Newsletter from the Trauma & Critical Care Section, June 2019
Dear colleagues in the area of Neurotrauma & Critical Care. Our EANS Section has, with huge help and input from our younger section members, put together a newsletter that I hope you will find interesting. It includes several relevant and recent clinical articles, as well as a strong preclinical article of importance to our field on Wallerian degeneration. Not- to-miss is the summary of the recent consensus meeting on decompressive craniectomy, very recently published in Acta. In addition, recent updates on pediatric TBI guidelines are addressed. We have also included articles on the role of procalcitonin in ventricular drain-related infections, and a recent study on surgical approaches in motor complete spinal cord injury. For those of us interested in sports-related concussion, there is a recent NEJM article on tau-PET in the evaluation of suspected chronic traumatic encephalopathy addressed here. One particular highlight of our newsletters is the clinical cases, and we are proud to present cases not only from our European setting (a traumatic PICA aneurysm), but also from a colleague in Syria, performing neurosurgery in a different, and from many aspects difficult setting, without a CT scanner.
The remainder of 2019 will be particularly interesting from a Neurotrauma perspective with many extraordinary events coming up, both European and international. I must particularly recommend the EANS meeting in Dublin (Sept 24-28), the 2nd EANS Trauma Update meeting (co-organized with the Pannonian symposium, Oct 3-4) and the 2nd Nordic Neurotrauma Conference in Lund, Sweden (Nov 18-20). Attached is a list of these events, and we all hope to meet many of the readers of this letter there. Guaranteed is truly up-to date trauma programs in all these events and invited lecturers/faculty who are among the true leaders in the field. As you see, some great meetings for 2020 are mentioned as well. In the fall, the Section plans to host the 1st webinar - so keep your eyes open for that. In all, European and EANS Neurotrauma research remains strong and we hope that even more groups join the increasing number of international collaborations on neurotrauma, such as the Global Neurotrauma Outcomes (GNOS) and Global NeuroSurg 1 (GNS) studies, and update on their progress is included in the present newsletter.
On behalf of the EANS Section for Trauma & Critical Care
Niklas Marklund, Lund, Sweden June 20th, 2019
Elham Rostami, on behalf of the young EANS Trauma “subsection” https://twitter.com/lablubin; https://twitter.com/EANSNeurotrauma; https://twitter.com/RostamiDr
Events in 2019
EANS2019, September 24-29, Dublin, Ireland. We have a good neurotrauma program here, consisting of two parallel session and one plenary session as well as two Masterclass session. There will be relevant topics for everyone interested in Neurotrauma. Many abstracts have been selected for e-poster or oral presentation - and who won the “best abstract” in Neurotrauma? Join us there and you will find out. Colleagues from the AANS, WFNS and local organizing committee are contributing to these sessions. Should not be missed! https://eans2019.com
The 2nd Nordic Neurotrauma Conference, November 18-20, Lund, Sweden. The 1st NNC was held in Lund in 2017 and was a huge success. In wintery Lund, an excellent program ranging from prehospital management, to sports concussion, to neurocritical care, to neurorehab, and to spinal injuries has been created. The organizers Niklas Marklund and Johan Undén cordially invite you to Lund, Sweden for this neurotrauma meeting, with many renowned lecturers invited, as well as a great social program. https://mkon.nu/nnc
Importantly - don´t miss the opportunity to come to beautiful Messina in Sicily, October 3-4 for the 2nd EANS Trauma & Critical Care Update meeting arranged by local host Prof. Germano, Andras Buki (Pecs, Hungary), and Niklas Marklund (Lund, Sweden). This meeting is combined with the Pannonian Symposium on CNS Injury previously held in Hungary. A great number of excellent speakers and experts in the neurotrauma field from across the globe will be there. See http://www.neurotrauma2019.eu/
Other important upcoming 2019 (and some 2020) events in Neurotrauma ICRAN 2019: International conference on recent advances in neurotraumatology March 07-10, 2019 Peshawar, Pakistan had to be postponed and will take place in Nov 14-17. https://icran2019.pk National Neurotrauma Symposium, Neurotrauma 2019, June 30- July 3, Pittsburgh, USA https://www.nationalneurotraumasociety.org/symposium/2019-pittsburgh
ICP 2019, September 08-12, 2019 Leuven, Belgium https://kuleuvencongres.be/icp2019/ ICRAN-NTSI 2020, which is a Joint Meeting of Neurotraumatology Committee of WFNS [International Conference of Research and Advances in Neurotraumatology (ICRAN)] and Annual Conference of Neurotrauma Society of India (NTSI), which is going to be held from August 20 to 22, 2020 at Bangalore, India. www.Icran-ntsi2020.com WFNS Congress, Beijing, China, September 9-12, 2019, has some interesting neurotrauma topics. Of course: International Neurotrauma Symposium (INTS), Melbourne, Australia, March 29 - April 2, 2020.
