Radiological parameters for surgical indication in traumatic brain injury

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1 Radiological parameters for surgical indication in traumatic brain injury Poster No.: C-1821 Congress: ECR 2011 Type: Educational Exhibit Authors: A. Elías Mas, C. Corbella Sala, S. Pasetto, F. Caiazzo, M. Garcia ; Barcelona/ES Keywords: Neuroradiology brain, CT, Decision analysis, Surgery, Trauma DOI: /ecr2011/C-1821 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 49

2 Learning objectives Computed tomography (CT) has become the mainstay in the investigation of patients with traumatic brain injury (TBI). Our objectives are to analyze the contribution this makes. In particular the important signs that will be crucial in the therapeutic-decision making process on CT are assessed. Page 2 of 49

3 Background TBI is the major cause of death and severe disability in young people in Europe. Often, early surgical treatment is necessary to avoid a poor outcome such as death or a persistent vegetative state. A non-enhanced CT head: Has a wide availability. Is a secure tenchinque that provides images in a short time. Provides accurate information of skull fractures, intra or extra-axial bleeds and their consequences within the brain. For all these reasons CT head is considered the first line study in patients with acute TBI.. The Classification of TBI lesions: In the literature, several classifications of TBI have been made. These can be divided into those with prognostic value and those without. Without prognostic value Primary lesions: these are produced at the moment of the impact Secondary lesions: these develop subsequently to the trauma Focal lesions Diffuse lesions With prognostic value Primary traumatic lesions: Meningeal lesions: epidural, subdural and subarachnoid haematoma, subdural hygroma and post-trauma arachnoid cyst Parenchymal lesions: axonal injury, intra-axial contusion/haematoma, brainstem damage and cranial nerves injury Vascular lesions Page 3 of 49

4 Skull fractures Epicranial injuries: wounds and haematomas Secondary traumatic lesions: Encephalomalacia Secondary stroke Infection Necrosis due to compression Brainstem bleeding (or Duret haematoma) Leptomeningeal cysts The traumatic brain injury classification with prognostic value is particulary relevant in those patients whose initial clinical examination is unremarkable but have a high risk of evolving into a progressive neurological deficit with poor clinical outcome. Providing prognostic value to the initial CT findings is the aim of the Traumatic Coma Data Bank (TCDB) classification. TCDB classification was first proposed by Marshall. Posteriorly, new alternative classifications have been proposed. The Traumatic Coma Data Bank Classification grades the severity of the injury as follows: (J. Neurosurgery) (fig1) Diffuse injury I. Normal CT scan. Diffuse injury II. Diffuse injury. The basal cisterns are present. There is displacement of the midline structures from 0 to 5 mm and / or dense lesions. No lesions of high or mixed density larger than 25 cc. Bony fragments or foregin body may be present. Diffuse injury III. Diffuse injury with Swelling. The basal cisterns are compressed or absent. There is displacement of the midline structures from 0 to 5 mm. Page 4 of 49

5 No lesions of high or mixed density larger than 25 cc. Diffuse injury IV. Diffuse injury with shift. There is displacement of the midline structures more than 5 mm. No lesions of high or mixed density larger than 25 cc. Evacuated focal lesion. Any mass lesion surgically evacuated. Not evacuated focal lesion VI. Any mass lesion of high or mixed density larger than 25 cc that has not been operated upon. We illustrate different methods to measure: The volume of the haematoma (fig 2) The shift of the midline structures (fig 3) The grade of the basal cistern compression (fig 4) Page 5 of 49

