Update: PulseRider Aneurysm Neck Reconstruction Device

PulseRider

http://www.pulsarvascular.com/
see Video

The PulseRider Aneurysm Neck Reconstruction Device is intended for use with embolic coils in the treatment of intracranial aneurysms originating on or near a vessel bifurcation.
In the early 1990’s, endovascular treatment using embolic coils for the treatment of intracranial aneurysms was established. Since then, there has been a significant body of peer-reviewed literature written by medical experts regarding the use, safety, and efficacy of these detachable embolic coils. With the publishing of the ISAT (Intracranial Subarachnoid Aneurysm Trial) trial data in 2005, which compared clinical outcomes of neurosurgical clipping and endovascular coiling, embolic coiling became the preferred method for treatment of the majority of unruptured intracranial aneurysms [ISAT 2003, Molyneux et al. 2005].
Since then, there has been a revolution in interventional neuroradiology which includes a shift toward catheter based procedures. Unfortunately, for a variety of reasons there are not always endovascular treatment options available to some patients with intracranial aneurysms, especially if the neck of the aneurysm is wide. Additionally there is a range of concerns relating to patient comorbidities, aneurysm geometry or the location of the lesion. Consequently there are many challenges, even today, when treating patients with such lesions. Hence there has been significant research in this arena to develop adjunctive devices to be used with embolic coils as well as sole therapy devices.


The PulseRider has an open cell frame. The unique frame configuration opens to conform to the vessel walls. The PulseRider is specifically designed to resolve the shortcomings of current endovascular devices by preserving luminal patency and hemodynamic flow through the parent vessel bifurcation, while minimizing exposed metal in order to encourage early endothelialization while securely retaining embolic agents within the aneurysm sac. The PulseRider is delivered through commercially available microcatheters using standard endovascular techniques. The implant is retrievable and may be repositioned by retracting it into the microcatheter at any time during or after deployment (prior to detachment). The implant is designed with an open frame to maintain luminal patency. It is deployed at the parent vessel bifurcation and across the aneurysm neck to provide a support framework, bridging the aneurysm neck while retaining embolic agents within the aneurysm. The PulseRider is electrolytically detached from the delivery wire.


In the early experience with the Pulse Rider device its use was safe and effective as an adjunct in the treatment of bifurcation aneurysms arising at the basilar apex or carotid terminus 1).


The safety and probable benefit of the PulseRider (Pulsar Vascular, Los Gatos, California) for the treatment of broad-necked, bifurcation aneurysms was studied in the context of the prospective, nonrandomized, single arm clinical trial-the Adjunctive Neurovascular Support of Wide-neck aneurysm Embolization and Reconstruction (ANSWER) Trial.
Aneurysms treated with the PulseRider device among sites enrolling in the ANSWER trial were prospectively studied and the results are summarized. Aneurysms arising at either the carotid terminus or basilar apex that were relatively broad necked were considered candidates for inclusion into the ANSWER study.
Thirty-four patients were enrolled (29 female and 5 male) with a mean age of 60.9 years (27 basilar apex and 7 carotid terminus). Mean aneurysm height ranged from 2.4 to 15.9 mm with a mean neck size of 5.2 mm (range 2.3-11.6 mm). In all patients, the device was delivered and deployed. Immediate Raymond I or II occlusion was achieved in 82.4% and progressed to 87.9% at 6-month follow-up. A modified Rankin Score of 2 or less was seen in 94% of patients at 6 months.
The results from the ANSWER trial demonstrate that the PulseRider device is safe and offers probable benefit as for the treatment of bifurcation aneurysms arising at the basilar apex or carotid terminus. As such, it represents a useful addition to the armamentarium of the neuroendovascular specialist 2).
1)

Spiotta AM, Chaudry MI, Turk AS, Turner RD. Initial experience with the PulseRider for the treatment of bifurcation aneurysms: report of first three cases in the USA. J Neurointerv Surg. 2016 Feb;8(2):186-9. doi: 10.1136/neurintsurg-2014-011531. Epub 2015 Jan 5. PubMed PMID: 25561583.
2)

Spiotta AM, Derdeyn CP, Tateshima S, Mocco J, Crowley RW, Liu KC, Jensen L, Ebersole K, Reeves A, Lopes DK, Hanel RA, Sauvageau E, Duckwiler G, Siddiqui A, Levy E, Puri A, Pride L, Novakovic R, Chaudry MI, Turner RD, Turk AS. Results of the ANSWER Trial Using the PulseRider for the Treatment of Broad-Necked, Bifurcation Aneurysms. Neurosurgery. 2017 Apr 25. doi: 10.1093/neuros/nyx085. [Epub ahead of print] PubMed PMID: 28449126.

Hyponatremia Following Transsphenoidal Surgery

Epidemiology

Delayed hyponatremia following transsphenoidal surgery is a known complication, with a peak incidence of 4-7 days post-operatively 1) 2) 3).
It is a common cause of hospital readmission, due to fluid retention resulting in reduction of plasma sodium concentration below physiologic levels 4).


In a database of 466 consecutive patients who underwent endoscopic transsphenoidal surgery at a tertiary care center between April 2006 and July 2014 was reviewed for 30-day causes for readmission, length of stay, level of care required, and average cost.
Twenty-nine readmissions were identified within the study period, indicating a 30-day readmission rate of 6.2%. Among all patients, rates of 30-day readmission were 2.1% for epistaxis, 1.5% for hyponatremia, 0.9% for cerebrospinal fluid leak, and 1.7% for other medical conditions. Average cost per readmission ranged from $6011 for hyponatremia to $24,613 for cerebrospinal fluid leak 5).

Etiology

The development of Delayed Symptomatic Hyponatremia (DSH) after transsphenoidal surgery has been ascribed mostly to elevations in the secretion of ADH following mechanical manipulation of the pituitary gland, or less frequently as a result of excessive urinary excretion of salt resulting in cerebral salt wasting syndrome (CSWS) 6).
Patients with Cushing’s disease were at a significantly higher risk than other patients to experience DSH 7) 8).

Clinical features

Patients can present with a range of symptoms, from minor nausea, vomiting headache to confusion, and in severe cases, seizures and death 9).

Management

Close symptom monitoring may be a reasonable alternative to routine screening 10).
Age, gender, tumor size, rate of decline of blood sodium, and Cushing disease are potential predictors of Delayed Symptomatic Hyponatremia (DSH) (defined as serum sodium level <135 mEq/L with associated symptoms) after postoperative day 3. By identifying patients at high risk for DSH, preventative efforts can be implemented in the perioperative setting to reduce the incidence of potentially catastrophic hyponatremia following transsphenoidal surgery 11).
Modern skull base surgeons suggest that improved visualization and identification provided by the endoscope can lead to greater visualization and reduced trauma to the posterior pituitary gland 12) 13) 14).

Systematic review

A systematic search of the literature was conducted using MEDLINE/PUBMED, EMBASE, and Cochrane databases. Inclusion criteria were 1) case series with at least 10 cases reported, 2) adult patients who underwent eTSS or mTSS for pituitary tumors, and 3) reported occurrence of Delayed Symptomatic Hyponatremia (DSH) (defined as serum sodium level <135 mEq/L with associated symptoms) after postoperative day 3. Data were analyzed using CMA V.3 Statistical Software (2014).
Ten case series satisfied the inclusion criteria for a total of 2947 patients. Various factors including age, gender, cerebrospinal fluid leak, and tumor size were investigated as potential predictors of DSH. DSH event rates for both mTSS and eTSS fell between around 4 and 12 percent and included a variety of proposed predictors.
Age, gender, tumor size, rate of decline of blood sodium, and Cushing disease are potential predictors of DSH. By identifying patients at high risk for DSH, preventative efforts can be implemented in the perioperative setting to reduce the incidence of potentially catastrophic hyponatremia following transsphenoidal surgery 15).