On going studies & Projects
The Global Neurotrauma Outcomes Study (GNOS) study and its update Traumatic brain injury (TBI) accounts for a significant amount of death and disability worldwide and the majority of this burden affects individuals in low-and-middle income countries. The GNOS study is the first global neurosurgical study that aims to provide a comprehensive picture of the management and outcomes of patients undergoing emergency surgery for TBI worldwide.
GNOS is a multi-center, international, prospective cohort study and any unit performing emergency surgery for TBI worldwide will be eligible to participate. Neurosurgeons from each participating unit will form a study team responsible for gaining local approval, identifying patients and conducting data collection. Team can consist of a mix of neurosurgeons, general surgeons, anesthetists, intensivists, trainees and medical students. The participation of residents and medical students is encouraged. Local teams of up to 4 people will sign up and select a 30-day recruitment period between October 2018 and October 2019 and collect data on all patients receiving emergency surgery for TBI during that period. Data will be collected via a secure online platform in anonymized form. All team members will be indexed on PubMed as collaborators on all publications resulting from the study.
The full protocol and other important information can be found here https://globalneurotrauma.com/protocol/
The study runs under the auspices of the WFNS and NIHR Global Health Research Group on Neurotrauma. It has already been endorsed by the Asian Australasian Society of Neurological Surgeons, Asian Congress of Neurological Surgeons, European Association of Neurosurgical Societies, Federación Latinoamericana de Sociedades en Neurocirugía, and Young African Neurosurgeons Forum.
GNOS Update
54 sites have already registered for the study
31 different countries
23 in Europe
15 in Africa
14 in Asia
2 in South America 38/54 sites (70%) have begun data collection.
10 sites (19%) have completed data collection.
The update has been presented by the principal investigator of the study, Professor Peter Hutchinson in the first Global Neurosurgery Symposium took place on January 18th and 19th at the Weill Cornell Medical College in New York, USA.
The more units participate, the more meaningful the results will be. So, please sign up here now https://globalneurotrauma.com/sign-up/. Importantly, the study period has now been extended until 31st of October 2019!
Updates on recent publications & Guidelines
Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Foundation Guidelines, Executive Summary Kochanek PM, et. Al. Pediatric Critical Care Medicine: March 2019 - Volume 20 - Issue 3 - p 280–289 Trauma Foundation’s Guidelines for the Management of Pediatric Severe Traumatic Brain Injury was published in March 2019. A total of 48 new studies were added. However, most recommendations are level III, supported by lower quality evidence but three level II recommendations could be added to the new guidelines. This Guidelines, also includes a companion article that presents a “Critical Pathway” algorithm of care for both first tier and second tier (refractory intracranial hypertension) approaches. The level II recommendations are as following: For ICP Control • Bolus hypertonic saline (3%) is recommended in patients with intracranial hypertension. Recommended effective doses for acute use range between 2 and 5 mL/kg over 10–20 min. To Improve Overall Outcomes • Prophylactic moderate (32–33°C) hypothermia is not recommended over normothermia. • Use of an immune-modulating diet is not recommended.
