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Traumatic brain injuries (TBI) are one of the most common consequences of traffic accidents. Patients with mild, moderate or severe brain injuries suffer from physical, cognitive, behavioral, emotional and social problems. Most of these problems have been a long standing focus amongst practitioners and researchers. Only recently a development has started that took interest in the quality of life outcome of TBI patients. The international members of this consensus meeting reviewed the literature on Quality of Life assessment after TBI and discussed the applicability of different measurements to this specific patient group.During the acute phase (T1;3 month after trauma) QoL it is difficult to assess due to the reduced consciousness of TBI patients. In the phase of rehabilitation (T2;one year after trauma) and in the post-rehabilitation phase (T3) repeated assessment of QoL is recommended.Several generic and disease-specific instruments possibly relevant to TBI patients or specifically developed for this group were assessed according to the existing evidence in the literature. Criteria for the evaluation of these instruments were: feasibility, specificity, validity, comprehensiveness, international availability, existence of norms, and psychometric quality. The cognitive impairment and the existential dimension were not sufficiently considered in most of the reviewed instruments.The family's and relatives' view of the patient's QoL should not be used as a proxy but provides an additional source of information in the acute phase. At T2 and T3, assessment of the patient's quality of life should include a generic as well as a disease specific instrument. Among the generic instruments the SF-36, the EuroQol and the WHO-QoL should be considered. The literature about specific instruments for patients with TBI like the EBIC is scarce. Therefore, the group could hardly give an empirically based recommendation. The need for further investigation on QoL instruments in TBI patients is strongly emphasized.

Treatment that results in death or survival with unacceptable disability should be minimized. A decision to limit treatment can sometimes be made within 48 hours. Failure to decide may deny intensive care to other patients who could benefit.

The strategy of head injury management should be to minimize avoidable mortality and morbidity by reducing secondary brain damage. Patients with severe injuries are a minority, and their main needs are maintenance of the airway and nutrition. Some patients with less severe injuries are at risk for developing intracranial hematoma, and these need CT scanning. Pharmacological interventions may improve the outlook for patients with diffuse injuries associated with brain swelling.

Features of patients transferred to a regional neurosurgical unit in coma after recent head injury were compared with a similar audit seven years previously. There were fewer avoidable adverse factors in the recent series, but some patients received inadequate care of the airway, while in some others major extracranial injuries were overlooked or poorly managed. Only 42% of the comatose patients had had an endotracheal tube inserted; half those in whom neither a tube nor an oral airway had been inserted were transported supine. Systemic hypoxia or hypotension [corrected] were associated with a poor outcome. Even when computed tomography scanners become available in more hospitals, many patients who are unconscious after head injury will still need to be transferred to a neurosurgical unit. Detailed guidelines should be agreed locally to minimise the hazards of transfer of unconscious patients between hospitals. A rota of experienced doctors and nurses at the sending hospital should be responsible for deciding how each individual patient should be managed during transfer, according to the guidelines. Continuing audit of such cases is needed to indicate whether revision of local practice is needed.

The ability to predict outcome in the early stages of severe head injury would have several uses. A computerized system which has been developed in Glasgow to assist clinicians in this task, based on information from over 2500 severely head-injured patients, is described, with particular attention to the testing of the statistical properties of the system, and, more importantly, the assessment of its clinical impact.