6 Images for this section: Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 6 of 49

7 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 7 of 49

8 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 8 of 49

9 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 9 of 49

10 Imaging findings OR Procedure details ACUTE EPIDURAL HAEMATOMA Radiological findings (Fig 1 and 2) The epidural haematoma is located in between the inner table of skull and dura mater. Typically, it has a convex shape. Due to the fixation of the dura at the cranial sutures, the epidural haematoma does not extend through sutures. It can cross the midline. In the acute phase it usually presents high attenuation. However, in patients with anemia it may present decreased attenuation. Physiopathology The epidural haematoma can result from injury to the middle meningeal artery, middle meningeal vein, diploe veins or from venous sinuses. As arterial blood flow is under higher pressure, damage to the middle meningeal artery poses a greater danger to the patient's life than from a venous injury. Epidural haematomas are frequently associated with bone fractures and are generally located in the temporal lobe or fronto-parietal region. Clinical presentation Classically, it presents as loss of consciousness, followed by a period of lucidity, and then subsequent neurological deterioration (which is usually caused by uncal herniation and mass effect of the haematoma). The lucid interval however occurs in less than half of the cases. Crucial radiological findings with prognostic value Most authors do not detect a relationship between the location of the epidural haematoma and the prognosis. However, the thickness and volume of the haematoma and the degree of deviation of the midline structures have been associated with the prognosis. Page 10 of 49

11 Surgical criteria in acute epidural haematoma In general Craniotomy for evacuation of an acute epidural haematoma has been historically one of the most effective procedures. It has resulted in almost eliminating the mortality. By contrast, in subdural haematomas and intraaxial contusions/ haematomas, surgery has not achieved such an improvement in the prognosis. The decision to operate on an acute epidural haematoma is based on the patient's score on the Glasgow Coma Scale, pupillary examination, comorbidities, age and CT findings. Epidural haematomas have a surgical indication if: They measure more than 30cc, regardless the patient's Glasgow Coma Scale. Epidural haematomas can be treated non-surgically with a follow-up scan and close neurological observation if: They measure less than 30 cc, less than 15 mm in thickness and there is less than 5 mm of deviation of the midline structures in a patient with a high score on the Glasgow Coma Scale without focal deficit. Radiological criteria In summary, according to surgical criteria of epidural haematoma, it is important to provide radiological information about: The volume of haematoma (more than 30 cc?) The thickness of the haematoma (more than 15 mm?) The degree of deviation of the midline structures (more than 5 mm?) ACUTE SUBDURAL HAEMATOMA Radiological findings (fig 3, 4, 5 and 6) They typically present as a crescent shape with a convex lateral edge and an inner concave edge distributed adjacent to the cortex. They are most common localized in the fronto-parietal convexity and, less frequently, parafacial, interhemispheric or tentorial regions. The acute subdural haematoma usually presents with a high attenuation. Page 11 of 49

12 However, when non-coagulated blood is present it can present with lower attenuation. This occurs in the hyperacute (actively bleeding) and chronic haematoma (many weeks old). Mixed density within the subdural collection may be related to active bleeding (hyperacute) or related to the presence of cerebrospinal fluid from arachnoid tears. Density of the haematoma may be lower in pateients suffering anemia. Patients with a coagulopathy should have special attention as haematomas can rapidly expand. Physiopathology Bleeding may be secondary to arterial or venous injury or bleeding from the cortical bridging veins which are localized in the subdural space. The cortical bridging veins are broken by shearing forces. Parenchymal lesions are frequently associated with acute subdural haematoma and therefore associated with a poor prognosis long-term. If the deviation of the midline structures is greater than the thickness of the haematoma it indicates a component of cerebral oedema and this is also associated with a poor prognosis. Prognostic findings There appears to be a relationship between CT findings and prognosis, but it is difficult to establish threshold values. Advanced age, low score on the Glasgow Coma Scale and signs of herniation are associated with a poor prognosis, but death cannot be predicted with certainty. Surgical criteria in acute subdural haematoma: In general Acute subdural haematomas are frequently associated with other intracranial lesions, and so the surgical decision should take into account the recommendations for both types of injuries. The surgical indications of acute subdural haematoma are based on the patient's Glasgow Coma Score, neurological status, CT findings, age and sometimes with the intracranial pressure. Surgical Criteria: Page 12 of 49

