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Functional outcomes at 12 months were a secondary outcome of the randomized DECRA trial of early decompressive craniectomy for severe diffuse traumatic brain injury (TBI) and refractory intracranial hypertension. In the DECRA trial, patients were randomly allocated 1:1 to either early decompressive craniectomy or intensive medical therapies (standard care). We conducted planned secondary analyses of the DECRA trial outcomes at 6 and 12 months, including all 155 patients. We measured functional outcome using the Glasgow Outcome Scale-Extended (GOS-E). We used ordered logistic regression, and dichotomized the GOS-E using logistic regression, to assess outcomes in patients overall and in survivors. We adjusted analyses for injury severity using the International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) model. At 12 months, the odds ratio (OR) for worse functional outcomes in the craniectomy group (OR 1.68; 95% confidence interval [CI]: 0.96-2.93; p = 0.07) was no longer significant. Unfavorable functional outcomes after craniectomy were 11% higher (59% compared with 48%), but were not significantly different from standard care (OR 1.58; 95% CI: 0.84-2.99; p = 0.16). Among survivors after craniectomy, there were fewer good (OR 0.33; 95% CI: 0.12-0.91; p = 0.03) and more vegetative (OR 5.12; 95% CI: 1.04-25.2; p = 0.04) outcomes. Similar outcomes in survivors were found at 6 months after injury. Vegetative (OR 5.85; 95% CI: 1.21-28.30; p = 0.03) and severely disabled outcomes (OR 2.49; 95% CI: 1.21-5.11; p = 0.01) were increased. Twelve months after severe diffuse TBI and early refractory intracranial hypertension, decompressive craniectomy did not improve outcomes and increased vegetative survivors.

Genetic risk factors for intracranial aneurysm (IA) are not yet fully understood. Genomewide association studies have been successful at identifying common variants; however, the role of rare variation in IA susceptibility has not been fully explored. In this study, we report the use of whole exome sequencing (WES) in seven densely-affected families (45 individuals) recruited as part of the Familial Intracranial Aneurysm study. WES variants were prioritized by functional prediction, frequency, predicted pathogenicity, and segregation within families. Using these criteria, 68 variants in 68 genes were prioritized across the seven families. Of the genes that were expressed in IA tissue, one gene (TMEM132B) was differentially expressed in aneurysmal samples (n=44) as compared to control samples (n=16) (false discovery rate adjusted p-value=0.023). We demonstrate that sequencing of densely affected families permits exploration of the role of rare variants in a relatively common disease such as IA, although there are important study design considerations for applying sequencing to complex disorders. In this study, we explore methods of WES variant prioritization, including the incorporation of unaffected individuals, multipoint linkage analysis, biological pathway information, and transcriptome profiling. Further studies are needed to validate and characterize the set of variants and genes identified in this study.

OBJECTIVE Nocardial brain abscesses are associated with significant morbidity and mortality rates. The optimal management remains unclear. We reviewed the surgical outcomes of patients treated with a relatively uniform policy at a single institution.METHODS Eleven patients were treated at the Royal

Objective Transcranial Doppler (TCD) flow velocity (FV) assessment may provide a useful index of autoregulatory impairment after severe head injury. It may define a therapeutic end point against which cerebral perfusion pressure (CPP) can be titrated. This study examines the relationship between cerebral blood flow (CBF) and TCD FV indices in a laboratory model before and after autoregulatory impairment. Methods CPP, CBF, and middle cerebral artery TCD FV were measured continuously in nine anesthetized and ventilated sheep. CPP was decreased by hemorrhagic hypotension. The process was repeated after impairment of autoregulation by cisternal infusion, which maintained CPP at 0 mm Hg for 15 minutes. Points of significant change (i.e., breakpoints) from baseline values for each of the measured flow parameters were identified by using a ratio of variance technique. Results Before any significant change in CBF or systolic TCD, diastolic TCD FV decreased (mean breakpoint, 69 mm Hg; range, 56-78 mm Hg) as CPP was reduced. This divergence of diastolic and systolic TCD FV, which occurred before autoregulatory failure, was associated with an increasing TCD pulsatility index (mean breakpoint, 63 mm Hg; range, 53-70 mm Hg). At diastolic TCD FV congruent with 10 cm/s, systolic TCD FV (mean breakpoint, 48 mm Hg; range, 46-53 mm Hg) and CBF (mean breakpoint, 49 mm Hg; range, 47-51 mm Hg) decreased rapidly, indicating autoregulatory failure. After autoregulatory impairment, the breakpoints for all four indices shifted to higher CPP values (mean, 16 mm Hg). Conclusion TCD FV assessment identified two CPP thresholds of autoregulatory loss. Before autoregulatory failure, an earlier phase of autoregulatory disturbance may be detected by divergent systolic and diastolic TCD FVs. It is important to note that this phase may be detected before CBF decreases. These TCD FV breakpoints depend on the state of autoregulatory impairment and may provide potential targets for CPP-directed therapy.