Case series

2017

Data from before and after delayed hyponatremia (DH) care pathway implementation were retrospectively reviewed. Patient demographics and clinical characteristics were compared. Readmission causes, clinical pathway failures, sodium trends, and symptoms were evaluated.
Before the DH care pathway implementation, 229 (55%) patients were treated (group 1); afterward, 188 (45%) were treated (group 2). Baseline characteristics were equivalent between groups, except for glucocorticoid supplementation, which was higher in group 2. The incidence of detected DH was significantly lower in group 1 (16/229, 7%) than group 2 (29/188, 15%) ( P = .006) likely due to the impact of routine screening in group 2. Ten group 1 patients (4%) were readmitted for hyponatremia and 6 (3%) were managed as outpatients. Eleven group 2 patients (6%) were readmitted and 17 (9%) were managed as outpatients. Readmission rates between groups were similar ( P = .49). Patients readmitted with severe hyponatremia experienced symptoms ≥24 h before presentation. The protocol failed to prevent readmission because outpatient management for mild or moderate DH (n = 4) failed, sodium levels precipitously declined after normal screening (n = 3), and severe hyponatremia developed after scheduled screenings were missed (n = 3).
Although more DH patients were identified after care pathway implementation, readmission rates were not reduced and clinical outcomes were not changed. Because DH onset timing varies, some patients have highly acute presentation, and most readmitted patients develop symptoms before reaching their sodium nadir, close symptom monitoring may be a reasonable alternative to routine screening 16).


Of 303 patients who had transsphenoidal surgery, 27 (8.9%) were readmitted within 30 days. Most of the 27 (15 [55.6%]) had delayed hyponatremia. Other causes were diabetes insipidus (4 [14.8%]), adrenal insufficiency (2 [7.4%]), and cerebrospinal fluid leak, epistaxis, cardiac arrhythmia, pneumonia, urinary tract infection, and hypoglycemia (1 each [3.7%]). Outpatient sodium screening was performed as needed. In cases of hyponatremia, the mean postoperative day of readmission was day 8 (range, 6-12 days) and the mean serum sodium was 119 mmol/L (range, 111-129 mmol/L). Numerous patient and surgical factors were examined, and no specific predictors of readmission were identified. We developed an outpatient care pathway for managing hyponatremia with the goal of improving readmission rates.
This study establishes a quality benchmark for readmission rates after transsphenoidal surgery for pituitary lesions and identifies delayed hyponatremia as the primary cause. Implementation of an outpatient care pathway for managing hyponatremia may improve readmission rates 17).

2013

A retrospective analysis of a single-institution prospective database was conducted; all patients undergoing TSS for lesions involving the pituitary gland were followed up in a multidisciplinary neuroendocrine clinic, and demographic, imaging, and clinical data were prospectively collected. Patients were examined preoperatively and followed up postoperatively in a standardized fashion, and their postoperative sodium levels were measured at Weeks 1 and 2 postoperatively. Levels of hyponatremia were rated as mild (serum sodium concentration 130-134 mEq/L), moderate (125-129 mEq/L), or severe (< 125 mEq/L). Routine clinical questionnaires were administered at all postoperative office visits. Postoperative hyponatremia was analyzed for correlations with demographic and clinical features and with immediate postoperative physiological characteristics. RESULTS: Over a 4-year interval, 373 procedures were performed in 339 patients who underwent TSS for sellar and parasellar lesions involving the pituitary gland. The mean (± SD) age of patients was 48 ± 18 years; 61.3% of the patients were female and 46.1% were obese (defined as a body mass index [BMI] ≥ 30). The overall prevalence of DPH within the first 30 days postoperatively was 15.0%; 7.2% of the patients had mild, 3.8% moderate, and 3.8% severe hyponatremia. The incidence of symptomatic hyponatremia requiring hospitalization was 6.4%. The Fisher exact test detected a statistically significant association of DPH with female sex (p = 0.027) and a low BMI (p = 0.001). Spearman rank correlation detected a statistically significant association between BMI and nadir serum sodium concentration (r = 0.158, p = 0.002) and an inverse association for age (r = -0.113, p = 0.031). Multivariate analyses revealed a positive correlation between postoperative hyponatremia and a low BMI and a trend toward association with age; there were no associations between other preoperative demographic or perioperative risk factors, including immediate postoperative alterations in serum sodium concentration. Patients were treated with standardized protocols for hyponatremia, and DPH was not associated with permanent morbidity or mortality. CONCLUSIONS: Delayed postoperative hyponatremia was a common result of TSS; a low BMI was the only clear predictor of which patients will develop DPH. Alterations in immediate postoperative sodium levels did not predict DPH. Therefore, an appropriate index of suspicion and close postoperative monitoring of serum sodium concentration should be maintained for these patients, and an appropriate treatment should be undertaken when hyponatremia is identified 18).

2011

Kinoshita et al. evaluated (i) the incidence of post-operative hyponatremia (serum Na levels ≤ 135 mEq/L) and the emergence of hyponatremic symptoms, and assessed (ii) the risk factors under a uniform protocol of i.v. infusion with steroid and electrolyte fluid. We examined 88 consecutive operated patients (female: 60; male: 28) with pituitary adenoma. Apart from reconfirming the effects of the purported risk factors, we focused on the degree of serum Na decline on post-operative hyponatremia. Although remained stable during early post-operative period (4 days after surgery), the serum Na levels subsequently decreased after post-operative day 4 in 81 of 88 cases (92.0%). Of 88 patients, 27 (30.7%) and 9 (10.2%) cases suffered from hyponatremia, and developed hyponatremic symptoms. Interestingly, the degree of serum Na levels decline (from pre-operative levels) indicated a useful independent risk factor for monitoring hyponatremic symptoms (p = 0.006) and the degree of decline tended to be greater in elder patients (> 60 years) (p = 0.0346). Serum Na levels should be monitored from, at least, post-operative day 7 to detect early development of hyponatremia. Special attention and recovery effort should be given to elder patients with marked serum Na level decline after surgery 19).

2008

The incidence and risk factors of symptomatic and asymptomatic hyponatremia were investigated in 94 patients who underwent transsphenoidal surgery and serum sodium level monitoring between January 2002 and December 2006. The records were retrospectively reviewed to determine the incidence and risk factors (age and sex, tumor size, endocrinologic findings) of hyponatremia. Postoperatively, the serum sodium levels of the patients were measured at least once within 2 or 3 days. Hyponatremia was found in 17 of the 94 patients, of whom 7 became symptomatic. The mean sodium level of symptomatic patients with hyponatremia at diagnosis was 123.5 mEq/l, compared with 129.8 mEq/l of asymptomatic patients. The serum sodium levels began to fall on mean postoperative day 7 and reached nadir on mean day 8. All 17 patients with hyponatremia were treated with mild fluid restriction. Four symptomatic patients with severe hyponatremia were treated with 3% hypertonic saline infusion in addition to fluid restriction. One symptomatic patient with severe hyponatremia was treated with fluid restriction only. All patients recovered within 5 days of management. Sex, tumor type, and tumor size did not correlate with development of delayed hyponatremia, but patients aged >/=50 years were more likely to develop hyponatremia. Postoperative hyponatremia after transsphenoidal surgery is more common than previously reported and may lead to fatal complications. Therefore, all patients should undergo serum electrolyte level monitoring regularly for at least 1 or 2 weeks after transsphenoidal surgery 20).

2007

Patients who underwent transsphenoidal surgery at the University of Southern California University Hospital between 1997 and 2004 had serum sodium levels drawn on an outpatient basis on postoperative Day 7. Patient records were retrospectively reviewed to determine the incidence of, and risk factors for, symptomatic and asymptomatic hyponatremia. Two hundred forty-one patients had routine serum sodium levels drawn as outpatients on postoperative Day 7. Twenty-three percent of these patients were found to be hyponatremic (Na < or =135 mEq/L). The overall incidence rate of symptomatic hyponatremia in the 241 patients was 5%. The majority of hyponatremic patients (80%) remained asymptomatic, whereas 20% became symptomatic. In patients with symptomatic hyponatremia, the mean sodium level at diagnosis was 120.5 mEq/L, compared with 128.4 mEq/L in asymptomatic, hyponatremic patients (p < 0.0001). Female patients were more likely to develop hyponatremia than male patients (33% compared with 22%, p < 0.03). Fifty-two percent of patients who had transient diabetes insipidus (DI) early in their postoperative course subsequently developed hyponatremia, compared with 21% of those who did not have DI (p < 0.001). Patient age, tumor type, and tumor size did not correlate with development of delayed hyponatremia. Outpatients with moderately and severely low sodium levels were 5 and 12.5 times more likely, respectively, to be symptomatic than were patients with mild hyponatremia.
Delayed hyponatremia occurs more frequently than was previously suspected in patients who have undergone transsphenoidal surgery, especially in female patients and those who have previously had transient DI. The majority of hyponatremic patients remain asymptomatic. Obtaining a serum sodium value on an outpatient basis 1 week after pituitary surgery is helpful in recognition, risk stratification, and subsequent intervention, and may prevent potentially serious complications 21).

