Perioperative Considerations and Positioning for Neurosurgical Procedures: A Clinical Guide

Perioperative Considerations and Positioning for Neurosurgical Procedures: A Clinical Guide

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There are relationships that exist between neuroanesthesia, neurosurgical procedures, individual patient pathology and the positioning of a patient for said procedure.  A comprehensive examination of these relationships, their association with patient morbidity/mortality and how to approach these issues in an evidence-based manner has yet to become available. Positioning related injuries have been documented as major contributors to neurosurgical/neuroanesthesiology liability.
This text examines these relationships. It provides considerations necessary to the correct positioning of a patient for a neurosurgical procedure for each individual patient and their individual pathology. In other words, this text will demonstrate how to construct the necessary surgical posture for the indicated neurosurgical procedure given the individual constraints of the patient within the environment of anesthesia and conforming to existing evidence-based practice guidelines. Sections will address physiological changes inherent in positioning in relation to anesthesia for neurosurgical procedures, assessment of patient for planned procedure, as well as considerations for managing problems associated with these relationships. Additional sections will examine the relationship between neurosurgical positioning and medical malpractice and the biomechanical science between positioning devices and neurosurgical procedures.
Neurosurgery and its patient population are in a constant state of change. Providing the necessary considerations for the neurosurgical procedure planned under the anesthesia conditions planned in the position planned, often in the absence of multicase study literary support, without incurring additional morbidity is the goal of this text.

Update: Posttraumatic epilepsy in children

Posttraumatic epilepsy in children

Posttraumatic epilepsy (PTE) after a traumatic brain injury occurs in 10%-20% of 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).

There is a a need for biomarkers in children following traumatic brain injury to reliably evaluate the risk of post-traumatic epilepsy 3).

Classification

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).

Treatment

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).

Case series

2018

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).

2017

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).

2015

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).

2013

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).

1) , 6)

Keret A, Shweiki M, Bennett-Back O, Abed-Fteiha F, Matoth I, Shoshan Y, Benifla M. The clinical characteristics of posttraumatic epilepsy following moderate-to-severe traumatic brain injury in children. Seizure. 2018 Mar 20;58:29-34. doi: 10.1016/j.seizure.2018.03.018. [Epub ahead of print] PubMed PMID: 29609147.
2) , 7)

Keret A, Bennett-Back O, Rosenthal G, Gilboa T, Shweiki M, Shoshan Y, Benifla M. Posttraumatic epilepsy: long-term follow-up of children with mild traumatic brain injury. J Neurosurg Pediatr. 2017 Jul;20(1):64-70. doi: 10.3171/2017.2.PEDS16585. Epub 2017 May 5. PubMed PMID: 28474982.
3) , 8)

Park JT, Chugani HT. Post-traumatic epilepsy in children-experience from a tertiary referral center. Pediatr Neurol. 2015 Feb;52(2):174-81. doi: 10.1016/j.pediatrneurol.2014.09.013. Epub 2014 Oct 12. PubMed PMID: 25693582.
4)

Arndt DH, Goodkin HP, Giza CC. Early Posttraumatic Seizures in the Pediatric Population. J Child Neurol. 2016 Jan;31(1):46-56. doi: 10.1177/0883073814562249. Epub 2015 Jan 6. Review. PubMed PMID: 25564481.
5)

Piccenna L, Shears G, O’Brien TJ. Management of post-traumatic epilepsy: An evidence review over the last 5 years and future directions. Epilepsia Open. 2017 Mar 17;2(2):123-144. doi: 10.1002/epi4.12049. eCollection 2017 Jun. PubMed PMID: 29588942; PubMed Central PMCID: PMC5719843.
9)

Pearl PL, McCarter R, McGavin CL, Yu Y, Sandoval F, Trzcinski S, Atabaki SM, Tsuchida T, van den Anker J, He J, Klein P. Results of phase II levetiracetam trial following acute head injury in children at risk for posttraumatic epilepsy. Epilepsia. 2013 Sep;54(9):e135-7. doi: 10.1111/epi.12326. Epub 2013 Jul 22. PubMed PMID: 23876024; PubMed Central PMCID: PMC3769484.

