complications. The incidence of symptomatic vasospasm was greater in patients with pulmonary complications (63%) than in patients without pulmonary complications (31%) (P = 0.001), and this association was independent of age and clinical grade at admission (odds ratio, 3.68; P < 0.001). Overall clinical outcomes were worse in patients with pulmonary complications (mean Glasgow Outcome Scale score, 3.3) than in patients without pulmonary complications (mean Glasgow Outcome Scale score, 4.0; P = 0.0001), but pulmonary complications were not an independent predictor of worse outcome when adjusted for age and clinical grade at admission (odds ratio, 1.38; P = 0.315). CONCLUSION: Patients who experience pulmonary complications after aneurysmal SAH have a higher incidence of symptomatic vasospasm than do patients without pulmonary complications. This most likely reflects both the failure to maintain aggressive hypervolemic and hyperdynamic therapy in patients with pulmonary compromise and the possible precipitation of congestive heart failure by hypervolemic therapy in patients with preexisting delayed ischemic neurological deficit. Although patients with pulmonary complications have worse overall clinical outcomes than do patients without pulmonary complications, this is attributable to older age and worse clinical grades at admission.     

Aneurysmal subarachnoid hemorrhage. Significance and complications

Despite substantial improvement in the management of patients with aneurysmal subarachnoid hemorrhage (SAH), including early aneurysm occlusion by endovascular techniques and surgical procedures, a significant percentage of patients with SAH still experience serious sequelae of neurological or cognitive deficits as a result of primary hemorrhage and/or secondary brain damage. Available neuromonitoring methods for early recognition of ischemia include, among others, measurement of brain tissue O(2) partial pressure, brain metabolism with microdialysis and monitoring of regional blood flow. The triple-H therapy (arterial hypertension, hypervolemia and hemodilution) is the treatment of choice of a symptomatic vasospasm and leads to an enduring recession of ischemic symptoms, if initiated early after the onset of a vasospasm-linked ischemic neurological deficit. Further promising therapy approaches are the administration of highly selective ET(A) receptor antagonists and intracisternal administration of vasodilators in depot form. This review summarizes the major neurological and non-neurological complications following aneurysm occlusion. Possible neuromonitoring techniques to improve diagnosis and therapy for treatment of symptomatic vasospasm as well as extracranial complications are discussed.     

Aneurysmatische Subarachnoidalblutung

Despite substantial improvement in the management of patients with aneurysmal subarachnoid hemorrhage (SAH), including early aneurysm occlusion by endovascular techniques and surgical procedures, a significant percentage of patients with SAH still experience serious sequelae of neurological or cognitive deficits as a result of primary hemorrhage and/or secondary brain damage. Available neuromonitoring methods for early recognition of ischemia include, among others, measurement of brain tissue O₂ partial pressure, brain metabolism with microdialysis and monitoring of regional blood flow. The triple-H therapy (arterial hypertension, hypervolemia and hemodilution) is the treatment of choice of a symptomatic vasospasm and leads to an enduring recession of ischemic symptoms, if initiated early after the onset of a vasospasm-linked ischemic neurological deficit. Further promising therapy approaches are the administration of highly selective ET_A receptor antagonists and intracisternal administration of vasodilators in depot form. This review summarizes the major neurological and non-neurological complications following aneurysm occlusion. Possible neuromonitoring techniques to improve diagnosis and therapy for treatment of symptomatic vasospasm as well as extracranial complications are discussed.     

Hyponatremia is predictable in patients with aneurysmal subarachnoid hemorrhage—clinical significance of serum atrial natriuretic peptide

Purpose  

Serum atrial natriuretic peptide (ANP) that is elevated after aneurysmal subarachnoid hemorrhage (SAH) causes diuresis and natriuresis (cerebral salt wasting) and might exacerbate delayed ischemic neurological deficit (DIND). We investigated relationships among hyponatremia, serum ANP elevation, and the onset of DIND after SAH.     

Early infarction detected by diffusion-weighted imaging in patients with subarachnoid hemorrhage

Purpose

Early infarction that occurs at the time of initial subarachnoid hemorrhage (SAH) due to rupture of an aneurysm is a poorly understood phenomenon. We investigate the frequency of early infarction using diffusion-weighted images (DWI) at the time of admission. We then discuss the pathogenesis of infarction.

Materials and methods

This study included 85 SAH patients who underwent serial DWI on admission. Early infarction detected by DWI and clinical features were investigated retrospectively.

Results

The overall incidence of DWI-detected early infarction at the time of SAH onset was 8% (7 of 85 cases). In all seven patients, early infarctions were asymptomatic on admission. Types of early infarction seen on DWI included infarcts occurring in the territory of the vessel harboring a ruptured aneurysm (solitary, three cases) and infarcts occurring outside the territory of the vessel (multiple, two cases; solitary, two cases). Six of seven patients eventually developed delayed ischemic neurological deficit (DIND) and computed tomography (CT)-detected and DWI-detected delayed extensive infarction. Four of seven patients with early infarction had an unfavorable outcome. The occurrence of DWI-detected early infarction on admission was significantly correlated with delayed angiographic vasospasm, DIND, CT-detected delayed infarction, DWI-detected delayed infarction, and unfavorable outcome.