The recommendations also include use of ICP monitoring to improve overall outcome with a threshold of <20 mmHg (level III). Hopefully the study Approaches and Decisions in Acute Pediatric TBI Trial (ADAPT) including 1,000 cases of severe pediatric TBI will generate higher quality results and stronger recommendations.
Ongoing research Topic in Frontiers Neurology/Neurotrauma Editors: Rostami E. Figaji A, Adelson D. https://www.frontiersin.org/research-topics/9385/pediatric-tbi---current-state-of-the-art-and- future-perspective Submit your papers in pediatric TBI deadline 1st of September.
Update on the International Consensus Meeting on the Role of Decompressive Craniectomy in the Management of Traumatic Brain Injury
Consensus statement from the International Consensus Meeting on the Role of Decompressive Craniectomy in the Management of Traumatic Brain Injury Hutchinson et al. Acta Neurochir (Wien). 2019 May 28. doi: 10.1007/s00701-019- 03936-y. [Epub ahead of print] The beneficial role of decompressive craniectomy (DC), a neurosurgical procedure that involves removal of a section of the skull and opening of the underlying dura, for the managements of patients with traumatic brain injury (TBI) is still controversial. Two randomised trials, DECRA in 2011 and RESCUEicp in 2016, assessed the effectiveness of DC following TBI yielding class 1 evidence. However, to provide general guidance on the use of DC following TBI and to identify areas of ongoing uncertainty, an international consensus meeting was organised in Cambridge, UK on the 28th and 29th September 2017. The meeting was under the auspices of World Federation of Neurosurgical Societies (WFNS), A/O Global Neuro and the NIHR Global Health Research Group on Neurotrauma. The consensus addressed six pre- specified themes: (1) primary DC for mass lesions, (2) secondary DC for intracranial hypertension, (3) peri-operative care, (4) surgical technique, (5) cranial reconstruction and (6) DC in low-and middle-income countries. The provided consensus statements could aid the clinicians as well as the researchers for the decision making and also to identify the areas of disagreement which require further studies. The full consensus statement: https://link.springer.com/article/10.1007%2Fs00701- 019-03936-y
The diagnostic value of procalcitonin in cerebrospinal fluid
in patient with external ventricular drain-associated infection Report on a prospective, multicentre, observational study Diagnosing and treating bacterial infections related to external ventricular drain (reported infection rate ranges between 1% and 42%) are important because the mortality rate and the incidence of neurological sequelae can be high in this condition [1]. However, defining central nervous infection in patient with external ventricular drain (EVD) may be a difficult task, and what is even more challenging is differentiating infection-induced inflammatory response from non-infection-induced in the ventricles. As conventional signs of infection (fever, headache, neck stiffness and confusion) are often unreliable in this patient population therefore microbiological tests and cerebrospinal fluid (CSF) analysis are used. Unfortunately the sensitivity of bacterial culture is low and microbiological examinations are equally time consuming, which makes an early diagnosis almost impossible. Microscopic and biochemical analysis of CSF may help diagnosing bacterial infection, although the sensitivity and specificity are not high enough to differentiate bacterial infection from sterile inflammation [2]. Therefore, it is necessary to identify more sensitive and specific biomarkers for the diagnosis of bacterial infection in patient with EVD. Procalcitonin (PCT) is a soluble protein which plasma levels in healthy individuals are quite low. It can be liberated into the circulation of patients in response to severe systemic inflammation, in particular by bacterial infection such as bacterial meningitis (BM) [3]. It has been shown that PCT concentration in both serum and CSF of BM patients is increased, and both can serve as diagnostic markers for BM detection. In addition, serum PCT exhibited a superior diagnostic value compared to CSF PCT [2]. But localised bacterial infection such as EVD-associated infection usually does not induce systemic inflammatory response and so serum PCT increase, hence serum PCT cannot be used to diagnose EVD-related bacterial infection [4]. Nevertheless it is still unknown whether locally liberated PCT in cerebrospinal fluid would be useful in this patient population. The aim of this prospective, observational study is to investigate the role of cerebrospinal fluid PCT in diagnosing external ventricular drain-related infection.
