54 research outputs found

    Correction to: the role of the complement system in traumatic brain injury: a review

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    Abstract After publication of the article [1], it was brought to our attention that Tables 1 and 2 were missing from the final manuscript, These tables can be seen below and have now been added to the revised version of the article

    Minimal invasive brain surgery for epilepsy; can it be the future?

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    Epilepsy affects 1–2% of the general population, of whom 30–40% may be considered drug resistant. In these patients, surgery is increasingly considered as the treatment of choice. However, conventional epilepsy surgery is invasive and associated with significant risks and overall intervention rates remain low. However, minimally invasive surgery, such as stereotactic radiosurgery and MRI-guided laser interstitial thermal surgery, have become popular alternative treatments, especially when a patient is not fit for a major open surgical procedure. In this month’s journal club, we will discuss three papers addressing these two modalities used in minimally invasive epilepsy surgery. The first is a clinical trial which randomizes patients with pharmacoresistant temporal lobe epilepsy to either stereotactic radiosurgery or open temporal lobectomy. The second is a systemic review and meta-analysis assessing outcomes of MRI-guided laser interstitial thermal therapy in the treatment of temporal epilepsies, extratemporal epilepsies and hypothalamic hamartoma. The last paper is a retrospective study comparing outcomes of MRI-guided laser interstitial thermal therapy and open temporal lobectomy

    Biomarkers for traumatic brain injury

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    Biomarkers for traumatic brain injury

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    Traumatic brain injury (TBI) poses a major public health problem. It is amongst the leading causes of mortality in young people in developed countries, and many survivors of TBI suffer from persistent disabilities. As a result, there remains an unmet clinical need for the development of more robust diagnostic and prognostic indicators of TBI. Axonal injury is a key driver of the ongoing pathological process following TBI, causing chronic neurological deficits and disability, and has been the focus of research in this area to date. A popular approach has been the investigation of body fluid (serum, CSF and saliva) biomarkers to assess axonal injury in the acute setting. Biomarkers can be any quantifiable product serving as a marker of physiological insult, and recent studies have highlighted several substances that appear both promising and clinically relevant. However, it is likely that eventually the optimal model for assessing axonal injury in TBI is likely to involve multi-faceted components, including multiple biomarkers and select advanced neuroimaging modalities. If successful, early and reliable identification of axonal injury post-TBI has the potential to enhance current care by increasing speed and accuracy of diagnosis, providing prognostic information, allowing patient stratification and efficient allocation of rehabilitation services, and providing better understanding if the underlying pathology, and discovery of potential therapeutic targets. In this article, we review three studies investigating candidate serum biomarkers of TBI, with a focus on their potential relationship with clinical outcomes within both human and animal models

    Ruptured pseudoaneurysm as a cause of spontaneous intracerebral bleed in a 3-month old infant

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    Ruptured intracranial aneurysms in infants are very rare but if missed can lead to poor outcomes. Spontaneously dissecting false aneurysms have been described only in a handful of cases. We report a case of a three-month old girl with deteriorating neurological function due to a ruptured distal middle cerebral artery pseudoaneurysm

    Risk factors for the development of seizures after cranioplasty in patients that sustained traumatic brain injury: a systematic review

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    Decompressive craniectomy (DC) is used for the treatment of raised intracranial pressure secondary to traumatic brain injury. Cranioplasty is a reconstructive procedure that restores the structural integrity of the skull following (DC). Seizures are a recognised complication of cranioplasty but its incidence and risk factors in TBI patients are unclear. Accurate prognostication can help direct prophylactic and treatment strategies for seizures. In this systematic review, we aim to evaluate current literature on these factors. A PROSPERO-registered systematic review was performed in accordance with PRISMA guidelines. Data was synthesised qualitatively and quantitatively in meta-analysis where appropriate. A total of 8 relevant studies were identified, reporting 919 cranioplasty patients. Random-effects meta-analysis reveals a pooled incidence of post-cranioplasty seizures (PCS) of 5.1% (95% CI 2.6–8.2%). Identified risk factors from a single study included increasing age (OR 6.1, p = 0.006), contusion at cranioplasty location (OR 4.8, p = 0.015), and use of monopolar diathermy at cranioplasty (OR 3.5, p = 0.04). There is an association between an extended DC-cranioplasty interval and PCS risk although it did not reach statistical significance (p = 0.062). Predictive factors for PCS are poorly investigated in the TBI population to date. Heterogeneity of included studies preclude meta-analysis of risk factors. Further studies are required to define the true incidence of PCS in TBI and its predictors, and trials are needed to inform management of these patients

