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Cerebral vasospasm has traditionally been regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral infarction and poor neurological outcome. However, data from recent studies argue against a pure focus on vasospasm as the cause of delayed ischaemic complications. Findings that marked reduction in the incidence of vasospasm does not translate to a reduction in DCI, or better outcomes has intensified research into other possible mechanisms which may promote ischaemic complications. Early brain injury and cell death, blood-brain barrier disruption and initiation of an inflammatory cascade, microvascular spasm, microthrombosis, cortical spreading depolarisations and failure of cerebral autoregulation, have all been implicated in the pathophysiology of DCI. This review summarises the current knowledge about the mechanisms underlying the development of DCI. Furthermore, it aims to describe and categorise the known pharmacological treatment options with respect to the presumed mechanism of action and its role in DCI.

Background: Inflammation is a recognised risk factor for the vulnerable atherosclerotic plaque. The aim of this study was to explore whether there is a difference in the degree of magnetic resonance (MR) defined inflammation using ultra small superparamagnetic iron oxide (USPIO) particles within carotid atheroma in completely asymptomatic individuals and the asymptomatic carotid stenosis contralateral to the symptomatic side. Methods: 20 symptomatic patients with contralateral disease and 20 completely asymptomatic patients underwent multi-sequence MR imaging before and 36 h after USPIO infusion. Images were manually segmented into quadrants and signal change in each quadrant was calculated following USPIO administration. Mean signal change was compared across all quadrants in the two groups. Results: The mean percentage of quadrants showing signal loss was 53% in the contralateral group compared with 31% in completely asymptomatic individuals (p = 0.025). The mean percentages showing enhancement were 44% and 65%, respectively (p = 0.024). The mean signal difference between the two groups was 8.6% (95% CI 1.6% to 15.6%; p = 0.017). Conclusions: Truly asymptomatic plaques seem to demonstrate inflammation but not to the extent of the contralateral asymptomatic stenosis to the symptomatic side. Inflammatory activity may be a significant risk factor in asymptomatic disease.

OBJECTIVE—To assess transcranial power Doppler and the effect of an intravenous ultrasonic contrast agent for detecting intracranial aneurysms in patients admitted with a subarachnoid haemorrhage METHODS—203 patients with subarachnoid haemorrhage were examined with the operator blind to the results of the admission CT and subsequent digital subtraction angiogram (DSA). In 98 cases patients were imaged using unenhanced transcranial power Doppler, and in 105cases, patients were imaged both using unenhanced and echo contrast enhanced (Levovist, Schering AG) transcranial power Doppler. RESULTS—DSA detected 168 intracranial aneurysms in 128 patients (24 patients had multiple lesions) and 75 patients had an aneurysm negative DSA. There was agreement between DSA and transcranial power Doppler in 87 intracranial aneurysms of which 20 were only detected after infusion of contrast agent. Without contrast infusion, transcranial power Doppler showed a sensitivity of 40% and specificity of 91%. A significant increase in detection was noted when using a contrast agent (χ2=9.49, p

Cerebral critical closing pressure (CCP) has been defined as an arterial pressure threshold below which arterial vessels collapse. Hypothetically this is equal to intracranial pressure (ICP) plus the contribution from the active tone of cerebral arterial smooth muscle. The correlation of CCP with ICP, cerebral autoregulation, and other clinical and haemodynamic modalities in patients with head injury was evaluated.intracranial pressure, arterial blood pressure (ABP) and middle cerebral artery blood flow velocity were recorded daily in ventilated patients. Waveforms were processed to calculate CCP, the transcranial Doppler-derived cerebral autoregulation index (Mx), mean arterial pressure (ABP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP).Critical closing pressure reflected the time related changes in ICP during plateau and B waves. Overall correlation between CCP and ICP was mild but significant (R=0.41; p0.0002). The mean difference between ABP and CCP correlated with CPP (R=0.57, 95% confidence interval (95% CI) for prediction 25 mm Hg). The difference between CCP and ICP, described previously as proportional to arterial wall tension, correlated with the index of cerebral autoregulation Mx (p0.0002) and CPP (p0.0001). However, by contrast with the Mx index, CCP-ICP was not significantly correlated with outcome after head injury.Critical closing pressure, although sensitive to variations in ICP and CPP, cannot be used as an accurate estimator of these modalities with acceptable confidence intervals. The difference CCP-ICP significantly correlates with cerebral autoregulation, but it lacks the power to predict outcome after head injury.