The aim of this study was to assess and quantitate topographically the effects of posttraumatic intravenous magnesium sulphate (MgSO4) on neuronal perikaryal APP antigen and messenger RNA (mRNA) expression in sheep brains 2 h after a controlled focal head impact. The percentage brain area with APP immunoreactive neuronal perikarya was 71, 56, 27.5 and 5.5%, respectively, in MgSO4-treated head-injured animals, head-injured animals without any treatment, MgSO4 treated nonimpacted animals, and nontreated nonimpacted control sheep. Although there was no statistically significant difference in APP immunoreactive neuronal perikarya in the MgSO4-treated HI group (mean 71%) compared to the HI group without any treatment (mean 56%), northern analysis showed that there was a 2.3-+/-0.2-fold increase in APP mRNA in the thalamus of treated impacted animals compared to untreated impacted animals (p < 0.005). However, MgSO4 treated nonimpacted control animals also showed a 1.6-+/-0.1-fold increase in APP mRNA compared to untreated nonimpacted controls (p < 0.005). MgSO4 therapy results in upregulation of neuronal APP mRNA and APP expression that is quantitatively greater following a focal head impact.

STUDY DESIGN Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI. OBJECTIVES To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia. SUMMARY OF BACKGROUND DATA Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury. METHODS The study group comprised 18 cases of spinal cord compression (17 due to fracture dislocation of the vertebral column and 1 iatrogenic compression from Harrington rods) and two normal control. All the cords were examined according to a standard protocol, and at least 10 segmental levels were immunostained using a monoclonal antibody to amyloid precursor protein and immunopositive AI was semiquantitated using a grading system to provide the axonal injury severity score (AISS). The focal injury at the site of cord compression (haemorrhage, haemorrhagic necrosis, ischaemic necrosis) was also semiquantitated to provide the focal injury area score (FIAS). AI occurring around the site of focal compression (focal axonal injury severity score or FAISS) was distinguished from AI distant to the focal injury (nonfocal axonal injury severity score or NFAISS). RESULTS All 18 cases showed widespread amyloid precursor protein immunoreactive axonal injury and the AISS ranged from 28 to 60%. In all cases, the FAISS was greater than the NFAISS and there was a statistically significant relationship between the AISS and the FIAS. CONCLUSION Acute spinal cord compression of sufficient severity to produce permanent paralysis causes widespread axonal damage that is maximal at the site of compression but also present throughout the length of the cord in segments far distant from the site of the focal injury.

“Syndrome of the trephined” or “sinking skin flap syndrome” is an unusual syndrome in which neurological deterioration occurs following removal of a large skull bone flap. The neurological status of the patient can occasionally be strongly related to posture. A 77-year-old male patient with an acute subdural hematoma was treated using a hemicraniectomy and evacuation of the hematoma. On the 9th postoperative day there was deterioration in sensorium associated with a sunken scalp flap and worsening midline shift on CT. A significant improvement in sensorium and a filling up of the scalp flap occurred after maintaining the patient's head in a dependent position. The patient subsequently made an excellent recovery following replacement of the bone flap. The pathophysiology of “syndrome of the trephined” or “sinking skin flap syndrome” is reviewed.

Continuous transcranial Doppler ultrasonography of the middle cerebral artery (TCD-MCA) has been proposed as a method of identifying the lower cerebral autoregulatory threshold. This study investigated the relationship between continuous TCD-MCA and cerebral blood flow (CBF) in sheep. Arterial blood pressure, intracranial pressure, CBF and left TCD-MCA were measured in 12 anaesthetized and ventilated merino sheep. Cerebral perfusion pressure (CPP) was reduced by haemorrhagic hypotension. Measurements were recorded continuously and breakpoint thresholds calculated by an analysis of variance. The TCD-MCA systolic velocity breakpoint (50 +/- 1.5 mmHg) did not significantly differ from the lower limit of autoregulation, identified by the CBF breakpoint (50 +/- 1.8 mmHg). The TCD-MCA diastolic velocity breakpoint occurred at a significantly higher level of CPP (64 +/- 2 mmHg) (P0.01). The relationship between TCD-MCA flow velocity and CBF thresholds has been described. Early divergence of flow velocity may represent a compensatory mechanism to maintain CBF.

