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Background: Despite the ubiquitous use of the Glasgow Coma Scale (GCS) worldwide, no study to date has objectively and quantitatively assessed its impact on the scientific literature and clinical practice. Therefore, we comprehensively analyzed scientific publications and clinical practice guidelines employing the GCS to gauge its clinical and academic impact, identify research hotspots, and inform future research on the topic., Methods: A cross-sectional bibliometric analysis was performed on Scopus to obtain relevant publications incorporating the GCS from 1974 to 2022. In addition, a systematic review of existing clinical practice guidelines in PubMed, Scopus, Web of Science, and Trip Database was performed. Validated bibliometric parameters including article title, journal, publication year, authors, citation count, country, institution, keywords, impact factor, and references were assessed. When evaluating clinical practice guidelines, the sponsoring organization, country of origin, specialty, and publication year were assessed., Results: A total of 37,633 articles originating from 3924 different scientific journals spanning 1974-2022 were included in the final analysis. The compound annual growth rate of publications referencing the GCS was 16.7%. Of 104 countries, the United States had the highest total number of publications employing the GCS (n = 8517). World Neurosurgery was the scientific periodical with the highest number of publications on the GCS (n = 798). The top trending author-supplied keyword was "traumatic brain injury" (n = 3408). The 97 included clinical practice guidelines most commonly employed the GCS in the fields of internal medicine (n = 22, 23%), critical care (n = 21, 22%), and neurotrauma (n = 19, 20%)., Conclusions: At the turn of the 50 th anniversary of the GCS, we provided a unique and detailed description of the "path to success" of the GCS both in terms of its scientific and clinical impact. These results have not only a historical but also an important didactic value. Ultimately our detailed analysis, which revealed some of the factors that led the GCS to become such a widespread and highly influential score, may assist future researchers in their development of new outcome measures and clinical scores, especially as such tools become increasingly relevant in an evidence-based data-driven age., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Competing Interests: Competing interests: The BMJ has judged that there are no disqualifying financial ties to commercial companies. The authors declare the following other interests: none. Further details of The BMJ policy on financial interests is here: https://www.bmj.com/sites/default/files/attachments/resources/2016/03/16-current-bmj-education-coi-form.pdf.

The Glasgow Outcome Scale-Extended (GOSE) has become one of the most widely used outcome instruments to assess global disability and recovery after traumatic brain injury. Achieving consistency in the application of the assessment remains a challenge, particularly in multi-center studies involving many assessors. We present a manual for the GOSE interview that is designed to support both single- and multi-center studies and promote inter-rater agreement. Many patients fall clearly into a particular category; however, patients may have outcomes that are on the borderline between adjacent categories, and cases can present other challenges for assessment. The Manual includes the general principles of assessment, advice on administering each section of the GOSE interview, and guidance on "borderline" and "difficult" cases. Finally, we discuss the properties of the GOSE, including strengths and limitations, and outline recommendations for assessor training, accreditation, and monitoring.

The Glasgow Outcome Scale (GOS) was first published in 1975 by Bryan Jennett and Michael Bond. With over 4,000 citations to the original paper, it is the most highly cited outcome measure in studies of brain injury and the second most-cited paper in clinical neurosurgery. The original GOS and the subsequently developed extended GOS (GOSE) are recommended by several national bodies as the outcome measure for major trauma and for head injury. The enduring appeal of the GOS is linked to its simplicity, short administration time, reliability and validity, stability, flexibility of administration (face-to-face, over the telephone and by post), cost-free availability and ease of access. These benefits apply to other derivatives of the scale, including the Glasgow Outcome at Discharge Scale (GODS) and the GOS paediatric revision. The GOS was devised to provide an overview of outcome and to focus on social recovery. Since the initial development of the GOS, there has been an increasing focus on the multidimensional nature of outcome after head injury. This Review charts the development of the GOS, its refinement and usage over the past 40 years, and considers its current and future roles in developing an understanding of brain injury.

