Category Archives: Neurotrauma

Chronic subdural hematoma complications

Chronic subdural hematoma complications

Failure of the brain to re-expand, pneumocephalus, incomplete evacuation, and recurrence of the fluid collection are the most frequently.

Brain herniation

Chronic subdural hematoma (CSDH) with brain herniation signs is rarely seen in the emergent department. As such, there are few cumulative data to analyze such cases.

Failure of postoperative cerebral reexpansion

A wide variation in postoperative drainage volumes is observed during treatment of chronic subdural hematoma (CSDH) with twist-drill or burr-hole craniostomy and closed-system drainage.

The postoperative drainage volumes varied greatly because of differences in the outer membrane permeability of CSDH, and such variation seems to be related to the findings on the CT scans obtained preoperatively. Patients with CSDH in whom there is less postoperative drainage than expected should be carefully observed, with special attention paid to the possibility of recurrence 1).

Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. A study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly 2).


Postoperative pneumocephalus

Remote cerebellar hemorrhage (RCH)

Epidural hematoma

After chronic subdural hematoma evacuation surgery, the development of epidural hematoma is a very rare entity.

Akpinar et al. report the case of a 41-year-old man with an epidural hematoma complication after chronic subdural hematoma evacuation. Under general anesthesia, the patient underwent a large craniotomy with closed system drainage performed to treat the chronic subdural hematoma. After chronic subdural hematoma evacuation, there was epidural leakage on the following day.

Although trauma is the most common risk factor in young CSDH patients, some other predisposing factors may exist. Intracranial hypotension can cause EDH. Craniotomy and drainage surgery can usually resolve the problem. Because of rapid dynamic intracranial changes, epidural leakages can occur. A large craniotomy flap and silicone drainage in the operation area are key safety points for neurosurgeons and hydration is essential 3).

Intracranial subdural empyema

A case of intracranial subdural empyema following chronic subdural hematoma drainage 4)


Kwon TH, Park YK, Lim DJ, Cho TH, Chung YG, Chung HS, Suh JK. Chronic subdural hematoma: evaluation of the clinical significance of postoperative drainage volume. J Neurosurg. 2000 Nov;93(5):796-9. PubMed PMID: 11059660.


Markwalder TM, Steinsiepe KF, Rohner M, Reichenbach W, Markwalder H. The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage. J Neurosurg. 1981 Sep;55(3):390-6. PubMed PMID: 7264730.


Akpinar A, Ucler N, Erdogan U, Yucetas CS. Epidural Hematoma Complication after Rapid Chronic Subdural Hematoma Evacuation: A Case Report. Am J Case Rep. 2015 Jul 6;16:430-433. PubMed PMID: 26147957.


Ovalioglu AO, Aydin OA. A case of subdural empyema following chronic subdural hematoma drainage. Neurol India. 2013 Mar-Apr;61(2):207-9. doi: 10.4103/0028-3886.111165. PubMed PMID: 23644343.

Book: Neurosurgical Intensive Care

Neurosurgical Intensive Care

Neurosurgical Intensive Care

List Price:$94.99


Decompression is still the mainstay of surgical intervention for neurosurgeons treating neurocritical care patients. However, during the last 20 years, an evolution away from a mechanistic approach has transformed neurocritical care into an increasingly multidisciplinary field. Neurosurgical Intensive Care, 2nd Edition reflects this new paradigm, authored by a neurosurgeon with contributions from experts in the fields of neurology, vascular neurology, interventional neuroradiology, anesthesiology, critical care, traumatology, nutrition, and advanced practice nursing.

Neuromonitoring advances have enabled customized interventions tailored to each patient’s unique circumstances. The critical care of neurosurgical patients has evolved from an emphasis on pulmonary care (ventilation and oxygenation) to a more nuanced understanding of cerebral protection measures required to manage a disrupted blood-brain-barrier. This edition encompasses advances in the use of ICP monitors, external ventricular devices, brain tissue oxygen monitoring devices, cerebral microdialysis, fluid and electrolyte correction, as well as the increasing use of continuous EEG in the ICU.