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

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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.

Neurosurgery Events Update

April


 VI Uruguayan Congress of Neurosurgery
4 – 7 April 2018
 http://www.sunc.com.uy

SBNS Spring Meeting – Torquay

April 11, 2018 — April 13, 2018

Torquay, UK

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11th Annual Cervical Spine Research Society Hands-On Cadaver Course

April 12, 2018 — April 14, 2018

St Louis, Missouri, USA

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SBNS (Society of British Neurological Surgeons) Spring Meeting – TORQUAY

11 – 13 April 2018 http://www.sbns.org.uk/index.php/conferences/plymouth-2018/ Call for Abstract 
 Brochure 


 

International Neurosurgery Resident Course – Amsterdam 2018 (INRC-Amsterdam 2018)
14 – 21 April 2018
 http://www.surgicalneurology.org
12th Annual Meeting of the Saudi Association of Neurological Surgery & 8th Neurosurgery Update Conference (SANS 2018)
15 – 16 April 2018
 http://www.sans.org.sa/index.php/event/sans-2018/


WFNS education course in conjunction with 4th ISMINS-Congress
19 – 21 April 2018
 http://www.congress-ph.ru/

Eurospine Spring Meeting 2018

April 26, 2018 — April 28, 2018

Vienna, Austria

Please see the website for further details.


 Surgical Approaches to Skull Base26 – 28 April 2018 http://www.cvent.com/d/ptqpwt


86th AANS Annual Scientific Meeting

April 28, 2018 — May 2, 2018

New Orleans, LA, USA

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May

26th Biennial Congress of the European Society for Pediatric Neurosurgery

May 1, 2018

Bonn, Germany

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Global Spine Congress 2018

May 2, 2018 — May 5, 2018

Singapore

Website: http://www.gsc2018.org


26th Biennial Congress of the European Society for Pediatric Neurosurgery

May 6, 2018 — May 9, 2018

Bonn, Germany

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34th Annual Meeting Cervical Spine Research Society – Europe

May 9, 2018 — May 11, 2018

Lisbon, Portugal

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45th ISSLS Annual Meeting

May 14, 2018 — May 18, 2018

Banff, Canada

Annual meeting of The International Society for the Study of the Lumbar Spine.

Website: http://www.issls.org


Israeli National Neurosurgical Society Annual Meeting

May 16, 2018 — May 18, 2018

Galilee, Israel

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SENEC 2018

May 16, 2018 — May 18, 2018

Toledo, Spain

22nd Congress of the SENEC.

Contact: secretaria@senec.es


ESOC 2018 – 4th European Stroke Organisation Conference

May 16, 2018 — May 18, 2018

Gothenburg, Sweden

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White Matter Dissection, Lectures + Hands-On Cadaver Course

May 23, 2018 — May 24, 2018

Graz, Austria

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aStroke Meeting Puglia 2018

May 24, 2018 — May 25, 2018

San Giovanni Rotondo, Italy

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Surgery Follows Function

May 25, 2018 — May 25, 2018

Graz, Austria

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WFNS Neurosurgical Anatomy Committee 2018: 3D Cinema Lectures – Advanced Management of Vascular and Brain Tumors
26 May 2018
 http://bit.ly/wfns2018
 Announcement 

June

69. Jahrestagung der DGNC / 69th Annual Meeting of the DGNC

03.06.2018  06.06.2018
Münster, Germany
http://www.dgnc-kongress.de  

15th Interdisciplinary Cerebrovascular Symposium

Magdeburg, Germany

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Microscopic and Endoscopic Approaches to the Skull Base

6 – 7 June 2018

 https://www.ircad.fr/training-center/course-calendar/?type=advanced&spec=neuro

 Brochure 


9th European Japanese Cerebrovascular Congress (EJCVC)

June 7, 2018

Milan, Italy

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2nd Congress of Mediterranean Association of Neurological Surgeons (MANS 2018)
19 – 20 June 2018
 http://www.mans2018.it
 Scientific Program 
 Brochure 

