Chronic subdural haematoma (CSDH) is an encapsulated collection of blood and fluid on the surface of the brain. Historically considered a result of head trauma, recent evidence suggests there are more complex processes involved. Trauma may be absent or very minor and does not explain the progressive, chronic course of the condition. This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. The characteristic membrane surrounding the CSDH has been identified as a source of fluid exudation and haemorrhage. Angiogenic stimuli lead to the creation of fragile blood vessels within membrane walls, whilst fibrinolytic processes prevent clot formation resulting in continued haemorrhage. An abundance of inflammatory cells and markers have been identified within the membranes and subdural fluid and are likely to contribute to propagating an inflammatory response which stimulates ongoing membrane growth and fluid accumulation. Currently, the mainstay of treatment for CSDH is surgical drainage, which has associated risks of recurrence requiring repeat surgery. Understanding of the underlying pathophysiological processes has been applied to developing potential drug treatments. Ongoing research is needed to identify if these therapies are successful in controlling the inflammatory and angiogenic disease processes leading to control and resolution of CSDH.

Background and Purpose— The goal of this study was to prospectively assess outcome and cost for poor-grade subarachnoid hemorrhage patients presenting to a regional neurosurgical center (Addenbrooke’s Hospital, Cambridge, UK) between 1994 and 2001. Outcome measures were clinical outcome at 6 months, number needed to treat (NNT) for favorable outcomes, and cost analysis. Methods— Poor-grade patients (World Federation of Neurological Surgeons grades 4 and 5) were transferred to the neurocritical care unit after intubation and ventilation. After resuscitation and drainage of ventricular cerebrospinal fluid for 24 hours, sedation was stopped, and patients were assessed clinically. Patients with a Glasgow Motor Score (GMS) ≥4 underwent angiography and surgical treatment of culprit aneurysms. Patients with a subsequent GMS of 6 were not deemed poor grade and were discounted from the study. Results— We deemed 166 ventilated patients genuinely poor grade (mean age, 53.4 years; 94 women [56.6%]). Of these, 88 patients (4<GMS<6; 53%) progressed to angiography and possible definitive treatment. Seventy-five patients had an identifiable aneurysm, but only 64 survived for treatment. Operative mortality was 31.3%, and of the 44 survivors, 22 (34.4% of operated patients) achieved a favorable outcome. Favorable outcomes were more frequently seen in women than men (21.3% versus 6.9%) but were unrelated to patient age. The NNT for 1 favorable outcome was 7 (male NNT, 15; female NNT, 5) at a cost of £84 336 per favorable outcome (female, £60 240; male, £180 720). Conclusions— Poor-grade aneurysmal subarachnoid hemorrhage is associated with a high mortality but a significant subset of patients can achieve favorable outcomes.

Aims: CSF leaks are not uncommon after a base of skull fracture. Currently there is no standardised algorithm for the investigation and management of post-traumatic CSF leaks. In this paper we aim to provide an evidence-based framework for managing post-traumatic CSF leaks. Methods: We searched the English literature over the past 45 years using CINAHL, EMBASE and MEDLINE for the terms (1) post-traumatic CSF leaks or fistulas, and (2) basilar or base of skull fractures, but excluded papers on post-operative and non-traumatic CSF leaks, and papers on paediatric post- traumatic CSF leaks. Results: The diagnosis of a base of skull fracture and any resultant CSF leak can be challenging. Therefore a combination of biochemical and radiological studies are needed to optimise the diagnosis of this condition. Post-traumatic CSF leaks are generally treated conservatively, and a majority of them resolve without further surgical management. However for patients who are refractory to such treatments, surgical closure of the CSF fistula is necessary. Surgical obliteration of CSF leaks can be challenging and requires the involvement of multiple surgical specialties such as neurosurgery, otolaryngology, and maxillofacial surgery. Conclusion: Although we have formulated a simple algorithm to aid the investigation and management of post-traumatic CSF leaks, there are still many important unresolved questions requiring further well powered studies to answer.

Introduction. In recent years craniectomy has been widely used in the management of traumatic brain injury and ischaemic stroke. The objective of this study was to evaluate the indications, techniques and outcomes for patients undergoing cranioplasty over a recent 7-year period in a geographically distinct population. Materials and methods. An observational study was performed retrospectively, with review of case records from 2004 to 2011. Demographic, clinical and outcome data were collected, and complications were classified as major and minor. A multi-variant analysis was performed to identify patient and management factors that influenced outcome. Results. Data were collected on a total of 87 cranioplasty patients with a median age of 42 and a mean follow-up time of 3 years and 10 months. The main indications for craniectomy were trauma (46%), infection (19%) intracranial haemorrhage (15%), tumour (13%) and ischaemic stroke (6%). Eight percent of patients had a synchronous craniectomy and cranioplasty, 14% had cranioplasty within 3 months of craniectomy, 21% within 3–6 months, 35% within 6–12 months, 14% over 1 year and 8% over 2 years later. The most frequently implanted cranioplasty material was titanium (53%), followed by autologous bone (26%) and acrylic (15%). Administration of prophylactic antibiotics was recorded in 97% of cases. Major complications occurred in 20% of patients, including 2 deaths (2%), 5 extradural haemorrhages (6%) and 9 infections (10%). A further 10% of cases experienced minor or cosmetic complications. Conclusions. Cranioplasty is often considered as a low-risk procedure following craniectomy. In our cohort, a 20% risk of major complications, including death, was identified. These findings contribute to the literature, emphasising that cranioplasty is a high-risk procedure. Whilst compelling reasons may guide the undertaking of craniectomy, it is essential that consideration is given to the significant subsequent risks of cranioplasty.

Chronic subdural hematoma (CSDH) is a common neurosurgical pathology, yet conflicting opinions exist concerning the pathophysiological processes involved. Many consider CSDH a product of an aged acute subdural hematoma (ASDH) secondary to trauma. Serial imaging, however, has demonstrated CSDH formation in patients without any initial ASDH. To understand the relevance of acute hemorrhage in a cohort of patients with CSDH, transformation from an ASDH were categorized as CSDH-acute transformed (CSDH-AT) and those without any acute hemorrhage at the outset as CSDH- de-novo (CSDH-DN). A cohort of 41 eligible patients with CSDH were included, with baseline imaging after trauma (or spontaneous ASDH) available for assessment of acute hemorrhage. Volumetric analysis of all subdural collections and measurements of baseline atrophy were performed. In 37% of cases, there was an ASDH present on baseline imaging (CSDH-AT), whereas 63% had no acute hemorrhage at baseline (CSDH-DN). The CSDH-ATs developed more rapidly (mean 16 days from baseline to diagnosis) and were smaller in volume than the CSDH-DNs, which developed at a mean delay of 57 days. In 54% of the CSDH-DNs, a subdural hygroma was present on baseline imaging, and there was a wide range of baseline cerebral atrophy. This study provides radiological evidence for two distinct pathways in the formation of CSDH, with CSDH-DN occurring more commonly and often involving subdural hygroma. Further work is needed to understand whether the pathological origin has implications for patient outcome.