1999

1571 patients with pituitary adenomas (238 Cushing’s disease, 405 acromegaly, 534 hormonally inactive adenomas, 358 prolactinoma, 23 Nelson’s syndrome, and 13 thyrotropinoma) were daily examined within a 10-day postoperative inpatient observation period. Prevalence of patterns of polyuria (> 2500 ml) and oliguria/hyponatraemia (< 132 mmol/l) were surveyed as well as predictors of postoperative morbidity. RESULTS: 487 patients (31%) developed immediate postoperative hypotonic polyuria, 161 patients (10%) showed prolonged polyuria and 37 patients (2.4%) delayed hyponatraemia. A biphasic (polyuria-hyponatraemia) and triphasic (polyuria-hyponatraemia-polyuria) pattern was seen in 53 (3.4%) and 18 (1.1%) patients, respectively. Forty-one patients (2.6%) displayed immediate postoperative (day 1) hyponatraemia. Altogether, 8.4% of patients developed hyponatraemia at some time up to the 10th day postoperative, with symptomatic hyponatraemia in 32 patients (2.1%). Risk analysis showed that patients with Cushing’s disease had a fourfold higher risk of polyuria than patients with acromegaly and a 2.8-fold higher risk for postoperative hyponatraemia. Younger age, male sex, and intrasellar expansion were associated with a higher risk of hypotonic polyuria, but this was not considered clinically relevant.
The analysis illustrates that disturbances in osmoregulation resulting in polyuria and pertubations of serum sodium concentration are of very high prevalence and need observation even after selective transsphenoidal surgery for pituitary adenomas, especially in patients with Cushing’s disease22).

1995

To clarify the frequency, presentation, and outcome of this poorly understood complication, Taylor et al. reviewed the database of 2297 patients who underwent transsphenoidal pituitary surgery between February 1971 and June 1993. Of 53 patients (2.3%) treated for symptomatic hyponatremia, 11 were excluded (2 received arginine vasopressin within 24 hours, 1 had untreated hypothyroidism, 4 had untreated adrenal insufficiency, and 4 had incomplete records). The remaining 42 patients (1.8%), 11 men and 31 women aged 21 to 79 years, presented 4 to 13 days (mean, 8 d) postoperatively with nausea and vomiting (20 patients), headache (18 patients), malaise (12 patients), dizziness (4 patients), anorexia (2 patients), and seizures (1 patient). Hyponatremia was unrelated to sex, age, adenoma type, tumor size, or glucocorticoid tapering. Although the clinical picture in our patients is consistent with SIADH, this was not supported by the antidiuretic hormone levels, which were normal or low-normal in the two patients in whom they were measured, suggesting the possibility that low serum sodium may not reflect SIADH. In all patients, hyponatremia resolved within 6 days (mean, 2 d); treatment consisted of salt replacement and mild fluid restriction in 37 patients and fluid restriction only in 4 (treatment unknown in 1). Delayed hyponatremia after transsphenoidal resection of pituitary adenoma is not as rare as previously thought, nor is it necessarily associated with SIADH or with hypoadrenalism during glucocorticoid tapering 23).
1) , 21)

Zada G, Liu CY, Fishback D, Singer PA, Weiss MH. Recognition and management of delayed hyponatremia following transsphenoidal pituitary surgery. J Neurosurg. 2007 Jan;106(1):66-71. PubMed PMID: 17236489.
2) , 7) , 22)

Hensen J, Henig A, Fahlbusch R, Meyer M, Boehnert M, Buchfelder M. Prevalence, predictors and patterns of postoperative polyuria and hyponatraemia in the immediate course after transsphenoidal surgery for pituitary adenomas. Clin Endocrinol (Oxf). 1999 Apr;50(4):431-9. PubMed PMID: 10468901.
3) , 6)

Kelly DF, Laws ER, Jr., Fossett D. Delayed hyponatremia after transsphenoidal surgery for pituitary adenoma. Report of nine cases. J Neurosurg. 1995;83(2):363-367.
4)

Bohl MA, Ahmad S, Jahnke H, et al. Delayed Hyponatremia Is the Most Common Cause of 30-Day Unplanned Readmission After Transsphenoidal Surgery for Pituitary Tumors. Neurosurgery. 2015.
5)

Hendricks BL, Shikary TA, Zimmer LA. Causes for 30-Day Readmission following Transsphenoidal Surgery. Otolaryngol Head Neck Surg. 2016 Feb;154(2):359-65. doi: 10.1177/0194599815617130. Epub 2015 Nov 17. PubMed PMID: 26577772.
8)

Sane T, Rantakari K, Poranen A, Tahtela R, Valimaki M, Pelkonen R. Hyponatremia after transsphenoidal surgery for pituitary tumors. The Journal of clinical endocrinology and metabolism. 1994;79(5):1395-1398.
9)

Whitaker SJ, Meanock CI, Turner GF, et al. Fluid balance and secretion of antidiuretic hormone following transsphenoidal pituitary surgery. A preliminary series. Journal of neurosurgery. 1985;63(3):404-412.
10) , 16)

Bohl MA, Ahmad S, White WL, Little AS. Implementation of a Postoperative Outpatient Care Pathway for Delayed Hyponatremia Following Transsphenoidal Surgery. Neurosurgery. 2017 Apr 25. doi: 10.1093/neuros/nyx151. [Epub ahead of print] PubMed PMID: 28449052.
11) , 15)

Cote DJ, Alzarea A, Acosta MA, Hulou MM, Huang KT, Almutairi H, Alharbi A, Zaidi HA, Algrani M, Alatawi A, Mekary RA, Smith TR. Predictors and Rates of Delayed Symptomatic Hyponatremia after Transsphenoidal Surgery: A Systemastic Review. World Neurosurg. 2016 Apr;88:1-6. doi: 10.1016/j.wneu.2016.01.022. Epub 2016 Jan 22. PubMed PMID: 26805685.
12)

Ammirati M, Wei L, Ciric I. Short-term outcome of endoscopic versus microscopic pituitary adenoma surgery: a systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2013;84(8):843-849.
13)

Gao Y, Zhong C, Wang Y, et al. Endoscopic versus microscopic transsphenoidal pituitary adenoma surgery: a meta-analysis. World J Surg Oncol. 2014;12(94).
14)

Cavallo LM, Dal Fabbro M, Jalalod’din H, et al. Endoscopic endonasal transsphenoidal surgery. Before scrubbing in: tips and tricks. Surg Neurol. 2007;67(4):342-347.
17)

Bohl MA, Ahmad S, Jahnke H, Shepherd D, Knecht L, White WL, Little AS. Delayed Hyponatremia Is the Most Common Cause of 30-Day Unplanned Readmission After Transsphenoidal Surgery for Pituitary Tumors. Neurosurgery. 2016 Jan;78(1):84-90. doi: 10.1227/NEU.0000000000001003. PubMed PMID: 26348011.
18)

Hussain NS, Piper M, Ludlam WG, Ludlam WH, Fuller CJ, Mayberg MR. Delayed postoperative hyponatremia after transsphenoidal surgery: prevalence and associated factors. J Neurosurg. 2013 Dec;119(6):1453-60. doi: 10.3171/2013.8.JNS13411. Epub 2013 Sep 20. PubMed PMID: 24053496.
19)

Kinoshita Y, Tominaga A, Arita K, Sugiyama K, Hanaya R, Hama S, Sakoguchi T, Usui S, Kurisu K. Post-operative hyponatremia in patients with pituitary adenoma: post-operative management with a uniform treatment protocol. Endocr J. 2011;58(5):373-9. Epub 2011 Apr 5. PubMed PMID: 21467692.
20)

Lee JI, Cho WH, Choi BK, Cha SH, Song GS, Choi CH. Delayed hyponatremia following transsphenoidal surgery for pituitary adenoma. Neurol Med Chir (Tokyo). 2008;48(11):489-92; discussion 492-4. PubMed PMID: 19029775.
23)

Taylor SL, Tyrrell JB, Wilson CB. Delayed onset of hyponatremia after transsphenoidal surgery for pituitary adenomas. Neurosurgery. 1995 Oct;37(4):649-53; discussion 653-4. Review. PubMed PMID: 8559292.