Endoscopy in Neurosurgery: the advanced three-day course

June 20, 2018 — June 22, 2018

London, UK

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ICRAN 2018
20 – 22 June 2018
 http://www.icran2018.it/
 Flyer 

13th European Low Grade Glioma Network

June 22, 2018 — June 23, 2018

Lisbon, Portugal

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Hydrocephalus Forum 2018

21.06.2018  23.06.2017
Potsdam, Germany

https://www.hydrocephalusforum.de/hydrocephalus-forum/


EANS Lyon Hands-On Course

June 25, 2018 — June 29, 2018

Lyon, France

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July


Seventh Annual World Course in Advanced Brain Tumour Surgery

July 12, 2018 — July 15, 2018

London, UK

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CAANS 2018 Congress

24 – 27 July 2018

 http://www.caanscongress.info/

 Announcement 


 

August

INTS 2018

August 11, 2018 — August 16, 2018

Toronto, Canada

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WFNS Symposium 2018

15TH – 19TH
AUGUST 2018

Hilton Kuala Lumpur,
Malaysia

http://wfns-symposia2018.com/


Prague Neurosurgical Week

August 29, 2018 — September 3, 2018

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September

EUROSPINE 2018

September 19, 2018 — September 21, 2018

Barcelona, Spain

For more information please visit http://www.eurospinemeeting.org/f130000847.html

October


Spine in XXI Century

October 4, 2018 — October 8, 2018

Nis, Serbia

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

First announcement.


CNS Annual Meeting

October 6, 2018 — October 10, 2018

Chicago, IL, USA


13th EANO Meeting

October 9, 2018 — October 14, 2018

Stockholm, Sweden

Annual Meeting of the European Association of Neuro-oncology

Website.


Surgical anatomy of the arm in relation to nerve injuries

October 11, 2018 — October 12, 2018

Leiden, The Netherlands

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EANS 2018

October 21, 2018 — October 25, 2018

Brussels, Belgium

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4th European Congress of NeuroRehabilitation (ECNR) 2017

October 25, 2018 — October 28, 2018

Lausanne, Switzerland

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ANTC 2017 – AIIMS NEUROTRAUMA CONFERENCE

October 27 — October 29

New Delhi, India

Taking place at the All India Institute of Medical Sciences.

Flyer.

November


Joint Global Neurofibromatosis Conference

November 2, 2018 — November 6, 2018

Paris, France

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SNO 2018

November 15, 2018 — November 18, 2018

New Orleans, LA, USA

Society for Neuro-Oncology (SNO) Annual Meeting 2018

Website.

2019


January


2nd International Conference on Complications in Neurosurgery

January 25, 2019 — January 27, 2019

Mumbai, India

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April


87th AANS Annual Scientific Meeting

April 13, 2019 — April 17, 2019

San Diego, CA, USA


September


EANS2019

September 24, 2019 — September 28, 2019

Dublin, Ireland

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WFNS 2019 Interim Meeting

(9/9/2019 – 12/9/2019) / Beijing, China

http://www.wfns2019.org/index/


October


EUROSPINE 2019

October 16, 2019 — October 18, 2019

Helsinki, Finland

Please click HERE for more information.


CNS Annual Meeting

October 19, 2019 — October 23, 2019

San Francisco, CA, USA


SNO 2019

November 20, 2018 — November 24, 2018

Phoenix, AZ, USA

Society for Neuro-Oncology (SNO) Annual Meeting 2019

Website.

Update: Intracranial chondroma

Intracranial chondroma

Intracranial chondroma are cysts of chondroid tissue, first reported by Hirschfeld in 1851 1)

Epidemiology

They are extremely rare and account for only 0.2% to 0.3% of all intracranial tumor2) 3).

They can be present at different regions within the cranial cavity especially the skull base 4)intrasellar 5),parasellar 6)intradural and especially falx 7).

Very occasionally observed in combination with intratumoral hemorrhage 8).

Despite a purported lack of any sex predilection there are reports of a slight female predominance 9).