Key Features

  • Straightforward summaries for each stage of patient care including bedside exams, neuroimaging, lab work, triage procedures, sedation and pain management, neuropharmacology, nutritional needs, administration of fluids, and more.
  • 159 tables and figures facilitate rapid evaluation and decision making.
  • Clinical pearls on a wide range of ICU scenarios – from pathophysiology and management of coma – to interventions for spinal cord injury, multisystem injuries, acute ischemic stroke, and pediatric cases.
  • Insights on how to handle family communication and spiritual needs, medical-legal issues, and discharge planning

This compact, highly practical handbook provides a stellar reference for managing critically ill neurosurgical patients in the ICU. It is a must-have resource for nurses, medical students, residents, fellows, and attending physicians who treat these patients.

Product Details

  • Published on: 2017-05-01
  • Original language: English
  • Dimensions: 5.00″ h x .0″ w x 8.00″ l,
  • Binding: Paperback
  • 576 pages

Update: Magnetic resonance imaging for chronic subdural hematoma

The Magnetic Resonance Imaging (MRI) examination better shows the location of the chronic subdural hematoma and evidences its dimensions much clearer together with the mass effect of the adjacent structures1).

Moreover, it is more useful in cases of bilateral chronic subdural hematoma and isodense chronic subdural hematomas. The MRI examination is superior to the CT examination as far as the membranes dimensions of the chronic subdural haematoma and the presence of the septa inside the haematoma are concerned, and in determining the size and internal structures of chronic subdural hematomas 2).

In these conditions the surgical approach could be modified 3).

Even though MRI has advantages, CT remains the procedure of choice in the acute setting because of shorter examination time, which is important in acutely ill patients, reliability in identifying other lesions 4).


Based on MRI, CSDHs can be classified into five types on both T(1)- and T(2)-weighted images: low, high, and mixed intensity, isointensity, and layered.

Usually, CSDHs are hyperintense on both T1- and T2-weighted MRI (the T1 values of CSDHs are significantly shorter than gray matter values and significantly longer than white matter values and the T2 values are significantly longer than both gray matter and white matter values) 5).

Axial T1-weighted magnetic resonance imaging demonstrates bilateral subacute subdural hematomas with increased signal intensity. Areas of intermediate intensity represent more acute hemorrhage into the subacute collections.

In the series of Hosoda et al. in many ways, MRI was superior to CT for demonstrating the hematomas. In general, chronic subdural hematomas were hyperintense on both T1- and T2-weighted MRI. The T1 values of chronic subdural hematomas were significantly shorter than gray matter values and significantly longer than white matter values. The T2 values were significantly longer than both gray matter and white matter values. These findings were consistent with previous reports. However, six hematomas (30%) were iso- or hypointense on T1-weighted images. Possible mechanisms responsible for the difference in intensity of chronic subdural hematoma on MRI are discussed, and the important role of methemoglobin formation is emphasized 6)

Case series


Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.

The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).

The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 7).


Preoperative MRI and postoperative computed tomography (CT) were performed and the influence of the preoperative use of antiplatelet or anticoagulant drugs was also studied. The overall recurrence rate was 9.3% (47 of 505 hematomas). The MRI T1-iso/hypointensity group showed a significantly higher recurrence rate (18.2%, 29 of 159) compared to the other groups (5.2%, 18 of 346; p < 0.001). Multivariate logistic regression analysis showed T1 classification was the solo significant prognostic predictor among various factors such as bilateral hematoma, antiplatelet or anticoagulant drug usage, residual hematoma on postoperative CT, and MRI classification (p < 0.001): adjusted odds ratio for the recurrence in T1-iso/hypointensity group relative to the T1-hyperintensity group was 5.58 [95% confidence interval (CI), 2.09-14.86] (p = 0.001). Postoperative residual hematoma and antiplatelet or anticoagulant drug usage did not increase the recurrence risk. The preoperative MRI findings, especially T1WI findings, have predictive value for postoperative recurrence of CSDH and the T1-iso/hypointensity group can be assumed to be a high recurrence risk group 8).