Since 1974, the Glasgow Coma Scale has provided a practical method for bedside assessment of impairment of conscious level, the clinical hallmark of acute brain injury. The scale was designed to be easy to use in clinical practice in general and specialist units and to replace previous ill-defined and inconsistent methods. 40 years later, the Glasgow Coma Scale has become an integral part of clinical practice and research worldwide. Findings using the scale have shown strong associations with those obtained by use of other early indices of severity and outcome. However, predictive statements should only be made in combination with other variables in a multivariate model. Individual patients are best described by the three components of the coma scale; whereas the derived total coma score should be used to characterise groups. Adherence to this principle and enhancement of the reliable practical use of the scale through continuing education of health professionals, standardisation across different settings, and consensus on methods to address confounders will maintain its role in clinical practice and research in the future., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

William Bryan Jennett, one of the leading figures in neurosurgery of the twentieth century, has died on 26 January 2008, at the age of 81. He made fundamental contributions to the field of traumatic brain injury (TBI) that still shape diagnosis, management and prognosis worldwide, in the second part of the last century. This paper is meant to gratefully acknowledge his contributions and to reflect on the implications that his work has for neurointensive care today. Starting from his early steps, we tried to highlight his fundamental work on diagnosis of severity in TBI, on rescue, treatment and prognosis of severe TBI. Moreover, his contribution in the definition of vegetative state, minimally conscious state and brain death has been emphasized. The contribution of Professor Bryan Jennett was in fact seminal in many aspects: the application of a common language in brain damage evaluation, where GCS and GOS are now universally employed; a critical approach to TBI diagnosis and treatment, in the search of proven better therapies; a quantitative approach to TBI prognosis, based on large clinical series and appropriate statistics; a strong commitment to the ethical implication of survival after severe injury, including the vegetative status; social responsibility in the diagnosis of brain death and in organ donors procurement. For these reasons, he can be considered one of the leading figures in neurosurgery and neurology of the twentieth century. This paper is meant to gratefully acknowledge his contributions and to reflect on the implications that his work has for neuro-intensive care today.

Background: Acute traumatic brain injury is a major cause of death and disability. Calcium channel blockers (calcium antagonists) have been used in an attempt to prevent cerebral vasospasm after injury, maintain blood flow to the brain, and so prevent further damage., Objectives: To estimate the effects of calcium channel blockers in patients with acute traumatic brain injury, and in a subgroup of brain injury patients with traumatic subarachnoid haemorrhage., Search Strategy: Handsearching and electronic searching for randomised controlled trials., Selection Criteria: Randomised controlled trials in patients with all levels of severity of clinically diagnosed acute traumatic brain injury., Data Collection and Analysis: Two reviewers independently assessed the identified studies for eligibility and extracted data from each study. Summary odds ratios were calculated using the Mantel-Haenszel method., Main Results: Six RCTs were identified as eligible for inclusion in the systematic review. The effect of calcium channel blockers on the risk of death was reported in five of the RCTs. The pooled odds ratio (OR) for the five studies was 0.91 (95% confidence interval [95%CI] 0.70-1.17). For the four RCTs that reported death and severe disability (unfavourable outcome), the pooled odds ratio was 0.85 (95%CI 0.68-1.07). In the two RCTs which reported the risk of death in a subgroup of traumatic subarachnoid haemorrhage patients, the pooled odds ratio was 0.59 (95%CI 0.37-0.94). Three RCTs reported death and severe disability as an outcome in this subgroup, and the pooled odds ratio was 0.67 (95%CI 0.46-0.98)., Reviewer's Conclusions: This systematic review of randomised controlled trials of calcium channel blockers in acute traumatic head injury patients shows that considerable uncertainty remains over their effects. The effect of nimodipine in a subgroup of brain injury patients with subarachnoid haemorrhage shows a beneficial effect, though the increase in adverse reactions suffered by the intervention group may mean that the drug is harmful for some patients.

Traumatic brain injury (TBI) remains a major public health problem globally. In the United States the incidence of closed head injuries admitted to hospitals is conservatively estimated to be 200 per 100,000 population, and the incidence of penetrating head injury is estimated to be 12 per 100,000, the highest of any developed country in the world. This yields an approximate number of 500,000 new cases each year, a sizeable proportion of which demonstrate significant long-term disabilities. Unfortunately, there is a paucity of proven therapies for this disease. For a variety of reasons, clinical trials for this condition have been difficult to design and perform. Despite promising pre-clinical data, most of the trials that have been performed in recent years have failed to demonstrate any significant improvement in outcomes. The reasons for these failures have not always been apparent and any insights gained were not always shared. It was therefore feared that we were running the risk of repeating our mistakes. Recognizing the importance of TBI, the National Institute of Neurological Disorders and Stroke (NINDS) sponsored a workshop that brought together experts from clinical, research, and pharmaceutical backgrounds. This workshop proved to be very informative and yielded many insights into previous and future TBI trials. This paper is an attempt to summarize the key points made at the workshop. It is hoped that these lessons will enhance the planning and design of future efforts in this important field of research.