Intracerebral location is extremely rare and has only been described in a few cases 10) 11) 12).

Etiology

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).

They grow slowly by expansion and mostly originate from rests of cartilaginous cells at sphenoethmoidal sutureand sphenooccipital suture 14).

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).

Clinical features

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.

Diagnosis

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).


Angiography shows displacement of vessels but no tumor stain 26) 27) 28).


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).

Differential diagnosis

Preoperatively, chondromas can be difficult to distinguish from meningiomas. They may also be confused with chordomas, craniopharyngiomas or even arterial aneurysms 31) 32)

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).

Treatment

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 approachsubtemporal 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).

In cases of convexity chondroma, it is additionally recommended to remove the dural attachment 36) 37) 38).

Outcome

Usually postoperative observation reveals no recurrence of the lesion after complete resection. An adjuvant therapy is not necessary and the long-term prognosis is good 39) 40) 41).

The malignant form, chondrosarcoma, generally occurs later in life, presenting mostly in the fifth and sixth decades 42).

Case series

2011

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).

1976

Four new cases are added to the previously recorded 122 cases 44).

Case reports

2018

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).

2017

Giant convexity chondroma with dural involvement: Case report and review of literature 46).

2013

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).

2012

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).

2011

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).

2007

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).

2003

A rare case of a chondroma arising from the convexity dura mater 53).

2001

A case of intracranial giant chondroma originating from the dura mater of the convexity 54).

2000

Intradural convexity chondroma: a case report and review of diagnostic features 55).

1993

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).

1991

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).

1990

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).

1989

A case is presented in which a solitary chondroma arose from the clivus of a patient with Ollier’s disease 60).

1983

Intradural chondroma: a case report and review of the literature 61).

1981

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).

1969

Osteochondroma of the base of the skull causing an isolated oculomotor nerve paralysis. Case report emphasizing microsurgical techniques 63).

1)

L. Hirschfeld, Sur une tumer cartilaginease du la base du crane (enchondroma), C. R. Soc. Biol. 3 (1851) 94–96.
2) , 42)

Berkmen YM, Blatt ES. Cranial and intracranial cartilaginous tumours. Clin Radiol. 1968 Jul;19(3):327-33. PubMed PMID: 5302924.
3)

Zulch KJ, Wechsler W. Pathology and classification of gliomas. Pro Neurol Surg. 1968;2:1–84.
4) , 14) , 29) , 35) , 51)

Higashida T, Sakata K, Kanno H, Tanabe Y, Kawasaki T, Yamamoto I. [Intracranial chondroma arising from the skull base: two case reports featuring the image findings for differential diagnosis]. No Shinkei Geka. 2007 May;35(5):495-501. Japanese. PubMed PMID: 17491346.
5)

Munemitsu H, Matsuda M, Hirai O, Fukumitsu T, Kawamura J. Intrasellar chondroma. Neurol Med Chir (Tokyo). 1981 Jul;21(7):775-80. PubMed PMID: 6170021.
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Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

by Alejandro A. Rabinstein MD FAAN

List Price: $138.99
This issue of Neurosurgery Clinics, edited by Alejandro A. Rabinstein, will focus on Neurocritical Care. Topics will include Anoxic-Ischemic Brain Injury, Practical Approach to Posttraumatic Intracranial Hypertension According to Pathophysiologic Reasoning, Management of Traumatic Brain Injury: An Update, Cortical Spreading Depression and Ischemia in Neurocritical Patients, Targeted Temperature Management in Brain-Injured Patients, Herpes Virus Encephalitis in Adults: Current Knowledge and Old Myths, Primary Acute Neuromuscular Respiratory Failure, Intensive Care Unit–Acquired Weakness, Recent Advances in the Acute Management of Intracerebral Hemorrhage, New Developments in Refractory Status Epilepticus, Acute Cardiac Complications in Critical Brain Disease, Nosocomial Infections in the Neurointensive Care Unit, Neurologic Complications of Solid Organ Transplantation, and Shared Decision Making in Neurocritical Care.