OBJECTIVE--To audit the outcome in patients with subarachnoid haemorrhage (SAH) after a change in management strategy. METHODS--A retrospective analysis of patients with aneurysmal subarachnoid haemorrhage over a 20 month period (phase 1) was followed by a prospective analysis of patients presenting during the next 20 months (phase 2) in which a protocol driven management regime of immediate intravenous fluid resuscitation and earlier surgery was pursued. Patients in this phase were grouped into those receiving early (within four days of subarachnoid haemorrhage) and late (after four days of subarachnoid haemorrhage) surgery. In phase 1, 75 out of a total of 92 patients underwent surgery on (median) day 12. From phase 2, 109 patients out of a total of 129 underwent surgery on (median) day 4, 58 of which had their surgery within 4 days of the subarachnoid haemorrhage. Patients in each phase/group were well matched for demographic features, site of aneurysm, and severity of subarachnoid haemorrhage. RESULTS--The surgical morbidity and mortality were no different in the two phases (P < 0.92; chi2 test). The management outcomes in the two phases of the study were also no different (P < 0.52). However, there was a significant reduction in the rebleed rate in patients undergoing surgery within four days of the subarachnoid haemorrhage in phase 2 (P < 0.0001) with an associated trend towards reduced incidence of postoperative ischaemia (P = 0.06) and mortality (P = 0.11). Operating earlier in phase 2 of the trial resulted in a lower total hospital inpatient stay of 15.8 (95% CI 13.1-18.5) days for survivors compared with 25.7 (95% CI 21.6-29.8) days in the late group (P < 0.00001; t test). CONCLUSIONS--surgical morbidity and mortality seemed independent of the timing of aneurysm surgery. Early surgery within four days was associated with a highly significant reduction in rebleed rate, and in the duration of total hospital inpatient stay.

Applanation tonometry is a non-invasive method of assessing the arterial blood pressure profiles in both the peripheral and systemic circulation. In this study the authors examined whether there were differences in these profiles in patients with trigeminal neuralgia. The carotid artery and derived aortic blood pressure waveforms were obtained using a pulse wave analysis system. The ratio of the pressure wave amplitude above the systolic shoulder to the total systolic blood pressure (augmentation index, AIx) was recorded. Thirty two patients with trigeminal neuralgia (16 male and 16 female) and 100 controls (50 male and 50 female) were recruited. Eleven patients had been treated by microvascular decompression, mean (SD) time from surgery 17 (24) months (range 3-86 months). For the patients with trigeminal neuralgia, the right and left carotid artery AIxs (mean (SD)) were 120.6 (21.7)% and 120.7 (19.1)% respectively. Corresponding values for the control group were 120.5 (19.3)% and 120.9 (19.5)%. The calculated AIx for the ascending aorta was 27.7 (10.1)% and 27.2 (10.5)% for the patients with trigeminal neuralgia and controls respectively. No significant differences were seen in either the right or left carotid artery (p=0.5 and p=0.6 respectively) or the derived ascending aorta (p=0.8). The results show that there does not seem to be a generalised increase in arterial stiffness in patients with trigeminal neuralgia.

Miller and Hayes have assembled chapters from 42 expert contributors renowned for their work in investigation of traumatic brain injury. They have divided the text into three main sections, basic science: overview; preclinical studies, and clinical directions. Organising the text in this way the authors have struck a theme …

Neurosurgical Management of Aneurysmal Subarachnoid Haemorrhage. Edited by iver a langmoen, tryggve lundar, rune aaslid, and hans-j reulen (Pp 177, DM140). Published By Springer-Verlag, Wien, 1999. ISBN 3 211 83256 4. The editors have gathered contributions on aneurysmal subarachnoid haemorrhage from several authors, each chapter dealing with a particular component of the subject and its up to date management. Chapters 1 to 3 cover the pathology, aetiology, and pathophysiology; the next two chapters are concerned with …