CT and MR images of 48 chronic subdural haematomas of 34 patients were reviewed retrospectively. The thickness measurements and imaging characteristics of haematomas were compared.

Levelling was observed in 25% of haematomas, and most of them (60%) had intrahaematomal membranes. All membranes could be delineated by MR imaging, whereas only 27% were defined by CT. Mixed density (52%) and T1 hyperintensity (59%) were commonly observed in membraned haematomas, but the difference was not statistically significant. Haematomas were measured significantly thicker on MR images. All patients had been treated with burr hole craniotomy and irrigation.

MR imaging is more sensitive than CT in determining the size and internal structures of chronic subdural haematomas 9).


Magnetic resonance imaging (MRI) and computerized tomography (CT) scans of 18 patients with 20 chronic subdural hematomas were compared. In many ways, MRI was superior to CT for demonstrating the hematomas. In general, chronic subdural hematomas were hyperintense on both T1- and T2-weighted MRI. The T1 values of chronic subdural hematomas were significantly shorter than gray matter values and significantly longer than white matter values. The T2 values were significantly longer than both gray matter and white matter values. These findings were consistent with previous reports. However, six hematomas (30%) were iso- or hypointense on T1-weighted images. Possible mechanisms responsible for the difference in intensity of chronic subdural hematoma on MRI are discussed, and the important role of methemoglobin formation is emphasized 10).


Williams VL, Hogg JP. Magnetic resonance imaging of chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):491-8. Review. PubMed PMID: 10918019.

2) , 9)

Senturk S, Guzel A, Bilici A, Takmaz I, Guzel E, Aluclu MU, Ceviz A. CT and MR imaging of chronic subdural hematomas: a comparative study. Swiss Med Wkly. 2010 Jun 12;140(23-24):335-40. doi: smw-12867. PubMed PMID: 20349366.


Iliescu IA. Current diagnosis and treatment of chronic subdural haematomas. J Med Life. 2015 Jul-Sep;8(3):278-84. Review. PubMed PMID: 26351527; PubMed Central PMCID: PMC4556906.


Adhiyaman V, Asghar M, Ganeshram KN, Bhowmick BK. Chronic subdural haematoma in the elderly. Postgrad Med J. 2002;78:71–5.


Fujisawa H, Nomura S, Kajiwara K, Kato S, Fujii M, Suzuki M. Various magnetic resonance imaging patterns of chronic subdural hematomas: indicators of the pathogenesis? Neurol Med Chir (Tokyo) 2006;46:333–9.

6) , 10)

Hosoda K, Tamaki N, Masumura M, Matsumoto S, Maeda F. Magnetic resonance images of chronic subdural hematomas. J Neurosurg. 1987 Nov;67(5):677-83. PubMed PMID: 3668635.


Fujitani S, Ishikawa O, Miura K, Takeda Y, Goto H, Maeda K. Factors predicting contralateral hematoma growth after unilateral drainage of bilateral chronic subdural hematoma. J Neurosurg. 2017 Mar;126(3):755-759. doi: 10.3171/2016.1.JNS152655. PubMed PMID: 27081904.


Goto H, Ishikawa O, Nomura M, Tanaka K, Nomura S, Maeda K. Magnetic resonance imaging findings predict the recurrence of chronic subdural hematoma. Neurol Med Chir (Tokyo). 2015;55(2):173-8. doi: 10.2176/nmc.oa.2013-0390. PubMed PMID: 25746312; PubMed Central PMCID: PMC4533403.

Update: Infantile acute subdural hematoma


Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered.

When trauma occur the motor vehicle accidents are the most frequent.

In the series of Loh et al. the most common cause of injury was shaken baby syndrome 1).

The accuracy of the history obtained from the caregivers of infants may be low in severe infantile head trauma. Therefore, medical professionals should treat the mechanism of injury obtained from caregivers as secondary information and investigate for possible abusive head trauma (AHT) in cases with inconsistencies between the history that was taken and the severity of the injury observed 2).

Chronic subdural effusions in infancy may arise from trauma, from various types of meningitis, from severe dehydration, or “idiopathically” 3).


