Incidence and effects of increased cerebral blood flow velocity after severe head injury: a transcranial Doppler ultrasound study I. Prediction of post-traumatic vasospasm and hyperemia.

Cerebral blood flow velocity was monitored in 50 patients with severe head injury (GCS 8 or less) within 24 h of injury and at least once daily thereafter, using transcranial Doppler ultrasonography (TCD). Delayed post-traumatic vasospasm occurred in 20, and cerebral hyperemia in another 15. Doppler velocities were higher in vasospasm, which also lasted significantly longer than hyperemia. The presence of visible blood on an early CT scan was of some value in predicting vasospasm only (accuracy 59%). Xenon-133 cerebral blood flow (CBF) was also measured within 24 h of injury. An abnormal early cerebral blood flow level, either above or below a narrow central range, was more effective than CT in predicting vasospasm or hyperemia (accuracy 80%), while the combination of an abnormal blood flow and hemorrhagic findings on CT scan helped to determine which of these would occur later. Patients with an abnormal early cerebral blood flow and hemorrhagic findings on CT were more likely to develop vasospasm--accuracy for prediction of vasospasm 73%. This distinction may be of great importance, since these different groups of patients may well need different management.

Incidence and effects of increased cerebral blood flow velocity after severe head injury: a transcranial Doppler ultrasound study II. Effect of vasospasm and hyperemia on outcome.

Cerebral blood flow velocities were measured in 50 severely head injured (Glasgow Coma Scale (GCS) 8 or less) patients using transcranial Doppler ultrasonography (TCD). Abnormally high TCD velocities were recorded in 35 patients; in 20 this was deemed to be due to vasospasm and in the other 15 to hyperemia. Patients who developed hyperemia also had the highest intracranial pressure (ICP) and the lowest cerebral perfusion pressure (CPP) of the three groups. Outcome was assessed at six months after injury using the Glasgow outcome scale and the disability rating scale. In the normal velocity group 87% of patients had a good outcome, compared with 47% of those with hyperemia and 40% of those with vasospasm. The highest velocity (HVEL), GCS, age, ICP and CPP were entered into a logistic regression analysis. HVEL, age and CPP were found to be the most significant predictors of outcome (chi 2 = 29.5; p < 0.0001). These factors predicted outcome with 82% accuracy, 86% sensitivity and 76% specificity. Routine monitoring of TCD velocity may be useful in detecting hyperemia and vasospasm after severe head injury, allowing appropriate treatment to be started as early as possible.

Aid to exposure of the upper basilar artery: technical note.

The author explains his method of retracting the tentorial edge during the subtemporal approach to the distal basilar artery. A modification of the ligature makes it unnecessary to tie a knot at depth.

Ectasia and fenestration of the anterior cerebral artery associated with persistent trigeminal artery: case report.

Multiple vascular anomalies in a 22-year-old patient who had signs and symptoms of vestibulocochlear dysfunction are reported. Angiography revealed a fenestration of the proximal segment of the left anterior cerebral artery, an ectasia of the left anterior and posterior cerebral arteries, and a persistence of the right trigeminal artery. The rarity of the association is documented, and the clinical significance is discussed.

Early experience with spiral CT in the diagnosis of intracranial aneurysms.

We report experience with 16 patients undergoing spiral CT Scans for the evaluation of cerebral aneurysms. There were 10 females and six males, aged between 36 and 73 years. The three-dimensional scanning was useful in five situations: (i) Suspicion of aneurysm on conventional scan. An aneurysm was found in one of four patients and later confirmed by angiography, and two showed arterial ectasia with no saccular aneurysm; the fourth again appeared to have an aneurysm, but this was not shown on angiography. (ii) Follow-up of previously detected aneurysms not planned for surgery. This has been done in three patients, the spiral CT findings correlating well with previous angiography. (iii) Follow-up of aneurysm remnants after surgery (three cases); findings correlate well with previous angiography, and clips cause no artefact problems. (iv) Detection of ruptured aneurysms. In two cases, small aneurysms were found that had been missed on angiography, and in a third, with doubtful angiographic findings, spiral CT was useful. (v) Investigation of patients with past treated aneurysms, or of relatives. Three subjects have been screened so far for that purpose; in one a small aneurysm has been found, and confirmed angiographically.