Conclusions

In the present study, DWI-detected early infarction at the time of SAH onset was correlated with the occurrence of delayed extensive ischemic lesions. We believe that performing DWI at the time of admission is useful for evaluating the primary ischemic insult, which might play an important role in the pathogenesis of early brain injury and delayed vasospasm-related complications.     

Smoking and subarachnoid haemorrhage: a case control study.

Retrospective and epidemiological studies have suggested that smoking increases the risk of developing aneurysmal subarachnoid haemorrhage (SAH). During 1990, 217 patients presenting to the Mersey Regional Neurosurgical unit with spontaneous SAH were prospectively studied. Smoking habits of patients with SAH were compared with age, sex and occupation matched controls. The relative risk of spontaneous aneurysmal SAH for smokers was twice that of non-smokers (p < 0.001). Management outcome at 6 months following aneurysmal SAH was similar for smokers and non-smokers (p = 0.43) but smokers had more postoperative pulmonary complications requiring ventilation. Significance was tested with chi-square tests.     

Role of bedside microdialysis in the diagnosis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage

OBJECT: Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH. METHODS: In 60 patients a microdialysis catheter was inserted into the brain parenchyma that is most likely to be affected by vasospasm directly after aneurysm clipping. Hourly analyses of glucose, pyruvate, lactate, and glutamate levels were performed using a bedside device. Blood-flow velocities were obtained using serial TCD measurements. Cerebral angiography was routinely performed on Day 7 after aneurysm clipping or earlier in cases of clinical deterioration (30 patients). In all patients the results of microdialysis monitoring, TCD ultrasonography, and angiography were correlated. The mean duration of monitoring was 7.3+/-2.5 days. In patients with acute ischemic neurological deficits (18 patients) immediate microdialysis-recorded alterations were observed if the probe was placed close to the malperfused region. In 13 of 15 patients with symptomatic vasospasm (delayed ischemic neurological deficit [DIND]), the microdialysis-recorded values revealed secondary deterioration. In terms of confirming DIND, microdialysis had the highest specificity (0.89, 95% confidence interval [CI] 0.78-1) compared with TCD ultrasonography (0.63, 95% CI 0.46-0.8) and angiography (0.53, 95% CI 0.35-0.7). For microdialysis, the positive likelihood ratio was 7.8, whereas this was significantly lower for TCD ultrasonography (1.7) and angiography (2.1). CONCLUSIONS: Although angiography also demonstrates vessel narrowing in asymptomatic patients, online microdialysis reveals characteristic metabolic changes that occur during vasospasm. Thus, online microdialysis may be used to confirm the diagnosis of vasospasm.     

Cisternal drainage after early operation of ruptured intracranial aneurysm

The authors reviewed 22 cases of intracranial aneurysm of the anterior part of the circle of Willis. All patients presented with the signs and symptoms of subarachnoid hemorrhage (SAH) and were in good neurological condition on admission. In all cases, early operation was performed to obliterate aneurysm. Subarachnoid blood clots were extensively removed and cisternal drainage was done. With topical application of povidone-iodine and intravenous administration of antibiotics, cisternal drainage continued for 14 days or more after the onset of SAH in 21 cases. Five patients developed symptomatic vasospasm, which was treated with hypervolemia and hypertension, and three received shunts later for chronic hydrocephalus. The overall result demonstrated that 21 patients were independent and had returned to their previous social lives. Therefore, it was strongly recommended that patients is good neurological condition after SAH secondary to ruptured intracranial aneurysm be treated with early operation, removal of subarachnoid clots, and long term application of cisternal drainage.     

Neurogenic pulmonary edema in patients with subarachnoid hemorrhage

Neurogenic pulmonary edema (NPE), leading to cardiopulmonary dysfunction, is a potentially life-threatening complication in patients with aneurysmal subarachnoid hemorrhage (SAH). We sought to assess the clinical presentation and risk factors for the development of NPE after SAH. The database contained prospectively collected information on 477 patients with SAH. Baseline characteristics, clinical and radiologic severity of the bleeding, localization of the ruptured aneurysm, and clinical outcome of patients with NPE were compared with those of patients without NPE. Further, in patients with NPE, intracranial pressure, serum cardiac biomarkers, and hemodynamic parameters during the acute phase were evaluated retrospectively. The incidence of NPE was 8% (39 of 477 patients). Most patients with NPE were severely impaired and all of them presented with radiologically severe hemorrhage. The incidence of NPE was significantly higher in patients with ruptured aneurysm in the posterior circulation. Elevated intracranial pressure was found in 67%, pathologically high cardiac biomarkers in up to 83% of patients with NPE. However, no patient suffered from persistent cardiac dysfunction. Compared with patients without NPE, patients with NPE showed poor neurologic outcome (Glasgow outcome scale 1 to 3 in 25% vs.77% of patients). In conclusion, patients with NPE have a high mortality rate more likely due to their severity grade of the bleeding. Morbidity and mortality due to cardiopulmonary failure might be reduced by appropriate recognition and treatment. The awareness of and knowledge about occurrence, clinical presentation, and treatment of NPE, are essential for all those potentially confronted with patients with SAH in the acute phase.     