13 An acute subdural haematoma greater than 10 mm thickness or deviation of the midline structures more than 5 mm should be evacuated surgically no matter what the patient's Glasgow coma Scale is. Surgical management shoud be carried out if in a comatose patient (Glasgow Coma Scale less than 9), the score decreases 2 points or more between the time of the TBI and admission to hospital and / or if the pateint presents unresponsive anisocoria and / or if the intracranial pressure exceeds 20 mmhg. These crieteria are valid even if the size of subdural haematoma is minor and the deviation of the deviation of the midline structures is less than 5 mm. Radiological criteria In summary, according to surgical criteria of subdural haematoma, it is important to provide radiological information about: The thickness of the haematoma (greater than 10mm?) The deviation of the midline structures (more than 5 mm?) PARENCHYMAL MASS LESIONS Classification Focal lesions: Likely surgical candidate: intraparenchymal acute and late haematoma, contusion Likely to have a conservative approach: infarction and diffuse axonal injury Diffuse lesions: cerebral oedema and swelling Acute intracerebral haematoma (fig 7) They often present as parenchymal high attenuation lesions surrounded by decresead hypodensity due to ooedema, which contributes to the mass effect. Page 13 of 49

14 They are often produced by the impact of the cerebral parenchyma with adjacent bony structures. For this reason they are usually localized in the frontal and temporal lobes. They can increase in size early after trauma. The ooedema tends to develop around the lesion over the first week or so, especially in young patients, contributing to mass effect. For this reason these lesions must be closely monitored until stabilized. If the lesion occurs in the temporal lobe, which it is contained within the middle cranial fossa, expansion tends to occur toward the brainstem and there is greater risk of transtentorial herniation. For this reason, the threshold size for surgical indication of lesions located in the temporal lobe is lower than in other locations. Patients with post-trauma coagulation disorder are more prone to intracranial haemorrhage. Delayed traumatic intracerebral haematoma Is defined by most authors as an injury that occurs in areas of the brain that appeared radiologically normal on the initial CT. It is strongly associated with death (16-72%, depending upon the article), especially if developed within 48 hours post TBI. Delayed traumatic intracranial haematoma is one of the reasons why the patient doesn't have the expected neurological recovery or has cognitive impairment. These patients have a poor prognosis if surgery is not performed promptly. In order to assure prompt surgical intervention, a strict neurological control is required in patients with initial abnormal CT head. Contusions (fig 8) These usually affect the cerebral cortex and the underlying white matter is spared. They are usually located in frontobasal and temporal regions. The association of a large contusion with subdural haematoma is referred as lobular burst. When they are located in the frontal and temporal lobe they are associated with high mortality and morbidity. Traumatic vascular lesions (infarction) (fig 9) There are several mechanisms that lead to post-traumatic cerebral infarction: Cerebral heniation is the main mechanism. Page 14 of 49

15 Carotid and/or vertebral artery dissection. Fat embolism. Vasospasm. Direct compression of brain parenchyma and compromise of the venous return produce ischaemic lesions that do not necessarily follow any arterial territory. - Global anoxia can lead to cerebral ooedema due to diffuse ischaemic injury. If skull base fractures are present, the possibility of carotid dissection or caroticocavernous fistulas should be considered. Diffuse axonal injury (DAI) (fig 10) It is usually secondary to high-energy impacts with abrupt accelerationdeceleration. It should always be suspected if there is discrepancy between neurologial deficit and unremarkable findings on the CT scan. This is because in most cases the DAI consists of multiple non hemorrhagic lesions. In these cases MRI should be performed. Intraventricular haemorrhage caused by injury in the periventricular ependyma cells may be the only CT finding. Classification (fig 11) Cerebral ooedema (fig 12) It is defined as focal or global loss of gray-white matter differentiation. Vasogenic ooedema tends to appear in the first days, while cytotoxic ooedema appears much quicker and can cause more mass effect (with effacement of basal cisterns and deviation of the midline structures more than 5 mm; If these two findings are present, intracranial pressure monitoring is required.) Swelling (fig 13) Cerebral ooedema and swelling present with mass effect, but in swelling the brain tissue density is preserved. Page 15 of 49