Nursing Care of the Pediatric Neurosurgery Patient

Nursing Care of the Pediatric Neurosurgery Patient

Nursing Care of the Pediatric Neurosurgery Patient

List Price:$149.00
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This updated third edition is a detailed reference for nurses and other health care providers who care for children with neurosurgical conditions. The explanations of pathophysiology, anatomy, neurodiagnostic imaging, and treatment options for each neurosurgical diagnosis will help to clarify the rationale behind the nursing care. Descriptions of presenting symptoms, history and findings on neurological examination will help nurses understand the neurological disorder and identify problems. New chapters have been added on skull and scalp anomalies, pediatric concussion, abuse head trauma and on neuroimaging. Each chapter includes case studies, impact on families, patient and family education, and practice pearls. Staff and student nurses working in clinics, critical care units, pediatric units, operating rooms, post-anesthesia care units, emergency departments, and radiology departments will benefit from the information presented. Although this book is written for nurses, child life therapists, physical and occupational therapists, medical students and neurosurgery residents will also find it helpful. Parents of children with neurosurgical disorders will also find it a useful resource in understanding their child’s condition.


Product Details

  • Published on: 2017-04-28
  • Original language: English
  • Number of items: 1
  • Dimensions: 10.25″ h x 7.25″ w x 1.50″ l,
  • Binding: Hardcover
  • 613 pages

Editorial Reviews

Review
From the reviews:
“…The attributes of this text result in a much wider appeal than to just pediatric neurosurgical nurses. This book will prove useful to anyone remotely interested in pediatric neurosurgery. I have no hesitation in recommending a copy be in every neurosurgical residency library. Hospitals will find this a useful textbook reference to place on the pediatrics floors for nurses and pediatric house staff to be able to quickly and concisely review any of the various neurosurgical subjects along with appropriate surgical interventions. Libraries will find this book is a must addition if they have patrons interested in neurosurgery. My only caveat is that I suspect this book will have a high disappearance (ie, “borrowing”) rate due to its value as a great educational tool.” (J.T. Goodrich, JAMA, November 2007)
“This book provides a one-of-a-kind clinical resource for nursing staff who work with this challenging population of patients. In addition to the easy-to-read text, this book includes 119 figures and 61 tables of valuable information to enhance nursing practice. … is written for nurses who are for pediatric neurosurgery patients but is also a tremendous reference for students and others in the healthcare profession. … This book will be a tremendous resource for me, and for the patients and staff with whom I work.” (Julie A Warren, Doody’s Review Service, August, 2007)
“The architecture of the book, subdivided in 12 multi-authored chapters, is quite solid, each contribution offering the basic knowledge necessary to understand the pathophysiology of a given disease, the essential of the surgical management, and the nurses’ considerations. Each chapter is nicely illustrated and enriched by numerous tables aimed at illustrating specific points, as well as providing further sources of information when needed … . Although this book is written by nurses, also medical students and neurosurgeons in training will find its reading quite useful.” (Concezio Di Rocco, Child’s Nervous System, Vol. 23, 2007)
From the Back Cover
This updated third edition is a detailed reference for nurses and other health care providers who care for children with neurosurgical conditions. The explanations of pathophysiology, anatomy, neurodiagnostic imaging, and treatment options for each neurosurgical diagnosis will help to clarify the rationale behind the nursing care. Descriptions of presenting symptoms, history and findings on neurological examination will help nurses understand the neurological disorder and identify problems. New chapters have been added on skull and scalp anomalies, pediatric concussion, abuse head trauma and on neuroimaging. Each chapter includes case studies, impact on families, patient and family education, and practice pearls. Staff and student nurses working in clinics, critical care units, pediatric units, operating rooms, post-anesthesia care units, emergency departments, and radiology departments will benefit from the information presented. Although this book is written for nurses, child life therapists, physical and occupational therapists, medical students and neurosurgery residents will also find it helpful. Parents of children with neurosurgical disorders will also find it a useful resource in understanding their child’s condition.
About the Author

Cathy C. Cartwright, MSN, RN-BC, PCNS, FAAN is a Pediatric Clinical Nurse Specialist and Director of Advanced Professional Practice at Children’s Mercy Hospital, Kansas City, Missouri. Prior to this position, she worked at the Children’s Hospital, University Hospitals and Clinics, Columbia, Missouri in a variety of positions, including Pediatric Clinical Nurse Specialist in Neurosurgery, Manager of Pediatric Services, Pediatric Outreach Coordinator, and Manager of the Pediatric Intensive Care Unit. She has received many awards, including the 2015 Magnet Nurse of the Year for Exemplary Professional Practice, an Excellence in Advanced Practice Award from the American Association of Neuroscience Nurses, March of Dimes Future of Nursing Award (Pediatric) and a Circle of Excellence Award (Management). She was President of the American Association of Neuroscience Nurses in 2009-10, having previously served on its Board of Directors. She has an extensive publication record and has given numerous national and international presentations.
Donna C. Wallace is currently a Pediatric Nurse Practitioner in the Neurosurgery Division of Banner Children Specialists, at Cardon Children’s Medical Center in Mesa, Arizona. Prior to that, she was a Nurse Practitioner for 16 years at the Barrow Neurological Institute in Phoenix, Arizona. Ms. Wallace has been a manager, and has also held several teaching positions. She has received several awards including the Mary Decker Mentorship Award, and the Excellence in Advanced Practice Award, from the American Association of Neuroscience Nursing (AANN). Additionally, she has served on the AANN Board of Directors.  Her passion for writing has resulted in numerous articles and lectures.

Update: Medulloblastoma

Epidemiology

It is the most common malignant pediatric intracranial tumor.

Classification

Medulloblastoma in children can be categorized into at least four molecular subgroups, offering the potential for targeted therapeutic approaches to reduce treatment related morbidities.
Medulloblastoma, genetically defined
Under the current consensus classification of medulloblastoma four principle subgroups are identified:
Medulloblastoma WNT activated
Sonic hedgehog Medulloblastoma and TP53 Mutant
Medulloblastoma non WNT/non SHH
Group 3 medulloblastoma
Group 4 medulloblastoma
Medulloblastoma, histologically defined
Medulloblastoma, classic
Medulloblastoma, Desmoplastic/nodular
Medulloblastoma with extensive nodularity.
The data show that medulloblastomas of Group 3/4 differ metabolically as measured using Magnetic resonance spectroscopy (MRS) when compared with SHH molecular subgroups. MRS is a useful and accurate tool to determine medulloblastoma molecular subgroups 1).
The evidence suggests that each of the four principle subgroups will likely have distinct ‘subsets’ that are biologically and clinically homogeneous as compared to other subsets from within the same subgroup. As the nature and number of subsets for each subgroup are currently unknown, the consensus classification suggests that each subset be named using a Greek letter (α, β, γ, etc.) until such time as they are sufficiently characterized to be named based on their molecular etiology 2).


see Cerebellar medulloblastomas
see Cerebellopontine angle medulloblastoma
see Multifocal medulloblastoma

Etiology

Several lines of evidence implicate granule neuron precursors (GNP) in the external granule layer (EGL) of the developing cerebellum as likely cells of origin for certain classes of medulloblastomas.
1). For example, cells that compose a preneoplastic stage of medulloblastoma colocalize with GNPs in the EGL and they express molecular markers of immature granule neurons ( 2). Another possible medulloblastoma cell of origin has been identified: a neural progenitor located in the cerebellar white matter and expressing both nestin and prominin ( 3). Signal transduction pathways that stimulate proliferation and inhibit differentiation of GNPs and other neural progenitor cells during development have been implicated in medulloblastoma. Thus, understanding the mitogenic functions of these pathways will yield insights into medulloblastoma formation.
The overexpression of proteins that normally stimulate proliferation of neural progenitor cells may initiate medulloblastoma formation. Two known mitogens for neural progenitors are the c-Myc oncoprotein and Sonic hedgehog (Shh), a crucial determinant of embryonic pattern formation in the central nervous system.
Several genes have been implicated in the development of medulloblastoma in children, including Patched-1 and Smoothened. The protein products of these genes function within the sonic hedgehog molecular signaling pathways, which are important in neural development and disease.