Diagnosis can be made by computed tomography or magnetic resonance imaging 4).

Large subdural hematoma of the right convexity up to 3 cm thick, which causes severe cerebral compression, with cingulate herniation and transtentorial herniation.

The hematoma shows liquid-liquid levels, with a higher density lower in relation to sedimented hematoma.

Signs of diffuse brain edema.


Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality 5).

Case series


Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome.

Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean = 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13-15), 12 (57%) had moderate (GCS 9-12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes.

Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality 6).


Hwang et al., reviewed a total of 16 infant head injury patients under 12 months of age who were treated in from 1989 to 1997. Birth head injury was excluded. The most common age group was 3-5 months. Early seizures were noted in 7 cases, and motor weakness in 6. Three patients with acute intracranial hematoma and another 3 with depressed skull fracture were operated on soon after admission. Chronic subdural hematomas (SDHs) developed in 3 infants. Initial CT scans showed a small amount of SDH that needed no emergency operation. Resolution of the acute SDH and development of subdural hygroma appeared on follow-up CT scans within 2 weeks of injury. Two of these infants developed early seizures. Chronic SDH was diagnosed on the 68th and 111th days after the injuries were sustained, respectively. The third patient was the subject of close follow-up with special attention to the evolution of chronic SDH in view of our experience in the previous 2 cases, and was found to have developed chronic SDH on the 90th day after injury. All chronic SDH patients were successively treated by subduro-peritoneal shunting. In conclusion, the evolution of chronic SDH from acute SDH is relatively common following infantile head injury. Infants with head injuries, especially if they are associated with acute SDH and early development of subdural hygroma, should be carefully followed up with special attention to the possible development of chronic SDH 7).


A retrospective analysis of the infantile acute subdural hematoma was made by Ikeda et al., with special reference to its pathogenesis.

In 11 of 15 cases, the hematomas were bilateral or a contralateral subdural fluid collection was present. In 7 of 11 patients who underwent operation the collection was bloody fluid and/or clotted blood. In 3 patients, a subdural membrane, as seen in adult chronic subdural hematoma, was found. In only 1 patient with unilateral hematoma was clotted blood present without subdural membrane. The thickest collection of clotted blood was in the parasagittal region. It is postulated that in most cases hemorrhage occurs after minor head injury, from the bridging veins near the superior sagittal sinus, into a pre-existing subdural fluid collection such as chronic subdural hematoma or subdural effusion with cranio-cerebral disproportion, and that infants without intracranial disproportion are unlikely to have acute subdural hematoma caused by minor head injury 8).


Aoki et al. report six Japanese cases of child abuse with subdural hematoma and discuss differences from those in the United States. The majority of abused children with subdural hematomas in Japan have suffered direct violence to the face and head, resulting in external signs of trauma. Failure to detect these external traces of trauma, however, might result in an incorrect diagnosis of infantile acute subdural hematoma attributed to accidental trivial head injury. Child abuse with subdural hematoma in the United States is frequently caused by whiplash shaking injury in which external signs of trauma may not be evident. In the United States, retinal hemorrhage and subdural hematoma together suggest child abuse; some cases of infantile acute subdural hematoma might be mistakenly diagnosed as child abuse. Thus, the constellation of retinal bleeding and subdural hematoma combined with the absence of visible signs of trauma is differently interpreted in the United States and Japan 9).


Twenty-six cases of infantile acute subdural hematoma treated between 1972 and 1983 were reviewed. The series was limited to infants with acute subdural hematoma apparently due to minor head trauma without loss of consciousness, and not associated with cerebral contusion. Twenty-three of the patients were boys, and three were girls, showing a clear male predominance. The patients ranged in age between 3 and 13 months, with an average age of 8.1 months, the majority of patients being between 7 and 10 months old. Most of the patients were brought to the hospital because of generalized tonic convulsion which developed soon after minor head trauma, and all patients had retinal and preretinal hemorrhage. The cases were graded into mild, intermediate, and fulminant types, mainly on the basis of the level of consciousness and motor weakness. Treatment for fulminant cases was emergency craniotomy, and that for mild cases was subdural tapping alone. For intermediate cases, craniotomy or subdural tapping was selected according to the contents of the hematoma. The follow-up results included death in two cases, mild physical retardation in one case, and epilepsy in one case. The remaining 23 patients showed normal development. The relationship between computerized tomography (CT) findings and clinical grading was analyzed. Because some mild and intermediate cases could be missed on CT, the importance of noting the characteristic clinical course and of funduscopic examination is stressed 10).