16 Brainstem injuries (fig 14 and 15) These usually present as a late onset. They are better assessed with MRI. Duret haemorrhage refears to brainstem hameorrhage secondary to transtentorial herniation. Surgical criteria in parenchymal lesions: In general The indication for surgical intraparenchymal lesions is controversial. Which patients with parenchymal lesions will benefit from surgery is not clearly defined and radiological criteria, patient's Glasgow Coma Scale, location of the lesion, the lesion volume, presence of intracranial hypertension, neurological deterioration etc should all be considered. Because it is a dynamic process, these lesions present changes over time. This fact makes it difficult to use initial CT findings as an independent parameter. Surgical criteria: - Intraparenchymal lesions larger than 50 cc. - Smaller parenchymal lesions but associated with mass effect evidenced by CT scan (deviation of the midline structures equal or more than 5 mm and / or compression of the basal cisterns) or with progressive neurological deterioration secondary to the injury or increased intracranial pressure refractory to the medical treatment. Patients can be treated non-surgically but with intensive monitoring and follow-up CTs: if they present with an intraparenchymous lesion but without neurological compromise, without signs of mass effect on CT scan and with controlled intracranial pressure. Radiological criteria In summary, according to surgical criteria of intracranial haematomas, it is important to provide radiological information about: The size of the lesion (greater than 50cc?) The deviation of the midline structures (more than 5 mm?) The state of the basal cisterns (compressed?, obliterated?) Page 16 of 49

17 INTRAVENTRICULAR HAEMORRHAGE (fig 16) It is often viewed as a hematocrit level at the posterior horns of the lateral ventricles. Unless there is hydrocephalus, it usually does not usually warrant surgery. Intraventricular haemorrhage secondary to trauma may be caused either by subarachnoid haemorrhage or by an intraparenchymal hemorrage with intraventricular extension. SUBARACHNOID HAEMORRHAGE (fig 17) This often manifests as blood in the convexity sulci, the Sylvian fissures or the basal cisterns. It is associated with a risk of late vasospasm and therefore ischemia. There is evidence that treatment with nimodipine (a vasodilator) improves prognosis in patients with subarachnoid haemorrhage. In some cases a ruptured aneurysm may be the cause of trauma. If suspected, CTAngiography should be performed in search of the aneurysm. Grading scores for subarachnoid haemorrhage. The higher the score, the worse the prognosis. - Hunt and Hess (based on the clinical observation) - Fisher Score (fig 18) - Fisher Score reviewed / modifyied by Claassen. It also considers the risk associated with the size of the subarachnoid haemorrhage and the intraventricular haemorrhage. (fig 19) POSTERIOR FOSSA LESIONS (fig 20) Posterior fossa lesions may not produce signs of progressive mass effect, but instead may rapidly evolve to coma and death. This is due to rapid mass effect of the lesion which is located in a limited compartment (posterior fossa). Posterior fossa lesions are more likely to produce brainstem compression. Recommendations for surgery for posterior fossa lesions Page 17 of 49

18 In general Intracranial pressure is rarely measured in the posterior fossa. Signs of mass effect in this compartiment include compression of the fourth ventricle, compresion of the basal cisterns and of obstructive hydrocephalus. Surgical criteria: Mass effect signs present on CT scan (compression of the fourth ventricle, compresion of the basal ciserns and of obstructive hydrocephalus) Neurological deterioration attributable to the injury. Lesions greater than 3 cm in diameter. Obstructive hydrocephalus should be treated with ventricular drainage with special attention to the gradient of drainage in order to prevent upward transtentorial herniation. Can be managed by close observation and follow-up images: Patients with lesions without significant mass effect on CT and without neurological damage. Radiological criteria In summary, according to surgical criteria of posterior fossa lesions, it is important to provide radiological information about: The fourth ventricle (compression?) The basal cisterns (compression?, obliteration?) The size of the lesion (greater than 3 cm in diameter?) Signs of obstructive hydrocephalus DEPRESSED CRANIAL FRACTURES (fig 21 and 22) Cranial fractures classification Is there laceration of the dura? No: simple (closed) Yes: complex (open) Page 18 of 49