Pathogenesis

Medulloblastoma, occurs with increased frequency in individuals with Fanconi anemia who have biallelic germline mutations in BRCA2.
Tumor necrosis-initiated complement activation stimulates proliferation of medulloblastoma cells 3).
Combined activation of the Shh/Ptc and IGF signaling pathways is an important mechanism in MB pathogenesis 4).
Both pathways are essential regulators of granule neuron precursors (GNP) proliferation during cerebellar development. In cultured GNPs, IGF signaling stabilizes the oncogenic transcription factor N-myc by inhibiting glycogen synthase kinase 3beta-dependent phosphorylation and consequent degradation of N-myc. However, determinants of Shh and IGF tumorigenicity in vivo remain unknown
Activation of the Sonic hedgehog (Shh)/Patched signaling pathway in the postnatal cerebellum is sufficient to induce medulloblastoma in mice. Activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway by insulin-like growth factor-II, inactivation of the p53 tumor suppressor protein, loss of DNA damage repair mechanisms, and ectopic expression of Myc oncoproteins cooperate with Shh/Patched signaling to enhance tumor formation in mice. Ectopic expression of alpha and beta interferons in the developing brain also induces Shh-mediated medulloblastoma formation, suggesting a possible role for antiviral response in the genesis of medulloblastoma 5).

Dissemination

Cerebrospinal fluid (CSF) dissemination to the cranio-spinal axis occurs in 30% to 40% of cases 6).
However, medulloblastoma primarily presenting with symptoms related to spinal metastasis is extremely rare 7) 8).
To date, there are only a limited number of cases that have been reported in the literature 9) 10) 11).

Diagnosis

It appears as a homogenously enhancing hyperdense mass on computed tomography scan and is associated with the clinical picture of posterior fossa syndrome. This unique clinic-radiological pattern in considered “typical” medulloblastoma, but medulloblastomas does not follow the typical clinic-radiological pattern in a significant number of children and adult cases and should be considered in all midline posterior fossa tumors, hemisphere and cerebellopontine angle despite having clinical and radiological features suggestive of other tumors. Definitive diagnosis requires histologic confirmation in all cases 12).

MRI

Tumor location and enhancement pattern were predictive of molecular subgroups of pediatric medulloblastoma and may potentially serve as a surrogate for genomic testing 13).
Enhancing medulloblastomas exhibited strong VEGFR1/2 and CD31 expression relative to nonenhancing tumors. There was no significant difference in perioperative complications or patient survival between the 2 groups.
These results suggest that in patients with medulloblastoma the presence of enhancement on MRI may correlate with increased vascularity and angiogenesis, but does not correlate with worse patient prognosis in the short or long term 14).
Apparent diffusion coefficient
Using only apparent diffusion coefficient (ADC) values measured on ADC maps. One hundred and three pediatric patients with pre-operative magnetic resonance imaging scans showing a posterior fossa tumor with histological verification were retrospectively identified from a ten-year period at a tertiary care medical center. A single observer measured the lowest ADC values in all tumors to determine the mean minimum ADC (ADCmin) value that provided greatest accuracy in distinguishing medulloblastomas from other tumors, which was determined to be 0.66×10(-3) mm(2)/s. Imaging studies, including ADC maps, from 90 patients were provided to two neuroradiologists, who provided a diagnosis, which was later dichotomized as medulloblastoma or other. Two medical students measured ADCmin within tumors and those with ADCmin < 0.66×10(-3) mm(2)/s were recorded as medulloblastoma; any other value was recorded as other. Diagnostic accuracy was measured. ADCmin values allowed a correct identification of lesions as either medulloblastoma or other in 91% of cases. After diagnoses by the two neuroradiologists were categorized as either medulloblastoma or other, their diagnoses were correct in 90% and 84% of cases, respectively. In 19 cases, at least one neuroradiologist was incorrect; the addition of ADC values to clinical interpretation would have allowed a correct diagnosis in 63% of such cases. Diagnostic accuracy based on ADC values by medical students was comparable to that of subspecialty-trained neuroradiologists. This findings suggest that the addition of ADC values to standard film interpretation may improve the diagnostic rate for these tumors 15).
Both ADCmin and nADC could serve as the basis for a CAD program to distinguish medulloblastoma from other posterior fossa tumors with a high degree of accuracy 16).

Differential diagnosis

Ewing’s Sarcoma peripheral primitive neuroectodermal tumor
Fourth ventricle ependymoma:
Usually arises from the floor of the 4th ventricle
Typically squeezes out the foramen of Luschka

Treatment

Genomics-based classification has identified four major subgroups and provides greater opportunity for developing targeted therapies more successful than current conventional therapy.

Surgery

Surgical resection is undertaken with the goal of gross total resection. Postoperative neuroimaging studies are compared with preoperative studies to determine the amount of residual disease.
The prognostic benefit of increased extent of resection for patients with medulloblastoma is attenuated after molecular subgroup affiliation is taken into account. Although maximum safe surgical resection should remain the standard of care, surgical removal of small residual portions of medulloblastoma is not recommended when the likelihood of neurological morbidity is high because there is no definitive benefit to gross total resection compared with near-total resection 17).
Cerebrospinal fluid is obtained from a lumbar puncture done at the conclusion of the surgical resection or 2 weeks after surgery in order to determine microscopic leptomeningeal spread. Children are enrolled, when possible, in open clinical trials.

Chemotherapy and radiation

Chemotherapy and radiation are given as per protocol. The goal of current treatment approaches is to tailor therapy based on clinical risk factors, with intensification of treatment for children with high-risk disease and reduction of radiation therapy for those with standard-risk disease.
Chemotherapeutic trials have been developed to assess the safety and efficacy of various multi-agent therapies to improve the poor results of high-risk patients and to allow reduction in the dose of radiation needed to cure standard-risk patients, which may allow a decrease in late cognitive sequelae. Currently, it is policy to evaluate all children with posterior fossa tumors characteristic of medulloblastoma with preoperative, staging neuroimaging studies of the craniospinal axis.

Outcome

Although surgery, radiation and high-dose chemotherapy have led to increased survival, one-third of patients succumb to their disease, and patients who survive suffer severe long-term side effects as a consequence of treatment.
Through analysis of several well-designed multi-institutional trials, much has been learned about the clinical factors that influence outcome in children with medulloblastomas. Age younger than 3 years, bulky residual disease postoperatively, and metastasis constitute adverse prognostic features and indicate patients who are considered “high risk” for recurrence with standard therapy using 3600 cGy craniospinal radiation in conjunction with a posterior fossa dose of 5400 cGy. Patients lacking these features are considered “standard risk.”
Evaluation of biologic predictors of outcome, which may further refine treatment stratification, is in progress.

Response Assessment

Lack of standard response criteria in clinical trials for medulloblastoma and other seeding tumors complicates assessment of therapeutic efficacy and comparisons across studies. An international working group was established to develop consensus recommendations for response assessment. The aim is that these recommendations be prospectively evaluated in clinical trials, with the goal of achieving more reliable risk stratification and uniformity across clinical trials. Current practices and literature review were performed to identify major confounding issues and justify subsequently developed recommendations; in areas lacking scientific investigations, recommendations were based on experience of committee members and consensus was reached after discussion. Recommendations apply to both adult and pediatric patients with medulloblastoma and other seeding tumors. Response should be assessed using MR imaging (brain and spine), Cerebrospinal fluid cytology, and neurologic examination. Clinical imaging standards with minimum mandatory sequence acquisition that optimizes detection of leptomeningeal metastases are defined.
Warren et al. recommend central review prior to inclusion in treatment cohorts to ensure appropriate risk stratification and cohort inclusion. Consensus recommendations and response definitions for patients with medulloblastomas and other seeding tumors have been established; as with other RANO recommendations, these need to now be prospectively validated in clinical trials 18).

Case series

2015

A total of 67 pediatric cases of newly diagnosed medulloblastoma were included in a study. All of the children were treated at Xinhua Hospital between January 2007 and June 2013. The authors retrospectively analyzed the clinical data, treatment modalities, and outcome. The male-to-female ratio was 2:1, and the patients’ median age at diagnosis was 51.96 months (range 3.96-168.24 months). The median duration of follow-up was 32 months (range 3-70 months).
At the most recent follow-up date, 31 patients (46%) were alive, 30 (45%) had died, and 6 (9%) had been lost to follow-up. The estimated 3-year overall survival and progression-free survival, based on Kaplan-Meier analysis, were 55.1% ± 6.4% and 45.6% ± 6.7%, respectively. Univariate analysis showed that standard-risk group (p = 0.009), postoperative radiotherapy (RT) combined with chemotherapy (p < 0.001), older age (≥ 3 years) at diagnosis (p = 0.010), gross-total resection (p = 0.012), annual family income higher than $3000 (p = 0.033), and living in urban areas (p = 0.008) were favorable prognostic factors. Multivariate analysis revealed that postoperative RT combined with chemotherapy was an independent prognostic factor (p < 0.001). The treatment abandonment rate in this cohort was 31% (21 of 67 cases).
There was a large gap between the outcome of medulloblastoma in Chinese children and the outcome in Western children. Based on this data, treatment abandonment was the major cause of therapeutic failure. Parents’ misunderstanding of medulloblastoma played a major role in abandonment, followed by financial and transportation difficulties. Establishment of multidisciplinary treatment teams could improve the prognosis of medulloblastoma in Chinese children 19).


