|VI Uruguayan Congress of Neurosurgery|
|4 – 7 April 2018|
Perioperative Considerations and Positioning for Neurosurgical Procedures: A Clinical Guide
List Price: $121.50
Posttraumatic epilepsy in children
Among children with moderate traumatic brain injury or severe traumatic brain injury, the presence of additional CT findings, other than skull fractures, seem to increase the risk of PTE. In the cohort of Keret et al, the occurrence of an early seizure did not confer an increased risk of PTE 1).
Mild traumatic brain injury (MTBI) was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population 2).
Literature recognizes several posttraumatic seizure subtypes based on time of presentation and the underlying pathophysiology: impact, immediate, delayed early, and late/posttraumatic epilepsy. Appropriate classification of pediatric posttraumatic seizure subtypes can be helpful for appropriate management and prognosis.
A review of Arndt et al focused on early posttraumatic seizures, and the subtypes of early posttraumatic seizure. Incidence, risk factors, diagnosis, seizure semiology, status epilepticus, management, risk of recurrence, and prognosis were reviewed. The integration of continuous electroencephalographic (EEG) monitoring into pediatric traumatic brain injury management may hold the key to better characterizing and understanding pediatric early posttraumatic seizures 4).
The aim of a rapid evidence review was to provide a synthesis of existing evidence on the effectiveness of treatment interventions for the prevention of PTE in people who have suffered a moderate/severe TBI to increase awareness and understanding among consumers. Electronic medical databases (n = 5) and gray literature published between January 2010 and April 2015 were searched for studies on the management of PTE. Twenty-two eligible studies were identified that met the inclusion criteria. No evidence was found for the effectiveness of any pharmacological treatments in the prevention or treatment of symptomatic seizures in adults with PTE. However, limited high-level evidence for the effectiveness of the antiepileptic drug levetiracetam was identified for PTE in children. Low-level evidence was identified for nonpharmacological interventions in significantly reducing seizures in patients with PTE, but only in a minority of cases, requiring further high-level studies to confirm the results 5).
During a median follow-up period of 7.3 years, 9 (9%) of 95 children with moderate-to-severe TBI developed PTE; 4 developed intractable epilepsy. The odds for developing PTE was 2.9 in patients with severe compared to moderate TBI. CT findings showed fractures in 7/9 (78%) of patients with PTE, compared to 40/86 (47%) of those without PTE (p = 0.09). Of the patients with fractures, all those with PTE had additional features on CT (such as haemorrhage, contusion and mass effect), compared to 29/40 (73%) of those without PTE. One of nine (11%) PTE patients and 10 of 86 (12%) patients without PTE had immediate seizures. Two (22%) children with PTE had their first seizure more than 2 years after the TBI.
Among children with moderate or severe TBI, the presence of additional CT findings, other than skull fractures, seem to increase the risk of PTE. In this cohort, the occurrence of an early seizure did not confer an increased risk of PTE 6).
Data were collected from electronic medical records of children 0-17 years of age, who were admitted to a single medical center between 2007 and 2009 with a diagnosis of MTBI. This prospective research consisted of a telephone survey between 2015 and 2016 of children or their caregivers, querying for information about epileptic episodes and current seizure and neurological status. The primary outcome measure was the incidence of epilepsy following TBI, which was defined as ≥ 2 unprovoked seizure episodes. Posttraumatic seizure (PTS) was defined as a single, nonrecurrent convulsive episode that occurred > 24 hours following injury. Seizures within 24 hours of the injury were defined as immediate PTS.
Of 290 children eligible for this study, 191 of them or their caregivers were reached by telephone survey and were included in the analysis. Most injuries (80.6%) were due to falls. Six children had immediate PTS. All children underwent CT imaging; of them, 72.8% demonstrated fractures and 10.5% did not demonstrate acute findings. The mean follow-up was 7.4 years. Seven children (3.7%) experienced PTS; of them, 6 (85.7%) developed epilepsy and 3 (42.9%) developed intractable epilepsy. The overall incidence of epilepsy and intractable epilepsy in this cohort was 3.1% and 1.6%, respectively. None of the children who had immediate PTS developed epilepsy. Children who developed epilepsy spent an average of 2 extra days in the hospital at the time of the injury. The mean time between trauma and onset of seizures was 3.1 years. Immediate PTS was not correlated with PTE.
In this analysis of data from medical records and long-term follow-up, MTBI was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population 7).