Case reports


An unusual case of ruptured infantile cerebral aneurysm. An eight-month-old infant was delivered to the hospital in poor condition, after convulsions, with no history of trauma. His emergent CT study revealed acute subdural hematoma. The clinical and radiological picture evoked suspicion that the hematoma was of aneurysmal origin. The infant was operated with special preparations and precautions appropriate for aneurysmal surgery, and has shown a good recovery. It is important to consider the possibility of vascular accident in infants with subdural hematoma of nontraumatic origin. A good outcome may be achieved when appropriate preparations are made prior to surgery 11).


Huang et al. the case of an infant with a traumatic acute subdural hematoma that resolved within 65 hours. A 23-month-old boy fell from a height of approximately 10 m. Brain computed tomography disclosed a left subdural hematoma with midline shift. The associated clots resolved spontaneously within 65 hours of the injury. Although they may mimic more clinically significant subdural hematomas, such collections of clots are likely to be located at least partly within the subarachnoid space. Their recognition may influence decisions regarding both surgical evacuation and the likelihood of non-accidental injury. Clinical and radiographic features distinguishing these “disappearing subdural hematomas” from more typical subdural hematomas are discussed 12)

Own case report

A 1 year old , according to anamnesis provided by the parents, they consulted in the last month for cough clinic with low expectoration, nasal congestion, Tº up to 38ºC of 24 hrs evolution. According to an emergency report: the previous week the patient presents right facial edema, of 2 days duration.

Scratch injuries in legs.

In the next days vomiting with progressive decay.

In the following hours after admission coma, respiratory arrest with bradycardia

Large subdural hematoma of the right convexity up to 3 cm thick, which causes severe cerebral compression, with cingulate herniation and transtentorial herniation.

The hematoma shows liquid-liquid levels, with a higher density lower in relation to sedimented hematoma.

Signs of diffuse brain edema.

In the surgical intervention xanthochromia appears at the beginning, later dark red liquid without clots. Later a subdural membrane is seen on the arachnoid surface, very characteristic of chronic subdural hematoma.

1) , 4) , 5) , 6)

Loh JK, Lin CL, Kwan AL, Howng SL. Acute subdural hematoma in infancy. Surg Neurol. 2002 Sep-Oct;58(3-4):218-24. PubMed PMID: 12480224.


Amagasa S, Matsui H, Tsuji S, Moriya T, Kinoshita K. Accuracy of the history of injury obtained from the caregiver in infantile head trauma. Am J Emerg Med. 2016 Sep;34(9):1863-7. doi: 10.1016/j.ajem.2016.06.085. PubMed PMID: 27422215.


Amacher AL, Li KT. Indirect trauma as a cause of acute infantile subdural hematomas. Can Med Assoc J. 1973 Jun 23;108(12):1530. PubMed PMID: 4714878; PubMed Central PMCID: PMC1941542.


Hwang SK, Kim SL. Infantile head injury, with special reference to the development of chronic subdural hematoma. Childs Nerv Syst. 2000 Sep;16(9):590-4. PubMed PMID: 11048634.


Ikeda A, Sato O, Tsugane R, Shibuya N, Yamamoto I, Shimoda M. Infantile acute subdural hematoma. Childs Nerv Syst. 1987;3(1):19-22. PubMed PMID: 3594464.


Aoki N, Masuzawa H. Subdural hematomas in abused children: report of six cases from Japan. Neurosurgery. 1986 Apr;18(4):475-7. PubMed PMID: 3703222.