Of 143 medulloblastoma patients, treated from 1991 to 2013, sufficient data were available for 130 patients (15 with Wnt, 30 with Shh, 30 with Group 3, and 55 with Group 4 medulloblastomas). Of these, 28 patients (22%) ultimately underwent CSF diversion surgery: 0% with Wnt, 29% with Shh, 29% with Group 3, and 43% with Group 4 tumors. Patients in the Wnt subgroup had a lower incidence of CSF diversion than all other patients combined (p = 0.04). Wnt patients had a lower Canadian Preoperative Prediction Rule for Hydrocephalus (mCPPRH) score (lower risk of CSF diversion, p = 0.045), were older, had smaller ventricles at diagnosis, and had no leptomeningeal metastases.
The overall rate of CSF diversion surgery for Shh, Group 3, and Group 4 medulloblastomas is around 30%, but no patients in the present series with a Wnt medulloblastoma required shunting. The low incidence of hydrocephalus in patients with Wnt medulloblastoma likely reflects both host factors (age) and disease factors (lack of metastases). The absence of hydrocephalus in patients with Wnt medulloblastomas likely contributes to their excellent rate of survival and may also contribute to a higher quality of life than for patients in other subgroups 20).

1995

Sure et al describe the incidence of secondary tumour manifestations in 66 patients of a single centre who underwent surgery for medulloblastoma between 1975 and 1990. No patient was excluded due to a poor postoperative course. Thirty-five patients showed evidence of secondary tumour growth. Of these, 17 suffered from local recurrence, and 27 developed metastastatic disease. The median latencies for secondary manifestations were 25 months for local recurrence (n = 17), 11 months for spinal metastases (n = 10), 15 months for supratentorial metastases (n = 8), 8 months for subleptomeningeal dissemination (n = 6), and 23 months for systemic metastases (n = 8). Two patients developed primary metastatic spread to the posterior fossa. Of 8 patients with supratentorial metastases, 6 developed fronto-basal lesions. In our patients, 89% of secondary lesions occurred within less than 3 years after primary diagnosis. 85% of patients with extra-axial tumour spread had been treated with a permanent shunt. Radical tumour resection and radiotherapy with 30 Gy to the neuraxis and 20 Gy boost to the posterior fossa was an important prognostic factor in this series. Patients with additional chemotherapy did not benefit significantly from this treatment. We conclude that optimal management of the primary lesions should aim at (i) total resection, (ii) avoid permanent shunting, and (iii) completion of the radiotherapy with inclusion of the medial frontobasal cisterns in the radiotherapeutic regimen. Our analysis suggests that adequate postoperative screening programmes should consist of 3-monthly scans of the neuraxis in the first three postoperative years and 6-monthly scans thereafter 21).
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Blüml S, Margol AS, Sposto R, Kennedy RJ, Robison NJ, Vali M, Hung LT, Muthugounder S, Finlay JL, Erdreich-Epstein A, Gilles FH, Judkins AR, Krieger MD, Dhall G, Nelson MD, Asgharzadeh S. Molecular subgroups of medulloblastoma identification using noninvasive magnetic resonance spectroscopy. Neuro Oncol. 2015 Aug 8. pii: nov097. [Epub ahead of print] PubMed PMID: 26254476.
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Taylor MD, Northcott PA, Korshunov A, Remke M, Cho YJ, Clifford SC, Eberhart CG, Parsons DW, Rutkowski S, Gajjar A, Ellison DW, Lichter P, Gilbertson RJ, Pomeroy SL, Kool M, Pfister SM. Molecular subgroups of medulloblastoma: the current consensus. Acta Neuropathol. 2012 Apr;123(4):465-72. doi: 10.1007/s00401-011-0922-z. Epub 2011 Dec 2. PubMed PMID: 22134537; PubMed Central PMCID: PMC3306779.
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Rao G, Pedone CA, Del Valle L, Reiss K, Holland EC, Fults DW. Sonic hedgehog and insulin-like growth factor signaling synergize to induce medulloblastoma formation from nestin-expressing neural progenitors in mice. Oncogene. 2004 Aug 12;23(36):6156-62. PubMed PMID: 15195141.
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Fults DW. Modeling medulloblastoma with genetically engineered mice. Neurosurg Focus. 2005 Nov 15;19(5):E7. Review. PubMed PMID: 16398471.
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Stanley P, Suminski N. The incidence and distribution of spinal metastases in children with posterior fossa medulloblastomas. Am J Pediatr Hematol Oncol. 1988;10:283–287. doi: 10.1097/00043426-198824000-00002.
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Meshkini A, Vahedi A, Meshkini M, Alikhah H, Naghavi-Behzad M. Atypical medulloblastoma: A case series. Asian J Neurosurg. 2014 Jan;9(1):45-7. doi: 10.4103/1793-5482.131077. PubMed PMID: 24891891; PubMed Central PMCID: PMC4038867.
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Perreault S, Ramaswamy V, Achrol AS, Chao K, Liu TT, Shih D, Remke M, Schubert S, Bouffet E, Fisher PG, Partap S, Vogel H, Taylor MD, Cho YJ, Yeom KW. MRI Surrogates for Molecular Subgroups of Medulloblastoma. AJNR Am J Neuroradiol. 2014 May 15. [Epub ahead of print] PubMed PMID: 24831600.
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Hervey-Jumper SL, Garton HJ, Lau D, Altshuler D, Quint DJ, Robertson PL, Muraszko KM, Maher CO. Differences in vascular endothelial growth factor receptor expression and correlation with the degree of enhancement in medulloblastoma. J Neurosurg Pediatr. 2014 Jun 6:1-8. [Epub ahead of print] PubMed PMID: 24905841.
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Pierce T, Kranz PG, Roth C, Leong D, Wei P, Provenzale JM. Use of apparent diffusion coefficient values for diagnosis of pediatric posterior fossa tumors. Neuroradiol J. 2014 Apr;27(2):233-44. doi: 10.15274/NRJ-2014-10027. Epub 2014 Apr 18. PubMed PMID: 24750714.
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Pierce TT, Provenzale JM. Evaluation of apparent diffusion coefficient thresholds for diagnosis of medulloblastoma using diffusion-weighted imaging. Neuroradiol J. 2014 Feb;27(1):63-74. Epub 2014 Feb 24. PubMed PMID: 24571835.
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Thompson EM, Hielscher T, Bouffet E, Remke M, Luu B, Gururangan S, McLendon RE, Bigner DD, Lipp ES, Perreault S, Cho YJ, Grant G, Kim SK, Lee JY, Rao AA, Giannini C, Li KK, Ng HK, Yao Y, Kumabe T, Tominaga T, Grajkowska WA, Perek-Polnik M, Low DC, Seow WT, Chang KT, Mora J, Pollack IF, Hamilton RL, Leary S, Moore AS, Ingram WJ, Hallahan AR, Jouvet A, Fèvre-Montange M, Vasiljevic A, Faure-Conter C, Shofuda T, Kagawa N, Hashimoto N, Jabado N, Weil AG, Gayden T, Wataya T, Shalaby T, Grotzer M, Zitterbart K, Sterba J, Kren L, Hortobágyi T, Klekner A, László B, Pócza T, Hauser P, Schüller U, Jung S, Jang WY, French PJ, Kros JM, van Veelen MC, Massimi L, Leonard JR, Rubin JB, Vibhakar R, Chambless LB, Cooper MK, Thompson RC, Faria CC, Carvalho A, Nunes S, Pimentel J, Fan X, Muraszko KM, López-Aguilar E, Lyden D, Garzia L, Shih DJ, Kijima N, Schneider C, Adamski J, Northcott PA, Kool M, Jones DT, Chan JA, Nikolic A, Garre ML, Van Meir EG, Osuka S, Olson JJ, Jahangiri A, Castro BA, Gupta N, Weiss WA, Moxon-Emre I, Mabbott DJ, Lassaletta A, Hawkins CE, Tabori U, Drake J, Kulkarni A, Dirks P, Rutka JT, Korshunov A, Pfister SM, Packer RJ, Ramaswamy V, Taylor MD. Prognostic value of medulloblastoma extent of resection after accounting for molecular subgroup: a retrospective integrated clinical and molecular analysis. Lancet Oncol. 2016 Mar 11. pii: S1470-2045(15)00581-1. doi: 10.1016/S1470-2045(15)00581-1. [Epub ahead of print] PubMed PMID: 26976201.
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Wang C, Yuan XJ, Jiang MW, Wang LF. Clinical characteristics and abandonment and outcome of treatment in 67 Chinese children with medulloblastoma. J Neurosurg Pediatr. 2016 Jan;17(1):49-56. doi: 10.3171/2015.5.PEDS1573. Epub 2015 Oct 9. PubMed PMID: 26451721.
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Schneider C, Ramaswamy V, Kulkarni AV, Rutka JT, Remke M, Tabori U, Hawkins C, Bouffet E, Taylor MD. Clinical implications of medulloblastoma subgroups: incidence of CSF diversion surgery. J Neurosurg Pediatr. 2015 Mar;15(3):236-42. doi: 10.3171/2014.9.PEDS14280. Epub 2014 Dec 19. PubMed PMID: 25525930.
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Update: Low grade glioma treatment