Park et al. performed a retrospective electronic chart review of patients who had suffered traumatic brain injury and subsequently evaluated at Children’s Hospital of Michigan from 2002 to 2012. Various epidemiologic and clinical variables were analyzed.
Patients who had severe traumatic brain injury and post-traumatic epilepsy had an abnormal acute head computed tomography. These patients had increased number of different seizure types, increased risk of intractability of epilepsy, and were on multiple antiepileptic drugs. Hypomotor seizure was the most common seizure type in these patients. There was a high prevalence of patients who suffered nonaccidental trauma, all of whom had severe traumatic brain injury.
This study demonstrates a need for biomarkers in children following traumatic brain injury to reliably evaluate the risk of post-traumatic epilepsy 8).
Children ages 6-17 years with one or more risk factors for the development of posttraumatic epilepsy, including presence of intracranial hemorrhage, depressed skull fracture, penetrating injury, or occurrence of posttraumatic seizure were recruited into a phase II study. Treatment subjects received levetiracetam 55 mg/kg/day, b.i.d., for 30 days, starting within 8 h postinjury. The recruitment goal was 20 treated patients. Twenty patients who presented within 8-24 h post-TBI and otherwise met eligibility criteria were recruited for observation. Follow-up was for 2 years. Forty-five patients screened within 8 h of head injury met eligibility criteria and 20 were recruited into the treatment arm. The most common risk factor present for pediatric inclusion following TBI was an immediate seizure. Medication compliance was 95%. No patients died; 19 of 20 treatment patients were retained and one observation patient was lost to follow-up. The most common severe adverse events in treatment subjects were headache, fatigue, drowsiness, and irritability. There was no higher incidence of infection, mood changes, or behavior problems among treatment subjects compared to observation subjects. Only 1 (2.5%) of 40 subjects developed posttraumatic epilepsy (defined as seizures >7 days after trauma). This study demonstrates the feasibility of a pediatric posttraumatic epilepsy prevention study in an at-risk traumatic brain injury population. Levetiracetam was safe and well tolerated in this population. This study sets the stage for implementation of a prospective study to prevent posttraumatic epilepsy in an at-risk population 9).
Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition
This book introduces the latest advances relating to the pathophysiology, biophysics, monitoring and treatment of traumatic brain injury, hydrocephalus, and stroke presented at the 16th International Conference on Intracranial Pressure and Neuromonitoring (the “ICP Conference”), held in Cambridge, Massachusetts, in June 2016 in conjunction with the 6th Annual Meeting of the Cerebral Autoregulation Research Network. Additionally, the conference held special sessions on neurocritical care informatics and cerebrovascular autoregulation. The peer-reviewed papers included were written by leading experts in neurosurgery, neurointensive care, anesthesiology, physiology, clinical engineering, clinical informatics and mathematics who have made important contributions in this translational area of research, and their focus ranges from the latest research findings and developments to clinical trials and experimental studies. The book continues the proud tradition of publishing key work from the ICP Conferences and is a must-read for anyone wishing to stay abreast of recent advances in the field.
|VI Uruguayan Congress of Neurosurgery|
|4 – 7 April 2018|
SBNS Spring Meeting – Torquay
April 11, 2018 — April 13, 2018
11th Annual Cervical Spine Research Society Hands-On Cadaver Course
April 12, 2018 — April 14, 2018
St Louis, Missouri, USA
11 – 13 April 2018 http://www.sbns.org.uk/index.php/conferences/plymouth-2018/ Call for Abstract
|International Neurosurgery Resident Course – Amsterdam 2018 (INRC-Amsterdam 2018)|
|14 – 21 April 2018|
|12th Annual Meeting of the Saudi Association of Neurological Surgery & 8th Neurosurgery Update Conference (SANS 2018)|
|15 – 16 April 2018|
|WFNS education course in conjunction with 4th ISMINS-Congress|
|19 – 21 April 2018|
Eurospine Spring Meeting 2018
April 26, 2018 — April 28, 2018
Please see the website for further details.
86th AANS Annual Scientific Meeting
April 28, 2018 — May 2, 2018
New Orleans, LA, USA
26th Biennial Congress of the European Society for Pediatric Neurosurgery
May 1, 2018
Global Spine Congress 2018
May 2, 2018 — May 5, 2018
26th Biennial Congress of the European Society for Pediatric Neurosurgery
May 6, 2018 — May 9, 2018
34th Annual Meeting Cervical Spine Research Society – Europe
May 9, 2018 — May 11, 2018
45th ISSLS Annual Meeting
May 14, 2018 — May 18, 2018
Annual meeting of The International Society for the Study of the Lumbar Spine.