19 Is there incongruity of the cranial vault? No: non-depressed Yes: depressed The presence of a skull fracture has been associated with increased incidence of intracranial injury, neurological deficit and a worse prognosis, especially in depressed open fractures. Recommendations for surgery for depressed cranial fractures In general Depressed closed fractures may be surgical if the extent of depression is more than the total thickness of the skull (although there is little basis for such an arbitrary threshold). The theoretical benefits are better asthetics, a decrease in post-traumatic epilepsy incidence and a reduction of a persistent neurological deficit. All patients with depressed open skull fractures have indications for surgery in order to prevent infection. Fractures that cross along venous sinuses and are not associated with bleeding are usually not touched unless it is necessary to repair the permeability of the venous sinus. Radiological criteria In summary, according to surgical criteria of cranial fractures, it is important to provide radiological information about: Type of fracture (open or closed? depressed?). When a fracture is depressed, it is important to note: The degree of depression (does it exceeds the thickness of the skull?) If there is evidence of dural penetration If there is involvement of the frontal sinus If there is a coexistent intracranial haematoma If there is pneumocephalus Page 19 of 49

20 PENETRATING BRAIN INJURY (fig 23 and 24) Recommendations for surgery in penetrating brain injury In general The management of penetrating brain injury includes treatment of intracranial hypertension, infection prevention, risk of vascular injury and seizures prophylaxis. There is increasing evidence that debriding the foreign body does not alter the risk of infection and does not improve prognosis. Debridement of the foreign body should only be performed when surgery is indicated for other reasons and the intracerebral fragment is easily resectable. The main indication for surgery is to prevent cerebrospinal fluid leakage. If the length of the wound passes through or near the Sylvian fissure, supraclinoid carotid, cavernous sinus or a greater venous sinus, there is a higher risk of developing a traumatic aneurysm or arteriovenous malformation and CT Angiography should be performed. The time course of development of these lesions is not clear, so repeating the CT Angiography study should be taken in consideration if no findings are present in the initial study. Radiological criteria In summary, according to surgical criteria of penetrating brain injury, it is important to provide radiological information about: The intracranial trajectory of the foreign body To determine if there is evidence of CSF leakage and the point of leakage To assess a possible vascular injury in order to perform a CT Angiogram Page 20 of 49

21 Images for this section: Institute of Neurological Sciences, Glasgow Page 21 of 49

22 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 22 of 49

23 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 23 of 49

24 Institute of Neurological Sciences, Glasgow Page 24 of 49

25 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 25 of 49

26 Institute of Neurological Sciences, Glasgow Page 26 of 49

27 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 27 of 49

28 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 28 of 49

29 Institute of Neurological Sciences, Glasgow Page 29 of 49

30 Institute of Neurological Sciences, Glasgow Page 30 of 49

31 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 31 of 49

32 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 32 of 49

33 Institute of Neurological Sciences, Glasgow Page 33 of 49

34 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 34 of 49

35 Institute of Neurological Sciences, Glasgow Page 35 of 49

36 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 36 of 49

37 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 37 of 49

38 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 38 of 49

39 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 39 of 49

40 Institute of Neurological Sciences, Glasgow Page 40 of 49

41 Radiologia, Hospital Universitari Mútua Terrassa - Barcelona/ES Page 41 of 49

42 Institute of Neurological Sciences, Glasgow Page 42 of 49

43 An Atlas and Practical Guide. Multidetector CT in Neuroimaging, Evelyn M Teasdale, Susan Aitken. Clinical Publishing Page 43 of 49

44 An Atlas and Practical Guide. Multidetector CT in Neuroimaging, Evelyn M Teasdale, Susan Aitken. Clinical Publishing Page 44 of 49

45 Conclusion Together with the degree of neurological compromise (Glasgow Coma Scale), radiological findings are crucial in the therapeutic and surgical decision-making process in patients with acutetbi. An adequate knowledge of these parameters by the radiologist leads to better quality of st patient care after TBI. This is even more important in the 21 century with the increasing use of teleradiology. Page 45 of 49