When the brain is examined within a few days of injury it can be surprisingly difficult to establish what has been the cause of death, or to determine with certainty which lesions are primary and which are secondary, apart from clear-cut complications such as intracranial haematoma or infection. Recent reports of continuous measurements of intracranial pressure after head injury (Lundberg, Troupp, and Lorin, 1965; Troupp, 1965 and 1967) suggest that many patients who die after head injury develop very high intracranial pressure before death without necessarily having a focal expanding lesion. The effect of a generalized increase in intracranial pressure on the brain is ultimately to produce a reduced perfusion of blood and the brain will then suffer hypoxic damage. In the belief that this may be one of the mechanisms contributing to brain damage after head injuries (and other lesions causing raised pressure) we have explored various aspects of the relationships between intracranial pressure and cerebral blood flow. The oxygen supply to the brain depends, as in any other tissue, on the equation: available oxygen = haemoglobin x oxygen saturation x blood flow. A reduced oxygen content of the blood is not uncommon after head injury, which makes the brain much more critically dependent on blood flow. Blood loss from associated injuries, which occurs in a third of all cases of head injury admitted to hospital, commonly gives a low haemoglobin. Respiratory difficulties are also frequent after head injury, either due to the unconscious state or to associated chest injuries, and as a result of ventilatory insufficiency the oxygen saturation is then reduced. Blood flow in the brain has a characteristic peculiar to its situation within a rigid closed cavity, namely, its susceptibility to surrounding tissue pressure. Indeed the supply of blood to the brain depends on cerebral perfusion pressure, which is the difference between systemic arterial pressure and intracranial pressure. Cerebral perfusion may be altered not only by systemic hypotension but also by raised intracranial pressure. Whilst hypotension is uncommon in patients suffering from head injury alone, the

SUMMARY The effects of the neuroleptanalgesic drug combinations, droperidol 5 mg+phnoperidine 1.5 mg, and droperidol 5 mg+fentanyl 0.1 mg, on the cerebrospinal fluid (c.s.f.) pressure, have been studied in patients with normal c.s.f. pathways during controlled ventilation. The influence of droperidol 5 mg+fentanyl 0.1 mg on intracranial pressure has also been investigated in patients with intracranial space-occupying lesions. In patients with normal c.s.f. pathways, droperidol and phenoperidine produced only small alterations in c.s.f. pressure in either direction, while a significant decrease in overall mean c.s.f. pressure. Similarly, in patients with intracranial space-occupying lesions, droperidol plus fentanyl produced decreases in c.s.f. pressure in all but one of the cases studied. The striking difference between the effect on c.s.f. pressure of these drugs and of the volatile anaesthetic agents could be of importance to the clinical anaesthetist dealing with head injuries or working in a neurosurgical unit, when under conditions of controlled ventilation these drugs could be used as adjuvants to nitrous oxide-oxygen anaesthesia.

Three weeks after admission to a maternity hospital for observation following minor antepartum haemorrhage, a primiparous patient aged 22 suffered a sudden left hemiplegia and became comatose. Congestive cardiac failure ensued and because of the subsequent severe hypoxaemia she was transferred to the hyperbaric oxygen unit at the Western Infirmary, Glasgow, where it was found possible to improve her condition by means of oxygen at increased pressure. A caesarean section was w successfully performed in the hyperbaric chamber, and a normal live female infant was delivered. Though the patient's general condition improved she never regained consciousness and died almost three months later. Necropsy confirmed the clinical diagnosis of cardiomyopathy of pregnancy with severe ischaemic changes in the brain.

Prognosis depends on establishing a relationship between the patient's state in the early stages and the ultimate outcome. Both the severity of the initial damage (including early complications) and the degree of recovery need to be defined, but practical and statistical considerations impose a limit on the number of variables which can be manipulated. Variables chosen should be those likely to be relevant, and pilot studies are more reliable than intuition in indicating which items should be included. Data chosen should be of a kind likely to be readily available for most patients and should not therefore depend on complex laboratory investigation. The most reliable indicant of initial severity appears to be the depth and duration of coma or altered consciousness, and a scale has been devised for measuring these. Measures of outcome should include separate assessment of mental and physical disability as well as the overall social consequence of the brain damage. Prognosis should be expressed as the probability (mathematically expressed) that a patient will reach certain defined outcome categories, five of which are recognized in the present study. Predictions should begin only after initial resuscitative measures are complete (say six hours after ictus); they need not be limited to the early stages but can include estimates of the degree of further improvement expected in the light of progress in the early weeks after injuries. New methods of management cannot be critically assessed unless factors influencing prognosis are reliably identified and can be matched in comparative patient groups. An estimate of prognosis is also required for the selection of patients for intensive treatment, both in the acute and in the rehabilitation stage. Without such data there is a tendency to deploy an unduly high proportion of scarce resources on patients who have little prospect of recovery; this may deny the best chance of recovery to patients with severe, but less overwhelming, brain damage.