Intradural extramedullary tuberculoma of the cervical spine. Case report.

A case is reported of a 45-year-old man who developed quadriplegia following a trivial motor-vehicle accident. Investigation including computerized tomography (CT) of the cervical spine revealed a large calcified lesion displacing the spinal cord and nerve roots, which proved to be a tuberculoma. The case is unusual in regard to the age of the patient, the size, location, and nature of the lesion, the mode of presentation, and the delineation of the lesion by CT scanning.

Double-blind, randomized, vehicle-controlled study of high-dose tirilazad mesylate in women with aneurysmal subarachnoid hemorrhage. Part I. A cooperative study in Europe, Australia, New Zealand, and South Africa.

OBJECT: Findings from previous multicenter clinical trials have suggested that tirilazad mesylate, a synthetic nonhormonal 21-aminosteroid, might be effective in preventing delayed cerebral ischemia following subarachnoid hemorrhage (SAH). This beneficial effect, however, was greater in males than females, possibly because of gender-related pharmacokinetic differences. The authors sought to assess the effects of administering a larger dose of tirilazad in women with SAH. METHODS: To test the efficacy of a higher tirilazad mesylate dose in female patients, a prospective randomized, double-blind, vehicle-controlled trial was conducted at 56 neurosurgical centers in Europe, Australia, New Zealand, and South Africa. Eight hundred nineteen patients were randomly assigned to receive either 15 mg/kg/day of tirilazad mesylate or a placebo containing the citrate vehicle. The two groups were similar in prognostic factors for delayed cerebral ischemia and overall outcome. High-dose tirilazad appeared to be well tolerated because no differences in the incidence of untoward medical events were noted between the two groups. Medical and surgical interventions were no different in the two treatment groups except for hyperdynamic therapy (intentional hypervolemia, induced hypertension, and/or hemodilution), which was more often used in the placebo-treated group to counteract symptomatic vasospasm (24% of patients given placebo compared with 18% of patients given tirilazad, p = 0.02). Mortality rates and overall outcome, assessed using the Glasgow Outcome Scale at 3 months post-SAH, were not different between the two groups, despite a significantly lower incidence of delayed cerebral ischemia in patients given tirilazad. Post hoc subgroup analysis by neurological grade also did not reveal significant differences in outcome, although a trend toward a lower mortality rate favoring the study drug was present in patients with neurological Grade IV and V at admission (32% compared with 37%). Symptomatic vasospasm occurred in 33.7% of the placebo-treated patients as opposed to 24.8% of the patients who were given tirilazad (p = 0.005). The severity of symptomatic vasospasm was also attenuated by administration of the study drug (severe symptomatic vasospasm was reported in 11% of the placebo-treated patients compared with 6% of patients in the tirilazad-treated group (p = 0.008). Clinical cerebral infarction from vasospasm was also reduced from 13% in the vehicle-treated group to 8% in the tirilazad-treated group (p < 0.04). CONCLUSIONS: The authors conclude that high-dose tirilazad mesylate is well tolerated in women with aneurysmal SAH. Although a significant reduction in the incidence of symptomatic vasospasm was observed in the treatment group, the primary end point (mortality rate at 3 months post-SAH) was not affected by the study drug. The use of other potentially effective rescue therapies (that is, hypervolemia, hemodilution, and induced hypertension) to counteract vasospasm may have been responsible for these contrasting observations between the two groups.

Clinical course and outcome of severe head injury in Australia.

The records of 159 severely head-injured patients (all in coma for longer than 6 hours) from Sydney, Australia, were studied. The clinical course, charted over a 2-week period, indicated that 60% of deaths occur by Day 3 and that 12% of patients remain in coma (Glagow Coma Scale (GCS) score less than 7) for more than 2 weeks. Overall, at long-term follow-up review more than 2 years after injury, 51% of patients were dead, 7% were severely disabled or vegetative, and 42% had a good to moderate recovery. Outcome of the patients in prolonged coma was assessed separately, with only one-third making a good or moderate recovery; two-thirds of the severely disabled patients came from this group. The high proportion of poor outcomes associated with prolonged coma suggests that this group of patients should be specifically targeted in research. One appropriate intervention with this group would be the restructuring and intensification of early rehabilitation. However, the GCS score lacks the precision needed for this type of study, and a better measure of recovery should be developed.