Israeli National Neurosurgical Society Annual Meeting
May 16, 2018 — May 18, 2018
May 16, 2018 — May 18, 2018
22nd Congress of the SENEC.
ESOC 2018 – 4th European Stroke Organisation Conference
May 16, 2018 — May 18, 2018
White Matter Dissection, Lectures + Hands-On Cadaver Course
May 23, 2018 — May 24, 2018
aStroke Meeting Puglia 2018
May 24, 2018 — May 25, 2018
San Giovanni Rotondo, Italy
Surgery Follows Function
May 25, 2018 — May 25, 2018
|WFNS Neurosurgical Anatomy Committee 2018: 3D Cinema Lectures – Advanced Management of Vascular and Brain Tumors|
|26 May 2018|
69. Jahrestagung der DGNC / 69th Annual Meeting of the DGNC
15th Interdisciplinary Cerebrovascular Symposium
6 – 7 June 2018
9th European Japanese Cerebrovascular Congress (EJCVC)
June 7, 2018
Endoscopy in Neurosurgery: the advanced three-day course
June 20, 2018 — June 22, 2018
|20 – 22 June 2018|
13th European Low Grade Glioma Network
June 22, 2018 — June 23, 2018
EANS Lyon Hands-On Course
June 25, 2018 — June 29, 2018
Seventh Annual World Course in Advanced Brain Tumour Surgery
July 12, 2018 — July 15, 2018
24 – 27 July 2018
August 11, 2018 — August 16, 2018
WFNS Symposium 2018
15TH – 19TH
Hilton Kuala Lumpur,
Prague Neurosurgical Week
August 29, 2018 — September 3, 2018
September 19, 2018 — September 21, 2018
For more information please visit http://www.eurospinemeeting.org/f130000847.html
Spine in XXI Century
October 4, 2018 — October 8, 2018
Association of Neurosurgeons of Russia
Russian Association of Spinal Surgeons
Serbian Neurosurgical Society
4th Meeting of the Serbian Neurosurgical Society
Joint Meeting with the Souteast Europe Neurosurgical Society
CNS Annual Meeting
October 6, 2018 — October 10, 2018
Chicago, IL, USA
13th EANO Meeting
October 9, 2018 — October 14, 2018
Annual Meeting of the European Association of Neuro-oncology
Surgical anatomy of the arm in relation to nerve injuries
October 11, 2018 — October 12, 2018
Leiden, The Netherlands
October 21, 2018 — October 25, 2018
4th European Congress of NeuroRehabilitation (ECNR) 2017
October 25, 2018 — October 28, 2018
ANTC 2017 – AIIMS NEUROTRAUMA CONFERENCE
October 27 — October 29
New Delhi, India
Taking place at the All India Institute of Medical Sciences.
Joint Global Neurofibromatosis Conference
November 2, 2018 — November 6, 2018
November 15, 2018 — November 18, 2018
New Orleans, LA, USA
Society for Neuro-Oncology (SNO) Annual Meeting 2018
2nd International Conference on Complications in Neurosurgery
January 25, 2019 — January 27, 2019
87th AANS Annual Scientific Meeting
April 13, 2019 — April 17, 2019
San Diego, CA, USA
September 24, 2019 — September 28, 2019
WFNS 2019 Interim Meeting
(9/9/2019 – 12/9/2019) / Beijing, China
October 16, 2019 — October 18, 2019
Please click HERE for more information.
CNS Annual Meeting
October 19, 2019 — October 23, 2019
San Francisco, CA, USA
November 20, 2018 — November 24, 2018
Phoenix, AZ, USA
Society for Neuro-Oncology (SNO) Annual Meeting 2019
Various theories have been proposed to determine the etiology of intracranial chondromas but none has succeeded to ascertain a definite cause of origin. The most commonly accepted explanation for skull base chondromas is embryonic remnants of chondrogenic cells along the base 13).
The chondromas arising from the dura matter, choroid plexus, and cerebral cortex have been proposed to develop from metaplasia of meningeal fibroblasts and perivascular meninges 15). Similarly, proliferation of ectopic embryologic rests of cartilage cells, traumatic displacement of cartilage elements or inflammatory cartilaginous activation of fibroblasts have been suggested to be the cause of development of intracranial chondromas 16).