No apologies are needed for returning to the subject of brain death and its definition. There has been so much public discussion that it is important for public confidence that the issues should be clarified. In the following two contributions - one from a professor of neurosurgery and the other from a lawyer - an attempt is made to convince doctors (if that is needed) and lay people alike that what appears to be a new bogy is not one at all but a confusion of thought arising from the use of new technology to treat brain-damaged patients. This, however, might not be the view of Mr Skegg (Journal of medical ethics, 2, 190) who, fearful of the situation, has argued for a statutory definition of death.

The overall objective of head injury care is to minimize the occurrence of avoidable mortality and morbidity. Most avoidable mortality is due to delayed diagnosis and management of intracranial hematoma or the overlooking of systemic extracranial events. Most avoidable morbidity is in mild and moderately disabled patients. Overall too much attention has probably been paid to very severely injured patients both in the acute stage and during rehabilitation.

Professor Jennett first defines the term `brain death' and the problems arising from a diagnosis of death, some the result of recent technological advances. The diagnosis is not necessarily connected with donor transplants, although in the popular mind this is still so. The criteria for establishing brain death and the sources of potential error in this diagnosis are outlined. The diagnosis of brain death can be made confidently, as is already common practice, and this should become standard good medical practice.

Mechanical ventilation frequently saves lives that are threatened by temporary respiratory failure; but when breathing stops due to irreversible brain damage ventilation only prolongs the process of dying, as organs serially cease to function. The possibility of extending from a few minutes to many days the interval between final failure of the brain and ultimate cardiac asystole emphasises that death is not an event, but a process.

The recovery process after acute brain damage has attracted little interest from either basic or clinical scientists who seem to be most concerned with the acute stage. Much might be learnt about the mechanisms of the nervous system from study of the recovery process. The number of patients with permanent brain damage is growing as the result of the increased survival rate from such common conditions as severe head injury and non-geriatric stroke. Response to this problem has largely come from other disciplines, and in the form of supportive care rather than scientific enquiry. Such an enquiry might seek to answer three outstanding questions. (1) What is the nature of the persisting disability? (2) Can more scientifically based rehabilitation, including physical, mental and social components, either accelerate the rate of recovery or reduce the degree of ultimate disability? (3) Can the ultimate outcome be predicted in the acute stage; and can the amount of further improvement be estimated in the later stages of recovery?

Thirty-one cases of ischaemic cerebral stroke occurring in association with childbirth were fully investigated. The pathological basis of non-haemorrhagic carotid territory strokes in pregnant or puerperal women proved to be similar to that in non-pregnant women of the same age group. Over 70% were due to occlusive cerebral arterial disease or ischaemic lesions unrelated to thrombosis of the intracranial venous system. Comparisons are made with some other reported series in which only a minority of the patients were investigated by angiography, but in which intracranial venous occlusion was assumed to be the primary lesion. It seems likely that many of these patients may also have suffered arterial rather than venous lesions.

The mode circulation time was measured using intravenously injected technetium 99(m) and a collimation system devised to discriminate between the right and left sides of the head. The results in 21 normal men were used as a basis of assessing the findings in 205 patients, made up of five diagnostic groups (ischaemia, haematoma, subarachnoid haemorrhage, intracranial tumour, and head injury). The average mode circulation time in the affected hemisphere for the three groups with vascular disease was increased, but even in these groups half the patients had a mode circulation time within 1 SD of normal mean; similar results were found for asymmetry between the hemispheres. In serial measurements in 45 patients no correlation was found between change in mode circulation time and the clinical state. That so many results are within the normal range limits the value of this method.