Giant intracranial aneurysms: diagnosis, management, and outcome.

The diagnosis, management, and outcome of a consecutive series of 25 patients with giant intracranial aneurysms are presented. Symptoms and signs directly or indirectly attributable to the intracranial mass effect accounted for presentation in 16 (64%) patients of whom seven had no focal neurological deficits. Nine patients (36%) presented after subarachnoid hemorrhage. Subarachnoid hemorrhage was frequently associated with intraventricular or intracerebral hemorrhage, a poor clinical grading at admission, and a high mortality (67%). Computed tomographic features of the giant aneurysms were usually characteristic; however, angiography was particularly useful in those in close proximity to the skull base. Nineteen patients had a surgical procedure directly or indirectly aimed at obliteration, isolation, or reinforcement of the giant aneurysm. Successful surgical obliteration or occlusion was obtained in 12 (63%) patients, while seven (37%) had only reinforcement or exploration of the aneurysm. The mortality associated with definitive surgical treatment was 5.6%, and major morbidity occurred in 17%. The good long-term outcome in 75% of the patients after occlusion of the giant aneurysm contrasted with the continuing mortality (43%) and morbidity (43%) in those patients in whom surgical obliteration of the aneurysm was not attained. Although advances in microsurgical instrumentation, anesthetic techniques, and innovative revascularization procedures have facilitated the surgical management of giant aneurysms, significant improvement in the high overall mortality associated with these aneurysms (36% in this series) will probably only be attained by diagnosis of giant intracranial aneurysms before they bleed.

Spiral CT scanning in the detection and evaluation of aneurysms of the Circle of Willis.

PURPOSE: To assess the utility of spiral computed tomography (CT) with three-dimensional reconstruction in defining aneurysms of the Circle of Willis. METHODS: Eighty-one patients with angiographic or surgical correlation were studied between 1993 and 1995, with surface rendered reconstructions of the arteries of the Circle of Willis. RESULTS: Spiral CT was useful in six clinical situations: further assessment in cases with CT suspicion of an aneurysm, follow-up of known untreated aneurysms or aneurysm remnants, subarachnoid hemorrhage (SAH) with negative angiography, a past or family history of aneurysms, and improved definition of aneurysm anatomy. Ten of fifteen patients with previous surgery had no significant artifacts on the spiral study. In 66 other patients studied in search of aneurysms, the sensitivity of detection was 95% and specificity 74%. Seventeen of nineteen aneurysms 3 mm or less in size and 38 of 39 larger were detected by spiral CT. Four of thirteen patients with SAH and previous negative angiography had aneurysms identified, which were confirmed at surgery. CONCLUSIONS: There is great promise in the use of spiral CT in demonstrating aneurysms of the Circle of Willis, including very small ones. Careful detailing of scan protocols and meticulous examination of multiplanar images are needed for maximum accuracy.

A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage Part II: Management.

This review examines prevention and treatment of delayed cerebral vasospasm after aneurysm haemorrhage, with emphasis on techniques for removal of cisternal blood, fluid loading and induced hypertension, and calcium antagonists. Most effective were fluids/hypertension and nimodipine, which reduced the incidence of DID by over half. Other drugs that may be useful are tissue plasminogen activator and the aminosteroids. A number of others have also been examined. For the treatment of DID, calcium antagonists, and fluid loading and hypertensive treatment are the most effective. Transluminal angioplasty is also proving to be useful. The combination of prophylaxis and treatment with fluids and nimodipine should reduce poor outcome resulting from vasospasm by two-thirds, from 21% untreated to less than 7%. In spite of the more or less proven efficacy of these measures, large numbers of cases are still being reported in whom no specific management is being used.

A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage Part III: Mechanisms of action of calcium antagonists.

The possible mechanisms by which calcium antagonists are effective in the management of cerebral vasospasm are discussed. They number seven: relaxation of spastic arteries or prevention of spasm; opening up of collateral channels; neuronal protection at the membrane level; intracellular actions in neurones or vascular cells; alterations of blood rheology; antimitogenic effects; and improved fluid management of patients. A number of more minor actions may also be involved. It is likely that more than one mechanism is involved in their protective effect, especially at different periods in the time course of vasospasm.