If you are interested in participating in or learn more about this study please contact: [email protected].
Reference: 1. AAB Jamjoom et al. J Neurol Neurosurg Psychiatry. 2018;89:120–126. 2. HY Shen et al. Clinical Biochemistry 2015;48:1079–1082 3. M. Meisner et al. Shock 2003;19:187-90 4. T. Hoshina et al. J Infect Chemother 21 (2015) 620e622
Extent of Spinal Cord Decompression in Motor Complete (American Spinal Injury Association Impairment Scale Grades A and B) Traumatic Spinal Cord Injury Patients: Post-Operative Magnetic Resonance Imaging Analysis of Standard Operative Approaches.
Bizhan Aarabi, et. Al. Journal of Neurotrauma. 2019 Mar 15; 36(6): 862–876. doi: 10.1089/neu.2018.5834
Severe traumatic spinal cord injury is often associated with unfavorable neurological outcome. Similar to decompressive craniectomy, spinal decompression is considered to lower the risks of secondary damage to the spinal cord in case of spinal cord compression. Rodent models of spinal trauma have shown that edema spreads from the primary lesion upwards and downwards along the spinal cord. This promotes compression of the unaffected segments of the spinal cord and secondary injuries leading to a potentially worse neurological outcome.
Several clinical studies have demonstrated the potential clinical effectiveness of spinal cord decompression. However, there was no evidence on sufficiency of various surgical techniques. The lack of objective visualization data on the extent of spinal decompression motivated this research.
A retrospective study, based on the results of pre- and post-surgical neurovisualization data, was performed in Walter Reed National Military Medical Center, which is Level 1 Trauma Center and University of Maryland School of Medicine. Of 1927 patients with blunt subaxial cervical spinal trauma 184 were included in the study. All of these patients underwent different surgical procedures for traumatic spinal cord injury and had high quality pre- and post-surgical MRI or CT scans. Neuroimaging was used to determine preoperative spinal cord compression and postoperative adequate spinal cord decompression. Surgical procedures were: anterior cervical discectomy and fusion with/without laminectomy, anterior cervical corpectomy and fusion with/without laminectomy and laminectomy with posterior stabilization alone. Statistical analysis showed that laminectomy, as a single or additional procedure, was the only associated with an adequate decompression verified by post-op MRI or CT scans.
A few limitations of the study are its retrospective format and probable selection bias. Moreover, the decision on the type of surgical intervention was subjective, and laminectomy was not routinely followed by a duraplasty. However, this is a very valuable paper showing the importance and sufficiency of laminectomy as a single or supplemental surgery for spinal cord decompression proved by neurovisualization data. A well- planned prospective study with a unified clinical, decision-making and visualization protocol is necessary to determine the treatment strategy for patients with traumatic spinal cord injury. Adequate decompression is likely to affect AIS grade conversion, and thus increases the chance of better long-term outcomes in severely disabled patients.