Preventable secondary injury remains disturbingly common and can only be reduced by highly organized and integrated services, and careful and continuous monitoring. Continuous non- or relatively non-invasive bedside monitoring of factors closely related to brain metabolism and function is becoming a practical reality. To the extent that the complex changes initiated by traumatic brain injury are ‘processes’ rather than ‘events’ it may become possible for components of injury to be halted or reversed. Pharmacological therapy given early after injury may be able to reduce the harmful events initiated by the injury. Head injury management is multidisciplinary. Improvements in head injury outcome have come about through better organisation of services — efficient retrieval, early investigation and removal of clots, and management in experienced intensive care units. Australian neurosurgeons have played a leading role in defining standards of care, in organizing services and in raising public health issues related to head injury. With the increasing and necessary involvement of other specialists and the greater dependence on technically demanding intensive monitoring and medical management, it is important that neurosurgeons remain at the forefront of the care of patients with head injury and not simply be reduced to managing the surgical complications on request.86

Axonal injury (AI), one of the principal determinants of clinical outcome after head injury, may evolve over several hours after injury, raising the future possibility of therapeutic intervention during this period. A new head impact model of AI in sheep was developed to examine pathological and physiological changes in the brain resulting from a graded traumatic insult. In this preliminary study 10 anesthetized and ventilated Merino ewes were used. Head injury was produced by impact from a humane stunner to the temporal region of an unrestrained head. Eight sheep were studied for 1, 2, 4, or 6 h after impact. Two sham animals (no impact, 6 h survival) were also examined. Arterial blood pressure, intracranial pressure, and cerebral blood flow were monitored continuously. A physiological index of injury severity was calculated by weighting the percentage shift from preinjury values for each monitored parameter over the first hour after injury. Immunostaining with amyloid precursor protein (APP) was used as a marker of axonal damage and the distribution of APP positive axons was recorded according to a sector scoring method (APPS). Widespread AI was identified in 7 of the 8 impacted animals, around cerebral contusions and in hemispheric white matter, central gray matter, brain stem, and cerebellum, and was detected as early as 1 h after injury. The degree of axonal injury (APPS) correlated well with an index of physiological response to injury (r = 0.83, p = 0.005).

✓ This 30-year-old woman presented with clinical symptoms and signs of intracranial hypertension and Parinaud syndrome secondary to ventriculoperitoneal shunt dysfunction. Magnetic resonance (MR) imaging revealed gross triventricular hydrocephalus with a large suprapineal recess due to aqueductal stenosis. Using an endoscopic approach, a ventriculostomy was performed within the floor of the dilated suprapineal recess. Following this procedure the patient experienced alleviation of all her neurological symptoms and signs. Postoperative MR imaging and cerebrospinal fluid flow studies demonstrated a functioning ventriculostomy. The anatomy of the suprapineal recess and its suitability for endoscopic ventriculostomy are discussed.

A prospective observational study was performed to assess the reliability of fibreoptic oximetric catheters and to identify the incidence and causes of jugular bulb oxygen desaturation in patients with acute closed head injury. There were twenty- five patients (30± 16 years) with GCS ≤8 in this study. Jugular bulb oximetry, mean arterial pressure, intracranial pressure, end-tidal CO2 and pulse oximetry were monitored continuously. Catheter calibration against a laboratory oximeter was performed post insertion and thereafter eight-hourly. Cerebral venous desaturation was defined as a jugular bulb oxygen saturation 10 minutes duration. There was a poor correlation for the first in vivo calibration (r2 = 0.602, P2 = 0.868, P Validation with a laboratory oximeter is essential prior to continuous jugular bulb oximetry. Sustained episodes of cerebral venous desaturation are frequent within the first 48 hours following acute head injury. Factors such as hypocapnia and cerebral hypoperfusion that primarily reduce cerebral blood flow are predominant.