A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage Part I: Incidence and effects.

Delayed ischaemia due to cerebral 'vasospasm' is a significant cause of morbidity and mortality after aneurysm haemorrhage. In a literature review more than 30 000 cases were found where vasospasm after subarachnoid haemorrhage (SAH) was discussed. The incidence of angiographic vasospasm was 43.3% overall, and 67.3% where angiography was done at a time of maximum expected spasm. Symptomatic vasospasm or delayed ischaemic deficit (DID) occurred in 32.5%. There was no difference in incidence and time course between preoperative and postoperative cases. 30% of those with DID died, and permanent neurological deficits occurred in 34%. A fatal outcome was much more likely in the presence of vasospasm, and a satisfactory outcome one third less likely. Vasospasm is thus the cause of death in about 10%, and of disability in slightly more cases of aneurysmal SAH. The extent of the problem has not changed significantly over three decades.

A review of cerebral vasospasm. Part IV. Post-traumatic vasospasm.

Cerebral vasospasm is increasingly recognized as contributing to ischaemia after head injury. The reported incidence of post-traumatic vasospasm (PTV) varies between 10% and 90%, probably largely because of differences in patient selection, in definitions of vasospasm and in methods of detecting spasm. In severe head injury, based on studies with similar criteria, the incidence is approximately 40%. PTV is often associated with traumatic subarachnoid haemorrhage (tSAH), but has been reported without tSAH. These two factors are independently associated with poor outcome, but the direct links between tSAH, vasospasm and outcome are uncertain. There is evidence that calcium antagonists improve outcome in patients with head injury and tSAH; aminosteroids may also be effective here. Other strategies such as maintaining normocapnia and control of blood volume and pressure may also be useful. Further investigation of large cohorts is required to clarify fully the significance of PTV, its relationship with tSAH and outcome and possible treatment modalities.

Aplasia of the posterior arch of the atlas.

A case of aplasia of the posterior arch of the atlas with persistence of the posterior tubercle in a 14-year-old youth is presented. The pathogenesis and clinical implications of the condition are discussed.

Early surgery for posterior circulation aneurysms following subarachnoid haemorrhage.

A retrospective analysis of 32 patients with posterior circulation aneurysms operated on within three days of subarachnoid haemorrhage is presented. The cases were treated at two Australian neurosurgery units over a five year period (1988-1992), both units having a policy of treating patients of all grades and all ages with early surgery. No patients suffered rebleeding. Five patients developed clinical vasopasm. Twenty-four patients (75%) had a good outcome (Glasgow Outcome Score 1-2), three had a poor outcome (GOS 3), and five died (16%). Of the five deaths, three presented as Hunt and Hess grade V. The results are considered in detail and the literature regarding the timing of surgery for posterior circulation aneurysms is reviewed.

Aggressive management of aneurysmal subarachnoid haemorrhage based on a papaverine angioplasty protocol.

The aim of this study was to analyse the results of intensive therapy unit management of aneurysmal subarachnoid haemorrhage incorporating angioplasty in the protocol. Two hundred consecutive patients were treated using a detailed protocol that included nimodipine, early aneurysm repair, and surveillance angiography. Angiography was performed on days 5 to 7 (or when the clinical state suggested the presence of vasospasm). If angiographic vasospasm was identified, irrespective of whether clinical vasospasm was present or absent, papaverine was selectively administered. In patients with vasospasm blood pressure was elevated to 160-180 mmHg and selective papaverine administration was repeated daily until vasospasm resolved. In cases requiring more frequent administration of papaverine, or in whom papaverine failed to adequately reverse spasm, balloon angioplasty was considered and for clinically refractory cases barbiturate coma was introduced. 43% of patients underwent papaverine administration and of these the average number of separate papaverine procedures was four (maximum 23). 26% of patients developed neurological deficits though to be due to vasospasm whilst 17% underwent papaverine angioplasty without clinical signs of vasospasm. Twelve patients (6%) were entered into barbiturate coma. There was a 5.5% mortality and no difference in outcome between patients who developed angiographic vasospasm and those who did not. For those developing clinical vasospasm, 71% were independent and 10% were dead at follow up compared with 84% reaching independent grades and 4% dead in those not developing clinical vasospasm. These differences failed to reach a significant difference. The average Intensive Therapy Unit stay for aneurysmal subarachnoid haemorrhage patients was 13.1 days with a mean cost to the hospital of $AUD 24,379. This protocol appears to be both a clinically and cost effective method of managing aneurysmal subarachnoid haemorrhage.