    Analysis of neuro-theatre utilisation and reasons for cancellation to improve efficiency and productivity

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    Aim: In neurosurgery, much emphasis has recently been placed on theatre cancellation and time utilization as a key hospital management performance indicator. We sought to evaluate our unit’s theatre throughput efficiency, and identify the causes of elective surgery cancellations. Methods: We retrospectively audited all scheduled elective neurosurgical procedures over a period of 9 months. Results: Mean theatre utilization time was 47.0%. The common causes of cancellations were lack of theatre time (32%), non-availability of beds in recovery room (18.6%), and insufficient preoperative patient preparation (5.5%). Discussion: Inefficiencies were noted in turnover of patients and inaccurate prediction of operative time. Our theatre utilization time is consistent with available literature, however cancellations of elective surgery waste valuable operative time and resources. Conclusions: A multi- dimensional approach must be taken to improve theatre utilization and reduce cancellation rates. A pre-assessment clinic has been introduced in order to reduce cancellation rates

    Profiling biomarkers of traumatic axonal injury: from mouse to man

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    Traumatic brain injury (TBI) poses a major public health problem on a global scale. Its burden results from high mortality and significant morbidity in survivors. This stems, in part, from an ongoing inadequacy in diagnostic and prognostic indicators despite significant technological advances. Traumatic axonal injury (TAI) is a key driver of the ongoing pathological process following TBI, causing chronic neurological deficits and disability. The science underpinning biomarkers of TAI has been a subject of many reviews in recent literature. However, in this review we provide a comprehensive account of biomarkers from animal models to clinical studies, bridging the gap between experimental science and clinical medicine. We have discussed pathogenesis, temporal kinetics, relationships to neuro-imaging, and, most importantly, clinical applicability in order to provide a holistic perspective of how this could improve TBI diagnosis and predict clinical outcome in a real-life setting. We conclude that early and reliable identification of axonal injury post-TBI with the help of body fluid biomarkers could enhance current care of TBI patients by (i) increasing speed and accuracy of diagnosis, (ii) providing invaluable prognostic information, (iii) allow efficient allocation of rehabilitation services, and (iv) provide potential therapeutic targets. The optimal model for assessing TAI is likely to involve multiple components, including several blood biomarkers and neuro-imaging modalities, at different time points

    High mobility group box protein 1 and white matter injury following traumatic brain injury: perspectives on mechanisms and therapeutic strategies

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    Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Despite significant medical advances over recent decades, many survivors of TBI develop long term neuro-cognitive deficits. Previously, only moderate and severe injuries were thought to account for the devastating consequences of TBI. However, there is increasing evidence that even milder injuries may result in problematic lifelong cognitive and affective disturbances. TBI is typically characterized by an an acute physical injury followed by a protracted innate neuro-inflammatory response. These reponses, mediated via neuronal, astrocyte and microglial cells, amongst others, and may result in widespread neuronal death and a micro-environment that is not conducive to brain repair (Manivannan et al., 2021). Whilst the primary physical injury often evades intervention from a medical perspective, the subsequent neuro-inflammatory response offers a potential therapeutic target. Nonetheless, effective pharmacological strategies continue to elude clinicians and scientists due to the complex underlying pathogenesis and difficulties of modelling such a heterogeneous disease. However, the majority of research to date has focused on investigating the effects of post-traumatic neuro-inflammation on grey matter injury rather than the consequences upon white matter (WM), which contributes greatly to cognitive dysfunction across many neurological diseases (Filly and Kelly, 2018). Herein, we will briefly discuss: (i) high mobility group box protein 1 (HMGB1) as a potential therapeutic target; (ii) the relevance of WM injury in TBI and current understanding of WM repair following injury; and (iii) perspectives on how HMGB1 may play a role
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