This paper reviews aspects of head injury management and research in the United Kingdom (UK). We discuss evidence about the scale and etiology of head injury in Britain and how this information has supported a triage-based approach, incorporating risk analysis. A Cohesive organization based upon nationally accepted, yet regionally flexible head injury management guidelines is important. Research in the United Kingdom has clarified the effect of head injury on the brain and how this can be reduced. This clarification follows from improved understanding of the neurobiology of injury, of secondary damage and recovery, and information gained from new techniques aimed at investigating events in patients. Outcome is an important perspective and we highlight the increasing focus upon recovery and the extent of disability after so called mild head injury. Although we retain a UK perspective, comparisons with aspects of European head injury emphasize the increasing importance of an international approach in the future.

The lack of a common, widely acceptable criterion for the definition of trivial, minor, or mild head injury has led to confusion and difficulty in comparing findings in published series. This review proposes that acute head-injured patients previously described as minor, mild, or trivial are defined as "mild head injury," and that further groups are recognized and classified as "low-risk mild head injury," "medium risk mild head injury," or "high-risk mild head injury." Low-risk mild injury patients are those with a Glasgow Coma Score (GCS) of 15 and without a history of loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is definitively less than 0.1:100. These patients can be sent home with written recommendations. Medium risk mild injury patients have a GCS of 15 and one or more of the following symptoms: loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is in the range of 1-3:100. Where there is one computed tomography (CT) scanner available in an area for 100,000 people or less, a CT scan should be obtained for such patients. If CT scanning is not so readily available, adults should have a skull x-ray and, if this shows a fracture, should be moved to the "high-risk" category and undergo CT scanning. High-risk mild head injury patients are those with an admission GCS of 14 or 15, with a skull fracture and/or neurological deficits. The risk of intracranial hematoma requiring surgical evacuation is in the range 6-10:100. If a CT scan is available for 500,000 people or less, this examination must be obtained. Patients with one of the following risk factors--coagulopathy, drug or alcohol consumption, previous neurosurgical procedures, pretrauma epilepsy, or age over 60 years--are included in the high-risk group independent of the clinical presentation.

In an attempt to examine in vivo the early metabolic consequences of severe acute head injury, 1H MRS was performed in four patients from 8 to 25 h (mean 15 h) following trauma. In three of these patients, decompressive surgery was performed 4-5 h prior to the MRS. High levels of lactate (area of lactate peak >50% of the mean areas of the NAA, choline-containing, and creatine-containing compound peaks) were found at 8 h posttrauma in the one patient who was not operated on and at 10 h posttrauma in one of the patients who underwent surgery. In the other two postoperative patients, at 18 and 25 h after trauma, lactate levels were found to be low (lactate peak <20% of the mean area of the other three peaks). In the one patient who had a follow-up at 6 days and who had the largest initial lactate levels, these remained high. These findings suggest that high levels of lactate may not be an inevitable consequence of severe head injury and that similar MRS studies should be performed on each individual patient before therapies to reduce lactate are considered. There appeared to be no correlation between the relative amounts of lactate and outcome.

Aims: To study the mechanism of action of steroids in patients with peritumorous oedema., Methods: To investigate early cerebral metabolic changes proton magnetic resonance spectroscopy (1H-MRS) was used before and 11 to 14 hours after treatment with dexamethasone (12 mg oral loading and 4 mg four times daily maintenance). Nine patients (two men, seven women, mean age 54) with pronounced oedema associated with various intracranial tumours (two astrocytomas, three meningiomas, two glioblastoma, and two metastases) were examined using MRI and MRS. SE1500/135 volume selected MRS (mean volume 21 ml) were performed on an oedematous region and a contralateral region. All spectra were acquired with and without water suppression. Metabolite peak area ratios were determined., Results: Regions of oedema had significantly (P < 0.01) higher unsuppressed water than the contralateral regions, as expected. There was no change at this early time point after dexamethasone. The ratio of the area of choline containing compounds to that creatine and phosphocreatine compounds was determined after which the serial ratios of these before and after were calculated (a serial ratio of 1.0 would indicate no change in the choline to creatine ratios after steroid administration). The mean serial ratios for the area of oedema were 1.02 (SEM 0.08) and 1.10 (0.08) for the contralateral volume of interest, indicating no significant changes. However, significant changes (P < 0.02) were found in the N-acetyl-aspartate (NAA)/choline serial ratios (0.86 (0.06) in the area of oedema, 1.20 (0.10) in contralateral brain) and the NAA/creatine serial ratios (0.86 (0.08) for the oedema, 1.25 (0.11) in contralateral brain)., Conclusions: Such rapid changes may be explained either by relatively large alterations in the relaxation characteristics of NAA or, more controversially, by actual changes in the amounts of NAA. It is proposed that steroids act primarily by causing early metabolic changes that are later expressed in improvements in intracranial volume relations.