Subarachnoid hemorrhage of unknown origin and the basilar artery configuration.

It is unclear whether the configuration of the basilar artery (BA) in patients with subarachnoid hemorrhage (SAH) of unknown origin is comparable to that in normal subjects or whether there are differences which may help to identify the origin. We studied the BA configuration in 57 patients with SAH of unknown origin (10%), who were identified in a prospectively collected series of 549 SAH patients consecutively admitted to our service over a 9-year period. There were 30 patients (53%) with non-perimesencephalic SAH and 27 with perimesencephalic SAH (47%). According to a standardized algorithm we determined, on straight anteroposterior digital subtraction angiography (DSA), the width of the proximal BA segment at the origin of the anterior inferior cerebellar artery and the width of the most distal BA segment between the superior cerebellar arteries and the posterior cerebral arteries. Based on these measurements we calculated the distal-proximal BA ratios and compared them to the ratios obtained in a control group of 31 patients who had DSA for reasons other than aneurysmal SAH. The mean ratio in patients with non-perimesencephalic SAH of unknown origin was 1.150 (range: 1.080-1.230). In patients with perimesencephalic SAH of unknown origin it was 1.156 (range: 1.120-1.250). In the control group the mean ratio was 1.163 (range: 1.125-1.200). There are no variations in the configurations of the BA which could possibly explain the cause of this type of SAH or clarify the origin of hemorrhage.

The effect and management of delayed vasospasm after aneurysmal subarachnoid hemorrhage.

Delayed cerebral vasospasm after aneurysm rupture is one of the major complications of subarachnoid hemorrhage. The purpose of this review was to determine the true incidence of vasospasm. All literature on cerebral aneurysms from 1960 onwards was reviewed, and the figures extracted from publications that mentioned vasospasm. Angiographic vasospasm, where patients were studied at the time of peak incidence, was reported in about two thirds of cases. Symptomatic vasospasm or delayed ischemia affects about one third. Untreated, nearly a third of those with ischemic deficits die and a similar proportion are left permanently disabled. Variations of Triple-H (hypervolemia, hypertension, hemodilution) therapy, used early after hemorrhage for prophylaxis of vasospasm, are associated with a decrease of nearly half in the incidence of delayed ischemia. When used as therapy outcome also appears better, with a reduction particularly in the death rate. Calcium antagonists have been widely used, especially nimodipine. In several controlled trials the incidence of delayed ischemia was significantly reduced. More importantly, the overall outcome of all subarachnoid hemorrhage patients was better with nimodipine prophylaxis. The 21-aminosteroid tirilazad mesylate has been the subject of several trials. In one the overall outcome of all patients was improved, but the effect was essentially in males only. Further studies with larger doses in females are being analyzed.

Treatment of symptomatic vasospasm with nimodipine.

Over a seven-year period, 130 patients with delayed ischaemia after cerebral aneurysm haemorrhage were treated with intravenous nimodipine. The delay from the last haemorrhage to the appearance of ischaemic symptoms was one to 18 days, and vasospasm was confirmed in most cases. Nimodipine treatment was started within three days of delayed ischaemic deficit (DID) onset, at a low dose increased quickly to 30-45 ug/kg/hr, and reduced gradually over the last day or two of the course. The duration of treatment was one to 27 days. Side effects were minor, and serious complications few. Hypotension occurred in 35 cases. During treatment, there were highly significant improvements in both clinical grade and Glasgow Coma Score. The final outcome was 98 good (Glasgow Outcome Score 1), 18 permanent deficits (eight GOS 2, ten GOS 3), and 14 dead. Ischaemia was directly involved in only half the deaths. These results are much better than the natural history (about 1/3 dead and 1/3 disabled), and a considerable improvement over fluid and hypertensive treatment (17% dead, 29% deficits), calculated from a literature review. Nimodipine is also safer than induced hypertension, especially pre-operatively.