Aoki N, Masuzawa H. Infantile acute subdural hematoma. Clinical analysis of 26 cases. J Neurosurg. 1984 Aug;61(2):273-80. PubMed PMID: 6737052.


Adeleye AO, Shoshan Y, Cohen JE, Spektor S. Ruptured middle cerebral artery aneurysm in an infant presenting as acute subdural hematoma: a case report. Pediatr Neurosurg. 2008;44(5):397-401. doi: 10.1159/000149908. PubMed PMID: 18703887.


Huang SH, Lee HM, Lin CK, Kwan AL, Howng SL, Loh JK. Rapid resolution of infantile acute subdural hematoma: a case report. Kaohsiung J Med Sci. 2005 Jun;21(6):291-4. PubMed PMID: 16035574.

Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition

The scope and purpose of the Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. is 2-fold: to synthesize the available evidence and to translate it into recommendations. This document provides recommendations only when there is evidence to support them. As such, they do not constitute a complete protocol for clinical use.

The intention is that these recommendations be used by others to develop treatment protocols, which necessarily need to incorporate consensus and clinical judgment in areas where current evidence is lacking or insufficient.

Carney et al. think it is important to have evidence-based recommendations to clarify what aspects of practice currently can and cannot be supported by evidence, to encourage use of evidence-based treatments that exist, and to encourage creativity in treatment and research in areas where evidence does not exist. The communities of neurosurgery and neurointensive care have been early pioneers and supporters of evidence based medicine and plan to continue in this endeavor. The complete guideline document, which summarizes and evaluates the literature for each topic, and supplemental appendices (A-I) are available online at 1).

4th edition

Free article of Neurosurgery

1) Carney N, Totten AM, OʼReilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2016 Sep 20. [Epub ahead of print] PubMed PMID: 27654000.

Book: Neurotrauma Management for the Severely Injured Polytrauma Patient

Neurotrauma Management for the Severely Injured Polytrauma Patient

Neurotrauma Management for the Severely Injured Polytrauma Patient

List Price : $129.00


This text addresses many of the questions which occur when medical professionals of various disciplines interact and have different plans and interventions, each with its own valid scientific and/or experience-based rationale:  Questions involving tourniquet placement, ideal fluids and volumes for resuscitation, VTE prophylaxis and many other management considerations. Straightforward decisions in the patient with a single diagnosis often conflict when applied to the neurologically injured polytrauma patients.

 Neurotrauma Management for the Severely Injured Polytrauma Patient answers as many of these questions as possible based on the current literature, vast experience with severe neurotrauma in the current conflicts in Afghanistan and Iraq, and the experience of trauma experts across the globe as well as proposes areas for future study where answers are currently less clear.

Product Details

  • Published on: 2017-01-13
  • Original language: English
  • Number of items: 1
  • Dimensions: 10.00″ h x .0″ w x 7.00″ l, .0 pounds
  • Binding: Hardcover
  • 340 pages

James M. Ecklund, M.D., F.A.C.S. serves as Chairman of the Inova Neuroscience Institute. Prior to joining Inova Medical Group, he served as Professor and Chairman of the Neurosurgery Program of the National Capital Consortium, which includes Walter Reed Army Medical Center, National Naval Medical Center and the Uniformed Services University. He is a retired colonel in the U.S Army and was deployed as a Neurosurgeon to both Afghanistan and Iraq. His program received the vast majority of American neurotrauma casualties.

Dr. Ecklund’s primary clinical and research interests include complex spine, cerebrovascular disease and neurotrauma with an emphasis on blast and penetrating injury. He directs a neurotrauma laboratory at the Uniformed Services University, has over 100 publications and abstracts, and has lectured throughout the world. He also has served on multiple oversight and advisory boards for the Veterans Administration, Department of Defense, National Institutes of Health, NATO, Neurotrauma Foundation, and Brain Trauma Foundation.