Tau Positron-Emission Tomography in Former National Football League Players Stern RA et al. N Engl J Med. 2019 May 2;380(18):1716-1725. doi: 10.1056/NEJMoa1900757. Epub 2019 Apr 10. https://www.nejm.org/doi/pdf/10.1056/NEJMoa1900757?articleTools=true In April 2019, the prestigious New England Journal of Medicine reported on pre- mortem neuroimaging findings of chronic traumatic encephalopathy (CTE) in former contact sport athletes. Stern and colleagues examined 26 former National Football League players (NFL) (age between 40-69 years), and compared positron-emission tomography (PET) findings of these athletes to 31 non-brain injured controls. To date, CTE is defined only neuropathologically by the deposition of tau aggregates in neurons, astrocytes, and cell processes in an irregular pattern around small vessels at the depths of cortical sulci. Tau aggregates are distributed mainly in the frontal, temporal, and parietal cortices. CTE is delineated from other tauopathies by its deviant tau accumulation pattern, and scarcity of amyloid-beta deposition. CTE has been linked to exposure to repetitive head impacts, such as those incurred in contact or collision sports. During the recent years, much research attention has been focused on elite contact sport athletes, especially in the United States. In the current PET study, NFL players with cognitive, mood, and behavioral symptoms represented with PET-positive tau aggregates bilaterally in the superior frontal and medial temporal regions, and the left parietal region. Tau accumulation was correlated with the total years of tackle football. However, these aggregates were not related to cognitive or neuropsychiatric test performance. The former NFL players did not differ from controls in relation to their cerebral amyloid-beta plaque burden. In conclusion, the published study sheds new light on the possible link between long- term repetitive head injuries and a pathognomic tau accumulation pattern. Further, it indicates that the cognitive difficulties reported by the former players were not related to Alzheimer’s disease amyloid-beta deposition. Though the study was executed rigorously, it was conducted with a rather small sample that is not widely representative, and the results should be generalized with caution. Furthermore, the study showed only between-group differences in PET measurements, and the analyses do not pertain to detection of tau pathology on an individual level.
Blocking Wallerian degeneration to ameliorate traumatic axonal injury of the brain Henninger et al. 2016. Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1. Brain. 138:1094-1105 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006226/pdf/aww001.pdf As neurosurgeons we have been traditionally taught to think of Wallerian degeneration as a process of distal nerve degeneration that occurs when a peripheral nerve is cut. This degeneration prepares the way for debris clearance and eventual regeneration. The histological finding of Wallerian degeneration was originally described in the 1850s by Augustus Waller who discovered the process in the hypoglossal nerves and studied the process in a frog model. What has become apparent in the intervening years is that Wallerian degeneration is actually an active axon death pathway that occurs in both the peripheral and central nervous system. It is an evolutionarily-ancient active self-destruct process akin to apoptosis but for the axon, and with its own unique molecular machinery and steps. In the early 1980s a spontaneous mutant mouse was discovered that slow Wallerian degeneration (Wlds). This unlocked the door to this fascinating area of neuroscience. Essentially, when the mouse had their sciatic nerves cut they did not degenerate but instead maintained their structural integrity and continued to conduct electrical impulses despite axon disconnection from the cell body. Fast-forward to the present day- and much meticulous genetic analysis including forward-genetic screening in Drosophila- have identified several key steps in the Wallerian degeneration pathway, and also begun to define its potential role in a number of diseases. One of the most important steps is the SARM1 gene. This encodes a Toll-Like Receptor Adaptor Protein whose activation is a downstream target in the Wallerian degeneration pathway. Blocking or genetically knocking out SARM1 markedly delays Wallerian degeneration. It has been hypothesised that traumatic brain injury, and in particular high velocity acceleration- deceleration injuries- cause axonal stretch and impair axonal transport- leading to SARM1 activation and hence Wallerian degeneration. The paper by Henninger et al was the first in vivo study in mice looking at the effects of SARM1 knockout in a cortical impact model. They found histological and behavioral evidence that SARM1 knockout ameliorated the effects of traumatic brain injury. They used a range of outcome measures including phosphorylated axonal neurofilament assays, proton magnetic resonance spectroscopy, and a neurobehavioral measurement scale. They concluded that anti- SARM1 therapeutics may be a viable approach to preserve neurological function after trauma. While these findings still need to be validated humans, and anti-SARM1 pharmacological agents developed, this is a promising new area of neurotrauma research.
Case Report A 34 year-old man, without relevant medical history, suffered a blunt severe head trauma due to an assault. On arrival of emergency medical services patient presented a GCS of 7 (motor response of 4 points). Systolic blood pressure was 125mmHg, heart rate of 103 bpm and peripheral oxygen saturation of 99%. Rapid sequence induction of anesthesia and orotracheal intubation was done before the patient was transferred to our trauma center. Upon arrival at our trauma center, primary and secondary survey did not reveal any other life-threatening injuries and the patient underwent head and body CT scans. No coagulopathy was noticed in his blood laboratory results. Main findings of his head CT scan were the presence of diffuse basal cistern subarachnoid haemorrhage (SAH) with a thick clot in left pontocerebellar angle and intraventricular haemorrhage (IVH) with secondary hydrocephalus (Figure 1). No fracture of the skull was found and no vascular lesion was observed in the angio-CT (Figure 2). Then, the patient was admitted to the intensive care unit.