Raised intracranial pressure (ICP) is the commonest cause of death in neurosurgical patients. It occurs in patients with head injury, haemorrhagic and thrombotic stroke, and space occupying lesions such as brain tumour. Intracranial mass lesions and the brain swelling that accompanies them raise ICP and distort the brain. It has been known for many years that anaesthetic agents may raise ICP’ and it is now commonplace for intensivists to care for patients suffering from severe head injury. Therefore, anaesthetists and intensive care specialists need to understand the principles of intracranial pressure dynamics. ICP monitoring provides the only sure way of confirming or excluding intracranial hypertension. If this is present, ICP monitoring provides the only reliable method of assessing whether therapy works and provides an early opportunity of switching to an alternative therapy should treatment fail. If increased ICP is not present, potentially dangerous treatment can be avoided. If the patient is paralysed or heavily sedated, conventional neurological observation is useless and ICP monitoring provides a means of determining the patient’s cerebral perfusion pressure (CPP) and an index of cerebral function.*

A false aneurysm of the pericallosal artery formed following resection of a colloid cyst. The aneurysm presumably resulted from arterial damage during surgery and its enlargement may have been facilitated by the surgical defect in the corpus callosum. A spherical hyperdense lesion on postoperative CT may indicate a false aneurysm.

While it is understood that raised intracranial pressure (ICP) after traumatic brain injury (TBI) may negatively impact on brain tissue oxygenation (PbtO2), few studies have characterized the inter-relationship between these two variables, particularly in a large animal model that replicates the human gyrencephalic brain. The current study uses an ovine model to examine the dynamics of ICP and PbtO2 after TBI.Five 2-year-old male Merino sheep were anesthetized with isoflurane and impacted in the left temporal region using a humane stunner. ICP and PbtO2 were then monitored over the following 4 h using a Codman ICP Express monitoring system and a LICOX brain tissue oxygen monitoring system, respectively. Two additional sheep were anesthetized and monitored as sham (uninjured) controls.Mean ICP 60 min following TBI was over 25 mmHg (p0.05 versus controls) and by 4 h, values were consistently greater than 30 mmHg (p0.001). With respect to PbtO2, values fell from mean control values of 52 +/- 11 to 20 +/- 4 mmHg by 60 min (p0.001) and by 4 h to 14 +/- 3 mmHg (p0.01). The sigmoidal relationship between the two variables included a negative linear correlation when ICP was between 13 to 27 mmHg.Our results suggest that TBI results in early changes in ICP that are associated with profound declines in PbtO2, and may indicate the need for earlier management of ICP after TBI.

Neurotrauma, in many countries and particularly in the younger age group kills more people than AIDS or cancer but unlike these diseases the causes are known and it is preventable. The costs to communities in terms of suffering and economics are enormous. The common causes are road traffic accidents, falls and violence. Neurotrauma affects particularly the developing world where it consumes already over stretched health resources. In the developed world steps to reduce the incidence of neurotrauma and to treat the victims have had some effect nevertheless it stills remains an endemic problem which does not receive the public awareness or the political support it deserves. For the victims there is general agreement on the principles of clinical management but often difficulties in applying early and effective care in countries with the greatest need because of shortage of facilities and expertise. To reduce the overall burden of neurotrauma demands actions which extend from the political to basic patient care. There have been remarkable advances in the understanding of acute brain and spinal cord injury and encouraging possibilities for effective neuroprotection, repair and regeneration but in the broader context prevention of neurotrauma is the urgent imperative. In this endeavour the neuroscientist has knowledge which informs and encourages policy makers to take the steps necessary to reduce injury. These steps require political will and community support for hard decisions which impact on the way people conduct their daily lives. The WHO predicts that unless there are changes in present policies and if there are no additional road safety countermeasures put in place, there will be a major increase in road traffic fatalities over the next 20 years and beyond (World Health Organisation. (2004). www.who.int).