Choosing the best treatment strategy for each patient with a diffuse low grade glioma, in other words optimizing the oncologic and functional balance, implies not only a full knowledge of the natural history of this chronic disease, but also an understanding of the adaptation of the brain in response to growth and spread of the glioma1).

The ideal management of suspected low-grade gliomas (LGGs) has historically been controversial in neurosurgery and neurooncology 2) 3) 4).
The management of low-grade glioma (LGG) still remains controversial because the effectiveness of early and extensive resection is unclear, and the use of radiation therapy or chemotherapy is not well-defined.

Surgery

Despite the lack of randomized controlled trials hampering the performance of appropriate metaanalysis, the increasing amount of evidence pointed toward an aggressive surgical strategy.
Although a large amount of data supports resection for symptomatic diffuse low-grade glioma (LGG), the therapeutic strategy regarding incidental LGG (ILGG) is still a matter of debate. Indeed, early “preventive” surgery has recently been proposed in asymptomatic patients with LGG, after showing that the extent of resection was larger than in symptomatic patients with LGG. However, the quality of life should be preserved by avoiding both neurological deficit and epilepsy 5).
The largest study in patients with low-grade gliomas, performed by Capelle et al. 6) , showed a strong impact of the extent of resection EOR on survival, especially when a radiological complete resection was obtained.
Although non-controlled series have a potential selection bias, similar results were found in a study with an unusual geographic and medical constellation that essentially eliminated the selection bias: two hospitals in Norway, each taking exclusive care of a large, stable population, followed different strategies for patients with low-grade glioma. One of the hospitals favoured a biopsy followed by a “wait-and-see” strategy, delaying further therapy until malignant progression while the other hospital preferred to perform maximal safe resection whenever possible. Outcome comparison between the two hospitals revealed that patients of the surgery-preferring hospital had a significantly better survival rate, suggesting that a proactive and aggressive treatment plan improves survival of low-grade glioma patients. Moreover, the rate of malignant transformation was twice as high in the “wait-and-see” cohort. Taken together, these findings support a proactive and radical surgical approach for low-grade gliomas rather than a “wait-and-see” strategy 7).
This surgery has to be performed with the appropriate armamentarium, which is the availability of intraoperative stimulation mapping, especially for those lesions occurring in cortical and subcortical eloquent sites.
According to the recently published guidelines, surgical treatment has been increasingly recognized as the initial therapeutic act of choice for patients diagnosed with a presumed low grade glioma, given that total resection can improve seizure control, progression free survival and overall survival, while reducing the risk of malignant transformation and preserving patients’ functional status 8).


Treatment options include observation, surgery, radiation, chemotherapy, or a combined approach, and management is individualized based on tumor location, histology, molecular profile, and patient characteristics. Moreover, in this type of brain tumor with a relatively good prognosis and prolonged survival, the potential benefits of treatment must be carefully weighed against potential treatment-related risks 9).
Patients with clinically and radiographically suspected LGG have two initial surgical options, biopsy or resection. Biopsy can provide a histological diagnosis with minimal risk but does not offer a direct treatment. Resection may have additional benefits such as increasing survival and delaying recurrence, but is associated with a higher risk for surgical morbidity. There remains controversy about the role of biopsy versus resection and the relative clinical outcomes for the management of LGG.
Evidence suggests that a greater extent of resection (EOR) extends malignant progression-free survival among patients with low-grade gliomas (LGGs). These studies, however, rely on the combined analysis of oligodendrogliomas, astrocytomas, and mixed oligoastrocytomas-3 histological subtypes with distinct genetic and molecular compositions 10).
The following electronic databases were searched in 2012 for the first version of the review: Cochrane Central Register of Controlled Trials (CENTRAL) (2012, Issue 11), MEDLINE (1950 to November week 3 2012), Embase (1980 to Week 46 2012). For this updated version, the following electronic databases were searched: Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 5), MEDLINE (Nov 2012 to June week 3 2016), Embase (Nov 2012 to 2016 week 26). All relevant articles were identified on PubMed and by using the ‘related articles’ feature.
Jiang et al. also searched unpublished and grey literature including ISRCTN-metaRegister of Controled Trials, Physicians Data Query and ClinicalTrials.gov for ongoing trials.
Jiang et al. planned to include patients of any age with a suspected intracranial LGG receiving biopsy or resection within a randomized clinical trial (RCT) or controlled clinical trial (CCT). Patients with prior resections, radiation therapy, or chemotherapy for LGG were excluded. Outcome measures included overall survival (OS), progression-free survival (PFS), functionally independent survival (FIS), adverse events, symptom control, and quality of life (QoL).
A total of 1375 updated citations were searched and critically analyzed for relevance. This was undertaken independently by two review authors. The original electronic database searches yielded a total of 2764 citations. In total, 4139 citations have been critically analyzed for this updated review.
No new RCTs of biopsy or resection for LGG were identified. No additional ineligible non-randomized studies (NRS) were included in this updated review. Twenty other ineligible studies were previously retrieved for further analysis despite not meeting the pre-specified criteria. Ten studies were retrospective or were literature reviews. Three studies were prospective, however they were limited to tumor recurrence and volumetric analysis and extent of resection. One study was a population-based parallel cohort in Norway, but not an RCT. Four studies were RCTs, however patients were randomized with respect to varying radiotherapy regimens to assess timing and dose of radiation. One RCT was on high-grade gliomas (HGGs) and not LGG. Finally, one RCT evaluated diffusion tensor imaging (DTI)-based neuro-navigation for surgical resection.
Since the last version of this review, no new studies have been identified for inclusion and currently there are no RCTs or CCTs available on which to base definitive clinical decisions. Therefore, physicians must approach each case individually and weigh the risks and benefits of each intervention until further evidence is available. Some retrospective studies and non-randomized prospective studies do seem to suggest improved OS and seizure control correlating to higher extent of resection. Future research could focus on RCTs to determine outcomes benefits for biopsy versus resection 11).


Based on results of three randomized clinical trials (RCT), radiotherapy (RT) may be deferred in patients with low risk low grade glioma (defined as age <40 years and having undergone a complete resection), although combined chemoradiotherapy has never been prospectively evaluated in the low-risk population. The recent RTOG 9802 RCT established a new standard of care in high-risk patients (defined as age >40 years or incomplete resection) by demonstrating a nearly twofold improvement in overall survival with the addition of PCV (procarbazine, CCNU, vincristine) chemotherapy following RT as compared to RT alone. Chemotherapy alone as a treatment of LGG may result in less toxicity than RT; however, this has only been prospectively studied once (EORTC 22033) in high-risk patients. A challenge remains to define when an aggressive treatment improves survival without impacting quality of life (QoL) or neurocognitive function and when an effective treatment can be delayed in order to preserve QoL without impacting survival. Current WHO histopathological classification is poorly predictive of outcome in patients with LGG. The integration of molecular biomarkers with histology will lead to an improved classification that more accurately reflects underlying tumor biology, prognosis, and hopefully best therapy 12).