46 Personal Information A. Elias, C. Corbella Sala, S. Pasetto, ; Department of Radiology, Hospital Universitari Mútua Terrassa (Barcelona) 1 1 F. Caiazzo, M. Garcia ; Department of Neurosurgery, Hospital Universitari Mútua Terrassa (Barcelona) Page 46 of 49

47 References 1. Marion DW. Evidenced-based guidelines for traumatic brain injuries. Prog Neurol Surg Chesnut RM. Care of central nervous system injuries. Surg Clin North Am Guidelines for the management of severe traumatic brain injuy. X. Brain oxygen monitoring and thresholds. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; J Neurotrauma Hiler M, Czosnyka M, Hutchinson P, Balestreri M, Smielewski P, Matta B, Pickard JD. Predictive value of initial computerized tomography scan, intracranial pressure, and state of autoregulation in patients with trauamtic brain injury. J Neurosurg Tong WS, Zheng P, Xu JF, Guo YJ, Zeng JS, Yang WJ, Li GY, He B, Yu H. Early CT signs of progressive hemorrhagic injury following acute traumatic brain injury. Neuroradiology Bremmer R, de Jong BM, Wagemakers M, Regtien JG, van der Naalt J. The Course of Intracranial Pressure in Traumatic Brain Injury: Relation with Outcome and CTcharacteristics. Neurocrit Care Oddo M, Gasche Y. Update on the management of severe traumatic brain injury. Rev Med Suisse Jacobs B, Beems T, van der Vliet TM, Borm GF, Vos PE. The status of the fourth ventricle and ambient cisterns predict outcome in moderate and severe traumatic brain injury. J Neurotrauma Zhu GW, Wang F, Liu WG. Classification and prediction of outcome in trauamatic brain injury based on computed tomographic imaging. J Int Med Res Page 47 of 49

48 10. Nelson DW, Nyström H, MacCallum RM, Thornquist B, Lilja A, Bellander BM, Rudehill A, Wanecek M, Weitzberg E. Extended analysis of early computed tomography scans of traumatic brain injured patients and relations to outcome. J Neurotrauma Jagoda AS, Bazarian JJ, Bruns JJ Jr, Cantrill SV, Gean AD, Howard PK, Ghajar J, Riggio S, Wright DW, Wears RL, Bakshy A, Burgess P, Wald MM, Whitson RR Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med Yuh EL, Gean AD, Manley GT, Callen AL, Wintermark M. Computer-aided assessment of head computed tomography (CT) studies in patients with suspected traumatic brain injury. J Neurotrauma James M. Provenzale Neuroradiology/Head and Neck Imaging Imaging of Traumatic Brain Injury: A Review of the Recent Medical Literature Am. J. Roentgenol., Jan 2010; 194: A new classification of head injury based on computed tomography. J. Neurosurgery Guidelines for the management of penetrating brain injury. J. Trauma Aarabi B, Alden TD, Chesnut RMD, et al. Gidelines for the management of penetrating brain injury. J Trauma Bullock MR, Chesnut R, Ghajar J, et al. Gidelines for the surgical management of traumatic brain injury. Neurosurgery Marshall LF, Marshall SB, Klauber MR, et al. A new classification of head injury based on computerized tomography. J Neurosurg Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery Page 48 of 49

49 20. Hukkelhoven CW, Steyerberg EW, Habbema JD, Farace E, Marmarou A, Murray GD, Marshall LF, Maas AI. Predicting outcome after traumatic brain injury: developement and validation of a pronostic score based on admission characteristics. J Neurotrauma Lee H, Wintermark M, Gean AD, Ghajar J, Manley GT, Mukherjee P. Focal lesions in acute mild traumatic brain injury and neurocognitive outcome: CT versus 3T MRI. J Neurotrauma 2008;25: Surgical management of penetrating brain injury. J Trauma Radiología Esencial. SERAM Editorial Médica Panamericana, S.A. 24. Classen J, Bernardini GL, Kreiter K, Bates J, Du YE, Copeland D, Connolly ES, Mayer SA. Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited. Stroke Sep;32(9): Page 49 of 49

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