Background: Due to the geographical remoteness of Darwin, which has no resident neurosurgeon, emergency transfer of patients for neurosurgery is usually impractical. In Darwin emergency neurosurgery must be undertaken by general surgeons. Methods: Data from the operating theatre, Emergency Department and Intensive Care Unit were prospectively recorded on all patients who underwent an emergency neurosurgical procedure between January 1992 and June 2004. Outcomes were assessed by retrospective case note review. Results: Three hundred and five neurosurgical procedures were performed upon 258 patients (average 26.5 procedures per year), including 130 craniotomies, 88 burr holes, 3 posterior fossa craniotomies, 2 decompressive frontal lobectomies, 4 decompressive craniectomies, 25 elevations of fracture and 33 ventricular drains only. Assault/domestic incident (31%) was a more common aetiology than motor vehicle accidents (29%). Outcome was best for extradural haematoma (82% good/moderate) and chronic subdural haematoma (84% good/moderate). In contrast, 44% with acute subdural haematoma and 77% with intracerebral haematoma died. Irrespective of type of bleed, Glasgow Coma Scale (GCS) score at presentation was a reliable predictor of outcome following surgery (61% correlation): 60% with GCS less than 9 died whereas 79% with GCS over 11 had a good recovery. Acute Physiology And Chronic Health Evaluation, version 2 and Simplified Acute Physiology Score, version 2 scores were also independent predictors of outcome. Time from presentation to operation for extradural haematoma and acute subdural haematoma was prolonged (more than 4 h) in 48% and was associated with worse outcome (P = 0.0001). Neither extremes of age nor the particular surgeon performing the operation affected outcome. Conclusions: General surgeons undertake a substantial number of procedures across a broad spectrum of emergency neurosurgery in Darwin. Outcomes following surgery appear acceptable.

The aim of these studies was to assess and quantitate the effects of cyclosporin-A (CyA) on brain APP messenger RNA and neuronal perikaryal APP antigen expression following controlled focal head impact in sheep. Impact results in a significant increase in both APP mRNA and neuronal perikaryal APP antigen expression. Post-traumatic administration of CyA (intrathecal 10 mg/kg) resulted in a reduction in APP mRNA and neuronal perikaryal antigen expression. At 2 h postinjury, CyA treatment caused a statistically significant (p0.05) 1.3 +/- 0.1-fold decrease in APP mRNA in the central gray matter of impacted sheep compared to untreated impacted sheep. A more profound reduction in APP mRNA synthesis (1.6 +/- 0.2 fold) was evident at 6 h (p0.05). The mean percentage brain area with APP immunoreactive neuronal perikarya at 6 h post-injury was 94.5% in untreated impacted animals, 10.0% in CyA-treated impacted animals, 5.5% in untreated nonimpacted animals, and 6% in CyA-treated non-impacted controls. These results demonstrate that CyA has a downregulatory effect on increased APP expression caused by TBI.

The authors report a 23-year-old man who was diagnosed with a brain stem malignant glioma following his first episode of generalised seizure. This was subsequently complicated by three separate documented episodes of intracranial haemorrhage. The literature is reviewed and the pathophysiological mechanisms of tumoural haemorrhage are discussed. It is speculated that significant intratumoural arteriovenous shunting may lead to recurrent haemorrhages.

Nocardial brain abscesses are associated with significant morbidity and mortality rates. The optimal management remains unclear. We reviewed the surgical outcomes of patients treated with a relatively uniform policy at a single institution.Eleven patients were treated at the Royal Adelaide Hospital between 1970 and 2001. Their clinical presentations, surgical treatment, and outcomes were reviewed.Clinical presentations most frequently involved focal neurological deficits (91%). Predisposing factors were identified for 63% of the patients. Nine patients were treated only with aspiration and long-term chemotherapy. Two patients underwent craniotomy and lesion excision. The majority of patients required either one or two procedures. There were no deaths in this series. Management complications were observed for three patients. Abscess aspiration was complicated by parenchymal hemorrhage and ventriculitis for one patient and temporary worsening of hemiparesis for two patients.Our results suggest that aspiration alone (repeated as clinically indicated) is a safe, efficacious treatment for the majority of patients with nocardial brain abscesses.