Figure 1
Figure 2 Case Continued A right frontal external ventricular drainage (EVD) was placed in the operating room for ICP monitoring and IVH treatment. Additionally, a brain tissue oxygen probe was placed on the ipsilateral side. Although the traumatic event was confirmed when he had his occiput bumped over and over against the wall, due to SAH distribution a cerebral angiogram was done on the second hospital day. A 1 mm aneurysm was found in the origin of the left PICA in the proximity of the initial intradural portion of the vertebral artery. Vertebral artery did not show signs of dissection and there was no other aneurysm or arterio-venous malformation noted. (Figure 3).
Figure 3 Therefore, Nimodipine infusion was started and cerebral perfusion pressure was optimized. ICP remained under normal values with second-tiered measures (sedation, muscle relaxant, normothermia, CSF drainage) and no ischemic episode was detected according with brain tissue oxygen probe. After 7 days, EVD was removed and an exteriorized ventriculo-peritoneal shunt was placed to avoid CNS infection. Two weeks after TBI, a follow-up cerebral angio-CT scan was performed and an increase of the diameter of the PICA aneurysm was evidenced (Figure 4).
Figure 4 Three days later, the aneurysm was treated by embolization with coils successfully. After sedation withdrawal, tolerance to closure of exteriorized ventriculoperitoneal shunt was assessed but patient`s level of consciousness declined. Finally, a programable ventriculoperitoneal shunt was placed on the 30th after TBI. The rest of ICU and neurosurgical unit hospitalization of the patient was uneventful. The patient has achieved a favorable outcome (GOSE 7) 6 months after TBI and serial MRI showed no remnant PICA aneurysm or another delayed lesion (Figure 5).
Figure 5
Case Discussion Traumatic cerebral aneurysms are rare, less than 1% of all intracranial aneurysms, and they are usually related to penetrating injury or contiguous skull fracture [1]. On the other hand, direct trauma with compression of the artery against the relatively fixed edges of the falx or tentorium may cause vascular injury leading to the formation of these aneurysms [2-4]. Because of that, the majority of traumatic aneurysm are located in the anterior circulation (paraclinoid internal carotid, distal anterior cerebral artery). Posterior circulation traumatic cerebral aneurysm accounts for less than 10% of all cases [5] and few cases of proximal PICA traumatic aneurysm have been previously reported [6-10] some of them with fatal end. False aneurysms are considered to be the most common histological type associated with TBI and result from disruption of all three layers of the vessel wall with formation. False aneurysms grow faster than true aneurysms, and their risk of re-bleeding is very high [11-13] They are associated to high mortality because of their delayed diagnosis until re-ruptured. The interval between the injury and their rupture ranged from a few hours to several years. We consider that the extensive intraventricular blood as well as the unusual pattern of SAH identified on computed tomography (CT) are very important findings that should be emphasized during TBI patient evaluation.
In the presence of intraventricular blood and posterior fossa SAH, traumatic VA–PICA aneurysms should be ruled out with cerebral angiography.
Although, the confirmation of its traumatic origin should include the absence of aneurysm in a preinjury angiographic study, in current practice, the history of the trauma, the young age of the patient, the site of the aneurysm being other than at branching points usually is enough. Sequential imaging in this case proves without a doubt that this is a trauma- induced aneurysm. While shrinkage and disappearance of them have been reported, this appears to be uncommon in the literature. Then, early diagnosis and treatment are recommended. The mortality rate varies between 32–54% in untreated cases, and 18–24% after surgical management. To the best of our knowledge, this is the only case with imaging demonstrating the evolution of a traumatic aneurysm and endovascular successful treatment.