Chemotherapy

Radiotherapy

Radiation therapy has been proven effective in increasing time to progression in LGG, and emerging data support a role for combined modality therapy incorporating chemotherapy.

Postoperative Radiotherapy

Early radiation therapy was associated with the following adverse effects: skin reactions, otitis media, mild headache, nausea, and vomiting. People with LGG who undergo early radiotherapy showed an increase in time to progression compared with people who were observed and had radiotherapy at the time of progression. There was no significant difference in overall survival between people who had early versus delayed radiotherapy; however, this finding may be due to the effectiveness of rescue therapy with radiation in the control arm. People who underwent early radiation had better seizure control at one year than people who underwent delayed radiation. There were no cases of radiation-induced malignant transformation of LGG. However, it remains unclear whether there are differences in memory, executive function, cognitive function, or quality of life between the two groups since these measures were not evaluated 13).
1)

Duffau H. Diffuse low-grade gliomas and neuroplasticity. Diagn Interv Imaging. 2014 Sep 10. pii: S2211-5684(14)00220-4. doi: 10.1016/j.diii.2014.08.001. [Epub ahead of print] PubMed PMID: 25218490.
2)

Keles GE, Lamborn KR, Berger MS: Low-grade hemispheric gliomas in adults: a critical review of extent of resection as a factor influencing outcome. J Neurosurg 95:735–745, 2001
3)

Lang FF, Gilbert MR: Diffusely infiltrative low-grade gliomas in adults. J Clin Oncol 24:1236–1245, 2006
4)

Wessels PH, Weber WE, Raven G, Ramaekers FC, Hopman AH, Twijnstra A: Supratentorial grade II astrocytoma: biological features and clinical course. Lancet Neurol 2:395–403, 2003
5)

de Oliveira Lima GL, Duffau H. Is there a risk of seizures in “preventive” awake surgery for incidental diffuse low-grade gliomas? J Neurosurg. 2015 Jun;122(6):1397-405. doi: 10.3171/2014.9.JNS141396. Epub 2015 Feb 27. PubMed PMID: 25723301.
6)

Capelle L, Fontaine, D, Mandonnet E, Taillandier L, Golmard JL, Bauchet L, et al. Spontaneous and therapeutic prognostic factors in adult hemispheric World Health Organization Grade II gliomas: a series of 1097 cases. J Neurosurg. 2013;118(6):1157–68.
7)

Jakola A, Mymel KS, Kloster R, Torp SH, Lindal S, Unsgard G. Comparison of a strategy favoring early surgical resection vs a strategy favoring watchful waiting in low-grade gliomas. JAMA. 2012;308(18):1881–8.
8)

Riva M, Bello L. Low-grade glioma management: a contemporary surgical approach. Curr Opin Oncol. 2014 Nov;26(6):615-21. doi: 10.1097/CCO.0000000000000120. PubMed PMID: 25279963.
9)

Forst DA, Nahed BV, Loeffler JS, Batchelor TT. Low-Grade Gliomas. Oncologist. 2014 Mar 24. [Epub ahead of print] PubMed PMID: 24664484.
10)

Snyder LA, Wolf AB, Oppenlander ME, Bina R, Wilson JR, Ashby L, Brachman D, Coons SW, Spetzler RF, Sanai N. The impact of extent of resection on malignant transformation of pure oligodendrogliomas. J Neurosurg. 2014 Feb;120(2):309-14. doi: 10.3171/2013.10.JNS13368. Epub 2013 Dec 6. PubMed PMID: 24313617.
11)

Jiang B, Chaichana K, Veeravagu A, Chang SD, Black KL, Patil CG. Biopsy versus resection for the management of low-grade gliomas. Cochrane Database Syst Rev. 2017 Apr 27;4:CD009319. doi: 10.1002/14651858.CD009319.pub3. [Epub ahead of print] Review. PubMed PMID: 28447767.
12)

Le Rhun E, Taillibert S, Chamberlain MC. Current Management of Adult Diffuse Infiltrative Low Grade Gliomas. Curr Neurol Neurosci Rep. 2016 Feb;16(2):15. doi: 10.1007/s11910-015-0615-4. PubMed PMID: 26750130.
13)

Sarmiento JM, Venteicher AS, Patil CG. Early versus delayed postoperative radiotherapy for treatment of low-grade gliomas. Cochrane Database Syst Rev. 2015 Jun 29;6:CD009229. doi: 10.1002/14651858.CD009229.pub2. PubMed PMID: 26118544; PubMed Central PMCID: PMC4506130.

85th AANS Annual Scientific Meeting

Download Program

The Opening Reception will be on Sunday, April 23, from 7-9 p.m., at Microsoft Square at L.A. LIVE.
7 a.m.-4:30 p.m.
Practical Clinics (Half- or Full-day Sessions)


7:30 a.m.-4:30 p.m.
International Symposium Join leaders from the AANS and various international neurosurgical organizations speaking in this year’s International Symposium. In addition to connecting with colleagues from around the world, attendees may also meet the 2017 International Lifetime Recognition Award recipient.


7:30 a.m.-4:30 p.m. Advanced Practice Providers (APPs) Plenary Session Nurses, nurse practitioners (NPs) and physician assistants (PAs) attendees are invited to this full-day session with presentations on spine, pain, coding and traumatic brain injury – all geared specifically for the APP.


7:00 a.m.-4:30 p.m. NEW Society of Neurological Surgeons (SNS) Chief Resident Course


1-4:30 p.m. Young Neurosurgeons Research Forum


5-6:30 p.m. AANS Opening Ceremonies: Global Issues in Healthcare and Innovations The Opening Ceremonies kick off the 2017 AANS Annual Scientific Meeting with presentations by Paul Farmer, MD, PhD; Michael M. Haglund, MD, PhD, MACM, FAANS, FCS (ECSA); Walter D. Johnson, MD, FAANS(L) and Vanessa Kerry, MD, MSc. They will be joined by Sanjay K. Gupta, MD, FAANS, CNN’s chief medical correspondent and Emory University assistant professor of Neurological Surgery who will moderate


7-9 p.m. Opening Reception at Microsoft Square Microsoft Square is an exciting, one acre, open-air plaza centrally located in the heart of L.A. LIVE, a premier destination in the downtown Los Angeles area.

Book: Color Atlas of Brainstem Surgery

Color Atlas of Brainstem Surgery

Color Atlas of Brainstem Surgery

List Price:$249.99
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The highly complex specialty of brainstem surgery requires many years of study, a focus on precision, and a passionate dedication to excellence to prepare the neurosurgeon for navigating significant anatomic challenges. Although the brainstem is technically surgically accessible, its highly eloquent structure demands rigorous surgical decision-making. An in-depth understanding of brainstem and thalamic anatomy and the safe entry zones used to access critical areas of the brainstem is essential to traversing the brainstem safely and successfully.
This remarkable, one-of-a-kind atlas draws on the senior author’s decades of experience performing more than 1,000 surgeries on the brainstem, thalamus, basal ganglia, and surrounding areas. Its content is organized by anatomic region, enabling readers to study separate subdivisions of the brainstem, each of which has its own unique anatomic and surgical considerations. From cover to cover, the atlas provides readers with technical guidance on approach selection, the timing of surgery, and optimization of outcomes-elucidated by more than 1700 remarkable color illustrations, dissections, clinical images, and line drawings.
Key Highlights

  • Beautifully detailed, highly sophisticated brain slices and dissections by Kaan Yagmurlu, who trained under the internationally renowned neuroanatomist and neurosurgeon Albert Rhoton Jr.
  • Color illustrations clearly labeled with callouts and other indicators of foci of interest delineate multiple safe entry zones to the brainstem
  • More than 50 detailed patient cases highlight each patient’s history of previous neurological disorders, presenting symptoms, preoperative imaging, diagnosis, the planned surgical approach, patient positioning, intraoperative and postoperative imaging, and outcome
  • Seven animations and more than 50 surgical videos elucidate approach selection, anatomy, and surgical outcomes of thalamic region and brainstem lesions

This illuminating atlas provides insights into the complexities of the hallowed halls of the brainstem. Neurosurgeons and neurosurgical residents alike who glean knowledge from the clinical pearls throughout each section will no doubt become more adept surgeons, to the ultimate benefit of their patients.


Product Details

  • Published on: 2017-04-15
  • Original language: English
  • Dimensions: 12.30″ h x 1.30″ w x 9.40″ l,
  • Binding: Hardcover
  • 416 pages
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