The presenting symptoms range from headaches to lower cranial nerve palsy. In some cases, proptosis, diplopia and varying degrees of visual activity impairment along with orbital extension have been reported. Patients often complain of forgetfulness and lack of concentration.
Generalized tonic–clonic seizures are also usually the presenting complaints in intracranial chondromas, which develop because of the gradual destruction of a large number of neurons that begin to fire at regular intervals. Focal neurological deficits may also result from mass effects of tumor.
Intracranial chondroma has also been reported as a component of Ollier’s multiple chondromatosis.
Pontine hemorrhage has also been associated with parasellar intracranial chondromas. Association of skull base chondromas has also been reported with Maffucci syndrome.
Intracranial chondromas may develop in a person at any age but they have been most frequently observed in the third decade.
Bone destruction occurs in over 50% of the cases, whereas irregular calcifications are seen in about 60%. Intracranial chondromas may also produce hyperostosis of the inner table of the skull 17) 18) 19).
On X-ray, intracranial chondromas represent hyperostosis of the internal table of the skull 20). enhanced intracranial pressure and calcified portions21). Intradural convexity chondromas possess carved, tufted, ring-shaped calcified areas 22).
MRI has become an important diagnostic tool for intracranial chondromas. Brownlee et al. reported variable signal intensity at different levels of MRI in a case of intracranial chondroma. At T1 they reported less intensity whereas at T2 the signal appeared to be of middle to high intensity 23).
They are typically DWI hypointense with high apparent diffusion coefficient (ADC) values while meningiomas are typically DWI hyperintense with low ADC values 24).
A study reported that intradural chondromas possess two different CT appearances. The usually found type 1 shows mixed density with minimal or moderate enhancements. The rare type 2 shows an innermost less dense area containing a cyst 25).
Chondromas showed low uptake in PET images, which might be useful for differentiation between chondromas and chordomas 29).
In the past pneumoencephalography revealed displacement of basal cisterns and the ventricular system. A radionuclide brain scan may show abnormal uptake in the tumor 30).
Tanohata et al. reported two instances of skull base chondromas that exhibited delayed contrast enhancement on CT after a high-dose of the contrast medium was administered. They suggested this CT feature to be employed in differential diagnosis of intracranial chondromas from meningiomas and neurinomas 33).
In symptomatic patients, operative resection is sensible. In most cases total removal of the tumor is possible and leads to full recovery. When the finding is merely incidental in older patients, a watchful waiting approach is acceptable, given the benign and slow-growing nature of the lesion 34).
The current popular surgical approach for parasellar lesions is transcranial such as the orbitozygomatic approach, subtemporal approach. In surgical removal of skull base chondromas, it is advisable to try to confirm the diagnosis preoperatively with characteristic image findings and to consider the best approach in each case to decompress the involved nerves without any complications 35).
Xin et al. retrospectively analyzed the clinical data of 30 patients (12 males and 18 females; mean age 35.4 years; age range 16-60 years) who had pathologically confirmed intracranial chondroma treated at our hospital from September 1996 to June 2008. Surgery was performed on all 30 patients: five patients underwent postoperative radiotherapy; 26 patients were followed up postoperatively for a mean duration of 45.8 months. The surgical approach was selected according to tumor location. Total resection was achieved in 11 patients, subtotal resection in 13, and partial resection in nine (three patients had recurrent chondroma). Follow-up showed that 21 patients recovered without recurrences, three had recurrence, and two patients died. The clinical manifestations included headache and multiple cranial nerve lesions. Imaging usually showed a well-demarcated extramedullary tumor, centrally located, without surrounding brain edema, partially calcified (73.3%) and with minimal vascularity, often accompanied by erosion and destruction of surrounding bone (56.7%). It is difficult to totally remove an intracranial chondroma, and it is not possible to differentiate a chondroma from a myxoma or chordoma at the cranial base on the basis of clinical manifestations and neuroradiological findings. Selection of the appropriate surgical approach is important for resection of the tumor 43).
Four new cases are added to the previously recorded 122 cases 44).
A 25-year-old male patient with a giant convexity chondroma with meningeal attachment in the right frontal lobe that was detected after a first generalized seizure. Based on the putative diagnosis of meningioma, the tumor was completely resected via an osteoplastic parasagittal craniotomy. The postoperative MRI confirmed the complete tumor resection. Histopathological analysis revealed the presence of a chondroma 45).