In the 25 years since the 'Talk and Die' paper there have been substantial advances in the management of patients with severe closed head injury. This paper discusses developments in understanding of primary and secondary injury. Current management focuses on preventing secondary brain injury. That this has been successful is illustrated by a fall in mortality in recent decades. Evidence based guidelines have set standards of management but they do not take into account variations between individuals, between regions of the brain and variations with time from injury. Various monitoring techniques such as transcranial doppler, jugular venous oxygen saturation and ICP waveform analysis attempt to set individual therapeutic endpoints and to target therapy appropriately. Primary injury is no longer seen as a single irreversible event occurring at the time of impact, but rather as a process initiated by the impact and evolving over subsequent hours and days. Experimental studies have identified agents which reduce the evolution of brain injury and improve outcome. An experimental model of brain injury developed by the Adelaide He ad Injury Group identifies diffuse axonal injury as a target for therapeutic manipulation. Magnesium has been shown in other studies to improve outcome after diffuse brain injury. This has now been linked with upregulation of beta amyloid precursor prote in. Although this and several other experimental therapies have shown great promise, they have not so far produced benefit in large clinical studies. Avoiding secondary insults will remain the goal of management for the foreseeable future. Halting the evolution of the primary injury remains a highly sought after goal. Although elusive so far, it is likely to be the next major advance in clinical care.

For over 25 years, we have recorded intraoperative nerve action potentials (NAPs) on ulnar entrapments selected for operation. As summarized in 1995 [2], one of the striking findings in more than 400 cases was that NAP amplitude and conduction velocity (CV) often began to decrease on the portion of the nerve just proximal to the olecranon notch area. Even more importantly, the conductive abnormalities were, almost always, maximal along the segment of nerve within the olecranon notch. It was infrequent (only five cases) for the abnormality to be maximal in the cubital tunnel region distal to the olecranon notch. These electrical findings corresponded with our observations of scar, thickening, or sometimes attenuation of the nerve in the notch region. This strongly suggests that when there is significant and symptomatic ulnar entrapment, the problem is usually in the area of the olecranon notch and that therefore, the best procedure, if the nerve is to be operated upon, is to move it away from there. Thus, it would seem that release of the portion of the cubital tunnel beneath the flexor carpi ulnaris alone may not suffice. Once transferred, the ulnar nerve is placed deep to the pronator teres (PT) and flexor carpi ulnaris (FCU). Thus, we do a submuscular transposition as originally proposed by Learmouth [3], and modified by Dellon [1] and more recently others, including ourselves [2,4].

Amyloid precursor protein (APP), a membrane spanning glycoprotein which plays an important role in neuronal growth and synaptic plasticity, is increased after traumatic brain injury (TBI) and has been used as a sensitive marker of neuronal damage in an adult sheep head impact model. We hypothesised that APP expression would similarly be increased in lambs, suggesting that in the immature injured brain APP is also upregulated as an acute phase response to trauma. Ten anaesthetised and ventilated 4-5 week old Merino lambs sustained a left temporal head impact from a humane stunner. At 2 h after impact, there was widespread and intense neuronal cell body APP immunoreactivity which was more widely distributed than axonal APP. APP messenger RNA (mRNA) expression was also markedly increased with a distribution similar to that of APP antigen. These results demonstrate that APP antigen and mRNA are sensitive early indicators of TBI in paediatric cases.

In order to determine whether axonal injury (AI) is a factor in cases of penetrating head injury, the brains of 14 patients who died shortly after sustaining a fatal gunshot wound (GSW) to the head were examined, and the presence of AI determined using immunohistochemical staining for amyloid precursor protein (APP). The distribution of AI was mapped throughout the cerebral hemispheres and brain stem. AI was present in all cases in a diffuse distribution distant to the missle track with severe involvement of the brain stem in all cases. There was no axonal APP immunoreactivity in the direct region of the missle track at the point of primary axotomy. The APP-positive AI in these cases is likely to be a mixture of primary and secondary AI as APP immunostaining is unable to distinguish primary AI due to mechanical deformation from AI secondary to hypoxic-ischemic damage.

Laboratory studies suggest the pulsatile component of the transcranial doppler (TCD) waveform may be useful in determining lower autoregulatory threshold. This study aimed to assess the effect of increasing CPP on jugular bulb oximetry (SjO2) and middle cerebral artery (MCA) TCD flow velocities in the early management of severe head injury.

Amyloid precursor protein (APP) has been shown to accumulate in traumatically injured axons as early as 1 hour after injury. This accumulation may be due to interruption of fast axoplasmic transport and/or upregulation of APP synthesis. The aim of this study was to examine the neuronal cell body response to head impact using APP immunostaining in a focal non-missile head impact model.