Morbidity and mortality after early aneurysm surgery — a prospective study with nimodipine prevention

Summary Based on the outcome in 116 consecutive patients who were subjected to early aneurysm operation combined with additional nimodipine treatment, and who were controlled by transcranial Doppler (TCD) sonography, a morbidity and mortality analysis was performed. Of the 84 patients who preoperatively were in Hunt & Hess grades III, 79 patients (94%) were considered to show a favourable (good-fair) late recovery, while one patient (1%) had a poor outcome, and four patients (5%) died. Of the 32 poor condition patients (H & H IV–V), 17 (53%) showed a favourable recovery, while seven (22%) had a poor outcome, and eight patients (25%) died. Altogether, 20 patients (17%) had an unfavourable (poor-dead) outcome. Only two of these patients showed delayed ischaemic deterioration, one as a consequence of a secondary occlusion of perforating branches from the basilar artery and one with decompensated vasospasm after the evacuation of an epidural haematoma and a longlasting severe systemic hypotension; both these patients died. In another six of the patients with an unfavourable outcome, this was mainly related to a complicated surgery. The unfavourable outcome was related to primary brain damage produced by the subarachnoid haemorrhage (SAH) in ten patients and in two patients to internal medical complications. In addition to the two patients who died following delayed deterioration, secondary neurological dysfunction occurred in 11 patients. In 10 of these patients transient neurological dysfunction was attributed to vasospasm or to a combination of vasospasm with intraoperative or postoperative complications. One further case of delayed deterioration was attributed to secondary occlusion of the internal carotid artery after a complicated operation. From these data we conclude that following early aneurysm operation combined with intravenous nimodipine treatment, vasospasm alone is no more a major clinical problem. Morbidity and mortality are mainly related to primary effects of the SAH and/or complicated surgery.     

Acute subdural haematoma due to ruptured intracranial aneurysms

Acute spontaneous subdural haematoma (SDH) is rarely associated with rupture of intracranial saccular aneurysm. We report our experience with four cases of non-traumatic SDHs secondary to rupture of an intracranial aneurysm and discuss the diagnosis and management of this condition. We retrospectively reviewed of four cases of acute SDH due to cerebral aneurysm rupture confirmed by cerebral angiography and surgery. Patients were evaluated using the Glasgow Coma Scale (GCS) and subarachnoid grade of the World Federation of Neurosurgical Societies (WFNS) and outcome with the Glasgow Outcome Scale (GOS). Of the 232 patients with non-traumatic subarachnoid haemorrhage (SAH) treated between 1993 and 2002, only four patients (1.72%) presented SDH due to aneurysmal rupture. The SAH grade on admission was grade IV in one patient and V in the other three. In all cases the aneurysm was located in the posterior communicating artery. Spontaneous acute SDH secondary to aneurysm rupture has been rarely reported. We suggested that timely SDH removal and aneurysmal clipping surgery should be performed in such patients, including those in poor neurological condition.     

Cognitive deficits after rupture and early repair of anterior communicating artery aneurysms

Summary In a retrospective follow-up study covering a time period of four years 18 patients operated upon early for an aneurysm of the anterior communicating artery (ACoA) and a control group of 21 patients with aneurysmal subarachnoid haemorrhage (SAH) from other sources than ACoA aneurysm and 9 patients with SAH of nonaneurysmal origin were subjected to neuropsychological examination. Both groups were comparable in their neurological condition on admission and in the severity of bleeding seen on CT-scan. Testing included memory functions, concentration, logical and spatial thinking, a Stroop-test, an aphasia screening test and a complex choice reaction task. Patients with SAH of a ruptured ACoA aneurysm did not differ significantly from the control group in any of the tests used. But there was a trend for the ACoA patients to have more memory problems than the patients with SAH of other origins. On the other hand the patients in the control group with aneurysmal SAH of other locations and with non-aneurysmal SAH had not significantly more problems with concentration and aphasia than the patients with ruptured ACoA aneurysm. These results, which differ from the common opinion of frequent occurrence of memory deficits in ACoA aneurysms are interpreted as a consequence of the changes in improved pre-, intra- and postoperative management in modern neurosurgery.