Giant convexity chondroma with dural involvement: Case report and review of literature 46).
A 55-year-old female presented to the emergency room with a complaint of aphasia. Her initial brain computed tomography scan showed an intracranial hemorrhage in the left frontal area. After surgery, histopathological examination confirmed the diagnosis of a chondroma. Intradural chondroma is a rare, slow growing, benign intracranial neoplasm, but is even rarer in combination with an intratumoral hemorrhage. Chondromas are generally avascular cartilaginous lesions. This case was thought to be caused by the rupture of abnormally weak vessels derived from the friable tumor. Intradural chondromas may be included in the differential diagnosis of intracranial tumors with acute hemorrhages. 47).
A 23-year-old Asian man presenting with intracerebral chondroma of the left frontal lobe, which was eroding the dura matter. The intracranial chondroma was completely removed by surgery 48).
A 45-year old female is presented with a solitary intracerebral chondroma located in the right frontal lobe with no meningeal attachment 49).
An intracranial chondroma with intratumoral and subarachnoidal hemorrhage 50).
Higashida et al. reported two cases of intracranial skull base chondroma and discussed the differential diagnosis and the treatment strategies. The first case was a 39-year-old male who presented with left exophtalmos, visual loss and oculomotor disturbance. MRI showed a huge tumor occupying the bilateral cavernous sinus. Partial removal of the tumor was performed through the left orbitozygomatic subtemporal approach. The second case was a 54-year-old male who presented with left hemiparesis. MRI showed a brain stem infarction with a huge tumor located at the right middle fossa. Partial removal was performed through the right orbitozygomatic subtemporal approach. In these two cases, the histopathological diagnosis of the tumors was benign chondroma and the size of residual tumors have not changed for one year without any additional therapy 51).
A Osteochondroma of the skull base 52).
A rare case of a chondroma arising from the convexity dura mater 53).
A case of intracranial giant chondroma originating from the dura mater of the convexity 54).
Intradural convexity chondroma: a case report and review of diagnostic features 55).
A rare case of chondroma originated from the dura mater of the cerebral convexity in a 16-year-old girl. Radiologic findings are reported with emphasis on computed tomography and magnetic resonance imaging scans, and histogenesis is briefly discussed 56).
A rare case of Maffucci’s syndrome associated with enchondroma at the skull base, left internal carotid artery aneurysm, and goiter is reported. Two other previously reported cases of Maffucci’s syndrome with associated aneurysms and the present case suggest that Maffucci’s syndrome may be associated with aneurysm 57).
A 8-year-old female with Ollier’s disease (multiple enchondromatosis) developed an intracranial chondroma arising from the clivus, which was diagnosed by both computed tomography and magnetic resonance imaging 58).
A rare case of parasellar chondroma accompanied by pontine hemorrhage is described. A review is made of the previously reported 6 cases of intracranial chondromas complicated with hemorrhage. A 21 year-old woman was admitted because of consciousness deterioration progressing to coma within a day, and right hemiparesis. CT scan showed a contrast-enhanced mass in the parasellar region and a hematoma in the brain-stem, which was clearly demonstrated by MRI to be abutted on the dorsal part of the tumor mass. The tumor was removed through frontotemporal craniotomy and confirmed histologically as chondroma. Postoperatively, the patient gradually regained consciousness and is hospitalized to rehabilitate hemiparesis 59).
A case is presented in which a solitary chondroma arose from the clivus of a patient with Ollier’s disease 60).
Intradural chondroma: a case report and review of the literature 61).
A case of a huge intracranial frontoparietal osteochondroma in a 20-year-old man is reported. The presenting symptoms were headache, vomiting, and blurred vision. Apart from papilledema, no other abnormal neurological signs were present. A specific preoperative diagnosis could not be reached from the information provided by plain skull films, angiography, and radionuclide scan. The findings on computed tomography were those of a high density mass interspersed with small foci of lower densities, producing a honeycomb appearance, and surrounded by deposits of nodular calcification. The postcontrast scan showed a moderate degree of enhancement with preservation of the precontrast honeycomb pattern. These particular features may enable a correct preoperative histological diagnosis to be offered with a high degree of probability 62).
Osteochondroma of the base of the skull causing an isolated oculomotor nerve paralysis. Case report emphasizing microsurgical techniques 63).