To compare continuous jugular venous bulb oximetry and cerebral near-infrared spectroscopy in patients with severe closed head injury.A prospective observational study.Intensive care unit of a major teaching hospital.Adults (n = 10) with severe closed-head injury (Glasgow Coma Scale score ofor = 8).None.Jugular venous bulb oximetry, cerebral near-infrared spectroscopy, and cerebral perfusion pressure were measured continuously. A total of 3,691 paired measurements of near-infrared spectroscopy and jugular venous bulb oximetry were analyzed. Poor correlation (r2 = .04) between paired measurements and wide limits of agreement (-13% to +21%) were demonstrated. The mean difference between measurements was +/- 4% and the standard deviation of the mean difference was +/- 8.69%. The data were subsequently grouped according to three clinically significant subgroups of jugular venous bulb oxygen saturation reflecting low (55%), normal (55% to 75%) and high (75%) saturation values. Poor correlation and wide limits of agreement between the two methods of measurement were observed in all groups. Values recorded by near-infrared spectroscopy did not significantly change between the groups, and 14 clinically significant episodes of jugular venous bulb desaturation were not detected by near-infrared spectroscopy.Tissue oxygen saturation determined by near-infrared spectroscopy does not reflect significant changes in cerebral oxygenation detected by the global measurement of jugular venous bulb oximetry. This finding may be explained by inadequate signal detection and inaccuracies in the algorithm used to filter out extracranial components. Until these technical difficulties are addressed, near-infrared spectroscopy, as measured by the machine assessed in this study, cannot be routinely recommended for assessment of cerebral oxygenation in patients with acute head injury.

The 1975 paper ‘patients with head injury who talk and die’ depended on the insight of Bryan Jennett who coined the phrase and saw the significance of this group of patients and the excellent neuropathological studies of a large series of fatal head injuries conducted by Hume Adams and David Graham – a type of study almost impossible to replicate. That paper highlighted the distinction between primary head injury, in this group minor, and secondary head injury which was fatal. The important implication of that paper was that the primary head injury itself was potentially survivable. An analysis of ‘talk and die’ patients might therefore be an important audit of a trauma system. Goldschlager et al. in a retrospective review over 10 years, identified 15 patients who died after being admitted with mild head injury to a major trauma centre. This is an incidence of 1.5% per year or >6% of all mild head injuries. The selection of patients is based on coronial reporting but the analysis is based on CT scans rather than neuropathology. The patients were mostly elderly and the majority died as the result of acute subdural haematomas or contusions with swelling.

SUMMARY In the past one hundred years the surgery for brain tumours has advanced further from the mists of mythology to the limits of technology. The surgeon can approach an operation with very detailed information about the site, shape and attachments of a tumour. Microsurgical techniques have improved the operative results for benign tumours such as the acoustic neuroma. The surgical laser, and CT guided biopsy may refine the treatment of some patients still further, but we are no closer to curing gliomas. For these tumours, and for incompletely removed benign tumours, we must await a non surgical cure.

✓ Two patients who suffered loss of vision due to spontaneous optic nerve hematomas are described. The hemorrhage was contained within the pial confines of the involved optic nerve, although there was some extension more posteriorly. The diagnosis of an intraneural cryptic arteriovenous malformation was histologically confirmed in one case and was supported by evidence in the other. Surgical evacuation by the subfrontal approach was undertaken and visual function improved.

The importance of the empty sella syndrome has increased with recent interest in pituitary micro-adenomas, trans-sphenoidal hypophysectomy and computerised tomography. Four cases of the empty sella syndrome which illustrate the clinical and radiological features are reported, and the literature is reviewed. Headache, visual symptoms and endocrine disturbances are commonly found in association with the empty sella syndrome, and the coexistence of pituitary micro-adenomas is well recognised. Symmetrical ballooning of the sella turcica without changes in configuration is the typical finding with plain radiography, but occasionally more extensive destructive changes in the region of the pituitary fossa may occur. Provided that the correct angulation, collimation and level of cut are chosen, computerised tomography now may be used to make a definitive diagnosis, making air encephalography unnecessary.

Shunt function testing by radionuclide injection and shunt pressure measurement was performed in 312 cases. In our experience the test has a sensitivity of 92% and accuracy of 89%. The diagnostic value of the components of the test are discussed. The test is a safe and integral part of the assessment of shunt function. The significance of shunt malfunction must of course be determined by clinical evaluation, measures of ventricular size by CAT scanning or ultrasound, and by continuous ICP recording. However the shunt function test combined with shunt pressure measurement is a safe and essential investigation of symptomatic shunt malfunction.