Leon E. Moores, MD, MS, FACS is the CEO of Pediatric Specialists of Virginia and the Associate Chair for Pediatric Programs at the Inova Neuroscience Institute. He retired as a Colonel from the US Army where he led as an Infantry Platoon Leader, Chief of Neurosurgery at Walter Reed, Chairman of the Department of Surgery at Walter Reed, Deputy Commander of the National Naval Medical Center, and Commander of the Fort Meade Medical System. Dr Moores also served two tours of duty in Afghanistan and Iraq.
Dr Moores’ clinical and research interests center on brain and spinal tumors in children, CNS infections in combat soldiers, and complex craniofacial reconstruction in severe head and facial trauma. He is a Professor of Surgery and Pediatrics at the Uniformed Services University, and a Professor of Neurosurgery at Virginia Commonwealth University.

Update: Vernet’s syndrome

In contrast to the majority of classic brainstem syndromes, the interpretation of Schmidt’s syndrome (ipsilateral palsy of the IX, X, XI, and XII cranial nerves with contralateral hemiparesis) and Vernet’s syndrome (ipsilateral palsy of the IX, X, and XI nerves with contralateral hemiparesis) is controversial. They are sometimes addressed as crossed brainstem syndromes but also as syndromes due to multiple cranial nerve lesions without contralateral hemiparesis. In this study, the historic descriptions and recent publications about Schmidt’s and Vernet’s syndromes were reviewed and critically analysed. We conclude that historic descriptions and later publications describe exclusively patients with extracerebral lesions of multiple cranial nerves. “Central” syndromes of Schmidt and Vernet caused by brainstem lesion appear not to exist. An extremely extensive lesion explaining these hypothetical unilateral brainstem syndromes is theoretically possible but, however, was apparently never observed in any of the known unilateral brainstem diseases 1).


Symptoms of this syndrome are consequences of this paresis. As such, in an affected patient, you may find:


soft palate dropping

deviation of the uvula towards the normal side


loss of sensory function from the posterior 1/3 of the tongue

decrease in the parotid gland secretion

loss of gag reflex

sternocleidomastoid and trapezius muscles paresis.


A variety of neoplasms, vascular insults, infections, and trauma have been reported to cause JFS 2).

The causes of Vernet syndrome are primary tumors such as Glomus jugulare tumors (most frequently), meningioma, vestibular schwannoma, cerebellopontine angle metastases, inflammation such as meningitis and malignant otitis externa, and sarcoidosis, Guillain-Barre syndrome 3).

Trauma 4) 5).

Cholesteatoma (very rare) 6).

Obstruction of the jugular foramen due to bone diseases 7).

Varicella-zoster virus 8).

Giant cell arteritis 9) 10).

Internal jugular vein thrombosis 11).

After carotid endarterectomy 12).

Large mycotic aneurysm of the extracranial internal carotid artery after acute otitis media 13).

Systemic erythematous lupus 14).

1) Krasnianski M, Neudecker S, Zierz S. [The Schmidt and Vernet classical syndrome. Alternating brain stem syndromes that do not exist?]. Nervenarzt. 2003 Dec;74(12):1150-4. Review. German. PubMed PMID: 14647918.
2) Robbins KT, Fenton RS. Jugular foramen syndrome. J Otolaryngol. 1980 Dec;9(6):505-16. PubMed PMID: 7206037.
3) Ha SW, Kim JK, Kang SJ, Kim MJ, Yoo BG, Kim KS, et al. A case of Vernet’s syndrome caused by non-specific focal inflammation of the neck. J Korean Soc Clin Neurophysiol. 2007;9:81–84.
4) , 5) Kim HS, Ko K. Penetrating trauma of the posterior fossa resulting in Vernet’s syndrome and internuclear ophthalmoplegia. J Trauma. 1996 Apr;40(4):647-9. PubMed PMID: 8614050.
6) Erol FS, Kaplan M, Kavakli A, Ozveren MF. Jugular foramen syndrome caused by choleastatoma. Clin Neurol Neurosurg. 2005 Jun;107(4):342-6. PubMed PMID: 15885397.
7) Erol FS, Kaplan M, Kavakli A, Ozveren MF.Jugular foramen syndrome caused by choleastatoma. Clin Neurol Neurosurg. 2005 Jun;107(4):342-6.
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