In a new, reproducible model of rodent focal cortical injury, we have shown that in the absence of early traumatic disruption of the microvasculature and subsequent hemorrhage, delayed perivascular protein leakage and polymorphonuclear leukocyte infiltration of the injured cortex occur. In this study we employed a sensitive quantitative autoradiographic technique (using alpha-aminoisobutyric acid as a tracer) to investigate the focal changes in microvascular permeability with time and to determine the effects of administration of a 21-aminosteroid (Tirilazad) initiated 5 min after induction of the cortical injury. At all time points studied, there was a significant increase in perilesional blood-brain barrier permeability in lesioned animals treated with vehicle, compared to shamoperated animals, with the most marked increase in blood-brain barrier permeability at 4 h postinjury (mean Ki +/- SE = 19.2 +/- 2.4/1000 min with cortical injury, 1.5 +/- 0.3/1000 min in shams) (mean volume +/- SE = 15.48 +/- 0.7 mm3). In animals with cortical injury treated with Tirilazad (10 mg/kg), there was a significant reduction in microvascular permeability at the site of injury (Ki = 3.1 +/- 0.5, p < 0.001) and a significant reduction in volume of increased permeability (4.86 +/- 0.7 mm3, p < 0.01) at 4 h postinjury. In this model of cortical injury, a delayed increase in microvascular permeability occurs, which is significantly attenuated by postinjury treatment with Tirilazad.

The clinical features, treatment, and outcome were reviewed for 48 patients with a haematoma and 71 patients with an infarct in the posterior fossa in order to develop a rational plan of management. Clinical features alone were insufficient to make a diagnosis in about half of the series. Patients with a haematoma were referred more quickly to the neurosurgical unit, were more often in coma, and more often had CT evidence of brain stem compression and acute hydrocephalus. Ultimately, 75% of the patients with a haematoma required an operation. By contrast, most patients with an infarct were managed successfully conservatively. Early surgical management in both cerebellar haemorrhage and infarct (either external ventricular drainage or evacuation of the lesion), associated with early presentation and CT signs of brain stem compression and acute hydrocephalus, led to a good outcome in most patients. Of the patients with cerebellar haematoma initially treated by external drainage, over half subsequently required craniectomy and evacuation of the lesion; but, in some cases, this failed to reverse the deterioration. In patients with a cerebellar infarct, external drainage was more often successful. The guidelines, findings, and recommendations for future management of patients with posterior fossa stroke are discussed.

Cortical contusions are one of the most common characteristics in head injury and are regarded by many as the hallmark of significant injury. No experimental study has clarified the roles of mechanical forces, haemorrhage and ischaemia in the process of progressive acute brain damage and later neurobehavioural dysfunction. We have devised a new, simple reproducible rodent model of focal cortical injury which employs a 'pure' mechanical/physical force applied through the intact dura. Using this model we have investigated the time course and pattern of changes in neurons, glia and microvasculature. With the exception of haemorrhage, this model closely reproduces the light- and electron microscopy features of human contusion. In the absence of perivascular haemorrhage we have demonstrated delayed perivascular protein leakage and polymorphonuclear-leukocyte infiltration of the damaged cortex. We postulate that a component of the delayed blood brain barrier breakdown demonstrated in human focal head injury (which may contribute to swelling and brain damage) is due to an acute inflammatory response, the magnitude of which is dependent on the amount of tissue injury.

We studied the efficacy of nimodipine in severely head-injured patients in a randomized study. Of 176 patients who received nimodipine, 2 mg/h iv for 2 day, 53% had a favorable outcome (moderate or good recovery). Of 175 control patients, 49% had a favorable outcome. This difference was not statistically significant but does not exclude the possibility that a study of a larger number of patients could show a clinically useful benefit.

Neuroimaging with CT and MRI is a basis for decision making in individual head-injured patients and also provides a classification of patients according to severity of damage, patterns of injury, pathophysiologic mechanisms and prognosis. Such classifications can be based on the intracranial lesions identified: subdural, extradural, and intracerebral hematomas, contusions, and shearing lesions, or indirect indications of raised intracranial pressure and brain swelling: shift, obliteration of the third ventricle and basal cisterns, and signs of ischemia. The appropriate classification for early diagnosis and acute decision making may differ from the assessment of severity of damage, prognosis and late sequelae. Parallel systems of classification, suitable for these purposes, are proposed.