The goal of managing patients with traumatic aneurysms is early diagnosis and treatment to
prevent delayed re-bleeding or other thromboembolic complications. .
Bibliography
1. Frusco MR, Harrigan MR (2011) Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury, Neurosurgery 68: 517–530. 2. Fleischer AS, Patton JM, Tindall GT (1975) Cerebral aneurysms of traumatic origin. Surg Neurol 4: 233–239 3. Asari S, Nakamura S, Yamada O, Beck H, Sugatani H, Higashi H (1977) Traumatic aneurysm of peripheral cerebral arteries. J Neurosurg 46: 795–803 4. Wortzman D, Tucker WS, Gershater R (1980) Traumatic aneurysm in the posterior fossa. Surg Neurol 13:329-332. 5. Quattrocchi KB, Nielsen SL, Poirier V, Wagner FC Jr (1990) Traumatic aneurysm of the superior cerebellar artery. Case report and review of the literature. Neurosurgery 27: 476–479 6. Meguro K, Rowed DW (1985) Traumatic aneurysm of the posterior inferior cerebellar artery. Neurosurgery 16: 666–668 7. Schuster JM, Santiago P, Elliott JP, Grady MS, Newell DW, Winn HR (1999) Acute traumatic posteroinferior cerebellar artery aneurysms: report of three cases. Neurosurgery 45: 1465–1468 8. Nishioka T, Maeda Y, Tomogane Y, Nakano A, Arita N (2002) Unexpected delayed rupture of the vertebral-posterior inferior cerebellar artery aneurysms following closed head injury. Acta Neurochir (Wien) 144(8):839-45. 9. Purgina B, Milroy CM (2015) Fatal traumatic aneurysm of the posterior inferior cerebellar artery with delayed rupture. Forensic Sci Int 247:e1-5 10. Binning MJ, Hauschild TB, Amini A, MacDonald JD (2009) Delayed post-traumatic saccular aneurysm of PICA in an adolescent. Acta Neurochir (Wien) 151(12):1647-8 11. Burton C, Velasco F, Dorman J (1968) Traumatic aneurysm of a peripheral cerebral artery: review and case report, J Neurosurg 28: 468–474 12. Lee SH, Moon JU, Choi SK, Choi MK, Lee J, Sung JY (2016) Pseudoaneurysm at the Distal Posterior Inferior Cerebellar Artery After Blunt Head Trauma: A Case Report and Review of the Literature. World Neurosurg 92:580.e11-580.e15. 13. Paiva WS, Andrade AF, Sterman Neto H, de Amorim RL, Caldas JG, Teixeira MJ (2012) Traumatic pseudoaneurysm of the superior cerebellar artery. J Trauma Acute Care Surg.;72:E115.
Neurosurgery in the battlefield We have the privilege to hear the story of a colleague from an underground hospital in Idlib, Syria. Dr Omar Abdallah, a neurosurgical trainee and volunteer with the Syrian American Medical Society share his story and a case illustrating the difficulties he faces everyday. His everyday life differs from most of the neurosurgeons that are members of the EANS. He has worked without access to a CT-scanner, operating table, performing explorative craniotomies on the hospital floor under falling bombs and with no possibility to put EVDs. You can read his story from his work in Aleppo here (link)
Case Right parietal ICH caused by penetrating brain injury in a half year old girl. A 6 months old baby girl came to the ER, and presented with DCL and general convulsions with a history of a penetrating brain injury. According to the parents the baby was conscious with no neurological deficit. Examinations showed a right dilated non-reactive pupil. Mild left hemiparesis. CT brain showed right posterior parietal ICH with surrounding edema, and a 2 mm metal shrapnel.
Near the midline. The baby underwent emergency right parietal craniotomy and the hematoma was evacuated successfully.
She was extubated three hours post-op, and had a mild left hemiparesis, which improved after one week.
Post op CT scan is not available, but the baby was discharged from the hospital on three days following surgery.